A Fundamental Consideration for Effective Healthcare Hygiene – Microbial Pathogenicity

By Paul J. Pearce, PhD

This column originally appeared in the May 2022 issue of Healthcare Hygiene magazine.

Although there have been no studies which definitively link the transmission of an active infectious organism from the environment to a patient, there are numerous references that the environment is a contributor to healthcare-associated infections (HAIs).

How does the environment contribute to microbial transmission? This is not definitely known. However, research findings have shown that a patient admitted to a room previously occupied by a methicillin-resistant Staphylococcus aureus (MRSA) – positive or a vancomycin-resistant Enterococci (VRE) are at a significantly increased risk of acquiring MRSA and VRE. Similar findings have been reported for patients occupying a room previously occupied by a patient with Clostridioides difficile.

How do microorganisms induce disease after a patient comes in contact with a pathogenic or potentially pathogenic microorganism?

Microbial Pathogenicity

Pathogenicity is the capacity of a microorganism to initiate disease. It requires the attributes of (1) transmissibility or communicability from one host or reservoir to a fresh host, (2) survival in the new host, (3) infectivity or the ability to breach the new host’s defenses, and (4) virulence, a variable that is multifactorial and defines the ability of a pathogen to harm the host. Virulence in the clinical sense is a manifestation of a complex bacterial–host relationship in which the capacity of the organism to cause disease is considered in relation to the resistance of the host.

Types of Bacterial Pathogens

Microbial pathogens can be classified into two broad groups, primary and opportunistic pathogens. Primary pathogens can establish infection and causing disease in previously healthy people with intact immunological defenses. However, these bacteria may more readily cause disease in people with impaired defenses. Opportunistic pathogens rarely cause disease in people with intact immunological and anatomical defenses. Only when such defenses are impaired or compromised, because of congenital or acquired disease or using immunosuppressive therapy or surgical techniques, are these bacteria able to cause disease. Many opportunistic pathogens, such as coagulase negative staphylococci and Escherichia coli, are part of the normal human flora and are carried on the skin or mucosal surfaces where they cause no harm and may have beneficial effects, by preventing colonization by other potential pathogens. However, introduction of these organisms into anatomical sites in which they are not normally found, or removal of competing bacteria using broad-spectrum antibiotics, may allow their localized multiplication and subsequent development of disease. The above classification is applicable to most pathogens; however, there are exceptions and variations within both categories of bacterial pathogens. Different strains of any individual bacterial species can vary in their genetic makeup and virulence. For example, the majority of Neisseria meningitidis strains are harmless commensal bacteria and considered opportunistic pathogens, however, some hypervirulent clones of the organism can cause disease in a previously healthy individual. Conversely, people vary in their genetic make-up and susceptibility to invading bacteria. For example, Mycobacterium tuberculosis is a primary pathogen but does not cause disease in every host it invades.

Steps in the Pathogenic Process (Pathogenesis)

The process of pathogenesis involves various steps beginning with the transmission of the infectious agent to the host, followed by colonization of a patient’s body (e.g., skin, blood, urine). After the colonization of the patient, the bacteria remain adherent at the site of colonization followed by invasion of the patient’s system(s). After invasion and surviving the patient’s immune system it is ready to cause the disease.

Steps involved in the pathogenesis of the bacteria include:

  1. Transmission
  2. Colonization
  3. Adhesion
  4. Invasion

Transmission: Potential pathogens may enter the body by various routes, including the respiratory, gastrointestinal, urinary or genital tracts. Alternatively, they may directly enter tissues through insect bites or by accidental or surgical trauma to the skin. Many opportunistic pathogens are carried as part of the normal human flora, and this acts as a ready source of infection in the compromised host (e.g., in cases of AIDS or when the skin barrier is breached). For many primary pathogens, however, transmission to a new host and establishment of infection are more complex processes.

Colonization: The establishment of a stable population of bacteria on the host’s skin or mucous membranes is called colonization. For many pathogenic bacteria, the initial interaction with host tissues occurs at a mucosal surface and colonization normally requires adhesion to the mucosal cell surface. This allows the establishment of a focus of infection that may remain localized or may subsequently spread to other tissues.

Adhesion: Adhesion is necessary to avoid innate host defense mechanisms such as peristalsis in the gut and the flushing action of mucus, saliva and urine, which remove non-adherent bacteria. For bacteria, adhesion is an essential preliminary to colonization and then penetration through tissues. Successful colonization also requires that bacteria acquire essential nutrients for growth. Many bacteria express pili (or fimbriae) which are involved in mediating attachment to mammalian cell surfaces. Different strains or species of bacteria produce different types of pili which can be identified based on antigenic composition, morphology and receptor specificity.

Invasion: Invasion is penetration of host cells and tissues (beyond the skin and mucous surfaces), and is mediated by a complex array of molecules, often described as “invasins.” These can be in the form of bacterial surface or secreted proteins which target host cell molecules (receptors). Once attached to a mucosal surface, some bacteria, e.g., Corynebacterium diphtheriae or Clostridioides tetani, exert their pathogenic effects without penetrating the tissues of the host. These produce biologically active molecules such as toxins, which mediate tissue damage at local or distant sites.

Paul J. Pearce, PhD, leads The Pearce Foundation for Scientific Endeavor. 



Manual of Environmental Microbiology, Fourth Edition. 2016. American Society for Microbiology.

Healthcare Environmental Cleaning. Second Edition. 2012. Association for the Healthcare Environment.

Pathogenesis of Bacterial Infections. 2020. https://nios.ac.in/media/documents/dmlt/Microbiology/

Interaction of Various Components of Staphylococcus aureus. Pearce, Paul J. 1973    www.thepearcefoundation.org



The Microbial Battlefront: Surfaces

By Rodney E. Rohde, PhD, MS, SM(ASCP) CMSV CM,MBCM, FACSc

This column originally appeared in the April 2022 issue of Healthcare Hygiene magazine.

A 2021 review article in Frontiers Bioengineering and Biotechnology discusses what I am calling the “microbial battlefront.” This so-called battlefront – the surface – alongside the many mechanisms of microbial attachment to surfaces has long been a topic of study. This interaction of microbes, particularly bacteria, with surfaces has far reaching and critical implications in a diverse range of areas, including infection and transmission dynamics, formation of biofilms, biofouling, and bioenergy to name just a few.

By definition, a biofilm is a three-dimensional structure formed because of microorganism’s surface sensing, initial adhesion to surfaces, followed by subsequent colonization and production of an extracellular polysaccharides matrix (EPS). The sticky and glue-like matrix substance is structured and act as “smart communities” by bacteria. Like enemies, the bacteria become entrenched, and the biofilm community creates actual channels much like trench warfare where there is a hidden and protected route from the external environment to the internal surface environment for delivery of nutrients and waste byproducts allowing for ongoing colonization and maturation for the embedded bacteria. Even more diabolical, once the microorganisms mature, they shed and move from the matured biofilm to join another biofilm community or to become a pioneer of a new one. True cunning by these microbial adversaries. Like any enemy or opposition, those of us in healthcare and other industries must work to better understand their makeup and mechanisms of action.

In the review article, the authors lay out the key research areas that help us to better understand the microbial battlefront – the surface. The two key areas discussed include surface properties and environmental factors. Briefly, I will highlight the primary areas with respect to the characteristics attributed to how they impact the healthcare environment.

Surface Properties
The authors primarily focus on the following surface properties: surface charge density, surface wettability, surface roughness, surface topography, and surface stiffness. Due to the general makeup of bacterial cell walls from carboxyl, amino, and phosphate groups, the overall bacterial surface is a negative charge. Generally, we see more adhesion and biofilm EPS accumulation on positively charged surfaces although some studies show trends for initial attachment and later biofilm formation can be variable. In terms of sterilization and disinfection, one might consider surface selection. The interactions between solid and liquid phases define surface wettability. The liquid phase “wets” the surface of a solid surface by maximizing its area in contact with the surface. Surfaces with low surface energy and liquids with high surface tension tend to reduce surface wettability and vice versa in this direct relationship.

While the authors state that broad generalizations can’t be made, there is an argument for engineered materials and surface treatments creating an extreme water contact angle – either superhydrophobic or superhydrophilic surfaces that can limit bacterial adhesion – playing a part in this battlefront. Surface roughness increases the surface area available for bacterial attachment and provides a scaffold for adhesion and can provide protection for bacteria versus shear forces which would help bound bacteria to resist being detached. Research consensus shows that as surface roughness increases, bacterial adhesion and biofilm formation also increases. Interestingly, bacteria are capable of sensing mechanical cues associated with natural and artificial physical features, such as the topography of surfaces. For example, topography alternations can affect the expression of bacterial adhesins.

Topography has important implications for “sheltering” of bacteria and stronger adhesion when the dimensions (e.g., space) is larger than a single bacterium. In a sense, the less topography helps to deter sheltering. Surface stiffness is an indication of if material is softer and more elastic or harder and less elastic. This review states that investigations on the underlying mechanism in this topic are not yet sufficient.

Environmental Factors
Fluid dynamics and bacterial motility are the primary focus areas regarding environmental factors. One might think about fluid dynamics in the sense of the human body – dental plaques are subject to salivary and gingival crevicular fluid flow and the way fluid flows in a catheter microenvironment. These hydrodynamic conditions can enhance or interfere with bacterial sensing and overall biofilm formation.

One study in the review showed that shear flow enhances biofilm formation by increasing the EPS production and strength of the EPS-matrix in Staphylococcus aureus. In other words, a strong flow likely triggers S. aureus to express more EPS genes for stronger attachment. Bacteria and other microbes can be broadly divided into motile and non-motile bacteria. At the simplest understanding of motility, motile bacteria can “search the environment” for the most suitable surface areas to attach to while non-motile bacteria must rely on gravity and other forces to participate in sensing. Generally, bacterial surface appendages such as flagella can play an important role in the adhesion by inducing a more dynamic response of motile bacteria to surface properties than non-motile bacteria. Once bacteria adhere to surfaces, motile bacteria can settle biofilms faster than non-motile bacteria by attracting free bacteria through chemotaxis and quorum sensing.

It is critical for those involved in healthcare and community infection control and prevention to understand the theoretical and applied research at the battlefront of microbes and surfaces. Likewise, the industries that play a role in the development of antibacterial and antimicrobial surfaces must continue to conduct robust research that looks at more complex surface and environmental factors. For example, the focus must shift from a single surface parameter and its effect on adhesion to efforts assessing the impact of multiple surface parameters on bacterial adhesion, including the effect of temperature.

For a complete understanding of this review, refer to the paper: Sherry, et. al. Implication of Surface Properties, Bacterial Motility, and Hydrodynamic Conditions on Bacterial Surface Sensing and Their Initial Adhesion in Front. Bioeng. Biotechnol., 12 February 2021. https://doi.org/10.3389/fbioe.2021.643722

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State University. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/


Update: The NCEZID and Candida auris

By Paul J. Pearce, PhD

This column originally appeared in the March 2022 issue of Healthcare Hygiene magazine.

The National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) works to protect people from emerging and zoonotic infections ranging from A to Z—anthrax to Zika. We live in an interconnected world where an outbreak of infectious disease is just a plane ride away.

Candida auris is an emerging fungal (yeast) pathogen that presents a serious global health threat. The Centers for Disease Control and Prevention (CDC) and NCEZID are concerned about C. auris for these main reasons:

1. It is often multidrug-resistant, meaning that it is resistant to multiple antifungal drugs commonly used to treat Candida infections. Some strains are resistant to all three available classes of antifungals.
2. It is difficult to identify with standard laboratory methods, and it can be misidentified in labs without specific technology. Misidentification may lead to inappropriate management. It has caused outbreaks in healthcare settings, so it is important to quickly identify C. auris in a hospitalized patient so that organizations can take special precautions to stop its spread.
3. C. auris is typically acquired in healthcare settings, so most healthy people are not at risk. It is passed from person-to-person through the hands of healthcare personnel or by contaminated medical devices like catheters or ventilators. Patients with C. auris may be put under special precautions, such as being placed in an isolation room. This may continue even after treatment because they may still have C. auris on their skin or other sites on their body. Practice proper hand hygiene and use of personal protective equipment (PPE) such as gloves, masks, and gowns. Patients should make sure to carefully follow instructions from their doctor regarding antifungal medications.
4. Frequently recommended and used environmental cleaners and disinfectants may not be effective in controlling or killing C. auris.

The NCEZID was established in 2010 with a mission and scientific activities that trace back to the earliest days of the CDC, including protecting against and responding to infectious disease outbreaks. NCEZID is responsible for the prevention, control, and management of a wide range of infectious diseases, including rare but deadly diseases such as anthrax and Ebola virus disease, as well as more common illnesses like foodborne disease and healthcare-associated infections. NCEZID is one of the agency’s principal sources of epidemiologic, clinical, and laboratory expertise for bacterial, viral, and fungal pathogens as well as infectious diseases of unknown origin. The nation relies on NCEZID to protect the country from more than 800 dangerous pathogens. C. auris falls in the category of emerging, opportunistic pathogens that is a threat to patients in healthcare settings.

Why is Candida auris a problem?
• It causes serious infections, such as bloodstream and other types of invasive infections, particularly in patients in hospitals and nursing homes who have many medical problems. More than 1 in 3 patients die within a month of being diagnosed with an invasive C. auris infection.
• It is often multidrug-resistant. Antifungal medications commonly used to treat other Candida infections often don’t work for C. auris. Some C. auris isolates are resistant to all three major classes of antifungal medications.
• It is becoming more common. Although C. auris was just discovered in 2009, the number of cases has grown quickly.
• It is difficult to identify. C. auris can be misidentified as other types of fungus unless specialized laboratory methods are used. Correctly identifying C. auris is critical for starting measures to stop its spread and prevent outbreaks.
• It can spread and cause outbreaks in healthcare facilities. Just like other multidrug-resistant organisms such as carbapenem-resistant Enterobacteriaceae (CRE) and methicillin-resistant Staphylococcus aureus (MRSA), C. auris can be transmitted in healthcare settings and cause outbreaks. It can colonize patients for many months, persist in the environment, and withstand some commonly used healthcare facility disinfectants.

What should I do if there is C. auris in my facility?
1. Check the CDC website for the most up-to-date guidance on identifying and managing C. auris: www.cdc.gov/fungal/candida-auris.
2. Report possible or confirmed C. auris test results immediately to your public health department.
3. Ensure adherence to CDC recommendations for infection control, including placing patients infected or colonized with C. auris on Transmission-Based Precautions and, whenever possible, in a single room; making sure gown and gloves are accessible and used appropriately; reinforcing hand hygiene as well as coordinating with environmental services (EVS) to monitor and ensure the patient care environment is cleaned using a disinfectant with an Environmental Protection Agency claim for C. auris or, if not available, for Clostridioides difficile. These products can be found at www.cdc.gov/fungal/candida-auris/c-auris-infection-control.html. Some disinfectants used in healthcare facilities (e.g., quaternary ammonium compounds [QACs]) may not be effective against C. auris, despite claims about effectiveness against C. albicans or other fungi. Work with the EVS team to monitor the cleaning process. Review EPA Lists N and P for disinfectants that are recognized as effective against C. auris.
4. After consulting with public health personnel, screen contacts of case-patients to identify patients with C. auris colonization. Use the same infection control measures for patients found to be colonized.
5. When a patient is being transferred from your facility (to a nursing home or other hospital), clearly communicate the patient’s C. auris status to receiving healthcare providers.

Paul J. Pearce, PhD, leads the Pearce Foundation for Scientific Endeavor.



Fish Aquariums: A Transmission Source

By Rodney E. Rohde, PhD, MS, SM(ASCP) CMSV CM,MBCM, FACSc

This column originally appeared in the February 2022 issue of Healthcare Hygiene magazine.

In September 2021, I reported on a Burkholderia pseudomallei (melioidosis) outbreak of four cases of from Georgia, Kansas, Minnesota and Texas. The first case (fatal) identified in March 2021 occurred in Kansas. The second and third cases, both identified in May 2021 in Minnesota and Texas, were hospitalized for extended time then discharged to transitional care facilities. The most recent case died in the hospital and was identified post-mortem in late July 2021 in Georgia. All cases had no history of traveling abroad from the United States. Melioidosis signs and symptoms are varied and nonspecific, and may include pneumonia, abscess formation, and blood infections.

All four melioidosis cases initially presented with symptoms ranging from cough and shortness of breath to weakness, fatigue, nausea, vomiting, intermittent fever, and rash on the trunk, abdomen, and face. Two cases, one fatal, had several risk factors for melioidosis, including COPD and cirrhosis. The other two cases had no known risk factors for melioidosis. Genomic analysis of the strains strongly suggested a common source (e.g., imported product or animal). The source is unknown to date despite environmental sampling, serological testing, and family interviews.

The Centers for Disease Control and Prevention (CDC) recently reported a 56-year-old woman, hospitalized on Sept. 20, 2019, likely acquired melioidosis via novel transmission of B. pseudomallei from a freshwater home aquarium in the December 2021 issue of Emerging Infectious Diseases. The Maryland woman is the first known person to have this severe tropical infection by this new transmission route.

The patient history showed diabetes and rheumatologic disease. She was hospitalized because of fever, cough, and chest pain with onset 2 days earlier. Her ongoing medications indicated immunosuppressives (methotrexate, azathioprine, and prednisone) until 1 month before she became symptomatic. Multiple blood cultures were taken on days 1-4 which grew B. pseudomallei, without evidence of endocarditis or intravascular seeding.

Other clinical data presented a thoracic radiograph on day 0 consistent with pneumonia. A non-contrast computed tomography (CT) scan on day 3 showed air space consolidation in the right lower lobe consistent with pneumonia. Other notable clinical laboratory results at presentation included an increased leukocyte count of 22,800 cells/μL (reference range 4,500 to 11,000 cells/μL) and a decreased sodium level of 125 mmol/L (reference range 135‒145 mmol/L).

Despite weeks of meropenem (Merrem), she developed evidence of a lung abscess, and trimethoprim/sulfamethoxazole (Bactrim) was added. Ultimately, the patient required a 12-week course of antibiotics for eradication therapy and resolution.
I started my career in public health at the Texas Department of State Health Services as a public health microbiologist and molecular epidemiologist in the Zoonosis Control Division. During that decade, I had the opportunity to spend two sessions with the CDC in the Rabies Laboratory as a Visiting Scientist. During those formative years of my professional career, I will always remember the critical and sometimes lifesaving advice to not forget about doing a deep dive on a patient history. The melioidosis case in Maryland is significant to that advice.

CDC epidemiologist Patrick Dawson, PhD, first author of the report, told Medscape Medical News that although outbreak investigators always ask about pet ownership, they have not explicitly asked about fish. In this case, the patient did not volunteer exposure to the fish. If I am being honest, I am not sure I would have either. Typically, physicians and epidemiologists know to ask about exposures from animals, the environment (e.g., soil, water, etc.) and travel. While we know fish can be a source of different microbial infections, since this patient had not mentioned it, the epidemiologists and others did not think about.

However, when there was a visit to patient's home, "one of the first things they saw was a few aquariums," Dawson said. Seeing the water and knowing "that most freshwater tropical fish in the U.S. are imported from Southeast Asia" led them to culture specifically for B. pseudomallei, which can be difficult for the microbiology lab to identify.

The investigative epidemiology team discovered she had bought her fish 6 months earlier. Through environmental sampling at the local pet store, they did not discover the bacteria there. Eventually, the team worked with the national brand to find where the fish originated. Ultimately, an exact matching isolate could not be identified after so many months had passed, but they found a positive PCR for B. pseudomallei in a water sample from imported fish in Los Angeles.

Advice for the public:
• Wash your hands before and after contact with an aquarium
• If you have cuts or wounds, wear gloves while working with an aquarium or cleaning fish
• If immunocompromised (including younger children), don’t handle fish or aquariums
• Aquatic zoonoses (infections from water) are important because an estimated 11.5 million U.S. households have pet fish, totaling about 139 million freshwater fish.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State University. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/


Eradicating the Deadliest Predators from the Microbial Jungle

By Paul J. Pearce, PhD

This column originally appeared in the January 2022 issue of Healthcare Hygiene magazine.

An article in the August 2020 edition of Healthcare Hygiene magazine, “A Better Way to Understand Your Microbial Jungle: What’s in There and How to Know It’s Gone,” highlighted the requirement to know the microbial enemies and deadliest predators that create the complex microbial jungle responsible for healthcare-associated infections (HAIs). The following describes the most common microorganisms that are associated with HAIs and effective methods, means and equipment that have been successfully used to eradicate these pathogenic microorganisms.

Acinetobacter is a group of bacteria commonly found in soil and water. Outbreaks of Acinetobacter infections typically occur in intensive care units and healthcare settings housing very ill patients. While there are many types or “species” of Acinetobacter and all can cause human disease, Acinetobacter baumannii accounts for about 80 percent of reported infections. Acinetobacter infections rarely occur outside of healthcare settings.

Healthcare facilities in several countries have reported that a type of yeast called Candida auris has been causing severe illness in hospitalized patients. In some patients, this yeast can enter the bloodstream and spread throughout the body, causing serious invasive infections. This yeast often does not respond to commonly used antifungal drugs, making infections difficult to treat. Patients who have been hospitalized in a healthcare facility a long time, have a central venous catheter, or other lines or tubes entering their body, or have previously received antibiotics or antifungal medications, appear to be at highest risk of infection with this yeast.

Vancomycin-intermediate Staphylococcus aureus (also called S. aureus) and vancomycin-resistant Staphylococcus aureus are specific staph bacteria that have developed resistance to the antimicrobial agent vancomycin. Persons who develop this type of staph infection may have underlying health conditions (such as diabetes and kidney disease), devices going into their bodies (such as catheters), previous infections with methicillin-resistant Staphylococcus aureus, and recent exposure to vancomycin and other antimicrobial agents.
Vancomycin-resistant Enterococci are specific types of antimicrobial-resistant bacteria that are resistant to vancomycin, the drug often used to treat infections caused by enterococci. Enteroccocci are bacteria that are normally present in the human intestines and in the female genital tract and are often found in the environment. These bacteria can sometimes cause infections. Most vancomycin-resistant Enterococci infections occur in hospitals.

Gram-negative bacteria cause infections including pneumonia, bloodstream infections, wound or surgical site infections, and meningitis in healthcare settings. They are resistant to multiple drugs and are increasingly resistant to most available antibiotics. Gram-negative infections include those caused by Klebsiella, Acinetobacter, Pseudomonas aeruginosa, and E. coli, as well as many other less common bacteria.

Clostridioides difficile (C. diff) causes life-threatening diarrhea. It is usually a side-effect of taking antibiotics. These infections mostly occur in people 65 and older who take antibiotics and receive medical care, people staying in hospitals and nursing homes for a long period of time, and people with weakened immune systems or previous infection with C. diff.

The 2020 National and State Healthcare-Associated Infections Progress Report provides a summary of select HAIs across four healthcare settings: acute care hospitals (ACHs), critical access hospitals (CAHs), inpatient rehabilitation facilities (IRFs) and long-term acute care hospitals (LTACHs). Data from CAHs are provided in the detailed technical tables but not in the report itself. The designation of CAH is assigned by the Centers for Medicare and Medicaid Services (CMS) to hospitals that have 25 or fewer acute-care inpatient beds and that maintain an annual average length of stay of 96 hours or less for acute-care patients. IRFs include hospitals, or part of a hospital, that provide intensive rehabilitation services using an interdisciplinary team approach. LTACHs provide treatment for patients who are generally very sick and stay, on average, more than 25 days.

The 2020 National and State Healthcare-Associated Infections Progress Report, along with the detailed technical tables, provides national- and state-level data about HAI incidence during 2020. The report is designed to be accessible to many audiences. National and state HAI reports will be made available for viewing, downloading, and printing from the Antibiotic Resistance and Patient Safety Portal. For detailed methods, references, and definitions, refer to the Technical Appendix and Glossary within this report. For more information, please visit CDC’s Healthcare-Associated Infection Data Reports website.

Paul J. Pearce, PhD, leads the Pearce Foundation for Scientific Endeavor.




What is Herd Immunity? A Public Health Expert and a Medical Laboratory Scientist Explain

By Rodney E. Rohde, PhD, MS, SM(ASCP) CMSV CM,MBCM, FACSc, and Ryan McNamara, PhD

Editor’s note: This content originally appeared on The Conversation blog.

The term herd immunity means that enough of a population has gained immunity to stifle a pathogen’s spread. You can think of herd immunity as being similar to fire starting in a field: If the field is dry and filled with weeds, the fire will catch and spread quickly. However, if the field is well-maintained with watering and trimming, the fire will fizzle out. Future embers that might land there will be far less likely to ignite.

The embers are much like SARS-CoV-2, the coronavirus that causes COVID-19.

Herd immunity can theoretically be achieved either through infection and recovery or by vaccination. The danger of trying to achieve herd immunity through infection is that many people will die or be forced to live with post-recovery disabilities. Moreover, research has shown that the immune response resulting from infection does not always provide strong enough long-term protection against COVID-19 and its evolving strains. Thus, public health experts still recommend vaccination against the coronavirus to achieve the strongest and most reliable protection.

When the COVID-19 pandemic erupted, scientists quickly began to develop vaccines so that populations could develop immunity to slow the fire-like spread of the coronavirus. In the meantime, nearly all countries mandated or encouraged social distancing, masking and other public health measures.

Unfortunately, the disjointed implementation of these efforts, coupled with large-scale surges and the emergence of the highly transmissible delta variant, has forced public health experts to recalculate what it would take to reach “herd immunity” for COVID-19.

Prior experience with respiratory pathogens that were comparable to the new coronavirus allowed public health experts to make educated estimates of what would be needed to reach the lower threshold of herd immunity for COVID-19. Initially they believed that around 70% of the population would need to be vaccinated to effectively slow or stop the spread of SARS-CoV-2.

But with the delta variant continuing to spread rapidly around the world, experts revised that estimate. Now, epidemiologists and other public health officials estimate that closer to 90% of the U.S. population would need to be vaccinated to reach herd immunity for COVID-19.

Viruses like those that cause polio and measles required decades of education and vaccination programs to achieve herd immunity and to ultimately eliminate them in the U.S. But given that new U.S. cases of COVID-19 continue to number in the tens of thousands daily, it’s become clear that COVID-19 is going to stick around.

There are several reasons it will take some time to achieve COVID-19 herd immunity. The COVID-19 vaccines are currently authorized for some age groups but not others. For perspective, roughly 90 percent of the U.S. population receives the measles, mumps and rubella vaccine – or MMR – as children, and 93 percent of the population is vaccinated against polio; both of these have been routine childhood immunizations for decades. Since children make up more than 20% of U.S. residents, the country likely cannot reach COVID-19 herd immunity without widespread childhood vaccination, even if all eligible adults were vaccinated.

As of Nov. 1, 2021, only 67.8 percent of the total U.S. population ages 12 and up that are vaccine-eligible had been fully vaccinated. Experts have attributed this to multiple factors including vaccine hesitancy and the politicization of the pandemic.

Of course, no vaccine is perfect. Vaccinated people can have breakthrough infections, although the COVID-19 vaccines continue to effectively reduce the most severe cases of COVID-19. In addition, research suggests that those who experience COVID-19 after vaccination may transmit the virus at lower transmission rates than those who are unvaccinated.

Rodney E. Rohde, PhD, MS, SM(ASCP) CMSV CM,MBCM, FACSc, is professor of clinical laboratory science at Texas State University.

Ryan McNamara, PhD, is a research associate of microbiology and immunology at University of North Carolina at Chapel Hill.


Abiotrophia defective: Quit Being So Difficult

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the November issue of Healthcare Hygiene magazine.

In 1961, Frenkel and Hirsch described strains of streptococci isolated from cases of bacterial endocarditis that grew only in the presence of other bacteria, around which they formed satellite colonies, or in media enriched with sulfhydryl compounds, such as cysteine. These nutritionally variant streptococci were eventually assigned the species Streptococcus defectivus (Latin for “deficient”) and S. adjacens (because it grows adjacent to other bacteria). Later research placed them in a new genus Abiotrophia (Greek a, “un-,” + bios, “life,” + trophe, “nutrition”) as A. adiacens and A. defectiva. The genus contains four species of coccus shaped species – A. adiacens, A. defective, A. balaenopterae and A. elegans. In 2000, Collins and Lawsons further differentiated A. adiacens, A. balaenopterae and A. elegans from A. defectiva by placing them into the new genus Granulicatella (Henry R. Etymologia: Granulicatella. Emerg Infect Dis. 2018;24(9):1704. https://doi.org/10.3201/eid2409.et2409 and Wikipedia).

In this column, I will focus on the Abiotrophia defectiva as it relates to important and dangerous cases of endocarditis. Infective endocarditis (IE) refers to an infection involving the endocardial surface of the heart.

Most IE cases are caused by viridans Streptococci or Staphylococci species. Abiotrophia defectiva is known to cause less than 1 percent of cases of IE. Though rare, it can cause life-threatening complications such as septic embolization, destruction of heart valves, and heart failure especially if not detected and treated quickly. A. defectiva is a part of the normal flora of the oral cavity, the urogenital and the intestinal tracts. For both physicians and medical laboratory professionals, this difficult bacterium causes many headaches and difficulties as to diagnosis and treatment. Though rare, nutritionally variant Streptococci (NVS) are estimated to cause approximately 5 percent to 6 percent of all cases of IE, including being a major cause of blood culture-negative IE. Importantly, this can result in early misdiagnosis or non-diagnosis.

Abiotrophia and Granulicatella spp. often appear as Gram-positive cocci in pairs or chains but can be pleomorphic. Sometimes however, they can appear more like coccobacilli or stain as Gram variable. Gram stain pleomorphism can be particularly apparent with suboptimal nutritional conditions. Gram stains consistent with a streptococcal-like morphology that are not detected by common used commercially available panels should raise suspicions for Abiotrophia or Granulicatella, among other organisms.

There have only been about 125 published cases of A. defective in the research literature. They do not synthesize pyridoxine, L-cysteine or other essential nutrients required for growth and depend on other bacteria (satellite) or enriched media for enhanced growth. The fastidious nature of this microbe often means that initial cultures appear to be sterile. A. defective is a pleomorphic organism, appearing as Gram-positive cocci, coccobacilli, and bacilli forms depending on the culture media. Literature suggests that due to the production of a considerable amount exopolysaccharides, the organism has a higher affinity for the endocardium and the ability to bind with fibronectin in the extracellular matrix, further contributing to their virulence.

Due to the difficulty in culturing this organism, one may need to utilize molecular diagnostic tools to raise sensitivity and specificity for quicker diagnosis, which can often lead to better patient outcomes. For example, Matrix-assisted laser desorption ionization–time of flight mass spectrometry (MALDI-TOF MS) with the Vitek MS using library v3.2 can assist in the detection of Abiotrophia defectiva. Clinical suspicion regarding this organism should arise in cases of culture-negative endocarditis and additional testing with supplemented media (e.g., chocolate agar) should be performed to encourage growth of colonies. Further, susceptibility testing may be required via broth microdilution at a reference laboratory and interpreted by Clinical and Laboratory Standards Institute (CLSI) guidelines for proper treatment.

Ultimately, A. defectiva and similar organisms require an approach through multiple paths for detection – including cultures, serology, histopathology, and molecular methods, with blood cultures being the critical foundation. If surgery is considered, histopathologic analysis and culture of the explanted heart valve is critical because it may assist with confirmation of valve involvement and help inform duration of antimicrobials. Often culture of the valve is negative which may be due to the use of antimicrobial therapy prior to surgery. Abiotrophia and Granulicatella may also cause “culture-negative” endocarditis when antimicrobial therapy is administered during or prior to the drawing of blood cultures.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State University. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Agrawal U, Prabhu MM. Abiotrophia defectiva: A Rare but Critical Cause of Infective Endocarditis. Cureus. 2019;11(12):e6492. 2019 Dec 28. doi:10.7759/cureus.6492

Dumm RE, Wing A, Richterman A, Jacob J, Glaser LJ, Rodino KG. 2021. The Brief Case: A variant on a classic—Abiotrophia defective endocarditis with discitis. J Clin Microbiol 59:e03093-20.https://doi.org/10.1128/JCM.03093-20.




Burkholderia cepacia Complex Triggers Recall

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the October 2021 issue of Healthcare Hygiene magazine.

In September's column, I discussed B. pseudomallei and the recent outbreak in four states. This genus, Burkholderia, unfortunately packs quite a punch with several species. A member of the Proteobacteria, its pathogenic members include a diverse group of species responsible for several dangerous and often deadly infections.

For our medical laboratory professionals, it can be difficult to isolate and differentiate in the typical clinical microbiology laboratory, which sometimes leads to issues of misidentification or other laboratory tests to assist in understanding the case. Finally, like many other groups of bacteria that I have written about this genus can create biofilms, which interact with environmental and human surfaces. Biofilms play a significant role in mediating cell-to-cell communication. During this type of interaction, bacteria release protein toxins in the environment. Cells with a corresponding protective protein (usually bacteria of the same strain) are not inhibited to grow or die. Lastly, recipient cells with the corresponding protein undergo gene expression changes and phenotype, which augments biofilm communities. Importantly, even if the recipient cell was not of the same bacterial strain this can happen showing the critical importance this genus can have in the environment.

Ultimately, biofilms create “persister” cells, which can share antimicrobial resistance and other factors detrimental to human health.

In this column, I will focus on the B. cepacia complex (Bcc) as it relates to outbreaks as a dangerous contaminant in water-based pharmaceutical products.

BCC and water-based products
On July 7, 2021, the Food and Drug Administration (FDA) advised drug manufacturers of non-sterile, water-based drug products that Burkholderia cepacia complex (Bcc or B. cepacia) continues to pose a risk of contamination. BCC is a group of Gram-negative bacteria comprising more than 20 species that has been linked to multiple instances of opportunistic infections. For example, Paroex® Chlorhexidine was recalled in 2020 due to objectionable microbial contamination including the BCC species B. lata. Inadequate design, control, or maintenance of pharmaceutical water systems have led to contamination with BCC and other water-borne opportunistic pathogens.

Multistate Outbreak of Burkholderia cepacia Infections Associated with Contaminated Ultrasound Gel
Following the FDA advisement in July, on Aug. 18, 2021, FDA requested healthcare providers, healthcare facility risk managers, and procurement staff to immediately stop using and discard all ultrasound gels and lotions manufactured by Eco-Med Pharmaceutical, Inc., due to risk of bacterial contamination with Bcc.
Background via Centers for Disease Control and Prevention (CDC)

CDC is assisting the FDA and several state and local health departments with ongoing investigations of this issue. Patients have developed Bcc infections, including bloodstream infections, after likely having undergone ultrasound-guided procedures in which MediChoice® M500812 ultrasound gel was used. This ultrasound gel was likely used to guide ultrasonography in preparation for or during placement of central and peripheral intravenous catheters, and transcutaneous procedures, such as paracentesis.

As of Aug. 18, 2021, CDC is aware of at least 59 patients in six states with Burkholderia stabilis infection. The species strain genetically matches the B. stabilis strain identified in four lots of MediChoice M500812 ultrasound gel. At least 48 cases are bloodstream infections, and many had undergone ultrasound-guided procedures prior to their infections. Ongoing investigations at the local public health level are being conducted to gather additional data on these cases.

Recommendations from CDC include:
• All healthcare facilities under manufacturer order should identify the affected products by lot number and immediately destroy or return products. Additionally, Eco-Med is instructing all healthcare facilities to immediately stop use and quarantine all lots of the ultrasound gels distributed under these brand names. Refer to https://eco-med.com/recall/ for additional information.
• CDC advises that healthcare facilities should always use single-use, sterile ultrasound gel packets for ultrasonography used in preparation for or during transcutaneous procedures.
o This includes avoiding use of bottles of nonsterile ultrasound gel for visualization prior to such procedures (such as vein marking, visualizing ascites).
o Healthcare facilities should also review facility practices related to ultrasound probe reprocessing to ensure they are aligned with manufacturer’s instructions for use and appropriate professional society guidelines.
• Healthcare facilities should completely clean and appropriately disinfect ultrasound devices and any warming devices that may have had contact with the product after removing the potentially contaminated ultrasound gel from use in the facility.
• Healthcare facilities should report any patient infections related to the use of potentially contaminated medical products to FDA’s MedWatch Adverse Event Reporting

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State University. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

American Institute of Ultrasound in Medicine (AIUM). Guidelines for Cleaning and Preparing External- and Internal-Use Ultrasound Transducers and Equipment Between Patients as well as Safe Handling and Use of Ultrasound Coupling Gel. March 5, 2021. Available at: https://www.aium.org/officialstatements/57


Sounding the Alarm About Burkholderia spp.

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

Editor's note: This column originally appeared in the September 2021 issue of Healthcare Hygiene magazine.

Burkholderia is a genus of Proteobacteria whose pathogenic members include a diverse group of species responsible for several dangerous and often deadly infections. Unfortunately, this group of bacteria can be difficult to isolate and differentiate in the typical clinical microbiology laboratory. Examples from this genus include the Burkholderia cepacia complex (Bcc), which attacks humans and Burkholderia mallei, responsible for glanders, a disease that occurs mostly in horses and related animals.

Burkholderia pseudomallei, the causative agent of melioidosis and a recent multi-state investigation of non-travel associated Burkholderia pseudomallei infections in four patients: Georgia, Kansas, Minnesota, and Texas—2021 via Centers for Disease Prevention and Control (CDC) Health Alert Network (CDCHAN-00448, August 9, 2021). Lastly, Burkholderia cepacia, an important pathogen of pulmonary infections in people with cystic fibrosis. This group is known for antibiotic resistance and a high mortality rate from their associated diseases, B. mallei and B. pseudomallei are considered to be potential biological warfare agents, targeting livestock and humans.

As many of you know, I have discussed many forms of antimicrobial resistance (AMR) in this column. Surfaces and biofilms intersect with AMR. Burkholderia research focused on interbacterial signaling has shown that contact-dependent growth inhibition plays a significant role in mediating cell-to-cell communication specifically in B. thailandensis. During this type of interaction, bacteria release protein toxins in the environment. Cells with a corresponding protective protein (usually bacteria of the same strain) are not inhibited to grow or die. Lastly, recipient cells that have the corresponding protein then undergo changes to gene expression and phenotype which advances community formation of biofilms. Unfortunately, this occurs even if the recipient cell was not of the same bacterial strain showing the critical importance this genus can have in the environment.

For this column, I will focus on B. pseudomallei and the recent outbreak in four states. In my next column (October), I will focus on the B. cepacia complex (Bcc) as it relates to outbreaks to a dangerous contaminant in water-based pharmaceutical products.

In a recent CDC Health Alert Network, four cases of melioidosis from Georgia, Kansas, Minnesota and Texas were identified and characterized. The first case (fatal) identified in March 2021 occurred in Kansas. The second and third cases, both identified in May 2021 in Minnesota and Texas, were hospitalized for extended periods of time before being discharged to transitional care facilities. The most recent case died in the hospital and was identified post-mortem in late July 2021 in Georgia. All cases had no history of traveling abroad from the United States. Melioidosis signs and symptoms are varied and nonspecific, and may include pneumonia, abscess formation, and blood infections.

All four melioidosis cases initially presented with symptoms ranging from cough and shortness of breath to weakness, fatigue, nausea, vomiting, intermittent fever, and rash on the trunk, abdomen, and face. Two cases, one fatal, had several risk factors for melioidosis, including COPD and cirrhosis. The other two cases had no known risk factors for melioidosis. Genomic analysis of the strains strongly suggests a common source (e.g., imported product or animal). The source is unknown to date despite environmental sampling, serological testing, and family interviews.

Importantly, B. pseudomallei may be misidentified by some automated identification methods in laboratory settings.

Recommendations from CDC include:
• Consider melioidosis diagnosis in patients with a compatible illness, even if they do not have a travel history to a disease-endemic country.
• Culture of B. pseudomallei from any clinical specimen is considered diagnostic for melioidosis. Ideal specimens for culture include blood, urine, throat swab, and, when relevant, respiratory specimens, abscesses, or wound swabs.
• When ordering specimen cultures to diagnose melioidosis, advise the laboratory that cultures may grow B. pseudomallei, and that appropriate laboratory safety precautions should be observed by the laboratory personnel.
• Laboratory testing involving automated identification algorithms (e.g., MALDI-TOF, 16s, VITEK-2) may misidentify B. pseudomallei as another bacterium. The isolate from the Texas case was initially misidentified as B. thailandensis by MALDI-TOF. Consider re-evaluating patients with isolates identified on automated systems as Burkholderia spp. (specifically B. cepacia and B. thailandensis), Chromobacterium violaceum, Ochrobactrum anthropi; and, possibly, Pseudomonas spp., Acinetobacter spp., and Aeromonas spp.
• Treat melioidosis with IV antibiotics (e.g., ceftazidime or meropenem) for at least two weeks. Depending on the response to therapy, IV treatment may be extended for up to eight weeks. Intravenous treatment is followed by oral trimethoprim-sulfamethoxazole (TMP/SMX) for three to six months to prevent relapse. Amoxicillin/clavulanic acid can be used in persons with a contraindication to, or who cannot tolerate, TMP/SMX. 5
• If B. pseudomallei is identified or an organism is suspicious for B. pseudomallei, contact your state or local public health department immediately. The health department can facilitate forwarding the isolate for confirmation to the closest reference laboratory and initiate a public health investigation.

For more information, see: https://emergency.cdc.gov/han/2021/han00448.asp

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State University. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Fungal Infections Worldwide are Becoming Resistant to Drugs and are More Deadly

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

Editor’s note: This piece originally was published June 28, 2021 in The Conversation and is reprinted under Creative Commons.

Say “fungus” and most people in the world would probably visualize a mushroom. But this fascinating and beautiful group of microbes has offered the world more than just foods like edible mushrooms. Fungi are also a source of antibiotics – for example, penicillin from penicillium – as well as the yeasts and other fermentation agents that make bread rise, give cheese its flavor and put the alcohol in wine and beer.

Many people may also not realize that some fungi can cause disease. However, athlete’s foot, thrush, ringworm and other ailments are caused by fungi, and some are serious risks to health and life. That’s why the rise of antifungal resistance is a problem that needs more widespread attention – one equal to the better-recognized crises of multidrug-resistant microbes like the bacteria that cause tuberculosis.

I’ve worked in public health and medical laboratories for over three decades, specializing in public health and clinical microbiology, antimicrobial resistance and accurate science communication and health literacy. I’ve been paying close attention to the growing resistance of a pathogenic fungus called Candida auris to limited and commonly used anti-fungal agents. Since fungi have traditionally not caused major diseases, the emergence of drug-resistant fungi that can cause serious illness rarely receives funding for medical research.

But the facts suggest that this needs to change.

Fungi-caused ailments are treated with specifically anti-fungal medications because these organisms are such a unique form of life. Fungi are spore-producing organisms, including molds, yeast, mushrooms and toadstools. Among their unique characteristics, fungi feed on organic matter by decomposing it, rather than ingesting it like animals do, or absorbing nutrients through roots, as plants do. Unlike bacteria, which have simple prokaryotic cells, or cells without a true nucleus, fungi have complex eukaryotic cells cells, which do have a nucleus surrounded by a membrane like animals and plants. In the multi-level taxonomy, or naming system, that biologists use to classify life forms, fungi are in their own kingdom under the domain of Eukarya.

Most fungal infections worldwide are caused by a genus of fungi called Candida, particularly the species called Candida albicans. But there are others, including Candida auris, which was first identified from an external ear canal discharge in 2009 in Japan, and given its name for the Latin term for ear, “auris.”

Candida normally lives on the skin and inside the body, such as in the mouth, throat, gut and vagina, without causing any problems. It exists as a yeast and is thought of as normal flora, or the microbes that are part of humans. Only if our bodies are immuno-compromised do these fungi become opportunistic and cause disease. That is what’s happening worldwide with multidrug-resistant C. auris.

Infections by C. auris, sometimes called fungemia, have been reported in 30 or more countries, including the United States. They are often found in the blood, urine, sputum, ear discharge, cerebrospinal fluid and soft tissue, and occur in people of all ages. According to the Centers for Disease Control and Prevention (CDC), the mortality rate in the U.S. has been reported to be between 30 percent to 60 percent in many patients who had other serious illnesses. In a 2018 overview of research to date about the global spread of the fungus, researchers estimated mortality rates of 30 percent to 70 percent in C. auris outbreaks among critically ill patients in intensive care.

Research data shows that risk factors include recent surgery, diabetes and broad-spectrum antibiotic and antifungal use. People who are immuno-compromised are at greater risk than those with healthy immune systems.

C. auris can be difficult to identify with conventional microbiological culture techniques, which leads to frequent misidentification and under recognition. This yeast is also known for its tenacity to easily colonize the human body and environment, including medical devices. People in nursing homes and patients who have lines and tubes that go into their bodies – like breathing tubes, feeding tubes and central venous catheters – seem to be at highest risk.

The Centers for Disease Control and Prevention have set C. auris infections at an “urgent” threat level because 90 percent are resistant to at least one antifungal, 30 percent to two antifungals, and some are resistant to all three available classes of antifungals. This multidrug resistance has led to outbreaks in healthcare settings, especially hospitals and nursing homes, that are extremely difficult to control.

For hospitalized COVID-19 patients, antimicrobial-resistant infections may be a particularly devastating risk of hospitalization. The mechanical ventilators often used to treat serious COVID-19 are breeding grounds and highways for entry of environmental microbes like C. auris. Further, according to a September 2020 paper authored by researchers Anuradha Chowdhary and Amit Sharma, hospitals in India treating COVID-19 have detected C. auris on surfaces including “bed rails, IV poles, beds, air conditioner ducts, windows and hospital floors.” The researchers termed the fungus a “lurking scourge” amid the COVID-19 pandemic. The same researchers reported in a November 2020 publication that of 596 COVID-19-confirmed patients in a New Delhi ICU from April 2020 to July 2020, 420 patients required mechanical ventilation. Fifteen of these patients were infected with candidemia fungal disease and eight of those infected (53%) died. Ten of the 15 patients were infected with C. auris; six of them died (60 percent).

With the options for effective antifungals narrowing, CDC is recommending a focus on stopping C. auris infections before they start. These steps include better hand hygiene and improving infection prevention and control in medical care settings, judicious and thoughtful use of antimicrobial medications, and stronger regulation limiting the over-the-counter availability of antibiotics.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State University. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Antibiotic Resistance and the Medical Laboratory

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

Editor's note: This column originally appeared in the July 2021 issue of Healthcare Hygiene magazine.

In the 2019 Antibiotic Resistance (AR) Threats Report (www.cdc.gov/DrugResistance/Biggest-Threats.htm), former Centers for Disease Control and Prevention (CDC) director, Robert R. Redfield, MD, discusses the radical change that has occurred over the history of antibiotic use from the 1940’s until today. In the foreword, he states to stop antibiotic resistance, the U.S. must:
• Stop referring to a coming post-antibiotic era—it is here. We are living in a time where miracle drugs no longer perform miracles and a microscopic enemy is ripping families apart. The time for action is now and we can be part of the solution.
• Stop playing the blame game. Each person, industry, and country can affect the development of antibiotic resistance. We each have a role to play and should be accountable to make meaningful progress against AR.
• Stop relying only on new antibiotics that are slow getting to market and that, sadly, these germs will one day render ineffective. We need to adopt aggressive strategies to keep germs away and infections from occurring in the first place.
• Stop believing that antibiotic resistance is a problem “over there” in someone else’s hospital, state, or country—and not in our own backyard. AR is in every U.S. state and in every country globally. There is no safe place from antibiotic resistance, but everyone can take action against it, from handwashing to improving antibiotic use.

Whether one is discussing AR or more generally antimicrobial resistance (AMR), together they represent a slow-burning global emergency. The World Health Organization (WHO), Centers for Disease Control and Prevention (CDC), and other agencies have predicted that AMR could lead to an economic impact of $100 trillion causing 10 million deaths annually by 2050 without action. AMR can become a slow-burning pandemic leading the world in mortality over longtime leaders like cancer and other health conditions.

How can we help? What can those of us who work in public health, the medical laboratory and healthcare do to help curb this global emergency?

In an April 2021 research study, Langford, et al. conclude that laboratory reporting of antibiotic susceptibility results for urine cultures is associated with empirical and directed prescribing of the reported antibiotics. Laboratories can play an important role in guiding appropriate antibiotic selection for urinary indications. Briefly, after a patient specimen is identified as a bacterial pathogen, the medical laboratory/clinical microbiology professional will perform an antibiotic susceptibility test (AST) on the pathogen. Testing determines the potential effectiveness of specific antibiotics on the bacteria and/or determines if the bacteria show resistance to certain antibiotics. Used properly, AST results help select the drug(s) that will likely be most effective in treating an infection.

This research study has important and practical findings for antibiotic stewardship programs (ASP). “Nudging” is a term used to describe the concept of modifying “choice architecture” to augment decision-making, without introducing incentives or inhibiting personal decisions by physicians (or other decision maker). Research shows that nudging is a promising intervention in the microbiology and medical laboratory. Selective reporting via nudging is a process whereby only certain culture and antibiotic susceptibility results are reported back to the clinician; the strategy aims to help guide appropriate antimicrobial prescribing. Selective reporting can take multiple forms, ranging from not reporting any susceptibility results at all to reporting only first-line antibiotics or agents with lower adverse risks. While national and international guidelines recommend the use of selective reporting, specific reporting policies are discretionary for individual laboratories, resulting in a high degree of variability.

Ultimately, the goal of nudging can influence how a physician does or does not select and/or utilize a particular antibiotic. Langford’s findings confirm their hypothesis that laboratory variability exists in selective reporting which influences antibiotic prescribing decisions. Approximately three-fold odds of directed antibiotic prescribing occurred when an antibiotic agent was listed on the susceptibility report and an association between laboratory antibiotic susceptibility reporting and prescribing in the empirical window. This suggests that the microbiology / medical laboratory can be highly influential in antibiotic prescribing choices, even when the prescriber is making decisions in the absence of a urine culture result (empirical or syndromic decisions).

Lastly, ongoing and growing development of rapid diagnostics (MALDI-TOF, PNA-FISH, qPCR, NGS, etc.) will continue to offer powerful discriminatory methods for pathogen identification and genes that may confer resistance to antimicrobial drugs. It is critical the experts on laboratory testing (medical laboratory professionals) are at the table for test selection and proper interpretation to aid physicians, pharmacists, and other healthcare professionals. Another important tool for hospitals to utilize will be the newly created doctorate of clinical laboratory science (DCLS). The DCLS will be the future of diagnostic management teams and laboratory test utilization at the intersection of open communication with the entire healthcare team, including physicians.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State University. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/


The Medical Laboratory Professional

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

Editor's note: This column originally appeared in the June 2021 issue of Healthcare Hygiene magazine.

In my recent, article “Who is doing all those COVID-19 tests? Why you should care about medical laboratory professionals” with The Conversation, I unpack why one should care about medical laboratory and public health professionals. Who do you think performs your medical laboratory tests for COVID-19 or any other test? If you answered “my doctor” or “my nurse” or a robot, you would be completely wrong. To put it bluntly, your life is in the hands of medical laboratory professionals. We perform an estimated 13 billion laboratory tests in the U.S. annually. That means that laboratory testing is the single highest-volume medical activity in the lives of Americans. Why should you care? Those 13 billion tests help drive approximately two-thirds of all medical decisions made by your doctor and other healthcare professionals from cradle to grave. There are only 337,800 practicing medical laboratory professionals for a population of just over 330 million people in the U.S.

As of May 14, 2021, our professionals have conducted 462,798,339 tests for COVID-19 infections since the pandemic began. What about all the other testing conducted each day? We are also running tests for people who are having babies, heart attacks, cancer, antibiotic-resistant infections, strep throat and other illness or diseases. Just because a novel virus showed up in our world and demanded to be tested for does not mean all other health issues stop.

A medical, or clinical, laboratory science degree often requires an average of five years of college education. Medical laboratory scientists all have bachelor’s degrees and have certification or a license to practice. I, and many of my colleagues, have a master’s degree, and a doctorate. These complex qualifications are reflected in our education and clinical background.

A degree in medical laboratory testing requires mastery of several areas of medicine including the study of hematology, molecular diagnostics, immunology, urine analysis, microbiology, chemistry, parasitology, toxicology, immunohematology (blood banking), coagulation and transfusion, and laboratory safety and operation. I often tell my students that this degree is like having to complete four majors.

Our profession can also start toward a laboratory science career at an entry level with a bit less education and clinical training – even as a technician, which requires only a two-year associate’s medical laboratory technician degree. These technicians often move up the career ladder by obtaining other degrees. Like any health care professional degree, ours is externally accredited through the National Accreditation Agency for Clinical Laboratory Sciences.

Currently there are an estimated 337,800 employed medical laboratory professionals in the U.S., according to the Bureau of Labor Statistics. This is an estimate, because without licenses in every state, an accurate number of practicing laboratory professionals is not available. But the demand for these professionals is expected to grow by 25,000 between 2019 and 2029, according to the Bureau of Labor Statistics. But that doesn’t include the number of jobs that will become vacant when workers retire or leave the profession during the pandemic.

What is frightening to me is that while the demand for clinical laboratory personnel is growing, the number of training programs is declining. Currently, there are 235 medical laboratory scientist and 240 medical laboratory technician training programs in the U.S. This is a 7 percent decline from the year 2000. In some states, there are no programs.

Fewer training programs, coupled with greater demand for laboratory professionals, could impact patient care, notes Jim Flanigan, executive vice president of the American Society for Clinical Laboratory Science. He is concerned by the lack of federal programs supporting medical laboratory education as compared to all other health programs. Vacancy rates are exceeding the number of medical laboratory scientist and medical laboratory technician graduates.

A number of other factors help explain our low workforce numbers. Training laboratory personnel is expensive, and there are few scholarship or loan programs available for prospective students. Salaries are also problematic. Compared to nursing, physical therapists or pharmacists, our professionals are paid 40 percent to 60 percent less on average for annual salaries.

The American Society for Clinical Laboratory Science is calling for expansion of the Title VII health professions program – which provides education and training opportunities in high-demand disciplines – to include medical (clinical) laboratory science. The organization also supports efforts to improve visibility of the profession by engaging in community outreach opportunities and by partnering with middle and high school STEM programs to show young people that laboratory medicine is a viable career path.

Lastly, with competition for laboratory personnel intensifying over the last year, turnover rates for some categories of laboratory personnel now exceed 20 percent. Because of the difficulty in finding qualified staff, medical laboratories are increasingly turning to temporary staff to handle the patient testing workload. In a sense, the pandemic has exacerbated a “free-agent” effect for traveling medical laboratory professionals that hurts continuity and quality in healthcare.

We hope that you see us and hear us. Your life or that of a loved one depends on it.

Originally published in The Conversation: https://theconversation.com/who-is-doing-all-those-covid-19-tests-why-you-should-care-about-medical-laboratory-professionals-151725

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Microplastics and Antibiotic Resistance

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the May 2021 issue of Healthcare Hygiene magazine.

Antibiotic and antimicrobial resistance (AMR) continues to be a slow burning pandemic. It is not as recognized as the SARS-CoV-2 / COVID-19 pandemic. Even before the current ongoing global pandemic, AMR was a major global emergency, and we must not forget about this very dangerous public health threat. Most experts agree that AMR is a multifaceted complex problem. Resistance happens when germs (any microbe) defeat the drugs designed to kill them. Any antibiotic or antimicrobial use—in people, animals, or crops—can lead to resistance. Resistant germs are a One Health problem—they can spread between people, animals, and the environment.

The Centers for Disease Control and Prevention (CDC) tells us that antibiotic resistance is one of the biggest public health challenges of our time. Each year in the United States, at least 2.8 million people get an antibiotic-resistant infection, and more than 35,000 people die. Fighting this threat is a public health priority that requires a collaborative global approach.

As many of you know, I have discussed many forms of AMR in this column. Surfaces and biofilms are intersect with AMR. Now, we have another hidden surface to consider regarding the problem of resistance. In a recent Elsevier Journal of Hazardous Materials Letters, researchers found certain strains of bacteria elevated antibiotic resistance by up to 30 times while living on microplastic biofilms that can form inside activated sludge units at municipal wastewater treatment plants.

These ultra-fine plastic particles, less than 5 m in length, are in everything from cosmetics, toothpaste and clothing microfibers, to our food, air and drinking water. News Medical reports that estimates show an average-sized wastewater treatment plant serving roughly 400,000 residents will discharge up to 2,000,000 microplastic particles into the environment daily. Researchers are still learning the environmental and human health impact of these ultra-fine plastic particles.

The authors of the study discuss that some research focuses on the negative impacts that millions of tons of microplastic waste a year is having on our freshwater and ocean environments. Only recently, have studies started looking into the role of microplastics in towns and cities’ wastewater treatment processes which means we do not really know much there. The wastewater treatment plants may be hotspots where various chemicals, antibiotic-resistant bacteria and pathogens converge. The authors believe this is what their study documents regarding microplastics serving as their (AMR) carriers and posing hazards to aquatic biota and human health if they bypass the water treatment process.

The study was designed to collect batches of sludge samples from three domestic wastewater treatment plants in northern New Jersey, inoculating the samples in the laboratory with two widespread commercial microplastics – polyethylene and polystyrene. Quantitative PCR and next-generation sequencing techniques identified the species of bacteria that tend to grow on the microplastics. These powerful molecular techniques allowed them to track and detect how the bacteria adapted and changed in real time.

The study revealed that three genes in particular – sul1, sul2 and intI1 – known to aid resistance to common antibiotics, sulfonamides, were up to 30 times greater on the microplastic biofilms than in the experimental controls after just three days. Further, when they spiked the samples with the antibiotic, sulfamethoxazole, it amplified the antibiotic resistance genes an additional 4.5 times. The authors think the presence of antibiotics would be necessary to enhance AMR genes in these microplastic-associated bacteria, but it seems microplastics can naturally allow for uptake of these resistance genes on their own. However, it does appear that the presence of antibiotics can have significant amplification.

The study revealed eight different species of bacteria were highly enriched on the microplastics. Two of those species were emerging human pathogens typically linked with respiratory infection, Raoultella ornithinolytica and Stenotrophomonas maltophilia. The most common strain found on the microplastics was, Novosphingobium pokkalii, and is likely a key initiator in forming the sticky biofilm that attracts such pathogens because it leads to breakdown of the plastic and expands the biofilm. The study also highlighted the role of the gene, intI1, a mobile genetic element chiefly responsible for enabling the exchange of antibiotic resistance genes among the microplastic-bound microbes.

Most people likely think that these tiny microplastic “bead-like” materials are unseen and not a problem. However, what this study has shown us is that microbes always find a way to develop a niche and take advantage of their environment and surfaces. When a bacterium like Novosphingobium accidentally attaches to a microplastic surface and secretes glue-like extracellular substances (biofilms), it can allow other bacteria to stick to surfaces and grow. More worrisome is that it will offer them the opportunity to exchange DNA. This is how the antibiotic resistance genes are being spread among the community. Ultimately, this study and others may bring new regulations on the use of microplastics in consumer products.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/



The Infection Prevention and Environmental Services Professions

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the April 2021 issue of Healthcare Hygiene magazine.

For those who know my career journey, you probably realize that I often advocate for several critical professions that often go unnoticed. For example, I write, speak and interview often to discuss the medical laboratory and how #WeSaveLivesEveryday in the shadows of healthcare. For this month’s article, I want to briefly discuss two other professions that many people do now know about, including many healthcare professionals.

In my 30-year career journey, I have worked in public health, medical laboratory and academia. I discovered very early in these paths that many individuals in the public as well as other professional environments did not understand or made aware of hidden professions that have profoundly important roles in saving lives. These two professions – infection prevention and environmental services – have ongoing powerful roles in preventing infections in healthcare and community settings.
The first profession I would like to discuss is the role of an infection preventionist (IP). I am starting with this career because I have several alumni from our Texas State University Clinical (medical) Laboratory Science Program who have gone on to amazing IP careers after their medical laboratory journey. In fact, these two careers have synergistic and complimentary coursework and healthcare environment education / training.

According to the Centers for Disease Control and Prevention (CDC), one in 25 hospitalized patients will get an infection because of the care they receive, and an estimated 75,000 patients will die each year. Because healthcare-associated infections (HAIs) are a threat to patient safety, many hospitals and healthcare facilities have made the prevention and reduction of these infections a top priority. The IP is on the frontlines of preventing HAIs as well as community infections in some career slants.

What does an IP actually do? How do you become an IP? According to the Association for Professionals in Infection Control and Epidemiology (APIC), IPs are the professionals who ensure that healthcare workers (physicians, nurses and others) and patients are doing everything they should to prevent infections. Most IPs are nurses, epidemiologists, public health professionals, medical laboratorians, microbiologists, doctors, or other health professionals who work to prevent germs from spreading within healthcare facilities. They look for patterns of infection within the facility; observe practices; educate healthcare teams; advise hospital leaders and other professionals; compile infection data; develop policies and procedures; and coordinate with local and national public health agencies.

Usually, when one decides to work in the field of infection prevention, they probably were working in one of the healthcare fields mentioned (nurse, medical laboratory, etc.) and find that they have a passion and talent for this area. This is how several of my alumni ended up working in the IP world. APIC discusses the ever-changing requirements of the profession demand that IPs constantly update their knowledge base and expand their skill set. The updated APIC Competency Model (May 2019) has four career stages, defined as follows: novice, becoming proficient, proficient, and expert. As one progress through these stages, typically when the proficient state is reached an individual will want to obtain the CIC® credential [see: https://www.cbic.org/CBIC/CIC-Certification/About-the-Examination.htm].

IPs are in the trenches of curbing and prevention life-threatening antimicrobial resistant HAIs and other dangerous pathogens. Truly, a wonderful career for those interested in this area.

The second career path that I love to discuss to raise awareness for is the environmental services professional (EVS). In a 2014 article, I wrote for Elsevier Connect titled “A secret weapon for preventing HAIs,” I mention that when I teach a microbiology class for future nurses or medical laboratory professionals, I often start a complex discussion of microbial control. As an aside, I happened to tell my students of what I believe to be an overlooked "secret weapon" in reducing and preventing HAIs in hospitals: the housekeepers – or more accurately, the environmental services staff.

After all, as I often tell my medical/clinical laboratory science students, "clean does not necessarily mean microbially clean." In other words, just because a healthcare or community setting looks and smells clean does not always mean that it is free from dangerous pathogens! These bugs do not read the textbooks when it comes to following any rules about infection prevention and control. We must all ensure that the EVS profession and its professionals are known and respected entities in controlling the chain of infection. Unfortunately, the environmental services staff rarely appear on the radar of hospital administrators except when there is a need for budget cuts. It is our job and professional duty to make sure EVS professionals remain on the radar of everyone involved in reducing HAIs and other pathogen transmission. I like to tell those who are not aware of EVS staff, #SurfacesMatter all the time to everyone. Learn more about this lifesaving profession with the CDC: https://www.cdc.gov/infectioncontrol/training/evs-battle-infection.html and other professional organizations.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/


AMR and COVID-19: The Intersection of the Pandemic

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the March 2021 issue of Healthcare Hygiene magazine.

For the past 15-plus years, I have discussed (screamed) about the dangers of empirical antibiotic use in treating infections. Most of us who conduct research in the realm of antibiotic and antimicrobial resistance (AMR), understand that there is a time when a physician or others in the healthcare team may need to utilize empirical treatment. For example, if an individual enters an emergency department and are suffering from sepsis leading to organ (e.g., kidney) failure. A physician must start that patient on a broad-spectrum antibiotic to protect their life. Unfortunately, the pandemic and prior has led to patient treatment with antibiotics minus a confirmatory laboratory test to identify the pathogen and the all-important antibiotic susceptibility test to predict effective antibiotic(s) use.

The ongoing SARS-CoV-2 pandemic has been at the forefront of everyone’s mind, including dominating healthcare and public health. Rightfully and arguably so, it is the most important global health emergency in the last century. However, just under the radar we find that the concern of treating COVID-19 patients may be amplifying an ongoing, slow-burning global pandemic that has been here decades – the antimicrobial resistance pandemic.

In a recent Open Forum Infectious Diseases study conducted in five hospitals in the Johns Hopkins Health System between March 1, 2020, and May 31, 2020 [Prevalence of Co-infection at the Time of Hospital Admission in COVID-19 Patients, A Multicenter Study], 1016 adult patients were evaluated for possible bacterial co-infection at time of presentation of COVID-19. Briefly, recent research tends to show that bacterial co-infection with COVID-19 is uncommon at the time of presentation. However, these data were based on microbiology results only. The investigators sought to develop and apply consensus definitions, incorporating clinical criteria to better understand the rate of co-infections and antibiotic use in COVID-19. Primary results indicated bacterial respiratory co-infections were infrequent (1.2 percent); one patient had proven bacterial community-acquired pneumonia (bCAP), and 11 (1.1 percent) probable bCAP. Two patients (0.2 percent) had viral respiratory co-infections. Yet, and frighteningly so, 69 percent of patients received antibiotics for pneumonia. Most were halted within 48 hours in patients with possible or no evidence of bCAP.

For emphasis, in everyday language this means that seven out of 10 patients were treated empirically with antibiotics when they did NOT have bacterial respiratory infections or bCAP. We can and must do better.

I recently discussed this issue in a Forbes article regarding a recent Bulletin from the WHO. Experts discussed dangers of the ongoing COVID-19 pandemic amplifying antibiotic resistance. Too many people have been receiving antibiotics when presenting with mild cases of COVID-19, but no pneumonia or even a moderate case with pneumonia. Antibiotics should not be used here. The article goes on to note that studies “published on hospitalized COVID-19 patients identified that while 72 percent (1,450/2,010) of patients received antibiotics, only 8 percent (62/806) demonstrated superimposed bacterial or fungal co-infections.” The WHO also reports that azithromycin is being widely used with the hydroxychloroquine treatment as problematic for AMR.

I go on to argue that the recent CDC 2019 Antibiotic Resistance Threats in the United States article, states that despite improvements in recent years, “the number of people facing antibiotic resistance in the United States is still too high. More than 2.8 million antibiotic-resistant infections occur in the US each year, and more than 35,000 people die as a result. In addition, nearly 223,900 people in the US required hospital care for C. difficile and at least 12,800 people died in 2017.” Likewise, public health experts from the United Nations, international agencies and others released a report in April of 2019 stating that if no action is taken, “drug-resistant diseases could cause 10 million deaths each year by 2050 and damage to the economy as catastrophic as the 2008-2009 global financial crisis. By 2030, antimicrobial resistance could force up to 24 million people into extreme poverty.”

Proactive, prevention of disease is much more cost effective and logical for the treatment of disease rather than being reactive. Simply stated, the nation’s (and world) public health system has been underfunded for decades. Until we get serious about prioritizing public health in an ongoing, logical, purposeful way, we will continue to fight these deadly causes with fewer people in the public health and medical laboratory spaces. People will be overworked and perhaps rushed on to the “battlefields” too soon because of non-sustained pipelines of highly trained professionals in the lean workforce. Cutting funding for new research on vaccines and creative ways of attacking disease will suffer. Cutting educational scholarships and programs for ushering in a new generation of these professionals is shortsighted. Utilizing simulations and modeling to try to prepare better for the next outbreak is critical.

Public health and healthcare funding is smart and pays dividends. It meets the long-standing adage of “an ounce of prevention is worth a pound of cure.”

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/




What Does a SARS-CoV-2 Variant Mean?

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

Editor's note: This column originally appeared in the February 2021 issue of Healthcare Hygiene magazine.

Just when we were all starting to breathe a (small) sigh of relief with the news of successful therapies (antivirals, steroids, and monoclonal antibodies) and multiple vaccines for the SARS-CoV-2 virus to help with prevention of a COVID19 infection, we started seeing new headlines about a new virus variant (strain) emerging in the United Kingdom (UK). Scientists and public health officials began reporting what appeared to be a COVID19 surge in December caused by a SARS-CoV-2 variant. While it is likely too early to know, this new strain appears to be transmitting faster than earlier strains.

The UK sequences 5 percent to 10 percent of all COVID-19 cases for epidemiological surveillance. In 117 of 255 sequenced cases, roughly 50 percent of them were detected to be in a unique phylogenetic cluster. In common language a distinct cluster of viruses just means that they are very similar to each other (genetically) versus to other strains of the virus. The “new” detected viruses were initially designated as Variant Under Investigation (VUI) – 202012/01 upon detection, but on further review given its rapid spread has been re-designated as Variant of Concern (VOC-202012/01) or B.1.1.7 (a name derived from its phylogenetic heritage). It is important to understand that the terms “variant,” “strain,” and “lineage” are synonyms. Currently, the general media and scientists are using them in addition, for their reporting.

Global reports (https://cov-lineages.org/global_report_B.1.1.7.html#table2link) by Public Health England have illustrated that the B.1.1.7 strain has quickly spread outside of England and the UK. At the time of writing this column, almost 50 countries have detected this new variant, including the United States. While the world still awaits the analysis of a stronger (more cases) data set for more certainty, early statistical modeling by the Centre for Mathematical Modelling of Infectious Diseases at the London School of Hygiene and Tropical Medicine implies the transmission of this variant may be 56 percent greater. The data also exhibits a higher Rt (reproductive rate is the number of secondary infections that occur from a single infection) of 0.7 versus 0.4 from early strains.

Is it normal for viruses to change?

Viruses, especially RNA viruses, change rapidly (mutate). All viruses do this over time and the coronaviridae (SARS-CoV-2 belongs) is no different. Mutations occur in the sequence of nucleic acids by base changes. Sometimes these mutation events during virus evolution will be “silent” which means the changes do not produce anything of concern to its host (in this case, humans).

On the other hand, sometimes the mutation is not silent and can result in the virus producing new or changed proteins or features that produce changes resulting in a new or related phenotype. Scientists refer to minor changes in a microbial phenotype as resulting in an antigenic drift, while major changes are known as an antigenic shift. A drift is usually less problematic, for example, because the human immune system will likely still recognize the microbe and mount a response.
Many people may understand this situation with the ongoing changes of influenza viruses, which means each year we receive (usually) a new cocktail of vaccine for protection due to flu virus mutations. Fortunately, coronaviruses mutate slower than other RNA viruses. The scientific community has already documented SARS-CoV-2 variants that differ from the original Wuhan strain and involved the well know spike protein that is critical for virus cell-mediated entry.

What are some of the major concerns about this variant?

While there are always concerns with virus mutation, I believe there are primary issues the scientific, public health and healthcare community should focus on. Probably the biggest concern on everyone’s mind is whether the new vaccines will be effective on B.1.1.7 strain. Preliminary data has not shown that B.1.1.7 causes more severe illness than other strains. Likewise, it appears that the mutations to the virus spike protein have not shown new vaccines will not provide immunological protection (efficacy) but we must continue to monitor data with continued efforts of understanding the effect, if any, on all vaccines produced for SARS-CoV-2.

My medical laboratory and public health colleagues are also concerned with how changes in the virus spike protein or other mutation events may affect the laboratory detection of new strains. Briefly, when a virus mutates, sometimes it can decrease the ability for a laboratory test (antigenic or molecular) to “pickup” the new strain that could create false negatives. Lastly, the Centers for Disease Control and Prevention (CDC) reports that only 51,000 of 17 million (0.3 percent) cases are sequenced in the U.S.

It is critical to our national and global public health security that we put into place a more comprehensive effort to sequence more virus specimens to follow viral changes. To address this concern, the CDC has launched the National SARS-CoV-2 Strain Surveillance program, requiring each state to send them at least 10 samples bi-weekly for sequencing and characterization, which will identify B.1.1.7 and any other SARS-CoV-2 variants.

Acknowledgement: Dr. Rose Lee, https://asm.org/Articles/2021/January/B-1-1-7-What-We-Know-About-the-Novel-SARS-CoV-2

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/


2020: It Has Been Quite a Year!

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the January 2021 issue of Healthcare Hygiene magazine.

When I look back over the past year, I remember seeing first reports of a new viral respiratory agent popping up in Wuhan, China. Like many experts, I mentally noted it and moved on to other items of my workweek. That was in December of 2019. How little we knew of the coming tsunami of change for not only the United States but the entire global population.
As I opened my email today, I noticed so many stories about the “year in review” – both good and bad. Understandably, the global COVID-19 pandemic caused by the novel SARS-CoV-2 virus dominated the headlines daily during the past year, there are both pandemic and other stories that we have all witnessed.

IntraHealth’s Katherine Seaton writes that these were some of the following major news items this past year. In January, WHO launches the first-ever Year of the Nurse and the Midwife. March brings us the news that COVID-19 is officially declared a pandemic. Who can forget May? George Floyd is murdered. In July, the Trump Administration announces the U.S. will withdraw from the World Health Organization. Here comes August when we learn that Africa becomes free of wild polio. In the fall, October lets us know that The World Food Program wins the Nobel Peace Prize. November brings the U.S. unforgettable election (with plenty of ongoing controversy) as it ushers in new leadership and a renewed focus on global health. As I type these words for my monthly column, December unfolds an amazing and developing medical and public health event – The U.K. and the U.S. administer their first coronavirus vaccines.

This pandemic is arguably the most significant and devastating public health event. Globally, it will be remembered as an event that changed how we view microbes. I, like many of my colleagues, have been screaming for decades about the dangers of these invisible invaders. Like 9/11 changed air travel, this pandemic will change how everyone views the invisible world of the microbe. Now, there are new ways of thinking about our space, or the surfaces we touch, and what being in an overly crowded space can feel like. We use terms and phrases like “flatten the curve,” “physical distancing,” “reproduction number,” “false positive / negative” and “twindemic” like they are normal, everyday language.

As I sit her today, Dec. 17, 2020, there are approximately 74,695,618 cases and 1,658,588 deaths globally. In the U.S. alone, there are 17,401,787 cases and 314,694 deaths. My amazing colleagues in the medical laboratory and public health laboratory have tested approximately 226,751,534 specimens for COVID-19. Amazingly, there are only 337,800 practicing medical laboratory professionals for a population of just over 330 million people in the U.S. As I wrote in my recent article, “Who is doing all those COVID-19 tests? Why you should care about medical laboratory professionals,” for The Conversation, I’ve worked in public health and medical laboratories for three decades, specializing in the study of viruses and other microbes while also educating the next generation of medical laboratory scientists. In 2014, I coined the phrase “the hidden profession that saves lives.” With COVID-19, these unsung professionals are now in the limelight. Unfortunately, this pandemic has led to a nationwide burnout of these professionals, causing dangerous shortages in the U.S. healthcare infrastructure. Other public health and healthcare professionals show dangerous shortages and burnout as well.

I also wrote that most people in the public do not understand who performs medical laboratory tests for COVID-19 or any other test. It is not your doctor, nurse or a robot. It is a medical laboratory or public health laboratory professional. To put it bluntly, your life is in the hands of medical laboratory professionals. We perform an estimated 13 billion laboratory tests in the U.S. annually. That means that laboratory testing is the single highest-volume medical activity in your life. Why should you care? Those 13 billion tests drive roughly two-thirds of all medical decisions from cradle to grave. Our professionals have mad respect for physicians, nurses, respiratory therapists, pharmacists and all healthcare professionals. We just want you to understand that we save lives every day even though you do not necessarily see us in the shadows of healthcare.
Yet, as I sit her, I am reminded that we have come together to produce not one, but multiple vaccines that will help us end this pandemic. Our collective creativity, insight and brilliance has led to monoclonal antibodies, antivirals, and ongoing medical interventions, which save countless lives. Yes, it has been one of the worst years of our lives. However, I also believe this year is one of the most monumental, phenomenal, and significant public health and healthcare achievements of all time. Let us turn the page to 2021 and get to work! Happy New Year, everyone!

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/


Let’s Go Campy(ing)

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the December 2020 issue of Healthcare Hygiene magazine.

According to the most recent 2019 CDC publication, Antibiotic Resistance (AR) Threats in the United States, Campylobacter causes an estimated 1.5 million infections and $270 million in direct medical costs every year. Of those infections, 29% have decreased susceptibility to fluoroquinolones (e.g., ciprofloxacin) or macrolides (e.g., azithromycin), the antibiotics used to treat severe Campylobacter infections. CDC ranks AR threats from high to low as urgent, serious, concerning and watched. Campylobacter currently sits in the serious threat rank.

Campylobacter (meaning "curved bacteria") is a genus of Gram-negative bacteria. These bacteria typically appear as comma- or S-shaped and are motile. The genus is pronounced as cam·pylo·bac·ter | (kam-pi-lō-ˈbak-tər). Some species can infect humans, sometimes causing campylobacteriosis, a diarrheal disease in humans. In many instances, these infections are self-limiting and do not require treatment unless one is immunocompromised. However, there is a growing issue of antibiotic resistance with this genus. There are about a dozen known Campylobacter spp. implicated in human disease. The primary human pathogens are C. jejuni (~80-90%) and C. coli (~5-10%) which are the most common.

Campylobacter causes an estimated 1.5 million illnesses each year in the United States. People can get this infection by eating raw or undercooked poultry or eating something that touched it. The most known source for Campylobacter is poultry. However, due to its large and diverse natural reservoir, the infection can also occur from eating other foods, including seafood, meat, and produce, by contact with animals, and by drinking untreated water. Sources of infection can also be direct contact with infected animals (e.g. chickens), which often carry Campylobacter asymptomatically. C. jejuni leads the cause of bacterial foodborne disease in many developed countries, including Europe and the United States.
In this article, I will introduce Campylobacter and information aimed at a general understanding of the characteristics of this pathogen in the environment. Primarily, I will utilize information obtained from the Centers for Disease Control and Prevention along with professional experience.

How does one prevent infection? Since Campylobacter spp. are found in such a large and diverse number of environments, including animal reservoirs there are a number of public health measures one should follow to prevent infection.
• Wash your hands!
• Keep certain foods separated; especially keep raw poultry away from other foods. Use separate cutting boards and clean them properly.
• Cook food properly, especially poultry (minimum internal temperature of 165°F). It is one of the top causes of Campylobacter illnesses in the United States. Poultry includes chicken, turkey, duck, goose, and other farmed birds.
• Drink pasteurized milk (raw milk can carry Campylobacter and other harmful germs that can make you very sick).
• Do not drink untreated water.
• Be careful with pets and livestock since they can carry Campylobacter and other germs.

Can an outbreak occur with this bacteria? Outbreaks are not commonly reported, considering how often people get sick from this bacterium, but the frequency has been increasing. Typically, poultry, raw milk, and untreated water have been the most commonly identified sources.
• In a very recent example of an outbreak, CDC and public health officials in several states are investigating a multistate outbreak of multidrug-resistant Campylobacter jejuni infections linked to puppies purchased from pet stores. To date, 30 people infected with the outbreak strain of Campylobacter jejuni, which causes diarrheal illness, have been reported from 13 states. Four hospitalizations have been reported and currently there has been no mortality.
• Epidemiologic and laboratory evidence indicate that contact with puppies, especially those at pet stores, is the likely source of this outbreak.
• Campylobacter bacteria isolated from clinical samples from ill people in this outbreak are resistant to commonly recommended, first-line antibiotics.

How is this organism diagnosed and what are the typical treatment options?
Campylobacter infection is diagnosed when a laboratory test detects Campylobacter bacteria in stool, body tissue, or fluids. The test could be a culture that isolates the bacteria or a rapid diagnostic test that detects genetic material of the bacteria (e.g. PCR testing). Sometimes a direct examination of a stool sample using contrast microscopy or Gram’s strain provides for a rapid presumptive diagnosis that must still be confirmed by stool culture. Blood cultures are often not performed and in most cases, one does not detect sepsis in this infection.

Campylobacter infections often do not need antibiotic treatment. Individuals experiencing an infection should drink extra fluids as long as diarrhea lasts. Some people with, or at risk for, severe illness might need antibiotic treatment including anyone 65 years or older, pregnant women, and the immunocompromised (e.g. AIDS or cancer patients receiving chemotherapy). Due to growing antibiotic resistance, some types of antibiotics may not work for some types of Campylobacter. When antibiotics are necessary, healthcare providers should use standard medical laboratory testing (antibiotic susceptibility testing) to help determine which type of antibiotics will likely be effective. If prescribed antibiotic(s), one should always take them exactly as directed by their physician. Campylobacter infections with decreased susceptibility are more common in low- and middle-income countries, putting travelers at risk for infections that may be harder to treat.
What are the symptoms of an infection? Campylobacter infections usually cause people to have diarrhea (often bloody), fever, and stomach cramps. Nausea and vomiting may accompany the diarrhea. These symptoms usually start two to five days after the person ingests Campylobacter and last about one week. Sometimes these infections cause complications, such as irritable bowel syndrome, temporary paralysis, and arthritis. Those individuals with weakened immune systems (e.g. blood disorder, AIDS, or chemotherapy patients), Campylobacter occasionally spreads to the bloodstream and causes a life-threatening infection.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

What About Flu During the COVID-19 Pandemic?

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

Editor's note: This column originally appeared in the November 2020 issue of Healthcare Hygiene magazine.

The Centers for Disease Control and Prevention has published Prevention and Control of Seasonal Influenza with Vaccines: Recommendations of the Advisory Committee on Immunization Practices — United States, 2020-2021 Influenza Season. This report updates the 2019–20 recommendations of the Advisory Committee on Immunization Practices (ACIP) regarding the use of seasonal influenza vaccines in the United States (MMWR Recomm Rep 2019;68[No. RR-3]). Routine annual influenza vaccination is recommended for all persons aged ≥6 months who do not have contraindications.

Why is it so important to receive the flu vaccine during the ongoing pandemic? For starters, global efforts to lower the transmission of SARS-CoV2 which is responsible for the COVID-19 illness, such as reduced travel, staying home, telecommuting for work and online education, have led to a reduction in the number of people taking advantage of routine physician visits for a number of services, including getting one’s vaccines up to date. Overall, healthcare is already under dangerous workloads and shortages in both healthcare professionals and healthcare PPE, as well as other essential medical items due to the pandemic. It is vital that everyone get their routine vaccinations during the COVID-19 pandemic to protect people and communities from vaccine-preventable diseases and outbreaks, including flu.

We can never perfectly predict how bad an upcoming flu season will be for a particular year. It is always critical to prepare for the upcoming flu season since we know that it can lead to high morbidity and mortality for certain populations. It will be even more important this year to reduce flu because it can help reduce the overall impact of respiratory illnesses on the population and thus lessen the resulting burden on the healthcare system during the COVID-19 pandemic. A flu vaccine may also provide several individual health benefits, including preventing one from getting flu, lowering the severity of a flu illness and reducing one’s chances of having to go to the hospital.

Influenza (flu) is an RNA virus that is notorious, and some might say diabolical, in its ability to mutate from year to year. RNA viruses (like SARS-CoV2) are unfortunately very smart and mischievous in this aspect. Flu, like SARS, also has the ability to live as a zoonotic agent. The flu virus has long been an inhabitant of swine, fowl, and humans, which continually allow for antigenic drift (small changes in the virus genome) and shift (major changes in the virus genome). It is a contagious respiratory illness, which can cause mild to severe illness resulting in hospitalization or death. Some people, such as older people, young children, and people with certain health conditions, are at high risk of serious flu complications. There are two main types of influenza (flu) virus: Types A and B. A third, Type C, is not clinically relevant to humans. The influenza A and B viruses that routinely spread in people (human influenza viruses) are responsible for seasonal flu epidemics each year. Here, I will focus on the types of influenza of medical and clinical importance aimed at a general understanding of the characteristics of this pathogen in the environment. Primarily, I will utilize information obtained from the Centers for Disease Control and Prevention (CDC) along with professional experience.

How does transmission occur with influenza? Flu viruses typically circulate in the United States each year, most commonly from the late fall through the early spring. Flu viruses spread mainly by tiny respiratory droplets made when people with flu cough, sneeze or talk. Respiratory droplets can move through the air to other hosts (people) and end up in their eyes, mouth or nose especially when they are nearby to each other. Likewise, flu viruses can be expelled in respiratory droplets and land on surfaces. People might touch these surfaces, and then rub their eyes, nose or mouth with their fingers. This action is known as indirect transmission and is less of a primary transmission route versus person-to-person (direct transmission). Thus, being aware of physical distance and high-touch surfaces, as well as hand hygiene are primary preventative measures for influenza much like SARS-CoV-2.

Could I get flu and COVID-19 at the same time? Yes. It is possible and “mixed infections” do occur with other microbial agents. Experts are still studying how common this might be for flu and COVID-19. Due to similar symptoms for both agents, it can be difficult to tell the difference between them based on symptoms alone.

So, is there a laboratory test that can detect both viruses? Yes. CDC has developed a test that will check for Type A and B flu, and SARS CoV-2, the virus that causes COVID-19 at the same time. This test will be used by U.S. public health laboratories and has been granted EUA by the Food and Drug Administration (FDA) to CDC.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

A Visit From an Old Nemesis, Streptococcus

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

Editor's note: This column originally appeared in the October 2020 issue of Healthcare Hygiene magazine.

Recently, a group of infectious disease scientists at Houston Methodist Hospital identified strains of group A streptococcus that are less susceptible to commonly used antibiotics like penicillin and other related beta-lactams. While this genus of bacteria has not been seen as worrisome in regards to antibiotic resistance, these findings remind us that the agent of strep throat, flesh eating disease, rheumatic fever, glomerulonephritis and other dangerous illnesses must never be overlooked or neglected when it comes to research, diagnosis and treatment. James M. Musser, MD, PhD, lead author of the study and chair of the Department of Pathology and Genomic Medicine at Houston Methodist Hospital and members of his department collaborated with nearly a dozen institutions across seven countries; discuss this research study in the Jan. 29, 2020 online issue of the Journal of Clinical Microbiology.

Streptococcus is a genus of gram-positive coccus (plural cocci) or spherical bacteria that belongs to the family Streptococcaceae, within the order Lactobacillales (lactic acid bacteria), in the phylum Firmicutes. The streptococcus bacteria are found in the form of twisted chains (“strepto”) of coccus (spheres, circular body). At present, there are over 50 medically significant species of this genus. Most streptococci are oxidase-negative and catalase-negative, and many are facultative anaerobes, which means that they are capable of growing both aerobically and anaerobically. In 1984, many bacteria formerly grouped in the genus Streptococcus were separated out into the genera Enterococcus and Lactococcus.

Many of the species found in the genus are known to be a part of the respiratory and salivary microbiome. Some species can survive on a dry surface for three days to six months. Here, I will focus on the streptococci of medical and clinical importance aimed at a general understanding of the characteristics of this pathogen in the environment. Primarily, I will utilize information obtained from the Centers for Disease Control and Prevention (CDC) along with professional experience.
How does transmission occur with these bacteria? These bacteria are transmitted primarily by direct contact with secretions from oral and nasal discharges of infected people or by coming into contact with wounds (sores) on the skin. Risk of transmission to a new host is highest when one comes into contact with an ill person exhibiting these conditions. In the medical setting, the most important groups are the alpha-hemolytic streptococci S. pneumoniae and Streptococcus viridans group, and the beta-hemolytic streptococci of Lancefield groups A and B (also known as “group A strep” and “group B strep”).

Which species are of medical significance and what primary diseases do they cause. This group of bacteria are taxonomically classified based on their hemolytic properties (ability to lyse red blood cells). The alpha-hemolytic species cause oxidization of iron in hemoglobin molecules within red blood cells which leads to incomplete or “partial hemolysis” causing a greenish color on blood agar. Beta-hemolytic species cause complete lysis of red blood cells appearing as wide areas clear of blood cells surrounding bacterial colonies (known as zones of hemolysis) on blood agar. The gamma-hemolytic species do not cause hemolysis (non-hemolytic). Rebecca Lancefield (scientist) developed a classification scheme known as the Lancefield groups, a serotype classification (that is, describing specific carbohydrates present on the bacterial cell wall). Within the Lancefield grouping, the beta-hemolytic streptococci are named Lancefield group A-W.
Species, primary host and their diseases include:
• S. pyogenes (human) – pharyngitis, cellulitis, erysipelas [Group A, beta hemolytic],
• S. agalactiae (human, cattle) – neonatal meningitis and sepsis [Group B, beta hemolytic],
• S. dysgalactiae (human, animals) – endocarditis, bacteremia, pneumonia, meningitis, respiratory infections [Group G],
• S. gallolyticus (human, animals) –urinary tract or biliary infections, endocarditis
• body aches [Group D],
• S. anginosus (human, animals) – subcutaneous/organ abscesses, meningitis, respiratory infections [viridans streptococci group, alpha hemolytic],
• S. sanguinis (human) – endocarditis, dental caries [viridans streptococci group, alpha hemolytic],
• S. mitis (human) – endocarditis [viridans streptococci group, alpha hemolytic],
• S. mutans (human) – dental caries [viridans streptococci group, alpha hemolytic], and
• S. pneumoniae (human) – pneumonia [Alpha hemolytic group].

How can physicians (clinicians) and medical laboratory (clinical microbiologists) help track this genus?
Clinicians and microbiologists evaluating pneumococcal or other streptococcus isolates with the following characteristics should contact their state or local health departments for further assistance:
• Pneumococci with potentially novel features, such as an unusual antibiotic susceptibility profiles, and
• Concern about outbreaks related to pneumococci, streptococci (other than pneumococci), or other catalase-negative, Gram-positive cocci.
The CDC is available to offer epidemiologic assistance to state and local health departments.

Prevention and treatment
A single-dose, 23-valent vaccine to prevent infection by the most common serotypes of S. pneumoniae is available in the United States (see CDC for vaccine recommendations). Antibiotic (chemoprophylaxis) therapy with penicillin for those with rheumatic heart disease from streptococcus may be given monthly (intramuscular) or daily (oral) for lifetime to prevent development of bacterial endocarditis on a damaged heart valve. Penicillin may also be necessary to control outbreaks of S. pyogenes (military, nurseries, households, etc.).

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Norovirus: It’s Not Just on Cruise Ships

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the September 2020 issue of Healthcare Hygiene magazine.

When one reads or hears about the noroviruses (NoV), they likely think about a rough voyage on a cruise ship. Norovirus illness may be called “food poisoning,” “stomach flu,” or “stomach bug.” They are the leading cause of foodborne illness and can be found in healthcare setting outbreaks as well as in community outbreaks. NoV may be referred to as the winter vomiting bug but it is not related to influenza (flu). These viral agents can survive for long periods outside a human host depending on the surface and temperature conditions. Since they are non-enveloped viruses, NoV survive for weeks on hard and soft surfaces. Studies show survival for months and possibly even years in contaminated still water. Typically, they will be viable on surfaces used for food preparation for up to a week after contamination.

NoV are a genetically diverse group of single-stranded positive-sense RNA, non-enveloped viruses belonging to the family Caliciviridae. According to the International Committee on Taxonomy of Viruses, the genus Norovirus has one species: Norwalk virus. Serotypes, strains and isolates include Norwalk virus, Hawaii virus, Snow Mountain virus, Mexico virus, Desert Shield virus, Southampton virus, Lordsdale virus, and Wilkinson virus. Noroviruses are genetically classified into at least seven different genogroups (GI, GII, GIII, GIV, GV, GVI, and GVII), which can be further divided into different genetic clusters or genotypes. GI and GII are responsible for most human acute gastroenteritis and other genogroups are found in bovine and mice.

Unfortunately, one of the hallmark characteristics of NoV is the incredible effectiveness in transmission and infection. Those who are experiencing an illness with this viral agent can shed billions of norovirus particles. It only takes a few virus particles to make other people sick. Vomiting, in particular, transmits infection effectively and appears to allow airborne transmission. Studies have shown that one person can infect up to 14 other people and there are numerous outbreaks involving hundreds (or more) of people especially in close quarters (cruise ships, daycares, schools, etc.).

This organism is notorious for its survival on surfaces in all environments. Here, I will introduce NoV and information aimed at a general understanding of the characteristics of this pathogen in the environment. Primarily, I will utilize information obtained from the Centers for Disease Control and Prevention along with professional experience.

How does this virus spread? This virus spreads easily and efficiently primarily via the fecal – oral route, including the following:
• eat or drink NoV contaminated food or drink,
• touch surfaces or objects contaminated with norovirus then put your fingers in your mouth, or
• have direct contact with someone who is infected with norovirus, such as by caring for them or sharing food or eating utensils with them,
• septic tank leaking at the source (into a well),
• when an infected person vomits or poops in the water,
• improperly treated water sources, such as not enough chlorine,

What are the common symptoms? NoV causes inflammation of the stomach or intestines (acute gastroenteritis). Symptoms usually develop 12 to 48 hours after exposure and resolve within 1 to 3 days. If you have norovirus illness, you can feel extremely ill, and vomit or have diarrhea many times a day. This can lead to dehydration, especially in young children, older adults, and people with other illnesses. Symptoms can include:
• diarrhea
• vomiting
• nausea
• stomach pain
• or less commonly, fever
• headache
• body aches

Can NoV be treated?
Since a virus causes this infection, there is not any specific treatment required if there are no complications such as dehydration. Severe dehydration may require hospitalization for treatment with fluids given through your vein (intravenous or IV fluids). One should watch for signs of dehydration in children who have norovirus illness. Children who are dehydrated may cry with few or no tears and be unusually sleepy or fussy.

What should one do for prevention of this infection?
This virus, and other microbes, may be transmitted to patients because of their persistence on environmental surfaces in the healthcare environment. As I have often mentioned, all #SurfacesMatter all the time to everyone in the war on pathogen transmission. NoV can live for long periods on environmental surfaces and shared equipment when they are not properly cleaned and disinfected. Likewise, the same applies in the community environment.
Practice proper hand hygiene by washing your hands thoroughly with soap and water
• especially after using the toilet or changing diapers,
• always before eating, preparing, or handling food (cook seafood thoroughly), and
• before giving yourself or someone else medicine.

Laboratory diagnosis
This virus (infection) is diagnosed by detecting viral RNA (genetic material) or viral antigen. Diagnostic tests are available at all public health laboratories and many clinical laboratories, and most use reverse transcription- real-time polymerase chain reaction (RT-qPCR) or immunoassays to detect norovirus.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Just What Do You Know About Gonorrhea?

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the August 2020 issue of Healthcare Hygiene magazine.

In the most recent publication of CDC’s Antibiotic Resistance Threats in the United States, 2019 (2019 AR Threats Report) the latest national death and infection estimates underscore the continued threat of antibiotic resistance in the United States. Did you know that there are 2.8 million antibiotic-resistant infections in the U.S. each year, and more than 35,000 people die as a result? While many of us have heard about MRSA and other more common antimicrobial threats, most people do not realize that Neisseria gonorrhoeae belongs to this threat category. This bug causes gonorrhea, a sexually transmitted disease (STD) that can result in life-threatening ectopic pregnancy and infertility, and can increase the risk of getting and giving HIV.

N. gonorrhoeae and Neisseria meningitidis are genetically very closely related human pathogens. The genus Neisseria is composed of 17 species that may be isolated from humans and 6 species that colonize various animals. The Neisseriaceae are a family of Beta Proteobacteria consisting of Gram-negative aerobic bacteria from multiple genera, including Neisseria, Chromobacterium, Kingella, and others. While there are numerous commensals in this genus, N. gonorrhoeae causes gonorrhea, and N. meningitidis is the cause of meningococcal meningitis. N. gonorrhoeae infections have a high prevalence and low mortality, whereas N. meningitidis infections have a low prevalence and high mortality.

Unlike several of my past month’s articles in which I discussed bugs that are typically found in the natural environment, N. gonorrhoeae has no reservoir outside of humans. N. gonorrhoeae also known as gonococcus (singular), or gonococci (plural) is a species of Gram-negative diplococci bacteria isolated by Albert Neisser in 1879. Most members of this genus are fastidious and require nutrient supplementation to be cultured in the laboratory. Neisseria spp. are facultatively intracellular and typically appear in pairs (diplococci) which classically look like coffee beans in a gram stain. They do not form endospores and are capable of twitching motility. They are obligate aerobes (requires oxygen to grow) which must be considered for culture.

How common is gonorrhea?
This disease, unfortunately, is very common. CDC estimates that approximately 1.14 million new gonococcal infections occur in the United States each year and as many as half occur among young people aged 15-24. In 2018, 583,405 cases of gonorrhea were reported to CDC. It is a STD via infection of the mucous membranes of the reproductive tract, including the cervix, uterus, and fallopian tubes in women, and the urethra in women and men. N. gonorrhoeae can also infect the mucous membranes of the mouth, throat, eyes, and rectum. Importantly, a mother can give the infection to her baby as the baby passes through the birth canal during delivery sometimes causing blindness.
How is gonorrhea diagnosed?

This STD bug, historically was diagnosed by traditional microbiology tests, including oxidase positive (possessing cytochrome c oxidase) and catalase positive (able to convert hydrogen peroxide to oxygen) as well as by its ability oxidize only glucose (negative for the other carbohydrates lactose, maltose, and sucrose). However, in today’s microbiology world this drug resistant STD is most commonly rapidly diagnosed by a molecular test.

Urogenital gonorrhea can be diagnosed by testing urine, urethral (for men), or endocervical or vaginal (for women) specimens using nucleic acid amplification testing (NAAT). It can also be diagnosed using gonorrhea culture, which requires endocervical or urethral swab specimens.

If a person has had oral and/or anal sex, pharyngeal and/or rectal swab specimens should be collected either for culture or for NAAT (if the local laboratory has validated the use of NAAT for extra-genital specimens).

What do you need to know about antibiotic resistance?
Gonorrhea has quickly developed resistance to all but one class of antibiotics, and half of all infections are resistant to at least one antibiotic. Tests to detect resistance are not always available at time of treatment. Gonorrhea rapidly develops resistance to antibiotics—ceftriaxone is the last recommended treatment. Gonorrhea spreads easily. Some men and most women are asymptomatic and may not know they are infected, increasing spread. Due to this growing problem, clinicians and patients should seek out information on treatment regimens.

How can gonorrhea be prevented?
• Latex condoms, when used consistently and correctly, can reduce the risk of transmission of gonorrhea
• Abstain from vaginal, anal, and oral sex
• Long-term mutually monogamous relationship with a partner who has been tested and is known to be uninfected

Healthcare providers with STD consultation requests can contact the STD Clinical Consultation Network (STDCCN). This service is provided by the National Network of STD Clinical Prevention Training Centers and operates five days a week. STDCCN is convenient, simple, and free to healthcare providers and clinicians. More information is available at www.stdccn.org

While not traditionally found in the natural environment, we must all continue to work to help fight this antibiotic resistant organism with respect to its overall impact on the growing global antimicrobial resistance threat.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

(Bio)filming in the Environment

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the July 2020 issue of Healthcare Hygiene magazine.

The Pseudomonads include many “true” Pseudomonas species as well as several other genera formerly classified with this group. Over 100 species once made up the genus Pseudomonas but in the past decade or so, many of these have been reclassified into other genera. Like last month’s bug, Acinetobacter, the bacteria found in this group are typically associated as natural residents of soil and water. They rarely cause infections in healthy people. However, there are several groups within the Pseudomonads that can cause medical problems, including the fluorescent Pseudomonas spp., Burkholderia spp., Brevundimonas spp., Stenotrophomonas maltophilia, and other less frequent ones occasionally found in clinical specimens and the hospital environment.

Pseudomonas aeruginosa is the most common infection-causing species and are usually encapsulated, Gram-negative, rod-shaped bacterium that can cause disease in plants and animals, including humans. P. aeruginosa is an opportunistic species especially with existing diseases or conditions – most notably cystic fibrosis (CF) and traumatic burns. It generally affects the immunocompromised but can also infect the immunocompetent as in hot tub folliculitis. Treatment of P. aeruginosa infections can be difficult due to its natural resistance to antibiotics.

This organism is notorious for its survival in all types of man-made and artificial environments. It can live in diverse atmospheres at normal or low oxygen levels. It is most famous for thriving in moist environments and subsequent colonization of surfaces via extensive biofilm production. In cases of human infection, its versatility enables the organism to infect damaged tissues or those with reduced immunity. Inflammation (general) and sepsis are common symptoms.

Colonization in critical body organs, such as the lungs, the urinary tract, and kidneys, can be fatal. CF patients will often deal with life-threatening “blue-green” phlegm from lung infections while burn victims will also exhibit the common pigmented skin infection.

In 2017, multidrug-resistant Pseudomonas aeruginosa caused an estimated 32,600 infections among hospitalized patients and 2,700 estimated deaths in the United States [Source: 2019 AR Threats Report]. Like many of the microbes I have discussed in my column, this one is considered a healthcare-associated infection (HAIs).

Here, I will introduce P. aeruginosa and information aimed at a general understanding of the characteristics of this pathogen in the environment. Primarily, I will utilize information obtained from the Centers for Disease Control and Prevention along with professional experience.

Those most at risk include patients in hospitals, especially those:
• CF patients
• on breathing machines (ventilators)
• with devices such as catheters
• with wounds from surgery or burns are in intensive care units
• premature infants and neutropenic cancer patients
• urinary tract infections (UTI)
• have prolonged hospital stays

Infection can be increased by many factors, including prior antibiotic exposure, ICU admission, use of a central venous catheter, and mechanical ventilation or hemodialysis use. P. aeruginosa can be transmitted to patients because of their persistence on environmental surfaces and because of biofilms on medical devices and equipment. As I have often mentioned, all #SurfacesMatter all the time, to everyone in the war on pathogen transmission. Pseudomonas spp. can live for long periods on environmental surfaces and shared equipment if they are not properly cleaned and disinfected.

Pseudomonas aeruginosa lives in the environment and can be spread to people in healthcare settings when they are exposed to water or soil that is contaminated with these germs. Resistant strains of the germ can also spread in healthcare settings from one person to another through contaminated hands, equipment, or surfaces. Recently, research has shown that this organism (and others) can create problematic, long-standing biofilms in sink drains and other water based environmental areas and surfaces.

Pseudomonas aeruginosa infections are generally treated with antibiotics. Unfortunately, in people exposed to healthcare settings like hospitals or nursing homes, Pseudomonas aeruginosa infections are becoming more difficult to treat because of increasing antibiotic resistance.

Depending on the nature of infection (UTI, soft skin, etc.), an appropriate specimen is collected and sent to a medical laboratory for identification. Typically, a Gram stain is performed, which should show Gram-negative “thin long” rods and/or white blood cells. P. aeruginosa produces colonies with a characteristic "grape-like" or "fresh-tortilla" odor on some growth media. In mixed cultures, it can be isolated as clear colonies on MacConkey agar (as it does not ferment lactose) which will test positive for oxidase. Confirmatory tests include production of the blue-green pigment pyocyanin on cetrimide agar and growth at 42°C. A Triple Sugar Iron slant is often used to distinguish non-fermenting Pseudomonas species from enteric pathogens.

Following identification and to specify the best antibiotic(s) to treat P. aeruginosa infections, the laboratory will perform an antibiotic susceptibility test which allows for growth against a set of antibiotics to determine which are active against the bacteria. The best antibiotic(s) is then chosen based on the activity of the antibiotic and other factors, like potential side effects or interactions with other drugs. For some multidrug-resistant types of Pseudomonas aeruginosa, treatment options might be limited.

How you can avoid getting an infection:
• Hand hygiene from healthcare professionals and patients (and others)
• Wash hands with soap and water or use alcohol-based hand sanitizer, particularly before and after caring for wounds or touching medical devices
• Allow environmental services (housekeeping staff) and healthcare staff to clean their room daily when in a healthcare setting

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Tuberculosis: It Keeps On Keeping On

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the June 2020 issue of Healthcare Hygiene magazine.

Tuberculosis is an ancient disease that infects about a third of our global population, and each year we see almost 9 million new cases. Mycobacterium is a genus of bacteria in the family Mycobacteriaceae with over 190 species. The genus is well known for two notorious species, M. tuberculosis (M. tb) and M. leprae (leprosy), as well as other species causing disease in mammals. Robert Koch, who received the Nobel Prize for his finding in 1905, first described M. tuberculosis, then known as the “tubercle bacillus”, in 1882.

The genus is characterized by an acid-fast, aerobic bacillus with a high cell wall content of high-molecular-weight lipids known as mycolic acid. A Gram stain will not penetrate these organisms due to this waxy mycolic acid, and as a result, they can appear Gram-negative or Gram-positive. Acid-fast stains such as Ziehl-Neelsen, or fluorescent stains such as auramine are used to identify the characteristic thin long curved rods that often exhibit “cording” (rods / bacilli wrapped around each other) morphology under microscopy. M. tuberculosis can be cultured in the laboratory on Middlebrook or Lowenstein Jensen media but they are considered slow growers. These bacteria divide about every 18–24 hours whereas other common bacteria (E. coli) divide about every 20 minutes. Visible colonies require weeks (3 – 8) for growth and can be distinguished from other mycobacteria by production of catalase and niacin. However, more rapid and accurate differentiation is obtained with MALDI-TOF or other molecular platforms.

Humans are the only known reservoir for Mycobacterium tuberculosis [prounounced mī-kō-bak-ˈtir-ē-əm \ too-bur-kyuh-loh-sis]. Historically, this microbe targets the lungs but TB bacteria can attack any part of the body such as the kidney, spine, and brain. It gets its name from the Latin word tuber, which is a botanical term for an underground structure consisting of a solid rounded outgrowth of a stem of a more or less rounded form. The tubercle is a diminutive of tuber and comes from the Latin, tuberculum, or a small swelling. Thus, tuberculosis is the condition of patients exhibiting small, round, firm and white swellings on the surface or within an organ, usually the lungs. Those infected with M. tuberculosis do not always become sick. Therefore, two TB-related conditions exist: latent TB infection (LTBI) and TB disease. Tuberculosis can be fatal if not treated properly.

Many believe that casual contact like shaking hands, touching bed linens or sitting on toilet seats, sharing food or drink, or kissing, can spread M. tuberculosis. However, this agent is an airborne organism originating from a person with TB disease and transmits it by coughing, sneezing, speaking, or singing. When in the lungs, M. tuberculosis is phagocytosed by alveolar macrophages, but they are unable to kill and digest the bacterium (intracellular). Treatment of TB infections has become difficult due to antibiotic resistance. Multidrug-resistant tuberculosis (MDR-TB) indicates resistance to both isoniazid and rifampin. Extensively drug-resistant tuberculosis (XDR-TB) indicates resistance to isoniazid, rifampin, a fluoroquinolone, and a second-line injectable drug.

In 2019, there are 8,920 provisionally reported TB cases in the United States (a rate of 2.7 per 100,000 persons). The complete 2019 TB surveillance data report will be available in late 2020. There are 60 jurisdictions (states, cities, and US territories) in the United States that report TB data to the CDC. It is estimated that up to 13 million people in the United States are living with latent TB infection. Like many of the microbes I have discussed in my column, this one is considered a healthcare-associated infection (HAIs). Here, I will introduce M. tuberculosis and information aimed at a general understanding of the characteristics of this pathogen in the environment. Primarily, I will utilize information obtained from the Centers for Disease Control and Prevention along with professional experience.

What are the common signs and symptoms for TB?
Those with TB disease will show symptoms that align with where in the body the TB bacteria are growing. TB bacteria usually grow in the lungs (pulmonary TB). TB disease in the lungs may cause symptoms such as
• persistent bad coughs (3 weeks or longer)
• chest pains
• coughing up blood or sputum (phlegm from deep inside the lungs)

Other symptoms of TB disease are
• weakness or fatigue
• weight loss
• loss of appetite
• chills / fever
• night sweats

Symptoms of TB disease in other parts of the body depend on the area affected. Those with latent TB do not feel sick, do not have any symptoms, and cannot spread TB to others.

Who is most at risk for these infections? Tuberculosis is an ongoing globally challenging disease to diagnose, treat, and control. While anyone can be infected by this bacteria, those individuals with health disparities and who are part of certain populations should be targeted with prevention and control efforts. These groups include, but are not limited to:
• African-American Community
• Asian Community
• Children under 15 years of age (also called pediatric tuberculosis)
• Correctional Facilities
• Hispanics/Latinos
• Homelessness
• International Travelers
• Pregnancy
• Health Disparities in TB (gender, race or ethnicity, income, comorbid medical conditions, or geographic location may be considered).

Generally, persons at high risk for developing TB disease fall into two categories: 1. Persons recently infected with TB bacteria, and 2. Persons with medical conditions that weaken the immune system (e.g. HIV, drug abuse, Diabetes mellitus, organ transplants, cancer, autoimmune diseases, etc.).

The majority of mycobacteria species are found in the environment across a range of soil types and water distribution systems, which act as a reservoir for potential human and animal infection. Due to its cell wall richness in lipids such as mycolic acid, M. tuberculosis is inherently resistant to desiccation and is a key virulence factor. It can withstand weak disinfectants and survive without moisture for weeks. As I have often mentioned, all #SurfacesMatter all the time, to everyone in the war on pathogen transmission. Mycobacterium spp. can live for long periods on environmental surfaces and shared equipment if they are not properly cleaned and disinfected.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

The Environment Can Be a Dangerous Place

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

Editor's note: This column originally appeared in the May 2020 issue of Healthcare Hygiene magazine.

Comprising about 50 species, Acinetobacter are mostly nonpathogenic environmental organisms. They are common in places like the soil and water. The most common infection-causing species is A. baumannii (pronounced AH-sin-neto-bacter) which is a pleomorphic aerobic gram-negative bacillus. These bacteria cause infections in the blood, urinary tract, and lungs (pneumonia), or in wounds in other parts of the body. It can also “colonize” or live in a patient without causing infections or symptoms, especially in respiratory secretions (sputum) or open wounds.

In 2017, Carbapenem-resistant Acinetobacter baumannii (CRAB) caused an estimated 8,500 infections in hospitalized patients and 700 estimated deaths in the U.S. They constantly find new ways to avoid antibiotics used to treat the infections they cause. Antibiotic resistance occurs when the germs no longer respond to the antibiotics designed to kill them. If they develop resistance to the group of antibiotics called carbapenems, they become carbapenem-resistant. When resistant to multiple antibiotics, they are multidrug-resistant. Carbapenem-resistant Acinetobacter are usually multidrug-resistant. Like last month’s column on Clostridioides difficile (C. diff), CRAB is considered a healthcare associated infections (HAIs).

Which patients are at increased risk for A. baumannii (CRAB)? Acinetobacter infections typically occur in people in healthcare settings. People most at risk include patients in hospitals, especially those who:
• are on breathing machines (ventilators)
• have devices such as catheters
• have open wounds from surgery
• are in intensive care units
• have prolonged hospital stays

Acinetobacter infection can be increased by many factors, including prior antibiotic exposure, ICU admission, use of a central venous catheter, and mechanical ventilation or hemodialysis use. Acinetobacter species can be transmitted to patients because of their persistence on environmental surfaces and because of colonization of the hands of healthcare workers. As I have often mentioned, all #SurfacesMatter all the time, to everyone in the war on pathogen transmission. Acinetobacter can live for long periods on environmental surfaces and shared equipment if they are not properly cleaned and disinfected.

Where is this microbe found? Are there special environmental niches for it?
A. baumannii is an aquatic organism and preferentially colonizes those environments. This organism is often cultured from hospitalized patients' sputum or respiratory secretions, wounds, and urine. In a hospital setting, Acinetobacter commonly colonizes irrigating solutions and intravenous solutions.
When these infections occur, they usually involve (multi-) organ systems with a high fluid content (e.g., urinary tract, respiratory tract, peritoneal fluid, CSF, etc.). Outbreaks from these infections are more often than isolated cases of nosocomial pneumonia. Infections may complicate continuous ambulatory peritoneal dialysis (CAPD) or cause catheter-associated bacteriuria.

What are the differences between colonization and infection?
Acinetobacter species tend to be of low virulence but capable of causing infection in organ transplants and febrile neutropenia. Most isolates recovered from hospitalized patients, particularly those recovered from respiratory secretions and urine, represent colonization rather than infection. Thus, one must exercise caution in determining whether the isolate is due to colonization or is a true infection. As an example, Acinetobacter isolated from the sputum of a ventilated patient is more likely to represent colonization than infection in the absence of fever, leukocytosis, increased respiratory secretions, need for additional respiratory support, or a new abnormality on chest imaging. The difference is critical for proper antibiotic stewardship.

Which laboratory tests are commonly used for diagnosis?
To identify the best antibiotic to treat a specific infection, healthcare providers will send a specimen to the medical laboratory for a typical culture workup and test any bacteria that grow against a set of antibiotics (antibiotic susceptibility test) to determine which are active against the microbe.

How can you avoid getting an infection?
• Hand hygiene: healthcare professionals and patients (and others) must keep their hands clean to avoid getting sick and spreading germs that can cause infections
• Wash hands with soap and water or use alcohol-based hand sanitizer, particularly before and after caring for wounds or touching medical devices
• Remind healthcare providers and caregivers to clean their hands before touching the patient or handling medical devices
• Allow environmental services (housekeeping staff) and healthcare staff to clean their room daily when in a healthcare setting

In addition to hand hygiene, healthcare providers should pay careful attention to recommended infection control practices, including rigorous environmental cleaning (e.g., cleaning of patient rooms and shared equipment), to reduce the risk of spreading these germs to patient. As a final reminder, environmental services professionals (and others who have responsibility for cleaning / disinfection) are the secret weapon in proactive prevention of antibiotic resistant and other pathogen transmission.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Exactly What is Clostridioides difficile (C. diff)?

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the April 2020 issue of Healthcare Hygiene magazine.

Clostridioides difficile (C. diff) is a bacterium that can cause symptoms ranging from diarrhea to life-threatening inflammation of the colon. It is a spore forming, Gram-positive anaerobic (does not prefer oxygen rich environments) bacillus that produces two exotoxins: toxin A and toxin B. Illness from C. diff. commonly affects the elderly in hospitals or long-term care facilities and typically occurs after use of antibiotics. However, studies show increasing rates of C. diff. infection among people traditionally not considered to be at high risk, such as young and healthy individuals who haven't used antibiotics or been in a health care facility. Generally, C. diff. considered a healthcare-associated infection (HAI).

Each year in the U.S., about a half million people get sick from C. diff., and in recent years, these infections have become more frequent, severe and difficult to treat. Recurrent C. diff. infections also are on the rise. It is a common cause of antibiotic-associated diarrhea (AAD). It accounts for 15 percent to 25 percent of all episodes of AAD. The range of diseases caused by this bacterium is known as C. diff. Infection (CDI).

In my personal experience of discussing HAIs, antibiotic resistant pathogens, and other microbes that are transmitted in the healthcare or community setting, I often try to put myself in the place of an individual that little experience or understanding of these pathogens. Effective science communication, and ultimately raising the health literacy of the public, is everyone’s job in healthcare.

Here, I will introduce C. diff. and information aimed at a general understanding of the characteristics of this pathogen in the environment. Primarily, I will utilize information obtained from the Centers for Disease Control and Prevention (CDC), along with professional experience.

Which patients are at increased risk for CDI? The risk for disease increases in patients with:
• antibiotic exposure (e.g., fluoroquinolones, third/fourth generation cephalosporins, clindamycin, carbapenems)
• gastrointestinal surgery/manipulation
• long length of stay in healthcare settings
• a serious underlying illness
• immunocompromising conditions
• advanced age
• other possible causes include Proton pump inhibitors, H2-blockers

Where is C. diff. found and what are the causes of CDI?
C. diff. bacteria are ubiquitous in the environment — in soil, air, water, human and animal feces, and food products, such as processed meats. A small number of healthy people naturally carry the bacteria (colonized) in their large intestines and do not have ill effects from the infection.

Spores from C. diff. are passed in feces and spread all over the environment (food, surfaces and objects) when people who are infected do not wash their hands thoroughly. Spores are primarily a way for bacteria to survive in harsh times or conditions. They persist for weeks or months. If you touch a surface contaminated with C. diff. spores, you may not realize you’ve swallowed the spore which can then become a viable bacteria.

Once established, C. difficile can produce toxins that attack the lining of the intestine. The toxins destroy cells, produce patches (plaques) of inflammatory cells and decaying cellular debris inside the colon, and cause watery diarrhea.

What are the differences between colonization and infection?
Colonization is more common than CDI. The patient exhibits no clinical symptoms (asymptomatic) but does test positive for the C. diff. organism or its toxin. With infection, the patient exhibits clinical symptoms and tests positive for the C. diff. organism or its toxin. The difference is critical with respect to understanding when an individual should be considered positive for CDI (confirmatory medical laboratory test AND clinical symptoms).

Which laboratory tests are commonly used for diagnosis?
Most people are not experts in the world (or language) of medical laboratory tests. The following is a list of common tests that are often utilized in a medical or public health laboratory to identify C. diff. and many pathogens. If you do not understand a test, ALWAYS ask for clarification. This will increase your health literacy.
• Molecular tests: FDA-approved PCR assays, which test for the gene encoding toxin B, are same-day tests that are highly sensitive and specific for presence toxin-producing C. diff.
• Antigen detection for C. diff: Rapid tests (<1 hour) that detect the presence of C. diff. antigen. Nonspecific and often used in combination with other tests.
• Toxin testing for C. diff:
o Tissue culture cytotoxicity assay detects toxin B only.
o Enzyme immunoassay detects toxin A, toxin B, or both A and B. Due to concerns over toxin A-negative, B-positive strains causing disease, most laboratories employ a toxin B-only or A and B assay.
o C. diff. toxin is unstable. The toxin degrades at room temperature and might be undetectable within two hours after collection of a stool specimen. False-negative results occur when specimens are not promptly tested or kept refrigerated.
• Stool culture for C. diff: Most sensitive test available, but it is often associated with false-positive results due to the presence of nontoxigenic C. diff. strains.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Uncovering the Novel Coronavirus

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

Editor's note: This column originally appeared in the March 2020 issue of Healthcare Hygiene magazine.

Novel outbreaks from any microbe are always of public health concern. The risk from these outbreaks depends on characteristics of the virus, including whether and how well it spreads between people, the severity of resulting illness, and the medical or other measures available to control the impact of the virus (e.g., vaccine or antivirals).

The novel coronavirus (SARS CoV2/COVID-19) is a serious public health threat. The fact that it has caused severe illness and sustained person-to-person spread in China is concerning, but it is unclear how the situation in other parts of the world will unfold.

With the growing concern over COVID-19, exactly what questions should healthcare professionals and others (EVS, medical laboratory, etc.) be asking.
1. How does SARS CoV2 spread? While there is much to learn regarding the transmission of this novel virus, spread is thought to occur from person-to-person via respiratory droplets among close contacts. Close contact can occur while caring for a patient, including:
• Being within 6 feet (2 meters) of a patient with COVID-19 for prolonged time periods.
• Direct contact with infectious secretions from a patient with 2019-nCoV. Infectious secretions may include sputum, serum, blood, and respiratory droplets.
If close contact occurs while not wearing all recommended PPE, there may be risk of infection.

2. How long (duration) can 2019-nCoV survive outside of a host? All viruses require a host to reproduce and survive. It is currently unclear if a person can get SARS CoV2 by touching a surface or object with virus on it and then touching his or her own mouth, nose, or their eyes. Some reports show coronavirus strains (229E) have survived more than three hours after drying onto porous and non-porous materials, including aluminum and sterile sponges; strain OC43 remained infectious up to one hour. Thus, it is prudent to remain vigilant in both the use of PPE and disinfection of surfaces in the control of SARS CoV2.

3. How can healthcare personnel (and other related professionals) protect themselves? According to the CDC, healthcare personnel caring for patients with confirmed or possible COVID-19 should adhere to CDC recommendations for infection prevention and control (IPC):
• Assess and triage patients with acute respiratory symptoms and risk factors to minimize chances of exposure, including use of facemasks on the patient and isolating them in an Airborne Infection Isolation Room (AIIR), if available.
• Use Standard Precautions, Contact Precautions, and Airborne Precautions and eye protection when caring for patients.
• Perform hand hygiene with alcohol-based handrub before and after all patient contact, contact with potentially infectious material, and before putting on and upon removal of personal protective equipment (PPE), including gloves.
• Practice proper use PPE in a manner to prevent self-contamination.
• Perform aerosol-generating procedures, including collection of diagnostic respiratory specimens, in an AIIR, while following IPC practices, including use of appropriate PPE.

4. What about environmental cleaning and disinfection? CDC states routine cleaning and disinfection procedures are appropriate for COVID-19 in healthcare settings. Products with EPA-approved emerging viral pathogens claims are recommended. Management of laundry, food service utensils, and medical waste should be performed in accordance with routine procedures.

5. What do we currently know about the human-to-human transmission of this novel coronavirus? More specifically, once one person is infected, does the coronavirus appear to be significantly contagious in a human-to-human context? The modes of human-to-human transmission of the virus are still being determined, but given current evidence, it is most likely spread by the following, according to the CDC.
• Through the air by coughing and sneezing
• Close personal contact, such as touching or shaking hands
• Touching an object or surface with the virus on it, then touching your mouth, nose or eyes before washing your hands
• In rare cases, fecal contamination

With current data available and my professional experience, I do not believe this novel virus is any more contagious than the influenza virus. At this time, both appear to have similar transmission rates (1.4 – 4) and case fatality rates (currently holding steady at about 2 percent). Of course, this could change, and it is why we must monitor the outbreak closely and rely on “confirmed and accurate” laboratory test results.

Everyone should pay attention to reputable sources and heed the advice of the government and public health experts. The U.S. Department of State has issued a level 4 “do not travel” advisory for China. Proper perspective is critical. There is no need to panic. We should all do our part in not becoming part of the problem as a “super-spreader” of inaccurate or unchecked information surrounding this virus outbreak.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Walking Through the Microscopic Valley of Death

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the February 2020 issue of Healthcare Hygiene magazine.

Have you ever stopped and thought about how fortunate we are to live during this time? I am talking about the advancement of healthcare in general and medical procedures/devices in particular. Take a moment to consider how an artificial hip or knee may have changed a loved one’s life. What about the diagnostic medical devices utilized for visualizing possible life-threatening conditions or disease? Truly, I think we all probably take these wonders of medical science for granted.

Globally, medical devices have prolonged our lives, as well as improved the quality of life for millions. Most of us probably think of replacement knees and hips, vascular stents and pacemakers as representative of these engineering marvels. Endoscopes and catheters, used for diagnostic and therapeutic procedures, are categorized as medical devices too since they are placed into the body and retain their original form. To clarify, a needle that is inserted into the body is classed as a medical device, but the solution injected through that needle is specifically classified as a pharmaceutical. Given that medical devices enter the body, the need to be free of contamination is paramount for patient safety.

Berkshire Corporation via U.S. Food and Drug Administration (FDA) guidelines explain contaminants and their removal well. Prior to the introduction of the device into the body (whether temporarily for diagnostic purposes or permanently for therapeutic purposes), we want it to be as free of contaminants as possible. Medical device contaminants can include traces of lubricants, oils, and other processing residues (e.g. polymers, adhesives), viables (microorganisms), and non-viables, such as particles and fibers. In the manufacturing process, medical devices are packaged and then terminally sterilized as the last step. The sterilization procedure does not remove contaminants; it only ensures that any viables left on the device cannot proliferate further–any residual surface contamination left on the device before sterilization remains after the process and can pose a risk to patient safety. Fortunately, simple wiping techniques employed with proper wipers and solvents prior to packaging and sterilization can produce a clean medical device.

The FDA Center for Devices and Radiological Health (CDRH) Microbiology and Infection Control states that with the increased use of medical devices and their promise to improve quality of life, preventing device-associated infection is a top public health priority. Every medical device is prone to microbial colonization and biofilm formation, resulting inevitably in device failure and patient harm. In addition, the association of colonized devices with development of drug resistant organisms is a serious and under-investigated area of importance. The Medical Device Biofouling and Biofilms Research Program addresses medical-device failure and patient harm caused by the combined effects of biofouling, colonization, and biofilms. Rather than study these phenomena as individual events, the research uses sophisticated high-throughput microfluidic approaches to assess how variables such as biofouling, cleaning and material properties affect bacterial adhesion and biofilm progression. The group uses optical and electron microscopy, surface plasmon resonance (SPR), and other biosensing and surface analysis methods to study biomolecular interactions at the interface of device, host and microorganism. In laymen’s terms, this group is trying to determine the best way(s) to understand not only what invisible inhabitants are found in the microscopic valley of death (aka surfaces), but how to best remove (clean and sterilize) them.

Some of the current research areas addressed include:
• Bacterial interactions with soft medical device materials (contact lenses, dermal fillers, ophthalmic surgical devices
• Development of better test methods and endpoint measurements for antimicrobial device technologies (wound dressings, catheters)
• Biofilm specific diagnostics (optical coherence tomography, biomarkers)
• Detection of biofouling and biofilm on reprocessed devices (endoscopes, surgical tools)
• Influence of material, device design, roughness, and presence of soil on cleanability
• Performance testing of one-way valves Intended to prevent cross-contamination and infections in patients
• Reprocessing flexible endoscopes
• Chemically defined clinically relevant test soils for cleaning validation of reusable medical devices

While medical advances and devices have advanced the health of civilization in ways we never fathomed, let us not forget that the microorganisms have outpaced human advancement every step of the way, including finding ways to survive the microscopic valley and surfaces of arguably every niche known.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

A Microbial Home for the Holidays?

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column originally appeared in the January 2020 issue of Healthcare Hygiene magazine.

The holidays are a time for family and friends to get together and share memories. These times often include visits to see grandparents and others in a variety of settings, whether it is the home or a long-term care or assisted living facility. Likewise, as we approach 2020, we often surround ourselves with not only loved ones, but others that have traveled from across a vast geographic landscape. These gatherings are full of wonderful times of reconnecting, sharing food and drink, and visits with old and new acquaintances.

The holidays are an amazing time and we should all enjoy them to the fullest. However, there is a bit of a dark side to holiday season. Our own microbial population also comes along with us and/or we encounter new microbial visitors in our travels. Exposure to more people than usual can increase our chances of becoming ill. So, during this holiday season, spending some time to take extra precautions may help keep you from catching someone else’s illness or if you are ill, preventing the spread to others.

One thing we do not want to give or receive during the holidays is an infection. One of the major concerns during the holiday season in North America is how this time of the year coincides with cold and flu season. Everyone catches a cold (usually a rhinovirus) from time to time and, for most people, a cold causes a week or so of feeling miserable: stuffy nose, headache, cough, and more, and then it goes away. The cough associated with a cold can last for a while longer, sometimes weeks if it is a particularly nasty one. However, some people can become seriously ill if they catch a cold. The virus can make them vulnerable to developing other illnesses, like bronchitis or even pneumonia, particularly among the very old, very young, or those who have weakened immune systems or chronic illnesses. Pneumonia is the most common cause of sepsis and septic shock, according to the American Thoracic Society.

Influenza is another easily spread virus in close quarters. The flu is not a gastrointestinal illness; there is no such thing as the stomach flu. Influenza is a serious respiratory infection. According to the Centers for Disease Control and Prevention (CDC), depending on the flu season, between 9.3 million and 49 million people in the U.S. are affected annually, with 140,000 and 960,000 flu-related hospitalizations, and up to 79,000 deaths each year. Grandparents visiting their grandchildren could be particularly at risk. Children are "super-spreaders" of flu and the over-65s are one of the "at-risk" groups that can develop health complications, such as pneumonia, if they catch it.

To make matters worse, the flu virus can live on surfaces (doorknobs and tables) — and potentially infect people — for 48 hours, according to the CDC. This serves as an important reminder that all surfaces matter in the war on healthcare associated infections (HAIs) and pathogen transmission. Remember, a home or community environment can serve as a reservoir too for any pathogen or antimicrobial resistant microbe such as respiratory syncytial virus (RSV), parainfluenza (croup), or even pertussis (whooping cough) to name a few others.

Flu may spread to others up to 6 feet away. Droplets can land in the mouths or noses of people who are nearby or inhaled into the lungs. Less often, a person may touch a surface contaminated with the flu virus, and then touch their mouth, nose or eyes. Someone with the flu is most contagious for the first three to four days after becoming sick. However, adults can infect others a day before symptoms are apparent and up to five to seven days after becoming sick. Young children and people with weakened immune systems are contagious for longer.

Gastroenteritis (GE) is another illness often mistakenly referred to as a “stomach flu.” GE occurs when a microbe infection irritates and inflames the gastrointestinal lining, resulting in nausea, vomiting, cramping, stomach pain, fever, and diarrhea. The infection spreads either through direct contact with someone who is already ill, through touching objects that have the bacteria or virus on it, or through contaminated food or drink. Because of the many ways it spreads, it is particularly important to be vigilant when you are at a large gathering.

To avoid giving or receiving these unwanted microbial “gifts,” one can do several things for prevention:
• Wash your hands and properly discard of tissues, etc.
• Ensure that cold food is kept cold and hot food hot.
• Get the seasonal flu vaccine (and other recommended vaccines).
• Stay away from gatherings if you are ill.
• Avoid others who are ill.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

KPC: The Beginning of the End?

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column, Under the Microscope, originally appeared in the November 2019 issue of Healthcare Hygiene magazine.

First appearing in the United States in the late 1990s, Klebsiella pneumoniae carbapenemase (KPCs)-producing bacteria have spread rapidly across hospitals and long-term care facilities in many countries. KPC-producing K. pneumoniae is by far the most commonly encountered carbapenem-resistant Enterobacteriaceae (CRE) species.

KPC-producing bacteria are a group of emerging highly drug-resistant Gram-negative bacilli causing infections associated with significant morbidity and mortality. With the rapid increase of infections caused by this microbe, they are now referred collectively as carbapenemase-producing Enterobacteriaceae (CPE) but one may see different acronyms – E. coli and K. pneumoniae are the primary pathogens. The type of carbapenemase enzyme detected in carbapenemase-producing Enterobacteriaceae isolates (e.g. KPC, Metallo-beta-lactamases [MBL], carbapenem-hydrolysing oxacillinase-48 [OXA-48], etc.) is a complex discussion that will not be the focus of this article. As Ambretti, et al. (2019) state, the relationship between CRE and CPE is one of broad but not complete overlapping, since most but not all CRE are CPE and vice versa. In fact, some CRE are not CPE and some CPE are not. However, these differences are important to understand with respect to diagnostics, treatment, prevention, and epidemiology.

Enterobacteriaceae, namely Escherichia coli and Klebsiella pneumoniae, are the most common human pathogens, causing infections that range from cystitis to pyelonephritis, septicemia, pneumonia, peritonitis and meningitis. The other Enterobacteriaceae causing infections in humans include Citrobacter species, Enterobacter species, Serratia marcescens, Proteus spp., and Providencia spp. These organisms persist and spread rapidly in healthcare settings by hand carriage as well as contaminated food and water. In common language, they are Enterics (gut-associated bacteria) and can be found virtually everyone, on every surface in a healthcare and community environment.

Several factors increase the risk of colonization and infection with CPE. Risk factors for CPE infection include severe underlying illness, prolonged hospital stay, the presence of invasive medical devices, and antibiotic use.

CPE infections are difficult to treat, since CPE are resistant to virtually all beta-lactam antibiotics and often contain additional mechanisms of resistance against second-line antibiotics such as aminoglycoside and fluoroquinolones. Studies have also shown emerging resistance to antibiotics of last resort (i.e., tigecycline or colistin), leaving very few therapeutic options. Certainly, we know selective pressure from colistin use is a major factor that drives resistance to this agent, as has also been shown for colistin resistance in other pathogens. It is not surprising with the surge of colistin use for CPE in hospitals during the global transmission of the agent.

Colistin resistance can emerge rather quickly once KPC-producing K. pneumoniae is utilized in healthcare and/or long-term care environments, and colistin is used to treat. Then, colistin-resistant, KPC-producing K. pneumoniae may directly colonize or infect patients who are not colonized with the colistin-susceptible counterparts, at least in the setting of ongoing selective pressure from high-level colistin use. This leads us to another set of questions. If susceptibility to colistin cannot be assumed, should clinical microbiology laboratories consider performing susceptibility testing of the isolates for colistin for all patients who receive this agent, instead of just those who are colistin experienced? In addition, from an infection prevention perspective, should patients colonized or infected with colistin-resistant strains be grouped (or isolated) from patients with colistin-susceptible strains?

CPE have been associated with adverse clinical and economic outcomes, including increased mortality, increased length of stay, delay in the institution of effective therapy, decreased functional status on discharge, and increased cost of health care. It is imperative that risk factors for infection with these organisms are clearly identified so that effective strategies can be developed to curtail the emergence and spread of these strains.

CPE and other resistant pathogens continually beg the question – have we reached the post-antibiotic era? CPE have developed the ability to become resistant to last-resort powerful antimicrobials known as carbapenems, which makes them more challenging to treat if they go on to cause infection. CPE are bacteria that are carried in the gut and are resistant to most, and sometimes all, available antibiotics.

CPE is shed in feces and transmitted by direct and indirect contact. A period of four weeks or more may elapse between that contact that results in acquisition of the organism and the time at which CPE becomes detectable in the sample. If CPE stays in the gut, it is mostly harmless. However, if it spreads to the urine or blood it can be fatal.  And, for those of us who know about contamination and environmental surfaces in healthcare, this becomes especially concerning. It has been reported that more than half of all patients who develop blood stream infections with CPE die because of their infection. Many believe that of all the superbugs seen, CPE is the hardest to kill. Is this the end for antibiotics?

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

HAIs: Everything Changes When It Happens to You

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column, Under the Microscope, originally appeared in the November 2019 issue of Healthcare Hygiene magazine.

The Centers for Disease Control and Prevention (CDC) estimates that on any given day, 1 in 25 hospital patients get a healthcare-acquired infection (HAI). Research suggests that a growing number of HAIs are caused by pathogens that are outsmarting the antimicrobials typically used to fight them. These are known as antibiotic resistant germs, sometimes referred to as superbugs.

HAI and antimicrobial resistance (AMR), in my professional opinion, is one of the most critical public health and healthcare issues of the 21st century. They have devastating effects on physical, mental/emotional, and financial health. In addition, they cost billions of dollars in added expenses to the healthcare system. The World Health Organization (WHO) predicts that by 2050, AMR will have a $100 trillion economic impact globally as a mortality of 10 million people. If one does the math, this means that approximately one new AMR infection will occur every three seconds! At this pace, AMR/HAIs will surpass cancer as the No. 1 killer by 2050.

When I answered the phone at home one evening in late December 2007 and heard the voice of a worried woman, the genesis of an idea for my future research path began to take shape. She was concerned about her husband, she said. The retired Utah couple had traveled over the holidays and the husband, a cancer patient, developed sores on his torso. They went to the emergency room, where a doctor diagnosed a staph infection and prescribed antibiotics but ordered no lab tests. The man’s condition worsened, so he went to his family doctor. After an examination and some laboratory tests, the doctor determined that the man had methicillin-resistant Staphylococcus aureus (MRSA) — an infection that cannot be treated with most typical antibiotics. Studies show that about 1 in 3 (33 percent) people carry S. aureus bacteria in their nose, usually without any illness and approximately 5 percent of patients in U.S. hospitals carry MRSA in their nose or on their skin.

I remember it like yesterday – such a vivid reminder of the confusion, concern, and plight of these individuals dealing with such a difficult healthcare problem. The wife of the patient from Utah had some basic knowledge about MRSA from media coverage and she was very concerned about what had happened to her husband at the emergency room given his immunocompromised state because of the cancer. She just wanted to know why this had happened and whether she or anyone else they had been in contact with should be concerned about transmission.

MRSA first emerged as a serious infectious threat in the late 1960s as the bacterium developed resistance to penicillin. Vancomycin has been used as treatment for MRSA, but now even vancomycin-resistant strains are emerging. Although the Staphylococci bacteria, including MRSA, commonly colonize the skin of healthy people, often posing little to no threat, these bugs are quick to exploit any opportunity to invade wounds, nasal passageways, or mucosal membranes where they can rapidly produce infections that can become life threatening.

Fortunately, we are doing better in the war on HAIs. Progress in the latest report is based on information from the National Healthcare Safety Network (NHSN) on central line-associated bloodstream infections (CLABSIs), catheter-associated urinary tract infections (CAUTIs), ventilator-associated events (VAEs), surgical site infections (SSIs), methicillin-resistant Staphylococcus aureus (MRSA) bloodstream infections, and Clostridioides difficile events. Nationally, among acute-care hospitals between 2016 and 2017, report highlights include:

  • About 9% decrease in CLABSIs
  • About 5% decrease in CAUTIs
  • About 3% decrease in VAEs
  • No significant changes in abdominal hysterectomy SSIs
  • No significant changes in colon surgery SSIs
  • About 8% decrease in MRSA bacteremia
  • About 13% decrease in C. difficile infections

Concerning HAIs like MRSA, I feel particularly dedicated because of my interaction with the people I’ve interviewed and advised (including my family and friends). It is with this knowledge that I often tell my students (future medical laboratorians and nurses), family, and public that if you do nothing else when a physician or other healthcare worker prescribes you an antibiotic empirically or tells you it’s “just a regular staph infection,” be sure to demand a culture/ID and antibiotic susceptibility test. It just may save your life or that of a loved one.

We can and must be better. If not, we all fail. We fail ourselves. We fail each other. And, we especially fail those patients who need our voice and advocacy – even those who don’t know what questions to ask!

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. Follow him on Twitter @RodneyRohde / @TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

Sitting at the Intersection of Microbes and Surfaces

By Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc

This column, Under the Microscope, originally appeared in the October 2019 issue of Healthcare Hygiene magazine.

It is my honor to join Healthcare Hygiene magazine as the expert columnist for “Under the Microscope.” In the coming months, this column will explore the imperatives relating to microbiology and its importance and application in the real-world healthcare environment, especially as it relates to surfaces, and the roles they play in pathogen transfer. I will also feature a monthly microbe on the growing list of deadly antimicrobial resistant microbes.

This past week, I received my weekly phone call from my parents. My dad is a retired railroad conductor who is from the #GreatestGeneration. He is one of the strongest people I know. My brother, sister and I grew up hearing him often say to us, “I don’t have time to be sick,” as he headed out on another train trip. Like many of us, our parents are our heroes.

We think of them as being invincible – until they are not.

Being a railroad conductor was a great career for my father. In my hometown of Smithville, Texas, most men wanted the job because it provided a strong and steady income for a family. It allowed my mom to be a stay at home mother who raised the three of us – also a full-time job! A railroad conductor is the boss of the train, not the engineer. Dad worked when there was still a caboose at the back of the train and I still remember the vivid stories of him telling us about “jumping on and off” of the caboose to walk the train for inspection. Unfortunately, those long walks past hundreds of railway cars meant that he was often walking at odd angles in hard rock. Well, thirty plus years of doing that wore out his knees and his ankles.

Finally, it became too much to bear and he received a medical retirement in his late 50s. A great career, yet, one that took a terrible toll on his body. Last night, dad called to let me know that one of his feet had been bothering him again. What started as a small “corn” on one of his feet opened up and started draining blood. For my father, he knows what this means, as he has had one knee replacement and multiple surgeries on both ankles to fuse bones with screws and pins.

He has now become my student with respect to trying to understand what the difference is between “regular staph infections versus #MRSA.” Dad has been in and out of the hospital the past several years receiving everything from incision and drainage procedures to full-blown surgery to remove an infected toe, tissue and bone. Likewise, he has become all too familiar with oral versus IV antibiotics from multiple classes of antimicrobials. Finally, he and mom have had long discussions with me about infection control and prevention in the healthcare and home/community setting because all #SurfacesMatter in the new post-antibiotic world of #superbugs and #antibioticresistance (#amr). It saddens me to see the confusion and sometimes surrender on their faces due to “another infection.”

While I cannot prove it, my professional opinion as an infectious disease microbiologist and medical laboratory professional leads me to believe that his problems started with the various metal components inserted into my dad’s knee and/or feet years ago – you see, ALL surfaces matter ALL the time.

Staphylococcus skin infections and the emergence of methicillin-resistant Staphylococcus aureus (MRSA) are a major health concern. Staphylococcus aureus and other species are typical normal flora for human skin. For the average person, this means that you have bacteria growing on your body and it is normal. That is what normal flora means. It grows on/in you and often can be a symbiotic (healthy) relationship. However, complications can arise if the bacteria enter the host through breaks in the skin. Whether exposure leads to infection depends on several factors: bacterial virulence; overall host status; amount of exposure or infectious dose; and the time of exposure as longer exposures increase the chance that bacteria will gain entry. Should entry occur and the host's immune system overwhelmed, symptoms can range from a minor skin infection to serious systemic infection. In some cases, severe infection can result in death.

MRSA first emerged as a serious infectious threat in the late 1960s as the bacterium developed resistance to the synthetic form of penicillin known as methicillin. In fact, even the discoverer of the miracle drug penicillin in 1928, Alexander Fleming, observed resistance to his wonder drug and warned society in the 20th century. Unfortunately, we did not listen.

Although the Staphylococci bacteria, including MRSA, commonly colonize the skin of healthy people, often posing little to no threat, these bugs are quick to exploit any opportunity to invade wounds, nasal passageways, or mucosal membranes where they can rapidly produce infections that can become life threatening. It is not surprising then, that MRSA has been the focus of intense scientific and political interest around the world and has frequently been labeled as a superbug in the popular media.

This tiny, microscopic organism is just one of many that have become resistant to commonly prescribed antibiotics. It can also remain viable for extended periods of time on different surfaces in the community and healthcare environment.
A perfect storm waiting for its next unaware victim, like my dad.

Join me in the coming months as I begin to show you what’s behind the curtain and Under the Microscope with respect to these deadly and often hidden microbes that can take a terrible toll on us and our loved ones.

Rodney E. Rohde, PhD, MS, SM(ASCP)CM SVCM, MBCM, FACSc, serves as chair and professor of the Clinical Laboratory Science Program at Texas State; associate director for the Translational Health Research Initiative; as well as associate dean for research in the College of Health Professions. He also is a member of the board of directors of the Healthcare Surfaces Institute. Follow him on Twitter @RodneyRohde /@TXST_CLS, or on his website: http://rodneyerohde.wp.txstate.edu/

The following article is from the October 2019 issue of Healthcare Hygiene magazine.

Candida auris: A Stealth Enemy With Environmental Persistence

By Kelly M. Pyrek

Public health entities such as the Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) have compiled lists of the problem pathogens that continue to represent some of the greatest challenges to infection prevention and control (IPC) efforts. Rising on that list is Candida auris, an emerging worldwide public health scourge that is growing in intensity as a healthcare-acquired organism. It is particularly fearsome because of its innate resistance to multiple anti-fungal drugs and its resilience in the face of traditional hygiene measures.

In contrast to other Candida species, C. auris is transmitted easily in the healthcare setting, and it is demonstrating the ability to persist both in the human host and on inanimate surfaces.
“Candida auris is an emerging fungus and one of the headaches with this species is it’s multidrug-resistant, meaning that it is resistant to multiple antifungal drugs commonly used to treat Candida infections,” confirms Rodney E. Rohde, PhD, MS, professor and chair of the Clinical Laboratory Science Program at Texas State University.

C. auris is also transcending traditional classification.

“Infection prevention experts tend to want to group pathogens into groups such as healthcare-acquired or community-acquired but when it comes to resistant organisms you really can't use those terms anymore,” Rohde says. “For instance, in some of the studies I have conducted with different organisms, what we used to think was only in the community, we see those strains or genotypes showing up in healthcare patients, and vice versa. So, even though microbiology and science tells us certain species are strictly found in the healthcare setting or strictly found in the community setting, in reality, it’s more of a global presence now due to so many vehicles and vectors that move in and out of healthcare settings.”

Rohde continues, “When we talk healthcare settings, we tend to only think hospitals, but we must think long-term care, outpatient and dialysis centers, clinics, and school and university health centers. I think it’s a communication problem; as scientists, we love to put things into pots and think we’ve described them adequately, and they are going to stay that way, but one of my favorite sayings is, organisms do not read the book of rules we’ve written for them. However, we teach it that way sometimes to try to make sense of it, but when you get into the real-world trenches, the truth is, we’re not able to do that. Organisms are crossing all boundaries.”

C. auris is insidious and still greatly unknown to hospitals and healthcare systems, much like the early days of Clostridium difficile. Experts are tending to agree that C. auris has operated under the radar. Rhodes and Fisher (2019) say that “Since its discovery, C. auris has caused a ‘stealthy pandemic,’ emerging across the globe and is now recorded in all continents except Antarctica. However, C. auris is thought to have been misidentified as C. haemulonii on several occasions, suggesting that C. auris has likely been circulating as a human pathogen before 2009.”

Candida auris as a newly recognized cause of fungal infection is catching healthcare professionals unawares, despite cases being reported for nearly a decade now. Since the first official isolation of Candida auris in 2009, scientific community has witnessed an exponential emergence of infection episodes and outbreaks in different world regions. According to the CDC as of June 30, 2019 (the most recent data available), there are 725 confirmed cases, plus an additional 1,474 patients have been found to be colonized with C. auris by targeted screening in 10 states with clinical cases.

“Candida, as a fungus, is an unusual and a difficult problem to deal with,” Rohde says. “It’s not typically something you would be looking for in a healthcare setting, and certainly not looking for it in the common population. But it is a factor when looking at the immunocompromised population in context of environmental and healthcare exposure; for example, could a patient have been working in a certain environment where fungi and yeast are present? But to have a fungus emerging and breeding in a healthcare setting is a novel challenge in our lifetime. So, I think we are trying to grasp what that means.”

He continues, “Microbiologists are very concerned about C. auris because you almost have to rethink everything from the laboratory perspective. If you are a clinician in a smaller facility or a rural hospital, you often must wait on sending specimens out to an off-site, more central clinical laboratory, and that eats up valuable diagnostic time. You can typically know pretty quickly if you have Staph or Klebsiella or any of these other multi-resistant organisms if you have access to rapid assays; but yeast and fungi are not typically, at least right now, on the radar for panel testing. Fortunately, it’s starting to get there, obviously, but if you don’t have a trained medical laboratory professional on staff who can look under a microscope or conduct some type of test to rule out yeast -- you could have some slippage with respect to turnaround time on a diagnosis, so there’s a significant challenge.”

Kenters, et al. (2019) confirms that C. auris is a budding yeast that forms white, pink, or purple colonies on CHROMagar and can be difficult to distinguish from C. glabrata: “Some strains form aggregates of cells while others do not. In contrast to most other Candida species, it grows well at higher temperature (40-42° C) … First attempts to identify C. auris using PCR directly from swabs, seem to produce frequent ‘false positive’ results -- positive in PCR, negative in culture swabs. The first report of three cases of nosocomial fungemia due to C. auris showed that this yeast is commonly misidentified as C. haemulonii and Rhodotorula glutinis using traditional phenotypic methods. These widely used routine identification methods for yeasts are based on phenotypic assimilation/fermentation tests using sets of carbon and nitrogen compounds. An investigation of 102 clinical isolates, previously identified as C. haemulonii or C. famata, showed that 88.2 percent of the isolates were in fact C. auris, when confirmed by ITS sequencing. Several studies have since reported that, in routine microbiology laboratories, C. auris remains a problematic, difficult to identify pathogen, because commercial biochemical identification systems lacked this yeast in their databases.”

“C. auris transmission might be happening in a healthcare facility where professionals are completely unaware; they haven’t been able to detect it, or they are just missing it due to false negatives, and it begs the issue of the importance of having access to clinical microbiology services,” Rohde says. “An expert in clinical microbiology and medical laboratory needs to be part of this equation -- and not just for Candida auris, but for all pathogens in the healthcare setting."

He continues, “People may argue with me on this, but physicians and others in healthcare who are responsible for patient outcomes, often do not have the kind of expertise, education and background to immediately identify problematic organisms; not to detract from their other medical diagnostic skills, but you cannot know intuitively which microbe is infecting a patient without a medical laboratorian conducting a test -- it’s just not going to happen. Unless of course you have those cases where a physician might have the training and the background to do so, but that’s rare. Unfortunately, healthcare has become so lean that many laboratories are being consolidated, with their full microbiology toolbox being moved to a central location. This makes sense from an economic perspective, but sometimes for clinicians, that’s not the best scenario.”

That becomes even more of an issue when considering the long list of risk factors for patients, including immunosuppressed state, significant medical comorbidities, central venous catheters, urinary catheters, recent surgery, parenteral nutrition, exposure to broad spectrum antimicrobials, intensive care unit admission, and residence in a high-acuity skilled nursing facility.

Sears and Schwartz (2017) point out that C. auris has been recovered in samples from blood, catheter tips, cerebrospinal fluid, bone, ear discharge, pancreatic fluid, pericardial fluid, peritoneal fluid, pleural fluid, respiratory secretions (including sputum and bronchoalveolar lavage), skin and soft tissue samples (both tissue and swab cultures), urine, and vaginal secretions. Clinically, it has been implicated as a causative agent in fungemia, ventriculitis, osteomyelitis, malignant otitis, complicated intra-abdominal infections, pericarditis, complicated pleural effusions, and vulvovaginitis. They add that, “Much like other Candida species, there is uncertainty about the ability of C. auris to cause true respiratory, urinary, and skin and soft tissue infections despite being isolated from such samples.”

Cortegiani, et al. (2019) observe that “It is likely that many cases are missed, due to its misidentification with other non-albicans Candida spp. (e.g., C. haemulonii) by common microbiological diagnostic methods. Most of the reports occurred in critically ill adults, with risk factors for invasive fungal infections, such as immunosuppression, surgery, or indwelling catheters. The most common form of infection was candidemia, with a crude mortality of nearly 30 percent, but up to 70 percent in some reports.”

Cortegiani, et al. (2019) emphasize the criticality of fighting C. auris in the intensive care unit (ICU): “Despite implementation of countermeasures to limit colonization and infections in ICUs, cases continue to be reported, with a tendency to an endemic pattern. This reflects the ability of C. auris to persist in the clinical environment, facilitating its transmission within the critical-care setting. Multidrug-resistant (MDR) pattern and has been frequently observed (around 40 percent) with serious and complex consequences for antifungal therapy.”

The researchers note that due to the progressive spread of C. auris and treatment-related concerns, attention should be focused on the following major issues: worldwide transmission, anti-fungal treatment resistance, resilience and mechanisms of transmission, Implementation of infection prevention and control measures, and surveillance.

Let’s review each issue:

Antifungal treatment resistance
Cortegiani, et al. (2019) note that, “To date, there are not established minimum inhibitory concentrations (MICs) breakpoints for susceptibility testing of C. auris. Antifungal susceptibility data from three continents demonstrated that nearly 40 percent were MDR, with strains being resistant to fluconazole (90 percent), amphotericin B (30 percent to 40 percent) and echinocandins (5 percent to 10 percent). Moreover, a small percentage were also resistant to all antifungals available. C. auris demonstrates a high propensity to develop antifungal resistance under selective pressure. Recent studies demonstrated mutations in ERG11 (encoding lanosterol demethylase, the target of azoles) and FKS1 genes (encoding 1,3-beta-glucan synthase, the target of echinocandins). The recommended antifungals for C. auris treatment are mainly based on in-vitro testing and on the most frequently retrieved resistance profiles. Echinocandins are the recommended first-line treatment, pending specific susceptibility testing. Lipid formulation of amphotericin B should be an alternative in patients not responding to echinocandins. Close monitoring to early detect therapeutic failures and evolution of antifungal resistance is needed. New antifungals (e.g., SCY-078, APX001A/APX001, and rezafungin) have been tested with success but they are not available to date for clinical use.”

Resilience and mechanisms of transmission
Cortegiani, et al. (2019) explain that, “Unlike others Candida species, C. auris can colonize different anatomical sites (e.g., skin, skin, rectum, axilla, stool) and contaminate hospital equipment and surfaces, creating a vicious cycle of acquisition, spreading, and infection, particularly in ICUs. Indeed, bed, chairs, and monitoring tools (e.g., pulse oximeters, temperature probes) were contaminated during outbreaks. Recently, Eyre et al. published the results of a patients’ and hospital environmental screening program in Oxford, UK, after 70 patients (66 admitted to a neuro-ICU) were identified as being colonized or infected by C. auris. Seven patients developed an invasive infection during hospital stay. C. auris was detected mainly on skin-surface axillary temperature probes and other reusable tools. In patients monitored with skin-surface temperature probes, the risk of C. auris infection/colonization was seven times higher. Adoption of specific bundles of infection control had no significant effects until removal of the temperature probes. Recent studies have confirmed that C. auris can form biofilms, with a high variation of capacity of production depending on the C. auris strain considered. Biofilm may present reduced susceptibility to hydrogen peroxide and chlorhexidine. Quaternary ammonium compounds and cationic surface-active products seem to be ineffective against C. auris. Chlorine-based products appear to be the most effective for environmental surface disinfection. Chlorine-based disinfectants (at a concentration of 1,000 ppm), hydrogen- peroxide, or other disinfectants with documented fungicidal activity are recommended for environmental cleaning by the European CDC (ECDC).”

Implementation of infection prevention and control measures
Cortegiani, et al. (2019): say that, “Usually, outbreaks follow an exponential increase in the number of affected patients. It is mandatory to trace contacts with the aim to achieve early identification and screening of possible colonized patients that might be responsible for persistence of C. auris. Patients potentially or already colonized should be placed in single rooms with contact isolation precautions. Screening should be applied for contacts and patients previously hospitalized in healthcare settings where C. auris isolation was confirmed. Hand hygiene (with alcohol or chlorhexidine handrubs), wearing of protective clothing, and skin and environmental/equipment decontamination should be performed to prevent ongoing transmission.”

Global surveillance
Cortegiani, et al. (2019) emphasize that the emergence of C. auris and progressive spread of infections caused by other resistant pathogens has strengthened the need for a surveillance network for antimicrobial resistance globally for critically ill patients’ safety. The researchers observe, “It is hard to predict future C. auris diffusion. There will be outbreaks also in countries in which C. auris has been not reported yet? Will new MDR clones continue to emerge? Will we be able to apply effective antifungal stewardship programs and control measures?”

So much about C. auris is still unchartered territory, and as Rhodes and Fisher (2019) observe, “The global emergence of C. auris testifies to the unmapped nature of Kingdom Fungi and represents a new nosocomial threat that will require enhanced infection control across diverse healthcare and community settings.” The researchers add, “Currently, nothing is known about the origins and initial emergence of C. auris; its propensity to survive on inanimate objects within the hospital alongside resistance to disinfection protocols suggests the existence of an unknown non-human environmental reservoir. However, similar to other Candida species, the true nature of C. auris’ ancestral reservoirs currently remains elusive. The detection of clonal C. auris isolates on multiple continents simultaneously with distinct geographical antifungal resistance mechanisms suggests at least four independent emergence events followed by clonal expansion and the ongoing evolution of resistance in response to antifungal therapy … As sequencing technology develops, it is likely rapid sequencing of C. auris isolates can be achieved in 48 hours or less leading to the potential for bedside diagnostics twinned with molecular epidemiology of nosocomial patterns of transmission. Currently, it is not often known when patients become colonized – whether from the hospital environment or endogenous carriers – and the extent of carriage in the community remains largely unexamined.”

Lockhart (2019) indicates that rapid identification of colonized patients followed by isolation and contact precautions can help stem the spread of resistant clones: “Real-time detection methods can not only rapidly identify colonized patients but may also contribute to the rapid detection of resistance. Besides the existing laboratory-developed tests, there is at least one commercially available PCR test for the rapid detection of C. auris. There are currently two real-time assays for detection of anti-fungal resistance in C. auris, one for detecting azole resistance and the other for echinocandin resistance, as well as a report that echinocandin resistance can be detected using MALDI-TOF. These rapid platforms may become essential for the rapid determination of appropriate therapy.”

Environmental Persistence of C. auris
Short, et al. (2019) are sounding the alarm about the environmental persistence of C. auris; in their study, they found show that the ability of this multidrug-resistant yeast to form cellular aggregates increases survival after 14 days, which coincides with the upregulation of biofilm-associated genes. The researchers also caution, “Additionally, the aggregating strain demonstrated tolerance to clinical concentrations of sodium hypochlorite and remained viable 14 days post treatment. The ability of C. auris to adhere to and persist on environmental surfaces emphasizes our need to better understand the biology of this fungal pathogen.”

The researchers explain, “A key attribute of its pathogenic repertoire is its ability to survive and persist in the environment, yet the methods employed by this multidrug-resistant pathogen to disseminate throughout healthcare environments are still not fully understood. This has profound implications for decontamination and infection control protocols. Therefore, understanding the mechanisms of spread and survival in the hospital environment is critical, particularly as it persists on hospital fomites, extensively colonize individuals, and to survive as biofilms. Although traditionally biofilms are associated with formation on an indwelling medical device or on a mucosal substrate, recent investigations have suggested that these communities can facilitate residence and survival upon surfaces within a clinical setting. Despite the lack of nutrients, these communities adapt to survive and display increased tolerance to both heat and conventional disinfection treatments compared to a free-floating, equivalent cell. C. auris has been shown to readily transmit between hospital equipment, such as reusable temperature probes, and patients suggesting limitations of current infection control strategies. Commonly used disinfectants have been shown to be highly effective when tested in suspension, yet our previous data indicate that adherent C. auris cells can selectively tolerate biocides, including sodium hypochlorite and peracetic acid, in a substrate-dependent manner.”

To test the theory of biofilm formation being employed as an endurance strategy of C. auris, Short, et al. (2019) performed survival studies using two phenotypically distinct isolates based on their ability to form cellular aggregates. The researchers report, “Similar to previous findings, C. auris was found to remain viable for at least two weeks within a dry environment, regardless of the organic material in which it was suspended. It was shown that aggregating cells survived considerably better than their single-cell counterparts in PBS (>2.5 log2 cfu/mL) and 10% FCS (>4 log2 cfu/mL).”

The researchers add, “To confirm a role for biofilms in facilitating environmental persistence, a panel of biofilm associated genes, selected according to our group's previous transcriptional characterization of C. auris biofilms, was assessed. These genes were highly expressed across both phenotypes; however, comparative analysis revealed increased expression of approximately two-fold of several of these genes, which are involved in adhesion, extracellular matrix (ECM) production, and efflux pumps. ECM production is a well-documented resistance mechanism in pathogenic fungal biofilms of Candida spp. Increasing ECM production could provide the necessary protection for C. auris to survive extended periods of desiccation and retain viability following terminal disinfection.”

Using Infection Prevention and Control to Fight C. auris
Case investigation by public health entities such as the CDC and others has demonstrated that C. auris patients within similar geographic regions commonly had overlapping stays in the same acute-care hospital or long-term care facility, further supporting healthcare exposure as a key method of transmission.

Given the risk of nosocomial transmission of this multidrug-resistant pathogen, Sears and Schwartz (2017) emphasize that, “…infection control measures are vital to slowing the spread of C. auris. CDC recommends that all hospitalized patients with C. auris infection or colonization be treated using both Standard Precautions and Contact Precautions and housed in a private room with daily and terminal cleaning with a disinfectant agent active against Clostridium difficile spores (Cadnum et al., 2017). Receiving healthcare facilities should also be notified prior to transfer of an infected or colonized patient. Infection control precautions should be maintained until a patient is no longer infected or colonized with C. auris although there is uncertainty as to how best to monitor for ongoing colonization (CDC, 2017). There are no clear data on the efficacy of decolonization measures for patients colonized with C. auris, however this has been attempted with chlorhexidine in healthcare facilities during outbreaks.”

Kean, et al. (2018) articulate one of the greatest worries about C. auris: “The ability of this organism to survive on surfaces and withstand environmental stressors creates a challenge for eradicating it from hospitals.”

An experience with surface cleaning and disinfection to help combat C. auris in a U.S. healthcare facility was documented by Marrs, et al. (2017) who reported on two patients with C. auris infections that were admitted to the University of Chicago Medicine (UCM). In their study, the researchers collected environmental samples to assess environmental contamination before and after cleaning. They sampled the following surfaces: Bathroom sink drain, bedside table, bedrail, mattress, chair and window ledge. Routine terminal cleaning included using a 10 percent sodium hypochlorite solution that was applied to high-touch surfaces of the patient room and bathroom. The enhanced terminal cleaning process also included removing and replacing privacy curtains, using a single UV disinfection cycle in the room and bathroom, as well as supervision of the process by the environmental services manager.

The researchers note that due to a delay in identification of C auris for the first patient, pre-cleaning samples were taken more than two weeks after the patient had been discharged. During the intervening weeks, multiple patients had occupied the room and there had been more than three routine terminal cleanings. None of these samples was positive for C auris. Pre-cleaning, in-residence samples indicated C auris contamination of multiple surfaces for the second patient. Because of transfers within the institution, there are three sets of post-cleaning cultures for the second patient. All post-cleaning environmental cultures were negative for both patients. The researchers concluded that while routine terminal cleaning may have been effective in removing C auris from surfaces in one patient’s room, the enhanced terminal cleaning strategy used here was effective in their facility.

In their study, Kean, et al. (2018) evaluated a panel of C. auris clinical isolates on different surface environments against the standard disinfectant sodium hypochlorite and high-level disinfectant peracetic acid. The researchers note that, “C. auris was shown to selectively tolerate clinically relevant concentrations of sodium hypochlorite and peracetic acid in a surface-dependent manner, which may explain its ability to successfully persist within the hospital environment.”

The implications for infection control are significant, and Kean, et al. (2018) add that, “Understanding the mechanisms of spread and survival of this pathogen in the hospital environment is therefore crucial, particularly as it may persist on plastics and steel, and survive as biofilms. Several recent investigations have confirmed that C. auris is capable of prolonged survival on surfaces and have shown that surface disinfection protocols have variable and unsatisfactory outcomes. Since it has been shown recently that 1,000 ppm of an active chlorine solution is highly effective against these organisms when tested in suspension, the interaction between the pathogen and surfaces is likely to be important in determining survival of C. auris in the hospital environment. Our own work confirms this, with C. auris biofilms being generally insensitive to a range of key antimicrobial agents, thus prolonging their survival capacity.”

Kean, et al. (2018) investigated the general disinfectant sodium hypochlorite (NaOCl), widely used for terminal cleaning within the hospital environment, and the high-level disinfection agent peracetic acid, on different substrate surfaces. Four C. auris isolates obtained from various clinical sites were used, and several test surface substrates were used: cellulose matrix, 304 stainless steel, and polyester coverslips.
The researchers report that, “Initially, a standard disinfectant challenge was performed against C. auris on different substrates relevant to the hospital environment. A cellulose substrate was included to act as control for porosity. All four C. auris were significantly killed by NaOCl challenge at 1,000 and 10,000 ppm, irrespective of substrate and strain, though differences were observed between these substrates. Complete eradication was only achieved on the cellulose substrate. On the non-porous materials, significant quantities of viable yeast cells were killed on the steel surface following NaOCl at all treatment parameters, with ∼2.5 log10 reduction, with no significant differences observed at each time-point and concentration tested. Notably, those isolates treated with 1,000 ppm for 5 minutes showed significantly more regrowth compared to the other test conditions. When C. auris was tested on a polymer substrate, 5-minute exposure at 1,000 ppm was the least effective overall; although significant activity was observed, 4.95 log10 was retained on the surface. However, following an increased contact time of 10 minutes, or increased concentration to 10,000 ppm, significantly enhanced activity was observed, with an approximate overall 3.5 log10 reduction. When comparing both increased treatment parameters, no significant differences were observed between the regimens, and no notable regrowth was detected.”

The researchers observe, “There was a significant difference in activity between polymer and steel, which could be explained by the general ability of Candida species to adhere and form biofilms that are inherently more resistant. Whereas the isolates on steel responded by ∼3 log10 equally to the treatment regimens, on plastic we demonstrated differential activity depending on concentration and time of exposure to NaOCl. Another study reported greater efficacy of chlorine-based products on steel, but differences in experimental design may explain this, e.g. products and inoculum. Taken together, these data suggest that the standard disinfection procedures are surface-dependent, and that the diversity of fomites in the hospital setting could pose a problem for disinfection.”
Kean and McKloud, et al. (2018) used a three-dimensional complex biofilm model to investigate the efficacy of a panel of antiseptic therapeutics, including povidone iodine (PVP-I), chlorhexidine (CHX) and hydrogen peroxide (H2O2). They hypothesized that the ability of C. auris to form biofilms may be a potential mechanism that results in reduced susceptibility to antiseptic agents.

Initially, the antiseptic efficacy of three agents was tested against four C. auris isolates. As Kean and McKloud, et al. (2018) report, “When biofilms were treated with PVP-I for 5 minutes, concentrations of 1.25-2.5 percent were required to inhibit biofilms, which is a 16- to 128-fold change compared with planktonic cells. Increasing the exposure time (10 and 30 minutes) was shown to increase susceptibility to 0.625-1.25 percent, which is an eight- to 64-fold change compared with planktonic cells. CHX was highly active against planktonic cells, whereas biofilms were less susceptible with MICs increasing 2- to 16-fold. Elevated biofilm MICs were also observed following H2O2 exposure, with concentrations ranging between 0.25 and >1 percent required to kill biofilms, i.e. a 16-fold increase in the planktonically-active concentration. Regardless of the antiseptic active used, minimal differences in susceptibility were observed between 24- and 48-hour biofilms.”

The researchers observe, “Interestingly, PVP-I, a commonly used pre-surgical wash, was shown to be equally active against both early and mature biofilms when assessed by culture. This agreement with other studies in which PVP-I demonstrated excellent fungicidal activity against C. auris. The use of 10 percent PVP-I for surgical skin preparation has been used clinically for C. auris, with no postoperative infection reported. An interesting finding from this study was the ineffectiveness of H2O2 against both planktonic and sessile cells of C. auris. This finding is inconsistent with previous studies in which H2O2 showed significant fungicidal activity. Discrepancies between these findings are likely due to the test methodologies employed, with vaporized H2O2 assessed in one of these studies.”

The researchers add, “Future studies assessing the efficacy of CHX diluted in alcohol may provide a potential anti-biofilm strategy for successful skin disinfection. Collectively these findings illustrate the need for a greater understanding of the survival strategies of C. auris. Considering the documented high transmissibility of C. auris between patients and the environment, the implementation of stringent infection prevention and control procedures, coupled with the biological understanding of the organism, will ultimately aid the intervention strategies for this emerging pathogen.”

It is quickly becoming evident that current evidence for pragmatic infection prevention and control (IPC) recommendations is lacking, according to Kenters, et al. (2019), who reviewed the epidemiology of C. auris and identified best practices to provide guidance and recommendations for IPC measures, based on available scientific evidence, existing guidelines and expert opinion. The IPC working group of the International Society of Antimicrobial Chemotherapy (ISAC) organized a meeting with infection prevention and mycology experts to review recommendations on IPC measures on C. auris in inpatient healthcare facilities for healthcare workers on the most common interventions including: screening, standard precautions, cleaning and disinfection, inpatient transfer, outbreak management, decolonization and treatment.

The working group identified these best practices to help combat C. auris:

1. Optimal diagnostics
It is crucial to identify and report C. auris correctly in order to provide optimal patient care, treatment and initiate appropriate IPC measures. All isolates should be susceptibility tested, from whatever body site, because of varying levels of resistance.

2. Patient screening upon admission
Outbreak investigations have revealed that screening sites most frequently culturing positive for C. auris were axilla, groin, rectum and urine. Other sites for screening, even if less sensitive to colonization are the nose, mouth, external ear canals, catheter urine and wounds. If a patient has open wounds and/or intravascular catheters they should be included for screening in addition to the swabbing sites. It is important to only swab open wounds if they are not sealed by wound dressing, as opening a sealed wound can cause a risk for patients to become colonized with C. auris if they are carriers. Risk groups admitted to the hospital are patients previously admitted into intensive care units in endemic countries and, transfers from hospitals known to have C. auris. Hospitals that have C. auris present should liaise with receiving hospitals infection control teams and ensure that appropriate is information is shared. If healthcare institutions have an existing surveillance screening protocol in place for patients at high-risk for colonization with MDRO, it might be more valuable to add C. auris to the existing testing panel in the lab, rather than to re-implement additional swabbing sites.

3. Infection prevention and control interventions
For healthcare facilities to be prepared for a first case of C. auris, it is important to have a screening protocol as well as adequate IPC procedures in place. Any detection of C. auris should be immediately reported to the IPC department, leading to timely implementation of strict IPC-related measures. Patients colonized or infected with C. auris should be isolated until discharge and flagged for at least one year after the first negative screening culture. When patients are transferred within the institution or to other healthcare facilities handing over of the patient C. auris status needs to be ensured. Patient contact screening of direct contacts should be initiated on the detection of a ‘first’ case, including those being discharged and this may involve tracking back throughout the patient admission if internal transfers have taken place. Every patient should be screened in the axilla and groin, including any other relevant sites (e.g. nose, urine, rectum, throat, wounds and catheter exit sites).

The following IPC measures should be implemented for any C. auris case:
- Standard precautions
Hand hygiene is key to prevent transmission of any microorganism, including C. auris. Special attention should be given to adequate compliance with hand hygiene while caring for patients in isolation. Hand hygiene should be performed at the point of care using alcohol-based handrub (ABHR). While ABHR is the preferable choice, water and soap should be used when hands are visibly soiled and a dedicated sink needs to be in place to wash hands.

- Patient environment
Patients colonized or infected with C. auris need to be placed in contact precautions in a single room, ideally with negative pressure, and preferably with an anteroom and in-suite bathroom/toilet. If the latter is not available, patients should use a dedicated washroom or a waterless washing product, as well as a dedicated commode. The use of an isolation room with anteroom might be preferable, not because airborne spread is assumed, but because compliance with isolation measures might possibly be higher, as the double doors function as a reminder. A flagging system indicating the isolation needs to be visible at the entry of the patient room and instructions for HCWs and visitors need to be available. All biomedical products and equipment should be used as disposables, or, if re-usable should be left in the patient's room until discharge and thorough disinfection. Sharing biomedical products and equipment to other wards poses a risk of additional transmission. For mattresses and pillows, HCWs should ensure that they are 100 percent sealed before using them for a C. auris patient and its integrity should be assessed upon discharge if they are to be used for another patient.

- Personal protective equipment (PPE)
It has become evident that the use of a long-sleeved gown and gloves are sufficient to enter the room of patients found positive for C. auris. Taking into consideration that people often (unconsciously) touch their face, a surgical mask could be considered to prevent colonization of healthcare staff, since one HCW has been found transiently positive in the nose in a previous outbreak.

- Environmental cleaning
Enhanced daily and terminal disinfection has been shown to be crucial to control the spread of C. auris within healthcare facilities. In addition, the frequency of cleaning and disinfection should be at least twice daily, of at least all high-touch surfaces. Terminal cleaning and disinfection of the rooms after patient discharge needs to be performed with great diligence. When selecting a product, users should keep in mind the toxicity of a product and select one that is safer to use near a patient. Innovative automated decontamination technologies, such as UV-C disinfection can be used to ensure optimal terminal cleaning of surfaces but are an additional safeguard and not a replacement of the routine cleaning method. Both methods – UV-C and HPV – require vigorous cleaning before being effective against microorganisms. If UV-C is used, the duration of exposure for efficacy is longer than that for vegetative bacteria and a cycle time effective for spores such as C. difficile should be selected.

Cleaning and disinfection of reusable equipment is particularly important, especially as these items may be decontaminated at the departmental level by clinical staff. Where possible, dedicated equipment should be used. If dedicated equipment is not an option equipment and devices must be disinfected thoroughly after every use in line with the manufacturer's instructions and considering materials compatibility. The surfaces of re-usable items should be periodically examined to check for surface integrity and the continued ability to be able to effectively decontaminate. Materials that cannot be disinfected should not be used or discarded after use. Where possible, single-use equipment is preferred to limit possible spread via inadequately disinfected equipment. Equipment that is cleaned by clinical staff should be audited to ensure that it is effective, and facilities may wish to consider whether formal training for clinical staff in decontamination has been or should be provided.

- Patient clothing
The role of patient clothing in the transmission of C. auris is unclear. In the experience of the hospitals dealing with outbreaks, patients were asked to use hospital garments or clothes that have been washed at high temperatures. The expert group was not able to give a recommendation on this topic. Seeing that C. auris has been found to survive on linen, it may be prudent to change bedding and patient attire daily if decolonization or skin suppression is being attempted.

- Patient movement in the facility
Transfer of colonized or suspected patients for C. auris should be done with great care. The treatment of patients should always come first, but if transfer can be prevented by using mobile equipment, this should be considered. When patients need to go to radiology, for example, they should ideally be placed at the end of the schedule to allow time for terminal decontamination of the area.

- Readmission of previous C. auris positive patient
If known, previous positive C. auris patients should be placed in contact isolation and screened on three consecutive days. Contact precautions may be stopped if all three screens are negative. Weekly screening is however recommended as C. auris may resurface after antibiotic therapy or other interventions such as chemotherapy. This is the minimum measure, as local MDRO-related guidelines that are stricter must be regarded.

- Outpatient management
Family members and healthcare providers can become colonized; however, this is of minimal risk to the “healthy” individual. There are no guidelines yet for management of C. auris-colonized patients; however, it is prudent that sharing items should be kept to a minimum in line with the principles for other fungal infections: in particular, towels and clothing should not be shared, as well as cosmetic items, creams, ointments, etc., even in the absence of studies demonstrating any effectiveness.

- Healthcare personnel education and training
Compliance with, as well as adequacy of using IPC measures is essential to prevent transmission of C. auris within the healthcare facility. To increase staff's awareness around IPC measures, on-site training and auditing is critical to contain C. auris. Training should focus on standard precautions, PPE, environmental cleaning and other IPC measures applied to control C. auris. In addition, compliance and correct execution of IPC measures should be monitored, and direct feedback to HCWs should be provided.

- Outbreak management
The index or any unexpected case colonized or infected with C. auris should be isolated in a single/isolation room and direct contacts should be placed in cohort isolation, with contact precautions and no new patients should be admitted to the affected room. Maintaining cohorts of “proven colonized”, “possibly colonized” and “no risk” patients is important under all circumstances, even if that would lead to lowered bed capacities, reduction of admitted patients or cancelation of operating procedures. As C. auris has been cultured from the hands of healthcare personnel, where possible they should be assigned to one of the cohorts, instead of working throughout the whole unit. If the outbreak is large, creation of a separate unit for all proven colonized patients might be advisable. Single use equipment or dedicated equipment should be used. A root cause analysis by Schelenz, et al. found that patients who had contact with a positive case or contaminated environment were likely to have contracted C. auris within just four hours of contact.

To confirm negative patients, three consecutive C. auris screenings should be negative. In the absence of published data, it is advisable to space out the three screening times (such as day 3-5-7), instead of doing them on day 1-2-3 or even all in a day. When de-isolated, weekly screening of the negative contact patients, until discharge, is recommended. Healthcare personnel have been identified as carriers in the nose and groin, so during an ongoing outbreak, screening of healthcare staff could be considered, as well as unannounced cultures from hands as an educational measure.

In an outbreak scenario, cleaning and disinfection should be increased to three times daily of at least all high-touch surfaces with a product effective against C. auris. Terminal cleaning and disinfection should be monitored with quality indicators that go beyond visual inspection, such as ATP or fluorescent markers, to ensure the quality of terminal cleaning and disinfection. If available, UV-C or HPV could be used after terminal cleaning and disinfection, as an additional assurance that the room has been adequately decontaminated and is safe for the next bed occupant.

No recommendations can be provided about to the effect of decolonizing patients; in theory, this may lead to a lower burden of yeast on the patient's skin and thus, a lower risk of transmission. This approach has been adopted in outbreaks; however, non-conflicted data are missing to draw that conclusion for C. auris. Currently, limited evidence on the use of topical agents for the control of skin colonization exists. In one UK major outbreak, 2 percent chlorhexidine washcloths or 4 percent chlorhexidine solution were used to control skin shedding as part of several interventions. However, despite daily CHX bathing, patients described in the UK continued to be colonized with C. auris. Chlorhexidine solutions may dry the skin in such a way that it may lead to prolonged colonization with C. auris. Some patients however remained persistently colonized, possibly due to recolonization from bedding, as Candida spp. have been demonstrated to survive on polyester textiles for up to eight days.
Mandatory national reporting of outbreaks in institutions should be considered, as well as mandatory reporting of infections with C. auris. In countries that do not have laws accounting for this, mandatory sharing of outbreak status data with regional healthcare providers is advisable.

References and Recommended Reading:
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