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Archive for the ‘Microbiology’ Category

Misdiagnosing Legionellosis or Legionnaires’ Disease Can Be Fatal. But Why Is It Still Common?

Yellow water is poured from the tap into the glass: standard Legionellosis testing procedure

by Chandana Balasubramanian

Pathogen of the month: Legionella

Doubt strikes fear into the hearts of many. But it is a powerful tool in the hands of medical professionals and researchers. Being uncertain is the impetus that drives truth-seeking peer-to-peer verification and differential diagnoses that can help save lives.

Take Legionnaires’ disease. It is one of the leading causes of pneumonia worldwide [1]. If left untreated without the right antibiotics, it can be fatal. In the United States alone, the economic burden of just one year of Legionnaires’ disease cases can be over 800 million US dollars [2].

Surprisingly, it is often overlooked. So much so that even the World Health Organization or WHO states, “Since many countries lack appropriate methods of diagnosing the infection or sufficient surveillance systems, the rate of occurrence is unknown. In Europe, Australia, and the USA, there are about 10–15 cases detected per million population per year [1].”

A great place to begin addressing these challenges is if clinicians are willing to embrace doubt when faced with diagnosing pneumonia-like symptoms.

What causes Legionnaires’ Disease or Legionellosis?

There were many historical events in 1976. NASA unveiled their first space shuttle, Apple Computers was born, and the first Rocky movie was released. Unfortunately, it was also the year a tragic event led to the discovery of Legionnaires’ disease.

On July 21st, 1976, 4000 delegates from the American Legion, America’s largest veterans’ service organization, traveled to Philadelphia for a convention. Within a few weeks, almost 200 got sick with an upper respiratory illness, and 29 died. It took nearly five months of investigations to identify the pathogen – Legionella – as the cause [3].

Legionnaires’ disease or Legionellosis is caused by the bacteria Legionella. It lives in water and soil and can cause health issues when it grows in showerheads and faucets, hot tubs, and in stagnant water and air conditioning systems in large buildings. We are susceptible to infection by Legionella when we inhale water droplets with the bacteria in it or come in contact with contaminated soil. Legionellosis is not spread through direct human-to-human transmission. It has an incubation period of 2 to 10 days.

Legionella is widely found in warm water environments, so most cases of Legionnaires’ occur in the summer and early autumn. Legionnaires’ is a public health issue. Cassell et al. caution that utmost care must be taken when COVID-19 restrictions are lifted worldwide. Going back to work or school in buildings left unoccupied or unused during lockdowns is a risk factor for Legionellosis [4]. 

Paterna, Valencia, Spain: 03.05.2020; The legionella training
Paterna, Valencia, Spain, 2020; The Legionella training

 

Why is Legionnaires’ Disease often misdiagnosed or overlooked?

According to Reller et al. [5], a wrong Legionellosis diagnosis is often due to:

  1.     The inability to distinguish Legionnaires’ disease from other types of pneumonia, clinically and radiographically,
  2.     Failure to order diagnostic tests for Legionella infection, and
  3.     Inadequacies in current diagnostic tests and protocols.

The majority of Legionnaires’ disease cases each year remain undiagnosed; the world still awaits better diagnostic tests and protocols for Legionellosis. But the issue of “failure to order diagnostic tests for Legionella infections” can be fixed. The Urine Antigen Test (UAT) and sputum tests prescribed for Legionella are inexpensive, so cost is not the issue.

The solution lies in training medical professionals to embrace doubt and challenge their confirmation biases. Clinicians who take a few minutes to input a patient’s pneumonia and accompanying symptoms on a robust, clinical decision support tool like GIDEON (Global Infectious Diseases and Epidemiology Network) can better understand how to proceed

For example, when the COVID-19 pandemic hit, experts cautioned clinicians to be on the alert for Legionellosis as well. The concern was that clinicians might repeatedly be testing community-acquired pneumonia patients for COVID-19 but not Legionellosis – which would delay diagnosis and treatment. Since initial clinical presentations for the two are similar, clinical decision tools can be extremely useful.

GIDEON, for example, has a built-in feature to help clinicians challenge their confirmation biases. A ‘Why Not?’ feature helps clinicians understand why a specific diagnosis does not show up on the list of probable causes of a patient’s symptoms.

Legionnaires’ disease, misdiagnosed as Malaria, can be fatal because malarial drugs do not work against Legionella. It is even more critical to get the right diagnosis early. 

 

Legionellosis Misdiagnosed as Malaria

Take the example of the agricultural expert from Israel wrongly diagnosed with malaria instead of Legionellosis. He had traveled to India to work on a farming project in 2005. A week later, when he returned to Israel, he developed fever, headache, vomiting, and muscle pain. In two days, he felt better, but the symptoms reappeared but with cough, shortness of breath, and rigors in tow. The patient was highly lethargic, hypotensive, and blood tests showed elevated bilirubin and creatinine levels.

Because of his recent travel to India, doctors thought it was Malaria. He was started on malarial medication while laboratory tests were being processed. But when blood smears proved negative for Malaria, his doctors wondered if it was Dengue.

Luckily for him, his doctors decided to challenge their cognitive biases and conducted a differential diagnosis. They entered the patient’s symptoms in the popular DDx or differential diagnosis tool, GIDEON. To their surprise, neither Malaria nor Dengue showed up as possibilities. But given the symptoms and the incubation period, Legionellosis turned out to be the prime (and accurate) suspect. This saved his life because standard malarial therapy does not work against Legionellosis.

Legionellosis diagnosis on GIDEON application - two devices

Conclusion

Misdiagnosing Legionnaires’ disease can be fatal, lead to a public health crisis, and add hundreds of millions to an already astronomically high healthcare burden. One of the main reasons it is often overlooked is that clinicians may not think about testing for Legionellosis when treating a patient with pneumonia.

Equipping clinicians with the right clinical diagnosis tools can help them validate their assumptions. Not only that, using a tool like GIDEON, clinicians can also challenge their confirmation biases and learn why a diagnosis does not apply to a specific set of symptoms.

Getting to the correct answer starts with harboring and encouraging healthy doubt in initial diagnoses. As the famous philosopher, Voltaire said, “Doubt is not a pleasant condition, but certainty is absurd.”

 

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References

[1] WHO, World Health Organization, “Fact Sheet: Legionellosis,” WHO, February 16th, 2018. [Online]. Available: https://www.who.int/news-room/fact-sheets/detail/legionellosis. [Accessed 08 07 2021].
[2] K. R. C. E. a. S. C. M. Baker-Goering, “Economic Burden of Legionnaires’ Disease, United States, 2014,” Emerg Infect Dis., vol. 27, no. 1, pp. 255-257, 2021.
[3] J. E. M. e. al., “Legionnaires’ disease: Isolation of a bacterium and demonstration of its role in other respiratory diseases,” N. Engl. J. Med., vol. 297, no. 22, pp. 1197-1203, 1977.
[4] K. Cassell, “Legionnaires’ disease in the time of COVID-19,” Pneumonia, vol. 13, 2021.
[5] L. R. e. al., “Diagnosis of Legionella Infection,” Clinical Infectious Diseases, vol. 36, no. 1, pp. 64-69, 2003.

Pathogen of the month: Mycobacterium tuberculosis

Mycobacterium tuberculosis (M. tuberculosis), a non-motile, obligately aerobic, intracellular bacterium known to cause Tuberculosis (TB), was discovered by Robert Koch in 1882 [1]. TB primarily affects the lungs along with the abdomen, bones, nervous system, reproductive system, liver, and lymph glands [2].

Pulmonary Tuberculosis ( TB ) : Chest x-ray show alveolar infiltration at both lung due to mycobacterium tuberculosis infectio
Pulmonary Tuberculosis ( TB ): Chest x-ray shows alveolar infiltration at both lungs due to Mycobacterium tuberculosis infection

 

Global Burden of Tuberculosis

The World Health Organization (WHO) has reported a 22% decrease in TB-related mortality between 2000-2015, with a gradual 1.5% decrease in the annual rate. However, despite this trend and successful control of disease transmission, TB continues to have a significantly higher rate of morbidity. In 2015, six countries (China, India, Nigeria, Pakistan, Indonesia, and South Africa) accounted for 60% of TB-related deaths [3].

 

Global cases of Tuberculosis between 1965-2019

Worldwide Tuberculosis cases and rates, 1965 - today

 

Pathogenicity of Mycobacterium tuberculosis

Mycobacterium tuberculosis is transmitted in the form of droplet nuclei exhaled by individuals affected with laryngeal/pulmonary TB. It enters the body via the nasal cavity/mouth and travels to the alveoli of the lungs, where it recruits macrophages to the lung surface, in turn transporting the bacteria to the deeper tissues [4]. Another round of macrophage recruitment to the originally infected locus forms an organized aggregate of differentiated macrophages and immune cells called a granuloma. The infected granuloma undergoes necrosis, promoting bacterial growth and transmission to the next host [5].

Diagnosis of TB

Some patients with TB may present with non-specific findings such as anemia, weight loss, fever of unknown origin, and fatigue; while others may be asymptomatic and show no abnormalities on physical examination [6]. Thus, the physician should collect body fluids/tissues for Acid-Fast bacilli (AFB) smear and culture.  Only a positive culture can confirm the diagnosis of TB.

Confirmatory and diagnostic tests for TB:

– Culture, followed by Ziehl-Neelsen (AFB) staining

– A Chest X-ray to confirm the diagnosis in case of positive culture, indicating active disease

– Gene-based tests and nuclear amplification to identify the bacterial strains using DNA-based molecular techniques, such as GeneXpert [7].

 

Ziehl-Neelsen staining

AFB staining is the traditional method of TB diagnosis, as it is inexpensive and provides rapid results [8]. Mycobacterium species retain dyes when heated and treated with acidified organic compounds. The most common acid-fast staining method for M. tuberculosis is the Ziehl-Neelsen stain method, in which a specimen is fixed, stained with carbol-fuchsin dye, and decolorized with an acid-alcohol mixture. After counter-staining the smear with methylene blue or a similar dye, AFB appear red against a contrasting blue background [9].  In general, a sputum sample must contain at least 10,000 organisms/mL to visualize these bacteria at 100x magnification. 

Symptoms and ways of infection of tuberculosis. Medical vector infographics, poster

Latent TB vs. Active TB

Latent TB represents the condition where the body’s immune system restricts the growth of M. tuberculosis bacterium, making the individual appear asymptomatic [10].

An individual with latent TB infection shows

– no symptoms.

– is not infectious (cannot spread TB).

– tests positive for TB blood/skin tests.

– may eventually develop active TB if the immune system weakens.

Active TB represents a condition where the body’s immune system is unable to restrict the growth of M. tuberculosis, rendering patients both ill and contagious. 

The symptoms of TB depend on the affected area.

a. General symptoms include:

  1. Night sweats
  2. Weight loss
  3. Prolonged fever
  4. Loss of appetite
  5. Fatigue

b. Symptoms of Pulmonary TB (infected lungs):

  1. Shortness of breath, which progressively worsens
  2. A persistent cough that produces phlegm and sometimes blood, persisting  > 3 weeks. 

c. Symptoms in the case when other areas of the body are infected:

  1. Swellings in the neck or other regions
  2. Pain in a joint or affected bone
  3. Abdominal pain
  4. Headache
  5. Confusion
  6. Seizures

 

Treatment

According to the World Health Organization (WHO), first-line treatment for TB may include combinations of five essential drugs: Rifampicin (R), Isoniazid (H), Pyrazinamide (Z), Ethambutol (E), and Streptomycin (S) [11].  Patients with TB undergo a standardized treatment for 6 to 9 months, including an initial two-month course of Rifampicin, Isoniazid, Pyrazinamide, and Ethambutol, followed by another 4-month course of Isoniazid and Rifampicin [12].

For patients with Multi Drug-Resistant Tuberculosis (MDR-TB), directly-observed therapy (DOT) is used. In DOT, drugs are administered at least six days/week under the direct observation of the physician [13, 14]

BCG vaccine

Bacillus Calmette-Guerin (BCG), a vaccine for TB, was introduced in 1921 to control tuberculosis in humans. It is administered at birth, primarily in regions with a high disease burden, such as India, South Africa, and Pakistan [15]. Widespread immunization using BCG vaccine has facilitated a reduction in TB cases globally [16].

 

Risk factors

Five-to-ten percent of people with latent TB who do not receive appropriate treatment will eventually develop active TB disease [17]

Individuals at a higher risk of contracting TB include:

– Those who have traveled to or are living in a country with a high prevalence of TB. 

– Those living in crowded conditions

– Those who have been in close contact with a person infected with TB

– Children ages <= 5 years who have tested positive for TB

– People who reside or work with persons at high risk for TB, such as those in hospitals, correctional facilities, homeless shelters, residential homes for HIV-infected individuals, and nursing homes

Additionally, immune dysfunction associated with diabetes mellitus, HIV infection, cancer chemotherapy, malnutrition, and advanced age is associated with an increased risk of contracting TB. 

Additional conditions associated with high risk for tuberculosis include silicosis, substance abuse, malignancy, organ transplantation, corticosteroid therapy, Crohn’s disease, and rheumatoid arthritis.

Tuberculosis and HIV

Co-infection by TB and HIV places a diagnostic and therapeutic burden on the health care system. HIV infection has been shown to increase the risk of reactivation of latent TB by 20-fold. [18].

 

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References

  1.     K. R, Die Aetiologie der Tuberculose [The aetiology of Tuberculosis.], Berlin: Berliner Klinische Wochenschrift, 1882.
  2. F. K. Dye C, Disease Control Priorities in Developing Countries, New York:: Oxford University Press, 2006.
  3. Z. J. B. Q. H. H. B. L. Y. J. L. Q. L. J. Pan Z, “The Gap Between Global Tuberculosis Incidence and the First Milestone of the WHO End Tuberculosis Strategy: An Analysis Based on the Global Burden of Disease 2017 Database.,” 2020.
  4. CDC, How TB Spreads, CDC, 2016.
  5. G. M. J. Jr., “Microbial pathogenesis of Mycobacterium Tuberculosis: dawn of a discipline,” Cell, no. 104, pp. 477-485, 2001.
  6. J. D. E, Mycobacterial diseases of the lung and bronchial tree: Clinical and laboratory aspects of Tuberculosis, Boston: Brown and Company, 1974.
  7. [Online]. Available: https://www.ncbi.nlm.nih.gov/books/NBK441916/.
  8. B. J. R. Elizabeth A. Talbot, Molecular Medical Microbiology, 2015.
  9. R. l. Kradin, Diagnostic Pathology of Infectious Disease, 2018.
  10. World Health Organization, Guidelines on the management of latent Tuberculosis infection, Geneva: WHO, 2015.
  11. World Health Organization, Implementing the WHO Stop TB Strategy: A Handbook for National Tuberculosis Control Programmes.
  12. Gideononline, “www.gideonoline.com,” Gideon, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/Tuberculosis-12470.
  13. A. F. Z. L. F. E. Terracciano E, [Tuberculosis: an ever present disease but difficult to prevent], Ig Sanita, 2020.
  14. M.-R. K. R. R. C. R. Chaulk CP, Eleven years of community-based directly observed therapy for Tuberculosis, JAMA, 1995.
  15. “www.journals.plos.org,” [Online]. Available: https://journals.plos.org/plosmedicine/article/figures?id=10.1371/journal.pmed.1001012.
  16. Z. a. Lancione, “Using data science to improve knowledge around a century old vaccine,” The BCG Atlas, 2020.
  17. CDC. [Online]. Available: https://www.cdc.gov/tb/topic/basics/risk.htm.
  18. G. C. G. R. N. P. Getahun H, “HIV infection-associated Tuberculosis: the epidemiology and the response,” Pubmed, 2010.

Pathogen of the Month: Vibrio cholerae, the Causative Agent of Cholera

Vibrio cholerae
This blog was writtern by Dr. Jaclynn Moskow

 

Vibrio cholerae (V. cholerae) is a species of Gram-negative facultatively anaerobic bacteria of curved rod-shaped with single polar flagella. V. Cholerae has been classified into approximately 200 serogroups. Strains belonging to serogroups O1 and O139 cause the vast majority of cholera cases (1).

Vibrio cholerae is found naturally in brackish riverine, estuarine, and coastal waters. Recognized hosts of the organism include algae, shellfish, chironomid egg masses, fish, waterfowl, amebae, and copepods (2). V. cholerae colonies can form biofilms on both biotic and abiotic surfaces – including on shells, zooplankton, macroalgae, ship hulls, and plastic pollution (3-5). 

 

Cholera Transmission and Disease Severity 

Cholera is primarily transmitted through the consumption of fecally contaminated water and food. Foodborne outbreaks are most frequently linked to fish, shellfish, crabs, oysters, clams, rice, millet gruel, and vegetables (6).

Most V. cholerae infections are asymptomatic or mild in nature. Individuals with asymptomatic infections may still shed bacteria in their feces and infect others (7). Approximately 10% of V. cholerae infections will progress to severe disease (8). In endemic settings, the most severe infections occur in children, while in epidemic settings, severe disease occurs in adults as frequently as it does in children (9). 

Individuals with blood type O are more likely to suffer from severe V. cholerae infection (10). The use of drugs that reduce stomach acid, such as antacids, histamine receptor blockers, and proton pump inhibitors, also increases the risk of severe infection (11). 

 

Vibrio cholerae bacteria on agar
Vibrio cholerae isolated from feces obtained from a patient with profuse diarrhea who had traveled to India. Photo courtesy of Nathan Reading

 

 

Signs and Symptoms of Cholera

Cholera has an average incubation period of 1-5 days. Patients will experience a sudden onset of painless, watery diarrhea that may be accompanied by vomiting. The diarrhea is often characterized as having a “rice water” appearance and fishy odor. Fever is uncommon in adults, but often present in children (12).

In severe cases, dehydration may lead to the rapid progression to acidosis and electrolyte imbalance. Coma may occur. Without the replacement of fluids and electrolytes, hypovolemic shock and death ensue (12).

If left untreated, cholera has a 25-50% mortality rate. Proper treatment reduces the mortality rate to less than 1% (13).

Cholera vector illustration. Labeled infection structure and symptoms scheme. Educational infographic with unsafe water and food vibrio microorganism that causes diarrhea, vomiting and dehydration.

Diagnosis and Treatment of Cholera

Cholera is diagnosed via stool culture. When a case is suspected, healthcare and medical laboratory personnel should follow stool precautions.

Mild and moderate cases of cholera can be successfully treated with oral rehydration salts, while severe cases require rehydration with intravenous fluids (14). The World Health Organization (WHO) recommends reserving antibiotics as a treatment for severe cases only, as antibiotic use has no proven effect on controlling the spread of the disease and may contribute to antimicrobial resistance (15). In severe cases, tetracycline, doxycycline, azithromycin, erythromycin, or ciprofloxacin may be used (12). Most people who recover from V. cholerae infection incur long-lasting immunity (16).

 

Cholera Prevalence

Cholera originated in India and spread across the world during the 19th century (17). Since that time, there have been seven cholera pandemics, including one that is ongoing today (18). 

Currently, approximately 1.3 billion people are at risk for cholera in endemic countries. An estimated 2.86 million cholera cases occur annually, resulting in an estimated 95,000 deaths (19).

Over the last decade, the countries reporting the most cases of cholera have included Yemen, Somalia, the Democratic Republic of Congo, Mozambique, Bangladesh, and Haiti. If you have a GIDEON account, click here to explore the Cholera outbreak map. Cholera is exceedingly rare in Europe and the United States.

 

Cholera cases by region, 1953 – 2018

Cholera-cases-by-region-1953-2018

 

Cholera Prevention

Cholera cases by region, 1953 - 2018

When traveling to an area where cholera is endemic, precautions should include adherence to proper hand hygiene, drinking only bottled water, and avoiding uncooked food.

Ongoing worldwide efforts to end the current cholera pandemic center on increasing access to clean water and sanitation and expanding accessibility to existing cholera vaccines.

 

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References 

(1) Morris, “Infections due to non-O1/O139 Vibrio cholerae”, Uptodate.com, 2019. [Online]. Available: https://www.uptodate.com/contents/infections-due-to-non-o1-o139-vibrio-cholerae

(2) “Cholera: Environmental Reservoirs and Impact on Disease Transmission”, One Health, pp. 149-165, 2014. Available: 10.1128/microbiolspec.oh-0003-2012

(3) B. Wucher, T. Bartlett, M. Hoyos, K. Papenfort, A. Persat and C. Nadell, “Vibrio cholerae filamentation promotes chitin surface attachment at the expense of competition in biofilms”, Proceedings of the National Academy of Sciences, vol. 116, no. 28, pp. 14216-14221, 2019. Available: 10.1073/pnas.1819016116

(4) C. Lutz, M. Erken, P. Noorian, S. Sun and D. McDougald, “Environmental reservoirs and mechanisms of persistence of Vibrio cholerae”, Frontiers in Microbiology, vol. 4, 2013. Available: 10.3389/fmicb.2013.00375 

(5) J. Moskow, “What Do Plastics Have To Do With Infectious Diseases and the Immune System?”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://www.gideononline.com/2021/04/22/what-do-plastics-have-to-do-with-infectious-diseases-and-the-immune-system/ 

(6) G. Rabbani, W. Greenough. “Food as a vehicle of transmission of cholera”, J Diarrhoeal Dis Res, vol. 17, no. 1, pp. 1-9, 1999

(7) J. Lewnard, M. Antillón, G. Gonsalves, A. Miller, A. Ko and V. Pitzer, “Strategies to Prevent Cholera Introduction during International Personnel Deployments: A Computational Modeling Analysis Based on the 2010 Haiti Outbreak”, PLOS Medicine, vol. 13, no. 1, p. e1001947, 2016. Available: 10.1371/journal.pmed.1001947

(8) Cholera – Vibrio cholerae infection: General Information”, Centers for Disease Control and Prevention (CDC0, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), 2020. [Online] Available: https://www.cdc.gov/cholera/general/index.html

(9) J. Harris, R. LaRocque, F. Qadri, E. Ryan and S. Calderwood, “Cholera”, The Lancet, vol. 379, no. 9835, pp. 2466-2476, 2012. Available: 10.1016/s0140-6736(12)60436-x

(10) J. Harris and R. LaRocque, “Cholera and ABO Blood Group: Understanding an Ancient Association”, The American Journal of Tropical Medicine and Hygiene, vol. 95, no. 2, pp. 263-264, 2016. Available: 10.4269/ajtmh.16-0440

(11) S. Handa, “Which classes of medications increase the risk of cholera infection?”, Medscape.com, 2018. [Online]. Available: https://www.medscape.com/answers/962643-54708/which-classes-of-medications-increase-the-risk-of-cholera-infection 

(12) “Cholera”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/cholera-10390

(13) J. Fournier and M. Quilici, “Choléra”, La Presse Médicale, vol. 36, no. 4, pp. 727-739, 2007. Available: 10.1016/j.lpm.2006.11.029 

(14) “WHO | WHO position paper on Oral Rehydration Salts to reduce mortality from cholera”, Who.int, 2021. [Online]. Available: https://www.who.int/cholera/technical/en/

(15) “Cholera”, Who.int, 2021. [Online]. Available: https://www.who.int/news-room/fact-sheets/detail/cholera 

(16) J. Harris, “Cholera: Immunity and Prospects in Vaccine Development”, The Journal of Infectious Diseases, vol. 218, no. 3, pp. S141-S146, 2018. Available: 10.1093/infdis/jiy414

(17) D. Lippi, E. Gotuzzo and S. Caini, “Cholera”, Paleomicrobiology of Humans, pp. 173-180, 2016. Available: 10.1128/microbiolspec.poh-0012-2015 

(18) S. Handa, “What are the 7 pandemics of cholera”, Medscape.com, 2018. [Online]. Available: https://www.medscape.com/answers/962643-54700/what-are-the-7-pandemics-of-cholera

(19) M. Ali, A. Nelson, A. Lopez and D. Sack, “Updated Global Burden of Cholera in Endemic Countries”, PLOS Neglected Tropical Diseases, vol. 9, no. 6, p. e0003832, 2015. Available: 10.1371/journal.pntd.0003832

Pathogen of the month: Staphylococcus aureus

by Dr. Jaclynn Moskow

Staphylococcus aureus, 20,000X magnification
Staphylococcus aureus, 20,000X magnification. Courtesy of Frank DeLeo, NIAID

 

Staphylococcus aureus (S. aureus) is a facultative anaerobic, gram-positive coccus. S. aureus is part of the normal flora of the body, found in the skin, upper respiratory tract, gut, and genitourinary tract – and most commonly in the anterior nares. Twenty percent of individuals are persistent nasal carriers of S. aureus, and an additional thirty percent are intermittent carriers (1).

Under certain conditions, S. aureus can be pathogenic, causing a variety of infections, including skin conditions, pneumonia, gastroenteritis, endocarditis, osteomyelitis, septic arthritis, meningitis, bacteremia, and sepsis. Individuals at increased risk include patients with diabetes, cancer, HIV/AIDS, and other conditions that compromise the immune system. Intravenous drug users may introduce the bacteria into various tissues and/or the bloodstream. Hospitalization is in itself a risk factor for S. aureus infection.

 

Staphylococcus Aureus Skin infections

S. aureus can cause a diverse array of skin infections, including folliculitis, impetigo, furuncles, carbuncles, cellulitis, and abscesses. S. aureus is the most common cause of skin infection in individuals with eczema, and many presumed cases of “eczema” are, in fact, inflammatory reactions to colonization by S. aureus (2). 

S. aureus is the most common agent of surgical site infections (3), and a common cause of infection in burn patients. Animal bites, including bites from dogs and cats, can also lead to S. aureus skin infections.

Staphylococcal scalded skin syndrome, also known as “Ritter’s disease”, is caused by exotoxin-producing strains of S. aureus – and is characterized by diffuse erythematous cellulitis followed by extensive skin exfoliation (4). Fever is common, and patients are most often neonates, children, immunocompromised individuals, and individuals with severe renal disease. It is thought that the latter are at an increased risk due to a decreased ability to excrete the exotoxins in urine (5). Healthy adults rarely develop the syndrome, as a result of having antibodies to the exotoxins. Staphylococcal scalded skin syndrome is intraepidermal. Necrosis of the full epidermal layer may also occur as a result of S. aureus infection and is known as toxic epidermal necrolysis – a more severe form of the disease.

Various topical and systemic antibiotics can be used to treat S. aureus skin infections including beta-lactams, macrolides, and aminoglycosides. Treatment may be complicated by antibiotic resistance.

 

Staphylococcus Aureus Pneumonia 

S. aureus is identified in three percent of community-acquired bacterial pneumonias (6), and 18% of hospital-acquired pneumonias (7). S. aureus is a cause of secondary bacterial pneumonia associated with influenza, and influenza has been shown to increase the adherence of S. aureus to host cells (8). One study showed that 33% of children admitted to the PICU during the 2009 H1N1 pandemic had a secondary bacterial coinfection, with S. aureus being the most common pathogen (9). S. aureus is also frequently isolated from the respiratory tract of children with cystic fibrosis (10).

 

Doctor examining a lung radiography
Staphylococcus aureus is one of the etiological agents of bacterial pneumonia

 

S.aureus can cause necrotizing pneumonia, characterized by necrosis, liquefaction, and cavitation of the lung parenchyma (11) – often accompanied by empyema and bronchopleural fistulae. Necrotizing pneumonia caused by community-acquired methicillin-resistant S. aureus (MRSA) strains which produce Panton valentine leukocidin (PVL) toxin has a mortality rate of 60% (12).

Treatment of pneumonia caused by S. aureus is based on testing for antibiotic susceptibility. Nafcillin, oxacillin, and cefazolin are often used to treat methicillin-sensitive S. aureus (MSSA), while vancomycin or linezolid is often used to treat MRSA (13).

 

Food Poisoning From Staphylococcus Aureus 

S.aureus is one of the most common causes of food-borne disease worldwide (14). Illness is characterized by a short incubation period (2h-4h), nausea, vomiting, intestinal cramping, and profuse watery, non-bloody diarrhea (15). The condition is generally self-limited, and symptoms typically resolve within 12 to 24 hours.

 

Staphylococcal food poisoning, outbreak-related cases and rates in the United States, 1952 – 2010

Toxic Shock Syndrome From Staphylococcus Aureus

S.aureus is the most common cause of toxic shock syndrome, a life-threatening syndrome resulting from staphylococcal toxin-1 (TSST-1). It is characterized by fever, hypotension, myalgia, macular erythema, desquamation (particularly of the palms and soles), and acute vomiting or diarrhea (16). Most cases are associated with the use of “super absorbent” tampons or staphylococcal wound infection. Case fatality rates of 5 to 10% are reported. The condition is generally treated with vancomycin in combination with clindamycin.

 

Staphylococcus Aureus Endocarditis

S.aureus is the leading cause of acute bacterial endocarditis. Of infections caused by S. aureus, endocarditis accounts for the highest mortality rates (17). Populations at high risk include IV drug users and patients with implanted medical devices such as prosthetic heart valves, grafts, pacemakers, and hemodialysis catheters (18). Treatment varies and depends on several factors, including antibiotic susceptibility, site of infection (left side versus right side), IV drug abuse status, and if a prosthetic valve is present (19).

 

Other Infections Caused By Staphylococcus Aureus

Staphylococcus aureus can also cause mastitis, urinary tract infections, osteomyelitis, meningitis, septic arthritis, and many infections associated with medical devices and implants.

 

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References 

(1) Wertheim HF, Melles DC, Vos MC, van Leeuwen W, van Belkum A, Verbrugh HA, Nouwen JL. The role of nasal carriage in Staphylococcus aureus infections. Lancet Infect Dis. 2005 Dec;5(12):751-62. doi: 10.1016/S1473-3099(05)70295-4.

(2) Nakamura Y, Oscherwitz J, Cease KB, Chan SM, Muñoz-Planillo R, Hasegawa M, Villaruz AE, Cheung GY, McGavin MJ, Travers JB, Otto M, Inohara N, Núñez G. Staphylococcus δ-toxin induces allergic skin disease by activating mast cells. Nature. 2013 Nov 21;503(7476):397-401. doi: 10.1038/nature12655. 

(3) Mellinghoff SC, Vehreschild JJ, Liss BJ, Cornely OA. Epidemiology of Surgical Site Infections With Staphylococcus aureus in Europe: Protocol for a Retrospective, Multicenter Study. JMIR Res Protoc. 2018 Mar 12;7(3):e63. doi: 10.2196/resprot.8177.

(4) “Staphylococcal scalded skin syndrome”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/staphylococcal-scalded-skin-syndrome-12245

(5) Ross A, Shoff HW. Staphylococcal Scalded Skin Syndrome. 2020 Oct 27. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. 

(6) Hageman JC, Uyeki TM, Francis JS, Jernigan DB, Wheeler JG, Bridges CB, Barenkamp SJ, Sievert DM, Srinivasan A, Doherty MC, McDougal LK, Killgore GE, Lopatin UA, Coffman R, MacDonald JK, McAllister SK, Fosheim GE, Patel JB, McDonald LC. Severe community-acquired pneumonia due to Staphylococcus aureus, 2003-04 influenza season. Emerg Infect Dis. 2006 Jun;12(6):894-9. doi: 10.3201/eid1206.051141.

(7) Kollef MH, Micek ST. Staphylococcus aureus pneumonia: a “superbug” infection in community and hospital settings. Chest. 2005 Sep;128(3):1093-7. doi: 10.1378/chest.128.3.1093.

(8) Morris DE, Cleary DW, Clarke SC. Secondary Bacterial Infections Associated with Influenza Pandemics. Front Microbiol. 2017 Jun 23;8:1041. doi: 10.3389/fmicb.2017.01041.

(9) Randolph AG, Vaughn F, Sullivan R, Rubinson L, Thompson BT, Yoon G, Smoot E, Rice TW, Loftis LL, Helfaer M, Doctor A, Paden M, Flori H, Babbitt C, Graciano AL, Gedeit R, Sanders RC, Giuliano JS, Zimmerman J, Uyeki TM; Pediatric Acute Lung Injury and Sepsis Investigator’s Network and the National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. Critically ill children during the 2009-2010 influenza pandemic in the United States. Pediatrics. 2011 Dec;128(6):e1450-8. doi: 10.1542/peds.2011-0774.

(10) Hurley MN. Staphylococcus aureus in cystic fibrosis: problem bug or an innocent bystander? Breathe (Sheff). 2018 Jun;14(2):87-90. doi: 10.1183/20734735.014718.

(11) Nicolaou EV, Bartlett AH. Necrotizing Pneumonia. Pediatr Ann. 2017 Feb 1;46(2):e65-e68. doi: 10.3928/19382359-20170120-02.

(12) Gillet Y, Vanhems P, Lina G, Bes M, Vandenesch F, Floret D, Etienne J. Factors predicting mortality in necrotizing community-acquired pneumonia caused by Staphylococcus aureus containing Panton-Valentine leukocidin. Clin Infect Dis. 2007 Aug 1;45(3):315-21. doi: 10.1086/519263.

(13) Clark SB, Hicks MA. Staphylococcal Pneumonia. 2020 Oct 1. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. 

(14) Kadariya J, Smith TC, Thapaliya D. Staphylococcus aureus and staphylococcal food-borne disease: an ongoing challenge in public health. Biomed Res Int. 2014;2014:827965. doi: 10.1155/2014/827965.

(15) “Staphylococcal food poisoning”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/staphylococcal-food-poisoning-12260

(16) “Toxic shock syndrome”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/toxic-shock-syndrome-12360

(17) Fernández Guerrero ML, González López JJ, Goyenechea A, Fraile J, de Górgolas M. Endocarditis caused by Staphylococcus aureus: A reappraisal of the epidemiologic, clinical, and pathologic manifestations with analysis of factors determining outcome. Medicine (Baltimore). 2009 Jan;88(1):1-22. doi: 10.1097/MD.0b013e318194da65.

(18) Fowler VG Jr, Miro JM, Hoen B, Cabell CH, Abrutyn E, Rubinstein E, Corey GR, Spelman D, Bradley SF, Barsic B, Pappas PA, Anstrom KJ, Wray D, Fortes CQ, Anguera I, Athan E, Jones P, van der Meer JT, Elliott TS, Levine DP, Bayer AS; ICE Investigators. Staphylococcus aureus endocarditis: a consequence of medical progress. JAMA. 2005 Jun 22;293(24):3012-21. doi: 10.1001/jama.293.24.3012. 

(19) Bille J. Medical treatment of staphylococcal infective endocarditis. Eur Heart J. 1995 Apr;16 Suppl B:80-3. doi: 10.1093/eurheartj/16.suppl_b.80.

What Do Plastics Have To Do With Infectious Diseases and the Immune System?

by Dr. Jaclynn Moskow

Plastic bottles and microplastics floating in the open ocean

 

Most people are aware that plastics are harmful to the environment. They pollute soil, air, and water and disrupt our ecosystems. Few people, however, are aware of the influence plastics may have on the spread of infectious diseases and on the function of our immune systems.

In recognition of Earth Day 2021, we will examine the ways in which polluting our planet with plastics may affect human health.

 

Plastics as a Breeding Ground for Pathogens

Microbes struggle to survive on certain surfaces, and thrive on others. Copper, for example, has anti-microbial properties (1); while plastic keeps some microbes alive longer than other common materials.

Influenza A and B viruses survive for longer periods on plastic surfaces than on cloth or paper (2). SARS-CoV-2 has been shown to survive longer on plastic than on glass, stainless steel, pigskin, cardboard, banknotes, cotton, wood, paper, tissue, or copper (3). Indeed, bacteria – and not only viruses – favor plastic. Methicillin-resistant Staphylococcus aureus (MRSA), for example, survives longer on plastic than on wood, glass, or cloth (4). There is thus concern for plastics serving as fomites, especially in high-risk settings such as hospitals.

But what about the plastics polluting our oceans? Are these free from pathogens? There are actually such complex microbial communities found on the plastics in our ocean that the term “plastisphere” was coined (5). A 2019 study examined the plastisphere of plastic nurdles from five European beaches (6). Escherichia coli (E. coli) and Vibrio spp. were found colonizing nurdles from all beaches examined. Vibrio spp. occur naturally in seawater, and researchers have speculated that fecally-contaminated water was likely the original source of the E. coli.

 

Environment pollution - plastic floating in the water
Plastisphere is a breeding ground for pathogens

 

A subsequent study conducted in 2020 analyzed biofilms found on plastic substrates in estuarine tributaries of Lower Chesapeake Bay (7). Vibrio spp. – specifically V. cholerae, V. parahaemolyticus, and V. vulnificus – were identified… all three of which can be pathogenic to humans. Concerningly, the authors noted that, “the concentration of putative Vibrio spp. on microplastics was much greater than in corresponding water samples.” They also found a high rate of antibiotic resistance amongst isolates, noting that “the potential for plastic in aqueous environments to serve as a vector for pathogenic organisms is compounded by the possibility for its dissemination of antibiotic-resistance genes.”

Several additional studies have confirmed the presence of Vibrio spp. on marine plastics found in various bodies of water across the world – and it is only a matter of time before additional pathogens will be identified as common residents of the plastisphere. 

 

Plastics and the Immune System

In addition to polluting our oceans, plastics are polluting our bodies. A team examined 47 liver- and adipose-tissue specimens from donated cadavers, and detected plastic micro- and nanoparticles in 100% of samples (8). Microplastics have been found in human placentas (9), and animal models indicate that nanoplastics can cross the blood-brain barrier (10). There is also evidence that when plastics accumulate in the body, they may be harmful to the immune system. 

Recent work has examined how immune cells behave in the presence of microplastics. Microplastics coated in blood plasma were placed in culture dishes containing immune cells. Within 24 hours, 60% of immune cells were destroyed. Under the same culture conditions, but in the absence of microplastics, only 20% of immune cells were destroyed (11).

Microplastics may also alter the immune system at the level of gene expression. When adult zebrafish were exposed to microplastics, alterations in the expression of 41 genes encoding proteins attributed to immune processes were observed (12).

The toxic effects of plastic do not appear to be limited to the immune system. In animal models, plastics are found to be potentially harmful to just about every cell type and organ system. Micro- and nanoplastics appear to be pro-inflammatory (13), are known to irritate the respiratory tract (14), can act as endocrine disrupters (15), may be neurotoxic (16), and appear to alter the gut microbiome (17). Such effects are observed even in the absence of controversial additives such as bisphenol A (BPA) and phthalates.

 

Ocean microplastics pollution cycle
Ocean microplastics pollution cycle

 

So What Can We Do?

Unfortunately, plastics are now ubiquitous. They are used in packaging materials, construction, textile manufacturing, automobiles, furniture, electronics, toys, medical devices, makeup, and even chewing gum. As a result, micro and nanoplasitics have contaminated our food chain and have been detected in cows milk (18), seafood (19), fruit and vegetables (20), honey and sugar (21), table salt (22), and tap water (23).

In 1960, an estimated half a million metric tons of plastic were produced each year, increasing to 348 million tons in 2017 (24). This compounding problem warrants immediate attention.

Some have suggested the use of fungi, bacteria, or worms to help dissolve plastic. Although the introduction of such organisms into the ecosystem is itself risky, solutions of this type may still be worth exploring.

Many investigators have been directing their efforts at designing biodegradable and compostable plastics and plastic alternatives. The assumption is that such materials would be less harmful to the environment and human health than traditional plastics – but there are many unknowns. One study concluded that the chemical processing required to create some existing bioplastics resulted in a greater amount of pollutants than the chemical processing used to create traditional plastics (25). Beyond this, there is no data on the interaction of biodegradable plastics with the human body.

A woman chooses a paper bag with food and refuses to use plastic on the background of the kitchen. The concept of environmental protection and the abandonment of plastic
Small everyday decisions count

 

While the “big-picture” solution remains elusive, there are easy steps that we can take to reduce our individual plastic footprints and lessen the potential for harm to our own bodies. We can avoid drinking and eating from plastic containers, abstain from using plastic bags, switch to wire hangers, wooden toys, etc. 

We only get one Earth, and we only get one body… and we must take great care of both. 

Happy Earth Day!

 

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References

(1) G. Grass, C. Rensing and M. Solioz, “Metallic Copper as an Antimicrobial Surface”, Applied and Environmental Microbiology, vol. 77, no. 5, pp. 1541-1547, 2010. Available: 10.1128/aem.02766-10 

(2) B. Bean, B. Moore, B. Sterner, L. Peterson, D. Gerding and H. Balfour, “Survival of Influenza Viruses on Environmental Surfaces”, Journal of Infectious Diseases, vol. 146, no. 1, pp. 47-51, 1982. Available: 10.1093/infdis/146.1.47

(3) D. Corpet, “Why does SARS-CoV-2 survive longer on plastic than on paper?”, Medical Hypotheses, vol. 146, p. 110429, 2021. Available: 10.1016/j.mehy.2020.110429

(4) C. Coughenour, V. Stevens and L. Stetzenbach, “An Evaluation of Methicillin-Resistant Staphylococcus aureus Survival on Five Environmental Surfaces”, Microbial Drug Resistance, vol. 17, no. 3, pp. 457-461, 2011. Available: 10.1089/mdr.2011.0007 

(5)E. Zettler, T. Mincer and L. Amaral-Zettler, “Life in the “Plastisphere”: Microbial Communities on Plastic Marine Debris”, Environmental Science & Technology, vol. 47, no. 13, pp. 7137-7146, 2013. Available: 10.1021/es401288x

(6) A. Rodrigues, D. Oliver, A. McCarron and R. Quilliam, “Colonisation of plastic pellets (nurdles) by E. coli at public bathing beaches”, Marine Pollution Bulletin, vol. 139, pp. 376-380, 2019. Available: 10.1016/j.marpolbul.2019.01.011

(7) A. Laverty, S. Primpke, C. Lorenz, G. Gerdts and F. Dobbs, “Bacterial biofilms colonizing plastics in estuarine waters, with an emphasis on Vibrio spp. and their antibacterial resistance”, PLOS ONE, vol. 15, no. 8, p. e0237704, 2020. Available: 10.1371/journal.pone.0237704

(8) “Methods for microplastics, nanoplastics and plastic monomer detection and reporting in human tissues – American Chemical Society”, American Chemical Society, 2021. [Online]. Available: https://www.acs.org/content/acs/en/pressroom/newsreleases/2020/august/micro-and-nanoplastics-detectable-in-human-tissues.html

(9) A. Ragusa et al., “Plasticenta: First evidence of microplastics in human placenta”, Environment International, vol. 146, p. 106274, 2021. Available: 10.1016/j.envint.2020.106274

(10) M. Prüst, J. Meijer and R. Westerink, “The plastic brain: neurotoxicity of micro- and nanoplastics”, Particle and Fibre Toxicology, vol. 17, no. 1, 2020. Available: 10.1186/s12989-020-00358-y

(11) “Nienke Vrisekoop on microplastic’s impact on human immune cells | Plastic Health Summit 2019 – YouTube” Available: https://youtu.be/b-8DZ2taGPA

(12) G. Limonta et al., “Microplastics induce transcriptional changes, immune response and behavioral alterations in adult zebrafish”, Scientific Reports, vol. 9, no. 1, 2019. Available: 10.1038/s41598-019-52292-5

(13) R. Lehner, C. Weder, A. Petri-Fink and B. Rothen-Rutishauser, “Emergence of Nanoplastic in the Environment and Possible Impact on Human Health”, Environmental Science & Technology, vol. 53, no. 4, pp. 1748-1765, 2019. Available: 10.1021/acs.est.8b05512

(14) A. Banerjee and W. Shelver, “Micro- and nanoplastic induced cellular toxicity in mammals: A review”, Science of The Total Environment, vol. 755, p. 142518, 2021. Available: 10.1016/j.scitotenv.2020.142518 

(15) F. Amereh, M. Babaei, A. Eslami, S. Fazelipour and M. Rafiee, “The emerging risk of exposure to nano(micro)plastics on endocrine disturbance and reproductive toxicity: From a hypothetical scenario to a global public health challenge”, Environmental Pollution, vol. 261, p. 114158, 2020. Available: 10.1016/j.envpol.2020.114158 

(16) M. Prüst, J. Meijer and R. Westerink, “The plastic brain: neurotoxicity of micro- and nanoplastics”, Particle and Fibre Toxicology, vol. 17, no. 1, 2020. Available: 10.1186/s12989-020-00358-y

(17) N. Hirt and M. Body-Malapel, “Immunotoxicity and intestinal effects of nano- and microplastics: a review of the literature”, Particle and Fibre Toxicology, vol. 17, no. 1, 2020. Available: 10.1186/s12989-020-00387-7

(18) G. Kutralam-Muniasamy, F. Pérez-Guevara, I. Elizalde-Martínez and V. Shruti, “Branded milks – Are they immune from microplastics contamination?”, Science of The Total Environment, vol. 714, p. 136823, 2020. Available: 10.1016/j.scitotenv.2020.136823

(19) M. Smith, D. Love, C. Rochman and R. Neff, “Microplastics in Seafood and the Implications for Human Health”, Current Environmental Health Reports, vol. 5, no. 3, pp. 375-386, 2018. Available: 10.1007/s40572-018-0206-z

(20) D. Yang, H. Shi, L. Li, J. Li, K. Jabeen and P. Kolandhasamy, “Microplastic Pollution in Table Salts from China”, Environmental Science & Technology, vol. 49, no. 22, pp. 13622-13627, 2015. Available: 10.1021/acs.est.5b03163 

(21) G. Liebezeit and E. Liebezeit, “Non-pollen particulates in honey and sugar”, Food Additives & Contaminants: Part A, vol. 30, no. 12, pp. 2136-2140, 2013. Available: 10.1080/19440049.2013.843025 

(22) D. Yang, H. Shi, L. Li, J. Li, K. Jabeen and P. Kolandhasamy, “Microplastic Pollution in Table Salts from China”, Environmental Science & Technology, vol. 49, no. 22, pp. 13622-13627, 2015. Available: 10.1021/acs.est.5b03163 

(23) H. Tong, Q. Jiang, X. Hu and X. Zhong, “Occurrence and identification of microplastics in tap water from China”, Chemosphere, vol. 252, p. 126493, 2020. Available: 10.1016/j.chemosphere.2020.126493 

(24) P. Wu et al., “Environmental occurrences, fate, and impacts of microplastics”, Ecotoxicology and Environmental Safety, vol. 184, p. 109612, 2019. Available: 10.1016/j.ecoenv.2019.109612 

(25) M. Tabone, J. Cregg, E. Beckman and A. Landis, “Sustainability Metrics: Life Cycle Assessment and Green Design in Polymers”, Environmental Science & Technology, vol. 44, no. 21, pp. 8264-8269, 2010. Available: 10.1021/es101640n

Occupational Infectious Diseases

by Dr. Jaclynn Moskow

Occupational health: Manufacturer working at storage tanks in brewery

 

In recognition of World Health Day 2021, which falls on April 7, the WHO points out that “some people are able to live healthier lives and have better access to health services than others – entirely due to the conditions in which they are born, grow, live, work, and age.”

Many of us spend a significant portion of our lives engaged in work. Unfortunately, certain working conditions put us at increased risk of poor health. For example, some occupations involve repeated exposure to respiratory irritants and carcinogens, while others are associated with musculoskeletal injury or hearing loss. Many professions put workers at risk of contracting an infectious disease.

Textbook of Occupational Medicine Practice (1) outlines five primary modes of transmission for occupational infections:

  1. Contact with animals and animal products (zoonoses)
  2. Exposure to vectors 
  3. Care of patients 
  4. Environmental sources, exposure to soils 
  5. Occupational skin infections

 

Occupational Zoonoses

Farmer with cow

Individuals who work with animals and animal products are at risk of contracting zoonotic diseases. Such occupations include farmworkers, ranch workers, butchers, veterinary workers, and zoo workers. There are currently over 200 recognized zoonoses (2).

Brucellosis is a zoonotic infectious disease caused by Brucella spp. Reservoirs for Brucella include pigs, cattle, sheep, goats, dogs, coyotes, and caribou. Brucellosis can be acquired via direct contact with these animals, or by processing their meat. Symptoms include prolonged fever, hepatosplenomegaly, lymphadenopathy, arthritis, and osteomyelitis (3). A study of occupationally acquired Brucella in Russia found that factors increasing the risk of infection include lack of awareness amongst workers regarding the disease and absence of regular inspections of working conditions (4).

Individuals who work with cats are at increased risk of acquiring bartonellosis, also known as “cat scratch disease.” As the name implies, the disease is caused by species of Bartonella and transmitted via cat scratches. Clinical manifestations include tender suppurative regional adenopathy and fever. Occasionally, systemic infection occurs involving such sites as the liver, brain, endocardium, and bones (5). A recent study of veterinary personnel detected Bartonella in 28% of subjects, compared to 0% of a control group (6).

A review of the incidences of campylobacteriosis and cryptosporidiosis in Nebraska between 2005-2015 identified occupational animal exposure as the cause in 16.6% and 8.7% of cases, respectively (7). Most of these cases were acquired by farmers, ranchers, and those working in animal slaughter and processing facilities; and the most common animal source was determined to be cattle. Additional occupational zoonotic infectious diseases include salmonellosis, Escherichia coli O157 infection, and Q-fever.

 

Occupational Infections Acquired Via Exposure to Vectors

Woman digging hole with shovel to plant saplings in forest. Forester planting new small trees in deforested area. Vector-borne diseases are occupational hazards for forestry workers.

Individuals working in areas infested with ticks, fleas, and mites are at an increased risk for infectious diseases carried by these arthropods. Occupations at risk include agricultural workers, forestry workers, military personnel, veterinary workers, and pest control workers.

Diseases that may be spread to workers via tick bites include Lyme disease, babesiosis, ehrlichiosis, Colorado tick fever, Rocky Mountain spotted fever, tularemia, and Powassan virus encephalitis. In the United States, Lyme disease is the most common tick-borne illness. It is caused by Borrelia spp. and characterized by the presence of erythema migrans, neurological, musculoskeletal, and cardiac manifestations.

Individuals working around fleas may acquire flea-borne (murine) typhus, caused by Rickettsia typhi, or Plague caused by Yersinia pestis. Additionally, exposure to mites could lead to the development of rickettsialpox, caused by Rickettsia akari, or scrub typhus, caused by Orientia spp.

 

Occupational Infections Acquired Via Care of Patients

Female nurse tying surgical mask in operation theater

 

Caring for patients while working in hospitals, ambulatory clinics, diagnostic laboratories, nursing homes, and the home carries an increased risk for several infectious diseases.

Each year, healthcare workers experience approximately 600,000–800,000 exposures to HIV, hepatitis B, and hepatitis C (8). Exposures may occur via needle-stick injury or via blood and other bodily fluids which accidentally contact mucous membranes. Healthcare workers can decrease their risk of contracting bloodborne pathogens by adhering to universal precautions.

Airborne pathogens are also of concern to healthcare workers. Respiratory diseases that can be acquired while caring for patients include tuberculosis, influenza, and COVID-19. Healthcare workers are also at increased risk of contracting methicillin-resistant Staphylococcus aureus (MRSA). Approximately 4.6% of healthcare workers carry MRSA (9), compared to 1% of the general population (10).

Vaccinations recommended to healthcare workers to help prevent occupationally acquired infections include hepatitis B, MMR, and influenza. 

 

Occupational Infections Acquired Via Exposure to Soils

Close-up low section of woman standing with fork on dirt

Individuals engaged in plowing, digging, and excavating soil at work may be exposed to a variety of infections. Such occupations include construction and demolition work, oil and gas extraction, agriculture workers, landscaping, and archaeology.

Workers exposed to soils are at an increased risk of endemic mycoses, including histoplasmosis, coccidioidomycosis, paracoccidioidomycosis, and blastomycosis. These infections are generally acquired by inhaling fungal spores that become airborne as the soil is disrupted. An example of this occurred between 2011 and 2014 when an outbreak of coccidioidomycosis occurred among workers constructing solar power-generating facilities in San Luis Obispo County, California. A total of 44 cases were documented, including nine hospitalizations (11). 

The paradigm disease associated with soil contact is tetanus, caused by Clostridium tetani. Tetanus is acquired when bacterial spores found in soil are introduced to the body via a breach in the skin. Clinical manifestations of tetanus include trismus (lockjaw), facial spasm, opisthotonos, recurrent tonic spasms of skeletal muscle, and tachycardia. Tetanus has a case fatality rate of 10 to 40% (12). Tetanus cases can be prevented through vaccination…and the CDC reports that the efficacy of the tetanus vaccine is nearly 100% (13).

 

Occupational Skin Infections

Butchers may catch occupational skin infections by exposure to raw meat

There are a wide variety of professions in which occupational exposure to skin infections may occur. These include farmers, fisherman, butchers, veterinary workers, aquarium workers, swimming pool cleaners, healthcare workers, and salon workers. 

Many occupational skin infections result from exposure to animals and animal tissue. For example, farmers and butchers are at an increased risk of contracting cutaneous anthrax, caused by Bacillus anthracis. Cutaneous anthrax usually begins with pruritus at the affected site and is followed by a small, painless papule that progresses to a vesicle. The lesion erodes and becomes necrotic, and secondary vesicles are sometimes observed. Lymphadenopathy, fever, and headache may also occur. When left untreated, approximately 20% of cases are fatal (14).

Erysipeloid, caused by Erysipelothrix rhusiopathiae, can also occur when working with animals and animal tissues. The infection is characterized by rash, local pain, swelling, and occasionally fever. One report described an outbreak of erysipeloid amongst workers at a shoe factory (15). The source of the bacteria was determined to be raw leather.

Exposure to water is another common source of occupational skin infections. Fish tank granuloma, an infection caused by Mycobacterium marinum, is often acquired by aquarium workers. Fishermen are at risk of contracting Vibrio vulnificus infection through contact with contaminated ocean water or fish.

Other infections of the skin that can be acquired at work are caused by fungi. Examples include candidiasis, dermatophytosis, chromomycosis, and sporotrichosis. Scabies, a parasitic skin infestation caused by a mite, is often reported among healthcare workers, daycare workers, and correctional facility employees.

 

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References

(1) D. Koh and T. Aw, “Textbook of Occupational Medicine Practice”, 2017. Available: 10.1142/10298

(2) “Other Neglected Zoonotic Diseases”, World Health Organization, 2021. [Online]. Available: https://www.who.int/neglected_diseases/zoonoses/other_NZDs/en/

(3) “Brucellosis”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/brucellosis-10260

(4) A. Tarkhov,  et al., “The Working Conditions At Animal Farm Complexes of Workers With Occupational Brucellosis”, Med Tr Prom Ekol, vol. 5, pp. 5-9, 2012.

(5) “Bartonellosis – Cat Borne”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/bartonellosis-cat-borne-10320

(6) P. Lantos et al., “Detection of Bartonella Species in the Blood of Veterinarians and Veterinary Technicians: A Newly Recognized Occupational Hazard?”, Vector-Borne and Zoonotic Diseases, vol. 14, no. 8, pp. 563-570, 2014. Available: 10.1089/vbz.2013.1512

(7) C. Su, D. Stover, B. Buss, A. Carlson and S. Luckhaupt, “Occupational Animal Exposure Among Persons with Campylobacteriosis and Cryptosporidiosis — Nebraska, 2005–2015”, MMWR. Morbidity and Mortality Weekly Report, vol. 66, no. 36, pp. 955-958, 2017. Available: 10.15585/mmwr.mm6636a4

(8) N. Swanson, C. Ross and K. Fennelly, “Healthcare-related Infectious Diseases1”, Emerging Infectious Diseases, vol. 10, no. 11, pp. e3-e3, 2004. Available: 10.3201/eid1011.040622_03

(9) W. Albrich and S. Harbarth, “Health-care workers: source, vector, or victim of MRSA?”, The Lancet Infectious Diseases, vol. 8, no. 5, pp. 289-301, 2008. Available: 10.1016/s1473-3099(08)70097-5

(10) “MRSA and the Workplace”, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, 2015. [Online]. Available: https://www.cdc.gov/niosh/topics/mrsa/default.html

(11) G. Sondermeyer Cooksey et al., “Dust Exposure and Coccidioidomycosis Prevention Among Solar Power Farm Construction Workers in California”, American Journal of Public Health, vol. 107, no. 8, pp. 1296-1303, 2017. Available: 10.2105/ajph.2017.303820

(12) “Tetanus”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/tetanus-12330

(13) “Tetanus”, Centers for Disease Control and Prevention, Epidemiology and Prevention of Vaccine-Preventable Diseases, 2008. Available: https://www.cdc.gov/vaccines/pubs/pinkbook/downloads/tetanus.pdf

(14) “Anthrax”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/anthrax-10100

(15) V Popugaĭlo VM, et al., “Erysipeloid as an occupational disease of workers in shoe enterprises”, Zh Mikrobiol Epidemiol Immunobiol, vol. 10, pp. 46-9, 1983.

Pathogen of the Month: Escherichia Coli (E. Coli)

by Dr. Jaclynn Moskow

Escherichia coli bacterium, E.coli, gram-negative rod-shaped bacteria, part of intestinal normal flora and causative agent of diarrhea and inflammations of different location, 3D illustration

 

Escherichia coli (E. coli) is a species of Gram-negative, rod-shaped, facultatively anaerobic bacteria. Many E. coli strains are a part of the normal flora of the gut microbiome. E. coli can also be found in the normal flora of the skin and genital tract (1).

Strains of E. coli that are part of the microbiome can be pathogenic under certain conditions – often when introduced to a new part of the body. Additionally, strains of E. coli that are not normally found in the microbiome can also cause significant disease (i.e., enterovirulent E. coli).

E. coli is the most common cause of urinary tract infection and biliary sepsis, and a common agent in travelers’ diarrhea, foodborne gastroenteritis, hemorrhagic colitis, and a wide variety of systemic infections (2).

 

Enterotoxigenic Escherichia Coli (ETEC)

Enterotoxigenic E. coli (ETEC) infection is the most common cause of diarrhea in children (4) and the leading cause of travelers’ diarrhea (5). It is transmitted via contaminated food and water. Symptoms commonly include watery diarrhea and abdominal cramping. Most cases are self-limited, but infection may be life-threatening in infants. 

 

Enteropathogenic Escherichia Coli (EPEC)

Enteropathogenic E. coli (EPEC) infection is a common cause of infantile diarrhea, although it can affect people of all ages. Like ETEC, diarrhea caused by EPEC infection is usually watery. The organism is also spread via the fecal-oral route, commonly via contaminated food and water. Infection is usually self-limited.

 

Uropathogenic E. Coli (UPEC)

Uropathogenic Escherichia coli (UPEC) cells adhered to bladder epithelial cell (BEC). Cells stained with methylene blue and fuchsine.
Uropathogenic Escherichia coli (UPEC) cells adhered to bladder epithelial cell (BEC). Cells stained with methylene blue and fuchsine. Author: Stefan Walkowski

 

E. coli strains that cause urinary tract infection are referred to as uropathogenic E. coli (UPEC). Individuals at increased risk of UPEC infection include neonates, sexually active women, geriatric individuals, and patients with indwelling urinary catheters.

Approximately 40% of adult women will experience cystitis at some point, with UPEC identified as the causative agent in 75-80% of cases (3). Untreated cystitis caused by UPEC infection can progress to pyelonephritis. Symptoms of cystitis/pyelonephritis may include dysuria, hematuria, increased urinary frequency, cloudy or foul-smelling urine, flank pain, vomiting, and fever.

Many different antibiotics are commonly used to treat UPEC infections, including penicillins, cephalosporins, fluoroquinolones, and trimethoprim-sulfamethoxazole. Treatment may be complicated by the increasing prevalence of antibiotic-resistant strains.

 

Shiga Toxin-Producing E. Coli (STEC)

Shiga toxin-producing E. coli (STEC) is also referred to as Verocytotoxin-producing E. coli (VTEC) or Enterohemorrhagic E. coli (EHEC). This variety of E. coli is most commonly associated with foodborne outbreaks in the developed world. Infection can be acquired from contaminated bovine meat, milk and dairy products, vegetables, fruit, and water (6).

Unlike ETEC and EPEC, infection with STEC usually causes bloody diarrhea. Treatment of diarrhea from STEC is supportive and includes fluid replacement. Infection with STEC can also cause hemolytic-uremic syndrome (HUS), most notably associated with E. coli O157:H7 strain. Nearly 40% of patients with STEC-HUS require temporary renal replacement therapy, and up to 20% will have permanent residual kidney dysfunction (2).

Worldwide, it is estimated that STEC infection causes approximately 2.8 million acute illnesses annually, 3900 cases of HUS, 270 cases of end-stage renal disease, and 230 deaths (7).

In 1993, E. coli O157:H7 made headlines when an outbreak occurred at the Jack-in-the-Box restaurant chain in the United States, affecting a total of 73 restaurant locations across 4 states. The source of this outbreak was determined to be contaminated hamburger patties. More than 700 people became ill, including 171 hospitalizations and four deaths (8). More recently, in 2019, the CDC issued a warning to avoid Romaine lettuce from the Salinas Valley region in California (9). They reported that E. coli O157:H7 infection from this vegetable affected 167 people across 27 states, with 85 hospitalizations, and 15 cases of the hemolytic uremic syndrome (10).

 

United States. E. coli – VTEC infection, cases and rates per 100,000

United States. E. coli - VTEC infection, cases and rates per 100,000

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Enteroaggregative E. Coli (EAEC)

Enteroaggregative E. coli (EAEC) infection is recognized as the second most common cause of traveler’s diarrhea (10). It can also cause both acute and chronic childhood diarrhea. EAEC infection has been associated with reduced growth acceleration and failure to thrive among children in developing countries (11). EAEC are also the strains most commonly associated with diarrhea among individuals with HIV/AIDS (12). Diarrhea caused by EAEC is usually watery in nature. In some cases, infection is self-limiting, while in other cases, antibiotics are warranted. Fluoroquinolones, especially ciprofloxacin, are widely considered the treatments of choice (13).

 

Enteroinvasive E. Coli (EIEC)

Enteroinvasive E. coli (EIEC) are strains that possess some of the biochemical characteristics of E. coli and have the ability to cause dysentery through an invasion mechanism similar to that of Shigella (14).  As in shigellosis, diarrhea caused by EIEC may be watery or bloody, and mucus is sometimes present. Infection is usually self-limiting. 

 

Diffusely Adherent E. Coli (DAEC)

Diffusely-adherent E. coli (DAEC) is the most recent diarrheagenic E. coli pathogroup to be identified. DAEC infection is associated with diarrhea in children, where the risk of infection increases with age. These organisms have also been identified as agents of diarrhea in travelers and in patients with HIV/AIDS.  Strains have also been isolated from patients with inflammatory bowel disease and colorectal cancer (15).

 

Meningitis/Sepsis-Associated E. Coli (MNEC)

Meningitis/Sepsis-Associated E. coli (MNEC) infection is a common cause of severe disease in neonates. MNEC infection has a case fatality rate of 15–40% and may result in severe neurological defects in survivors (16). Third-generation cephalosporins are the recommended treatments for neonatal MNEC infection (17). Rarely, MNEC infection occurs in adults, particularly in those who are immunocompromised. 

 

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References

(1) S. Baron, Medical microbiology. Galveston, Tex.: University of Texas Medical Branch at Galveston, 1996. [Online]. Available: https://www.ncbi.nlm.nih.gov/books/NBK7617/

(2) “Escherichia coli”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/microbes/bacteria/escherichia-coli-1850

(3) H. Mobley, E. Hagan and M. Donnenberg, “Uropathogenic Escherichia coli”, EcoSal Plus, vol. 3, no. 2, 2009. Available: 10.1128/ecosalplus.8.6.1.3

(4) A. Mirhoseini, J. Amani and S. Nazarian, “Review on pathogenicity mechanism of enterotoxigenic Escherichia coli and vaccines against it”, Microbial Pathogenesis, vol. 117, pp. 162-169, 2018. Available: 10.1016/j.micpath.2018.02.032

(5) “Enterotoxigenic E. coli (ETEC)”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), 2014. [Online]. Available: https://www.cdc.gov/ecoli/etec.html

(6) “Pathogenicity assessment of Shiga toxin‐producing Escherichia coli (STEC) and the public health risk posed by contamination of food with STEC”, European Food Safety Authority, 2020. [Online]. Available: https://www.efsa.europa.eu/en/efsajournal/pub/5967

(7) Majowicz et al., “Global Incidence of Human Shiga Toxin–Producing Escherichia coliInfections and Deaths: A Systematic Review and Knowledge Synthesis”, Foodborne Pathogens and Disease, vol. 11, no. 6, pp. 447-455, 2014. Available: 10.1089/fpd.2013.1704

(8) “Jack in the Box E. Coli Outbreak – 25 Years Later”, Canadian Institute of Food Safety, 2021. [Online]. Available: https://www.foodsafety.ca/news/jack-box-e-coli-outbreak-25-years-later

(9) “The Final Update on the Multistate Outbreak of E. coli 0157:H7 Infections”, Centers for Disease Control and Prevention, 2020. [Online]. Available: https://www.cdc.gov/media/releases/2020/s0115-ecoli-outbreak.html

(10) H. Brüssow, “ESCHERICHIA COLI | Enteroaggregative E. coli”, Encyclopedia of Food Microbiology, pp. 706-712, 2014. Available: 10.1016/b978-0-12-384730-0.00387-6

(11) B. Hebbelstrup Jensen et al., “Enteroaggregative Escherichia coli in Daycare—A 1-Year Dynamic Cohort Study”, Frontiers in Cellular and Infection Microbiology, vol. 6, 2016. Available: 10.3389/fcimb.2016.00075

(12) A. Medina et al., “Diarrheagenic Escherichia coli in Human Immunodeficiency Virus (HIV) Pediatric Patients in Lima, Perú”, The American Journal of Tropical Medicine and Hygiene, vol. 83, no. 1, pp. 158-163, 2010. Available: 10.4269/ajtmh.2010.09-0596

(13) B. Hebbelstrup Jensen et al., “Characterization of Diarrheagenic Enteroaggregative Escherichia coli in Danish Adults—Antibiotic Treatment Does Not Reduce Duration of Diarrhea”, Frontiers in Cellular and Infection Microbiology, vol. 8, 2018. Available: 10.3389/fcimb.2018.00306

(14) M. Beld and F. Reubsaet, “Differentiation between Shigella, enteroinvasive Escherichia coli (EIEC) and noninvasive Escherichia coli”, European Journal of Clinical Microbiology & Infectious Diseases, vol. 31, no. 6, pp. 899-904, 2011. Available: 10.1007/s10096-011-1395-7

(15) M. Meza-Segura and T. Estrada-Garcia, “Diffusely Adherent Escherichia coli”, Escherichia coli in the Americas, pp. 125-147, 2016. Available: 10.1007/978-3-319-45092-6_6

(16) D. Wijetunge et al., “Characterizing the pathotype of neonatal meningitis causing Escherichia coli (NMEC)”, BMC Microbiology, vol. 15, no. 1, 2015. Available: 10.1186/s12866-015-0547-9

(17) Z. Zhao, X. Hua, J. Yu, H. Zhang, J. Li and Z. Li, “Duration of empirical therapy in neonatal bacterial meningitis with third-generation cephalosporin: a multicenter retrospective study”, Archives of Medical Science, vol. 15, no. 6, pp. 1482-1489, 2019. Available: 10.5114/aoms.2018.76938

Reviewing Fungal Infections

by Dr. Jaclynn Moskow

Candida auris fungi, emerging multidrug resistant fungus, agent of fungal infection
Candida auris, an emerging multidrug-resistant fungus

 

Fungi are similar in many ways to bacteria – both have a cell nucleus and complex cell walls. Unlike bacteria, species of fungi include both single-celled organisms (yeasts) and multicellular forms (molds). Molds resemble plants and often consist of filaments, spores, root structures, etc. Fungal infections (mycoses) include candidiasis, dermatophytosis, blastomycosis, coccidioidomycosis, histoplasmosis, cryptococcosis, paracoccidioidomycosis, aspergillosis, zygomycosis, and pneumocystosis.

 

Candidiasis

Candidiasis refers to infections caused by yeasts of the genus Candida. Candida is the most common cause of fungal infections worldwide; and is part of the normal flora of the mouth, GI tract, vagina, and skin. Candidiasis occurs when an imbalance in the amount of Candida in these areas results in signs and symptoms of inflammation, or when Candida colonizes parts of the body in which it is not normally present. All forms of candidiasis are more common in individuals who are immunocompromised. 

Vulvovaginal candidiasis fungal infection, commonly referred to as a “yeast infection,” is estimated to affect 70-75% of women at least once during their lifetimes (1). Symptoms may include itching, burning, soreness, redness, swelling, pain during intercourse or urination, and a thick, white discharge that is usually odorless and may resemble cottage cheese. Factors that predispose to vulvovaginal candidiasis include the use of antibiotics, douches, and other vaginal products, diabetes, hormonal changes such as those seen with pregnancy and menopause, contraceptives, immune deficiency, including HIV / AIDS, and certain genetic factors. A variety of topical and systemic azole agents can be used for treatment.

Oropharyngeal candidiasis commonly referred to as “thrush,” occurs from Candida overgrowth on the lining of the mouth, tongue, gums, tonsils, and lips. The condition may cause visible white or yellow patches, soreness, an unpleasant taste, and occasionally a “cotton-like sensation.” It is much more common in infants and toddlers than in adults. Predisposing factors in adults include smoking, dentures, antibiotic and corticosteroid use, and hormonal changes. 80-90% of HIV patients will experience oropharyngeal candidiasis (2). Proper dental hygiene may help protect against oropharyngeal candidiasis. Various azole mouthwashes, gels, and lozenges can be used for treatment, as well as oral antifungal medications.

Common sites of cutaneous candidiasis include the axilla (armpit), the area under the breast, the groin region, the intergluteal cleft, and on the hands and feet. Candida is a common cause of “diaper rash.”

Invasive candidiasis (“deep candidiasis”) occurs when Candida affects the bloodstream, heart, brain, eyes, bones, or other organs. It may occur in patients that are immunocompromised, or as a result of fungal infection introduced by vascular lines, prosthetic cardiac valves, and urinary catheters. Systemic symptoms may result, including fever, chills, pain, hypotension, and neurological deficits. The condition can be fatal. One strain, in particular, Candida auris, poses a threat in hospitals, as it is often multidrug-resistant and difficult to identify using standard laboratory methods (3).

 

Dermatophytosis

Dermatophytosis (“tinea”) is a fungal infection of keratinized tissue, including the skin, hair, and nails. Fungal causes include Ascomycota, Euascomycetes, Onygenales: Epidermophyton, Microsporum, Trichophyton, Trichosporon spp., and Arthroderma (4). Dermatophytosis is contracted by contact with infected humans or animals, or contact with contaminated objects, flooring, or soil.

Trichophyton mentagrophytes - an agent of fungal infection
Fungus Trichophyton mentagrophytes

 

The nomenclature of these conditions derives from the body region that is affected. For example, Tinea manuum is a dermatophyte infection of the hands, while Tinea barbae is an infection of the beard or mustache. Tinea pedis affects the feet, Tinea unguium the nails, Tinea cruris the groin, Tinea corporis the trunk, Tinea capitis the scalp, and Tinea faciei the non-bearded area of the face. 

Tinea corporis is commonly referred to as “ringworm.” It presents as a red, annular, scaly patch, often with central clearing. The condition is usually pruritic and is very common – especially among children. High rates are seen in Africa, India, and urban areas of the Americas (5). A common source of adult infection is through handling puppies and kittens. A wide variety of creams, ointments, gels, and sprays are available for treatment.

Tinea pedis is commonly referred to as “athlete’s foot”; and is the most common form of dermatophytosis in adults (6). The condition can cause itching, stinging, and burning of the feet – often with redness, blisters, and peeling. Tinea pedis is often acquired from wet floor surfaces such as showers, locker rooms, and pool areas. Wearing foot protection in these areas can help prevent transmission. 

The same fungal species that cause Tinea pedis can also cause Tinea cruris, commonly known as “jock itch.” Tinea cruris presents as a red, pruritic, and often annular rash in the crease of the groin. The condition may spread to the upper thigh in a “half-moon” shape. The condition can be acquired by sharing contaminated towels or clothing. Both Tinea pedis and Tinea cruris usually respond well to topical antifungals.

 

Endemic Mycoses

Endemic mycoses refer to a diverse group of fungal infections found in distinct geographical regions. They can cause significant morbidity and mortality in immunocompromised individuals, and may also affect healthy people. 

Blastomycosis is caused by the fungus Blastomyces. It mainly affects people living in regions of the United States and Canada surrounding the Ohio and Mississippi River valleys and the Great Lakes (7). Blastomycosis is acquired through inhalation of spores, often after participating in activities that disturb the soil. Symptoms are “flu-like” and may include fever, fatigue, muscle aches, night sweats, and cough. A chronic disease may affect the lungs, skin, bones, joints, genitourinary tract, or central nervous system. Amphotericin B is the treatment of choice.

Coccidioidomycosis (“Valley Fever”) is caused by Coccidioides immitis and Coccidioides posadasii. The condition is found in the Southwestern United States and parts of Mexico and Central and South America. Like blastomycosis, coccidioidomycosis follows the inhalation of spores from the soil. Symptoms are similar to coccidioidomycosis and are flu-like. A rash on the upper body or legs is commonly encountered. Most people with coccidioidomycosis improve without treatment, but fluconazole and similar antifungals can be used (8).

Fungus Coccidioides immitis, saprophytic stage, 3D illustration showing fungal arthroconidia. Pathogenic fungi that reside in soil and can cause fungal infection Coccidioidomycosis, or Valley fever
Coccidioides immitis, an agent of fungal infection Coccidioidomycosis (aka Valley fever), saprophytic stage.

 

Histoplasmosis, caused by Histoplasma, is acquired by inhaling spores – usually from soil containing bird- or bat-droppings.  The condition is found in the Ohio and Mississippi River valleys and parts of Central and South America, Africa, Asia, and Australia (9).  Histoplasmosis is also characterized by a flu-like illness and is usually self-limiting. 

Cryptococcosis is caused by various species of Cryptococcus, yeasts that are found in the soil and on certain trees. Cryptococcus gattii is found in California, Oregon, Washington, Canada, Australia, Papua New Guinea, and South America (10). Cryptococcus neoformans is found in all countries. Cryptococcus is often associated with pneumonia or meningitis. The current global incidence is estimated at 1 million cases per year, with 50% mortality (11). Most of these cases occur in individuals with HIV / AIDS. Treatment consists of Amphotericin B and Flucytosine, followed by Fluconazole.

Paracoccidioidomycosis is caused by Paracoccidioides, found in parts of Central and South America (12). It can cause lesions in the mouth and throat, rash, lymphadenopathy, fever, cough, and hepatosplenomegaly. Talaromycosis, formally known as sporotrichosis, is an endemic mycosis caused by Talaromyces marneffei and other species. The condition is found in Southeast Asia, Southern China, and Eastern India (13). Clinical manifestations include fever, cough, lymphadenopathy, hepatosplenomegaly, diarrhea, and abdominal pain.

 

Mold Infections

Most people inhale mold spores every day without becoming ill, but occasionally severe disease can result. Infection by Aspergillus (aspergillosis) may present as an allergic reaction. The fungus can also cause infection of the sinuses and lungs. Formation of “fungal ball” (aspergillomas) may occur in patients with pre-existing lung diseases. Aspergillus can also infect the eyes, skin, cardiac valves, brain, gastrointestinal tract, and genitourinary tract. Treatment options include Voriconazole, Amphotericin B, and Isavuconazole (14).

Aspergillus (mold) under the microscopic view. Aspergillus is an agent of fungal infection.
Aspergillus spp. under a microscope

 

Zygomycosis (“mucormycosis”) is caused by a group of molds called Mucormycetes. This fungal infection is commonly associated with hyperglycemia, metabolic (diabetic, uremic) acidosis, corticosteroid therapy, and neutropenia, transplantation, heroin injection, and administration of deferoxamine (15). Common sites of infection include the paranasal sinuses and contiguous structures, cranial nerves, cerebral arteries, lungs, and skin. Treatment may include intravenous Amphotericin B, followed by oral Posaconazole or Isavuconazole.

Other molds that can cause allergies and infections in humans include Stachybotrys chartarum, Alternaria alternata, Lomentospora prolificans, Scedosporium apiospermum, Cladosporium, and Penicillium.

Pneumocystis jirovecii, an agent of Pneymocystis pneumonia
Pneumocystis jirovecii, an agent of Pneumocystis pneumonia fungal infection

Pneumocystis pneumonia

Pneumocystis pneumonia (PCP) is caused by the fungus Pneumocystis jirovecii.  Until recent years, the organism had been classified as a protozoan parasite. Pneumocystis pneumonia usually occurs in individuals with severe immune suppression, including HIV / AIDS.  Presenting symptoms include shortness of breath, fever, and a nonproductive cough. Extrapulmonary infection is rare but can occur. Treatment options include Sulfamethoxazole / Trimethoprim, Pentamidine, Dapsone + Trimethoprim, Atovaquone, or Primaquine + Clindamycin (16).

 

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References

(1) Sobel JD. Vulvovaginal candidosis. Lancet. 2007 Jun 9;369(9577):1961-71. doi: 10.1016/S0140-6736(07)60917-9.

(2) Patil S, Majumdar B, Sarode SC, Sarode GS, Awan KH. Oropharyngeal Candidosis in HIV-Infected Patients-An Update. Front Microbiol. 2018 May 15;9:980. doi: 10.3389/fmicb.2018.00980.

(3) “General Information about Candida auris”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), 2019. [Online]. Available: https://www.cdc.gov/fungal/candida-auris/candida-auris-qanda.html

(4)”Dermatophytosis”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/dermatophytosis-10600

(5) M. Handler, “What is the global incidence of tinea capitis (scalp ringworm)?”, Medscape.com, 2020. [Online]. Available: https://www.medscape.com/answers/1091351-36134/what-is-the-global-incidence-of-tinea-capitis-scalp-ringworm

(6) Ilkit M, Durdu M. Tinea pedis: the etiology and global epidemiology of a common fungal infection. Crit Rev Microbiol. 2015;41(3):374-88. doi: 10.3109/1040841X.2013.856853.

(7) “Blastomycosis”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), 2020. [Online]. Available: https://www.cdc.gov/fungal/diseases/blastomycosis/index.html

(8) “Treatment for Valley Fever (Coccidioidomycosis)”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), 2019. [Online]. Available: https://www.cdc.gov/fungal/diseases/coccidioidomycosis/treatment.html

(9) “Histoplasmosis”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), 2020. [Online]. Available: https://www.cdc.gov/fungal/diseases/histoplasmosis/index.html

(10) “C. gattii Infection Statistics”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), 2020. [Online]. Available: https://www.cdc.gov/fungal/diseases/cryptococcosis-gattii/statistics.html

(11)”Cryptococcosis worldwide distribution”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/cryptococcosis-10530/worldwide

(12) “Paracoccidioidomycosis”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), 2020. [Online]. Available: https://www.cdc.gov/fungal/diseases/other/paracoccidioidomycosis.html

(13) “Talaromycosis (formerly Penicilliosis)”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), 2020. [Online]. Available: https://www.cdc.gov/fungal/diseases/other/talaromycosis.html

(14) “Aspergillosis”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/aspergillosis-10140

(15) “Zygomycosis”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/zygomycosis-12670

(16) “Pneumocystis pneumonia”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/pneumocystis-pneumonia-11850

Dr. Oli prepares medical students for real-life situations

Multi ethnic group of medical students in uniform looking on the x-ray sitting at the desk in the modern classroom
Dr. Oli has created the “GIDEON diagnostic game” where students take on different roles to diagnose a disease

 

Due to the COVID-19 pandemic, universities all over the world had to accelerate their digital teaching programs. This has created a greater need for online tools that support the challenges of preparing students for life after graduation. This is especially true when teaching medical students – it is critically important future health professionals are taught practical and critical thinking techniques that are based on real-life situations.

Dr. Monika Oli has been speaking with Times Higher Education about the challenges of teaching microbiology online and how GIDEON can bring value to the virtual classroom. Dr. Oli explains that traditional teaching techniques may focus on identifying a few pathogens found in most laboratories, which can create “a completely artificial scenario which would never happen in the real world”.

How can a future medical doctor learn to differentiate between diseases with similar symptoms, such as Rocky Mountain Spotted Fever and Lyme disease? In a real-world scenario, you can’t “just open page 510 of the textbook and diagnose the patient…You have to think outside the box” and this is where Dr. Oli brings GIDEON in.

Dr. Oli has created the “GIDEON diagnostic game” where students take on different roles – epidemiologist, doctor, microbiologists, etc. – and use GIDEON’s Bayesian analysis-driven diagnostic tools to help create the list of likely diseases. This is followed by exploring the database to determine the best treatment plan and even speculating whether the patient would have survived or not in a given scenario!

The game proved to be very popular with students. But Dr. Oli didn’t stop there, she further encouraged future medics to analyze issues relevant today by building an exam around secondary infections of COVID-19.

“Many COVID-19 patients get secondary infections that are bacterial, so I built my whole exam around it. Students were given data and had to use GIDEON to analyze the secondary infection, how it should be treated, whether it will contribute to COVID-19 resistance, so the role play continued even during the exams.”

If you are a teacher looking for new ways to engage and challenge your students, GIDEON might be the right tool for the job. Try it free!

Read the original Times Higher Education article here

 

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The Gut Microbiome and Its Role in Health and Disease

by Dr. Jaclynn Moskow

Intestinal bacteria, Gut microbiome helps control intestinal digestion and the immune system, Probiotics are beneficial bacteria used to help the growth of healthy gut flora
The gut microbiome helps control intestinal digestion and the immune system.

 

It is difficult to overstate the importance and complexity of the gut microbiome. Humans live in symbiosis with hundreds (and possibly thousands) of species of bacteria (1). Additionally, archaea, fungi, viruses, and protozoa are also present in our gut. In fact, only about 10% of the cells within our bodies are “ours” and contain human DNA. The remaining 90% of cells we carry with us are microbial. The exact makeup of the gut microbiome varies greatly from individual to individual and is influenced by variables that include diet, exercise, medication use, sleep, stress, hormonal changes, aging, and disease. Associations have been found between the composition of the microbiome and obesity, diabetes, hypertension, heart disease, autoimmune disorders, allergies, mood disorders, and more.

 

Why Do We Have a Gut Microbiome?

The bacteria in our gut participate in the digestion, absorption, and metabolism of proteins and carbohydrates and in the breakdown of endogenous intestinal mucus. They also synthesize vitamin K2 and various B group vitamins; and they influence the development of gut-associated lymphoid tissues and the development of cells of the immune system (2), and serve to limit the colonization of pathogenic bacteria. The majority of these bacteria are anaerobic. Common genera include Escherichia, Bifidobacterium, Lactobacillus, and Enterococcus.

 

The Gut Microbiome and COVID-19

A recent study examined the connection between the gut microbiome and COVID-19. Researchers found that patients hospitalized for COVID-19 had an increase in certain bacterial species and a decrease in others when compared to a control group, even after antibiotic use was accounted for (19). They found a negative correlation between disease severity and concentrations of Faecalibacterium prausnitzii and Eubacterium rectale. Patients were monitored for 30 days post-recovery, and the observed changes persisted. The researchers postulated that these changes may contribute to the persistence of symptoms and multi-system inflammation that is sometimes seen with patients who have recovered from COVID-19.

 

Gut flora vector illustration. Flat tiny gastrointestinal microbe person concept. Abstract digestive stomach living organisms for healthy life. Lactobacilli, coli and intestinal system environment.

 

The Gut Microbiome and Obesity

In recent years, many studies have examined associations between the gut microbiome and obesity. When germ-free mice are colonized with gut bacteria from obese mice, they gain weight; but when they are colonized with gut bacteria from lean mice, they do not gain weight (3). Mice also gain weight when they are colonized with bacteria from obese humans. In a discordant twin study, colonization from obese twins caused mice to gain weight while colonization from their lean siblings did not (4). Some believe the ratio of Bacteroidetes to Firmicutes may play a significant role in obesity. One study found that as obese individuals lose weight, the concentration of Bacteroidetes increases (5). Furthermore, genetically obese mice contain a higher proportion of Firmicutes than thin mice consuming the same diet, and thin mice contain more Bacteroidetes than obese mice consuming the same diet (6). When researchers employed machine learning to study this topic, they concluded that the association between the Bacteroidetes / Firmicutes ratio and obesity is relatively weak and that existing studies lack significant sample sizes (7). The science is far from settled.

 

The Gut Microbiome and Diabetes 

Studies have also investigated the link between the gut microbiome and diabetes. Some speculate that in individuals who are genetically susceptible to type 1 diabetes, it is ultimately a shift in the gut microbiome that triggers the onset (8).  The gut microbiome of children with type 1 diabetes has been found to be less diverse than that of children without the disease (9). A recent review of 42 studies that examined the gut microbiome and type 2 diabetes found Bifidobacterium, Bacteroides, Faecalibacterium, Akkermansia, and Roseburia to be negatively associated with type 2 diabetes; and Ruminococcus, Fusobacterium, and Blautia to be positively associated (10). Other work has shown that when individuals with metabolic syndrome were given fecal transplants from healthy donors, insulin-resistance improved (11).

 

The Gut Microbiome, Hypertension, and Cardiovascular Disease

The ratio of Bacteroidetes to Firmicutes has also been implicated in hypertension. Consuming milk fermented with Lactobacilli can lower blood pressure in some cases, and Lactobacilli produce peptides that can inhibit ACE1 (12).  The same bacterial species found within the atherosclerotic lesions of individuals with cardiovascular disease are found in their gut (13). Additionally, Akkermansia muciniphila may have a cardioprotective effect. Researchers observed that when mice were fed a Western diet, they experienced a decrease in Akkermansia muciniphila and an increase in atherosclerotic lesions. When these same mice were recolonized with Akkermansia muciniphila, a reversal in atherosclerotic lesions was observed (14). 

 

The Gut Microbiome, Autoimmune Disorders, and Allergies

Components of the gut microbiome may be involved in eliciting or quelling immune responses that lead to the development of autoimmune disorders and allergies. Antibodies directed against a yeast species, Saccharomyces cerevisiae,  have been found in patients with rheumatoid arthritis, systemic lupus erythematosus, antiphospholipid syndrome, and Crohn’s Disease (15). Individuals with these conditions show an increase in the numbers of certain bacterial species and a decrease in other species –  as do individuals with multiple sclerosis, Sjögren’s syndrome, and celiac disease. The ratio of Clostridium difficile to Bifidobacterium in infants has been associated with food and aero-allergies, and high levels of fecal Escherichia coli in infants are associated with IgE-mediated eczema (16).

 

The Gut Microbiome and Neuropsychiatric Disorders

The central nervous system and enteric nervous system (together known as the gut-brain axis) are both influenced by the gut microbiome. Bacteria in the gut can directly secrete neurotransmitters, including serotonin, dopamine, norepinephrine, GABA, and histamine. Several studies have shown that patients with bipolar and major depressive disorder have an increase in Actinobacteria and Enterobacteriaceae, and a decrease in Faecalibacterium (17). Mice treated with Lactobacillus rhamnosus have reduced anxiety/depression-like behavior and altered expression of GABA receptors (18). Differences in microbiome composition have also been noted in patients with schizophrenia, Parkinson’s disease, and an autism spectrum disorder.

 

Fecal microbiota transplant (FMT) stool transferring bacteria microbes
Fecal microbiota transplantation (FMT)

 

Fecal Microbiota Transplantation and Clostridium Difficile Colitis

Fecal microbiota transplantation (FMT) is currently being used as a treatment for Clostridium difficile colitis. In fact, FMT is more effective than vancomycin at treating recurrent Clostridium difficile colitis. Most commonly, FMT is performed via colonoscopy. Nasoduodenal tubes, nasogastric tubes, and enemas can also be used. FMT made headlines in 2019 when a transplant recipient died, and several others became seriously ill, after becoming colonized with multi-drug resistant Escherichia coli. This led the FDA to recommend new safety measures for FMTs, including screening donors for risk factors associated with carrying multi-drug-resistant organisms and testing all donor stools for such organisms.

 

Optimizing the Microbiome

In many regards, studying the gut microbiome often leads to more questions than answers. When a change in bacterial levels is observed in a disease state, it is sometimes difficult to know whether that change contributed to the disease state or merely resulted from it. Anyone who seeks to convince you that they know the perfect solution to optimizing gut health is misleading you. While a host of food products and health supplements are touted to enhance the gut microbiome, in most cases the details of this “enhancement” are not defined. As additional studies are conducted, we will gain a better understanding of this vast topic and will likely see an increase in the utilization of fecal transplants in treating various diseases.

 

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