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Archive for the ‘Microbiology’ Category

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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References

(1) Almeida A, Mitchell AL, Boland M, et al. A new genomic blueprint of the human gut microbiota. Nature. 2019 Apr;568(7753):499-504. Available: 10.1038/s41586-019-0965-1.

(2) Wu HJ, Wu E. The role of gut microbiota in immune homeostasis and autoimmunity. Gut Microbes. 2012 Jan-Feb;3(1):4-14. Available: 10.4161/gmic.19320.

(3) Turnbaugh PJ, Ley RE, Mahowald MA, et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature. 2006 Dec 21;444(7122):1027-31. Available: 10.1038/nature05414. 

(4) Ridaura VK, Faith JJ, Rey FE, et al. Gut microbiota from twins discordant for obesity modulate metabolism in mice. Science. 2013 Sep 6;341(6150):1241214. Available: 10.1126/science.1241214.

(5) Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial ecology: human gut microbes associated with obesity. Nature. 2006 Dec 21;444(7122):1022-3. Available: 10.1038/4441022a.

(6) Ley RE, Bäckhed F, Turnbaugh P, et al. Obesity alters gut microbial ecology. Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):11070-5. Available: 10.1073/pnas.0504978102.

(7) Sze MA, Schloss PD. Looking for a Signal in the Noise: Revisiting Obesity and the Microbiome. mBio. 2016 Aug 23;7(4):e01018-16. Available: 10.1128/mBio.01018-16.

(8) Zheng P, Li Z, Zhou Z. Gut microbiome in type 1 diabetes: A comprehensive review. Diabetes Metab Res Rev. 2018 Oct;34(7):e3043. Available: 10.1002/dmrr.3043.

(9) Giongo A, Gano KA, Crabb DB, et al. Toward defining the autoimmune microbiome for type 1 diabetes. ISME J. 2011 Jan;5(1):82-91. Available: 10.1038/ismej.2010.92.

(10) Gurung M, Li Z, You H, et al. Role of gut microbiota in type 2 diabetes pathophysiology. EBioMedicine. 2020 Jan;51:102590. Available: 10.1016/j.ebiom.2019.11.051.

(11) Vrieze A, Van Nood E, Holleman F, et al. Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. Gastroenterology. 2012 Oct;143(4):913-6.e7. Available: 10.1053/j.gastro.2012.06.031.

(12) Jose PA, Raj D. Gut microbiota in hypertension. Curr Opin Nephrol Hypertens. 2015 Sep;24(5):403-9. Available: 10.1097/MNH.0000000000000149.

(13) Tang WH, Kitai T, Hazen SL. Gut Microbiota in Cardiovascular Health and Disease. Circ Res. 2017 Mar 31;120(7):1183-1196. Available: 10.1161/CIRCRESAHA.117.309715.

(14) Li J, Lin S, Vanhoutte PM, et al. Akkermansia Muciniphila Protects Against Atherosclerosis by Preventing Metabolic Endotoxemia-Induced Inflammation in Apoe-/- Mice. Circulation. 2016 Jun 14;133(24):2434-46. Available: 10.1161/CIRCULATIONAHA.115.019645.

(15) De Luca F, Shoenfeld Y. The microbiome in autoimmune diseases. Clin Exp Immunol. 2019 Jan;195(1):74-85. Available: 10.1111/cei.13158.

(16) Pascal M, Perez-Gordo M, Caballero T, et al. Microbiome and Allergic Diseases. Front Immunol. 2018 Jul 17;9:1584. Available: 10.3389/fimmu.2018.01584.

(17) Huang TT, Lai JB, Du YL, et al. Current Understanding of Gut Microbiota in Mood Disorders: An Update of Human Studies. Front Genet. 2019 Feb 19;10:98. Available: 10.3389/fgene.2019.00098.

(18) Bravo JA, Forsythe P, Chew MV, et al. Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve. Proc Natl Acad Sci U S A. 2011 Sep 20;108(38):16050-5. Available: 10.1073/pnas.1102999108.

(19) Yeoh YK, Zuo T, Lui GC, et al. Gut microbiota composition reflects disease severity and dysfunctional immune responses in patients with COVID-19. Gut. 2021 Jan 11:gutjnl-2020-323020. Available: 10.1136/gutjnl-2020-323020.

Examining Salmonella Typhi and Typhoid Fever

by Dr. Jaclynn Moskow

Typhoid fever refers to the disease caused by Salmonella typhi (Salmonella enterica subsp. enterica serovar Typhi), a facultative anaerobic Gram-negative bacillus. Both typhoid fever and its close relative paratyphoid fever are sometimes referred to as “enteric fever.” As the name enteric fever implies, the illness is often characterized by gastrointestinal symptoms and fever.

Green houseflies feeding on ripe mango using their labellum to suck the meat

Transmission

Humans are the only natural reservoir for Salmonella typhi, and transmission occurs via the fecal-oral route. Transmission may occur after eating food that was prepared by someone carrying the bacterium or after using a contaminated toilet and failing to follow proper hand hygiene. Transmission can also occur by drinking water contaminated by sewage, or by eating food prepared in contaminated water. Flies can carry the bacteria from sewage to food.

The average incubation period for typhoid fever is 15 to 21 days, but symptoms may develop as soon as 5 days post transmission or as late as 34 days. Both children and adults contract typhoid fever. In some outbreaks, typhoid fever has primarily affected school-aged children, with cases in infants and toddlers being quite rare. In recent years, very young children have also proven extremely susceptible to the disease.[1]

Chronic Carriers and the Case of Typhoid Mary

Salmonella typhi may continue to shed in feces after a patient has recovered from the disease, and such individuals may become asymptomatic carriers of the bacteria. Approximately five percent of people who contract Salmonella typhi infection will become chronic carriers. 25% of carriers experienced no signs or symptoms of the disease.[2]  Females are more likely than males to become chronic carriers.  In chronic carriers, Salmonella typhi takes refuge in macrophages [3] and the gall bladder.

The most infamous carrier of typhoid fever was Mary Mallon, also known as “Typhoid Mary.” Mary was born in Ireland and immigrated to New York at the turn of the 20th century. She worked as a cook for eight affluent families, seven of which contracted Typhoid Fever.[4] These high-profile infections eventually led to an investigation and to Mary’s forced quarantine. After her release, she defied orders and continued to work as a cook, using various aliases. She stopped working for private clients and worked instead at several public restaurants as well as at Sloane Maternity Hospital.

51 cases of typhoid fever were traced to Mary, including three fatalities. [5] It is likely that Mary actually infected and killed many times this amount. In 1915, she was located and detained a second time, eventually dying after a period of 23 years in forced quarantine. Mary never believed she was the source of any infections, as she had no symptoms of the disease.

Signs and Symptoms

Typhoid fever can have a very nonspecific clinical presentation. Generally, initial enterocolitis develops, without associated fever. Patients may experience constipation or diarrhea, associated with abdominal pain and vomiting. Hematochezia may occur. Hepatosplenomegaly is present in 50% of cases and jaundice may also develop. Some patients develop cholecystitis or pancreatitis.

A short asymptomatic phase may proceed with the onset of fever.  Once fever develops, it often follows a “step-ladder” pattern, rising and subsequently falling before rising again. Additional flu-like symptoms may include chills, diaphoresis, headache, sore throat, cervical lymphadenopathy, cough, and myalgia. Pneumonia may develop and bradycardia is often noted. During the second week of illness, 30% of patients develop a rash referred to as “rose spots.” Initial leukocytosis is often seen, followed by leukopenia. Thrombocytopenia, coagulopathy, and hepatic dysfunction may also be noted.

Some patients will go on to develop an intestinal perforation, generally in the 3rd or 4th week of illness. Intestinal perforation is more common in males than in females. Typhoid fever is dangerous for pregnant women, with 70% of untreated cases ending in miscarriage. Additionally, transmission from mother to fetus and subsequent neonatal typhoid can occur.

Systemic inflammation may lead to such complications as myocarditis, endocarditis, pericarditis, and mycotic aneurysm. Some patients develop meningitis or encephalitis. Spondylitis/spondylodiscitis, rhabdomyolysis, and hemophagocytic lymphohistiocytosis have also been seen – as have endophthalmitis, cranial nerve palsy, and Guillain-Barre syndrome.

Typhoid fever can induce neuropsychiatric symptoms. Encephalopathy occurs in 21% of cases. Psychosis or confusion occurs in 5 to 10%. Seizures and coma occur less commonly. The term “typhoid state” (from the Greek word “typhos” –  meaning “clouded”) is sometimes used to refer to changes in mental status.

Without treatment, symptoms of typhoid fever will generally resolve in approximately one month. About ten percent of patients with typhoid fever will experience relapse, more common among those who received treatment than those who did not. Typhoid fever is more severe among patients with HIV infection, malaria, and sickle cell anemia. Long-term carriers have a higher incidence of cancers of the gallbladder, pancreas, colon, and lung. The case-fatality rate for untreated typhoid fever is approximately 15% – vs. 0.8% with treatment.

Illustration of typhoid fever

Diagnosis and Treatment

Diagnosis is made via culture of blood, urine, sputum, or bone marrow. Stool cultures are often negative except in very late infection. Previously, the Widal test was used to detect serum antibody titers against Salmonella typhi O and H antigens. However, this test has a high rate of both false negatives and false positives and is thus unreliable. 

Both Ceftriaxone and Azithromycin can be used to treat typhoid fever. Fluoroquinolones are no longer recommended, in view of the emergence of resistant strains. Corticosteroids may be used when there is evidence of widespread systemic involvement. Health-care personnel should follow stool precautions. Most carriers can be cured with antibiotics. Carriers with cholelithiasis usually remain positive after antibiotic treatment and will require cholecystectomy.

Prevalence 

Over the last three decades, typhoid fever has affected between 11 to 21 million people per year, worldwide.  Incidence has been declining in many countries. 

Typhoid, estimated cases worldwide 1990 - today

The countries reporting most cases include Bangladesh, China, India, Indonesia, Laos, Nepal, Pakistan, and Vietnam. High rates also occur in Africa and Central and South America. If you have a GIDEON account, click to explore the typhoid fever outbreak map. 

The CDC reports that approximately 350 people in the United States receive treatment for typhoid fever each year and that as many as 5,700 people are likely to be infected.[6]  Most cases in the United States result from travel to endemic areas. Occasionally, cases arise from other sources, such as from contaminated imported food. A review of outbreaks in the United States can be found here.

Prevention

Cases of typhoid fever and other waterborne diseases will decline as access to clean water increases and as sanitary conditions improve.  The CDC recommends receiving a typhoid fever vaccine prior to travel to countries with high incidence. Both oral and injectable vaccines are available – both with approximately 50 to 80% efficacy in preventing disease. When traveling, precautions should include adherence to proper hand hygiene, drinking only bottled water, and avoiding uncooked food.

Paratyphoid Fever and Typhus

Typhoid fever is clinically similar to Paratyphoid fever and some forms of Typhus. Paratyphoid fever is a form of enteric fever caused by a Salmonella paratyphi (Salmonella enterica serotypes Paratyphi A, Paratyphi B, or Paratyphi C). Clinically, it may be indistinguishable from typhoid fever and it is transmitted via the same routes. Salmonella paratyphi causes fewer cases of enteric fever than Salmonella typhi

Typhus refers to diseases caused by Rickettsia typhi, Rickettsia prowazekii, and Orientia tsutsugamushi.  Typhus is transmitted by fleas, mites, or lice. During the 19th century, typhoid and typhus were believed to be two forms of a single disease. Like typhoid fever, typhus usually causes flu-like symptoms and a rash, and often with gastrointestinal symptoms. The various forms of typhus are less common than typhoid – and are each reported in specific geographical regions. 

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References

[1] A Sinha, S Sazawal, R Kumar, et al., “Typhoid fever in children aged less than 5 years”, Lancet, vol. 28, num. 354, pp. 734-7, 1999. Available: 10.1016/S0140-6736(98)09001-1

[2] C Parry, T Hien, G Dougan, et al., “Typhoid fever”, N Engl J Med, vol. 347, num. 22, pp. 1770-82, 2002. Available: 10.1056/NEJMra020201

[3] N Eisele, T Ruby, A Jacobson et al., “Salmonella require the fatty acid regulator PPARδ for the establishment of a metabolic environment essential for long-term persistence”, Cell Host Microbe, vol. 14, num. 2, pp. 171-182, 2013. Available: 10.1016/j.chom.2013.07.010

[4] Marineli F, Tsoucalas G, Karamanou M, Androutsos G. Mary Mallon (1869-1938) and the history of typhoid fever. Ann Gastroenterol. 2013;26(2):132-134. [Online]. Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959940/

[5] “’Typhoid Mary’ Dies Of A Stroke At 68. Carrier of Disease, Blamed for 51 Cases and 3 Deaths, but Immune”, The New York Times, November 12, 1938. [Online]. Available: https://www.nytimes.com/1938/11/12/archives/typhoid-mary-dies-of-a-stroke-at-68-carrier-of-disease-blamed-for.html

[6] Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), “Typhoid Fever and Paratyphoid Fever: Questions and Answers”. [Online]. Available: https://www.cdc.gov/typhoid-fever/sources.html 

Pathogen of the Month: Yersinia Pestis

by Dr. Jaclynn Moskow

The most researched pathogen on GIDEON in January was Yersinia pestis, a facultative anaerobic, Gram-negative, coccobacillus. It is the causative agent of the Plague and responsible for some of the most deadly pandemics in history.  While Yersinia pestis is no longer a cause of mass mortality, outbreaks do still occur. Over the last decade, there have been up to 2,000 cases per year reported to the World Health Organization, and likely thousands more unreported.[1]

Yersinia pestis illustration
Yersinia pestis – the agent of Plague

Transmission

Rodents are the natural reservoirs for Yersinia pestis, including rats, mice, squirrels, chipmunks, voles, prairie dogs, and marmots. The bacteria can also be transmitted to a wide variety of other mammals, including rabbits, coyotes, sheep, and cats. There are currently animals carrying Yersinia pestis on all continents except for Oceania.[2]

Fleas transmit Yersinia pestis from animals to humans, and flea bites are the most common route of infection for humans. Humans can also become infected by coming into contact with fluid or tissue. For example, this could happen when a hunter skins a diseased animal. When respiratory infection occurs, Yersinia pestis can become airborne and spread between humans. In rare cases, Yersinia pestis has been contracted via ingestion of infected meat. Dr. Berger discusses transmission here

Both children and adults are at risk of becoming sick with Plague, and there does not appear to be a significant difference in infection rates between men and women.

Yersinia pestis in history

Yersinia pestis likely emerged around 6,000 years ago, evolving from a close relative – Yersinia pseudotuberculosis. [3] The first major Plague pandemic occurred in the 6th century and is known as The Justinian Plague. The disease spread throughout Europe, Asia, and North Africa by way of ship. Its death toll is disputed, with some researchers estimating it claimed half the world’s population and others believing it was less severe.[4]

The second major Plague pandemic occurred between 1346 and 1353, once again striking Europe, Asia, and North Africa. This outbreak, known as The Black Death, took the lives of 75 to 200 million people. It decimated cities quickly upon arrival, sometimes killing over half the population in just a few weeks. In Ragusa, a Venetian port city, incoming sailors were isolated for 40 days, a practice which was known as a “quarantino” …the origin of the word “quarantine”.[5]

Images of physicians wearing bird-like beak masks are often associated with The Black Death. Microbes had yet to be discovered, and many doctors believed Plague was transmitted through smell. To combat this smell, the beak mask had a space for flowers, herbs, and spices. This mask, however, was actually not invented during The Black Death, but rather during a different Plague outbreak in 1619. After the Black Death subsided, Plague outbreaks continued in Europe every few years for the next 300 years, culminating with “The Great Plague” of London in 1665.

 

 

The next significant Plague pandemic occurred in 1894, originating in China, spreading through Asia and Europe, and eventually arriving in the United States in 1900. In 1894 Swiss physician Alexandre Yersin and Japanese physician Kitasato Shibasaburō simultaneously discovered the bacterial origin of Plague. Yersin named the bacterium Pasteurella pestisSoon after, fleas were identified as a vector of transmission. Pasteurella pestis was renamed Yersinia pestis in 1944. Notable 20th-century plague outbreaks occurred in Los Angeles between 1924 to 1925 and in Vietnam from 1965 to 1975.

Bubonic Plague

There are 3 main types of Plague, with Bubonic Plague being the most common type. Bubonic Plague is transmitted via flea bites or via the handling of tissue or fluids. It has an incubation period of 2-to-6 days. Bacteria multiply in lymph nodes close to the site of infection. A maculopapular lesion may appear at the infection site. The lymph nodes become painful and swollen and are known as “Buboes.” Buboes are usually inguinal (60% to 90%), axillary (30%), cervical (10%), or epitrochlear (10%). Other symptoms of Bubonic Plague are flu-like, including fever, headache, chills, pharyngitis, muscle aches, extreme weakness, and tachycardia. Without treatment, Bubonic Plague has a mortality rate of around 50-60%. With treatment, this drops to about 10%. Human to human transmission of Bubonic Plague is extremely rare.

 

Bubonic plague transmission - illustration

 

Pneumonic Plague

Pneumonic Plague occurs when Yersinia pestis enters the lungs. This can happen from inhaling respiratory droplets, or from the bloodstream during untreated Bubonic Plague. The incubation period when the bacteria is inhaled is 1-to-3 days. Pneumonic Plague presents with fever, headache, weakness, tachycardia, coughing, chest pain, and shortness of breath. Hemoptysis is common. With treatment, it has a fatality rate of around 15%. Untreated Pneumonic Plague is almost always fatal.

Septicemic Plague

When Yersinia pestis enters the bloodstream, Septicemic Plague can occur. This may happen directly from a flea bite, or as a complication of untreated Bubonic or Pneumonic Plague. Septicemic Plague may begin with flu-like symptoms. Additionally, it may cause nausea, vomiting, diarrhea, abdominal pain, and sometimes hematemesis and/or hematochezia. Acrocyanosis, ecchymosis, petechiae, and digital gangrene may be noted. Septicemic Plague may progress to cause meningitis, osteomyelitis, kidney failure, DIC, and septic shock. The fatality rate is around 28% with treatment and around 100% if untreated.

Rare forms of Plague include cutaneous, pharyngeal, meningeal, and gastrointestinal.

Diagnosis and treatment

A presumptive diagnosis of Plague may be made through isolation of Yersinia pestis from pus, blood, sputum, or other infected material. 

When Plague is suspected, treatment should be initiated prior to laboratory confirmation. Gentamicin, Streptomycin, Doxycycline, and Chloramphenicol are all effective. Patients with Plague should be isolated. When Pneumonic Plague is suspected, standard respiratory droplet precautions should be followed. Individuals exposed to Plague patients should begin prophylaxis. 

Prevalence

Today, there are approximately 1,000 to 2,000 reported cases of Plague globally each year – and 100 to 200 deaths.

Plague deaths worldwide, GIDEON graph

 

About 95% of current Plague cases occur in Madagascar and the Democratic Republic of Congo.  Brazil, Myanmar, Peru, Vietnam, and The United States also report cases almost every year. If you have a GIDEON account, click to explore Plague outbreak map

According to the CDC, about 7 people in the United States contract Plague each year, with the areas reporting cases usually being Northern New Mexico, Northern Arizona, Southern Colorado, Southern Oregon, Western Nevada, and various rural and semi-rural parts of California.

In 2009, University of Chicago scientist Malcolm Casadaban contracted Plague while conducting vaccine research and unfortunately died. Between 2019 and 2020 there were at least 5 cases of Plague in China linked to eating marmot meat and a few others of unknown origin.

 

Prevention

People who live in areas with Plague outbreaks can take precautions to minimize the risk of infection. The CDC recommends the following:

  • Reduce rodent habitat around your home, workplace, and recreational areas. Remove brush, rock piles, junk, cluttered firewood, and possible rodent food supplies, such as pet-  and wild anima- food. Make your home and outbuildings rodent-proof.
  • Wear gloves if you are handling or skinning potentially infected animals to prevent contact between your skin and the plague bacteria. Contact your local health department if you have questions about disposal of dead animals.
  • Use repellent if you think you could be exposed to rodent fleas during activities such as camping, hiking, or working outdoors. Products containing DEET can be applied to the skin as well as clothing and products containing permethrin can be applied to clothing (always follow instructions on the label).
  • Keep fleas off of your pets by applying flea control products. Animals that roam freely are more likely to come in contact with plague infected animals or fleas and could bring them into homes. If your pet becomes sick, seek care from a veterinarian as soon as possible
  • Do not allow dogs or cats that roam free in endemic areas to sleep on your bed.

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References

[1] Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Vector-Borne Diseases (DVBD), “Plague: Frequently Asked Questions”. [Online]. Available: https://www.cdc.gov/plague/faq/index.html#cases

[2] World Health Organization, “Plague”. [Online]. Available: https://www.who.int/health-topics/plague#tab=tab_1

[3] C Demeure, O Dussurget, G Mas Fiol, et al., “Yersinia pestis and plague: an updated view on evolution, virulence determinants, immune subversion, vaccination, and diagnostics”, Genes Immun, vol. 20, num. 5, pp. 357-370, 2019. Available: 10.1038/s41435-019-0065-0

[4] L Mordechai, M Eisenberg, T Newfield, et al., “The Justinianic Plague: An inconsequential pandemic?”, Proc Natl Acad Sci, vol. 116, num. 51, pp. 25546-25554, 2019. Available: 10.1073/pnas.1903797116

[5] P Mackowiak, P Sehdev, “The Origin of Quarantine”, Clinical Infectious Diseases, vol. 35, num. 9, pp. 1071–1072, 2002. Available: 10.1086/344062

All you need to know about waterborne diseases

by Dr. Jaclynn Moskow

Woman scientist takes a water sample from polluted pond.

 

Waterborne diseases are contracted through exposure to contaminated water including drinking water, water used in food preparation, and swimming water. 

They can be caused by bacteria, viruses, and parasites. Below is a partial list of waterborne disease pathogens, their microbial classification, and their resulting illnesses.

Bacteria, virus, and a parasite icon

Classification Microorganism Disease
Bacterium Campylobacter spp. Campylobacteriosis
Bacterium Escherichia coli E. Coli Diarrhea
Bacterium Legionella pneumophila Legionnaires’ Disease
Bacterium Salmonella enterica Salmonellosis
Bacterium Salmonella typhi Typhoid fever
Bacterium Shigella spp. Shigellosis
Bacterium Vibrio cholerae Cholera
Parasite Cryptosporidium spp. Cryptosporidiosis
Parasite Cyclospora cayetanensis Cyclosporiasis
Parasite Entamoeba histolytica Amoebiasis
Parasite Giardia lamblia Giardiasis
Parasite Naegleria fowleri Primary Amoebic Meningoencephalitis (PAM)
Parasite Schistosoma spp. Schistosomiasis
Virus Adenovirus Adenovirus
Virus Hepatovirus A Hepatitis A
Virus Norovirus Norovirus
Virus Rotavirus Rotavirus

 

WHO IS MOST AFFECTED BY WATERBORNE DISEASES?

The vast majority of waterborne diseases are contracted by individuals who lack access to safe and sanitized water for drinking and personal hygiene. This problem is pervasive around the globe. 

According to the World Health Organization (WHO), 2.2 billion people do not have access to safe drinking water, which equates to 1 in 3 people on the planet. Additionally, 4.2 billion people lack access to adequate sanitation facilities such as hygienic toilets.[1] This lack of access to safe water and sanitation results in 4  billion cases of waterborne diseases annually and 3.4  million deaths.[2] 

Increasing access to clean water worldwide is the single most critical step we can take to prevent morbidity and mortality from these devastating diseases.

Delivery of humanitarian aid and water by military helicopter

 

Symptoms of waterborne diseases are primarily gastrointestinal and include fever, nausea, vomiting, and diarrhea. 88% of all deaths that occur as a result of diarrhea can be attributed to these infections.[3]  90% of diarrhea deaths involve children under the age of five years.[4] Children are particularly susceptible to waterborne diseases, in part because their naive immune systems have not yet encountered most pathogens. 

Another group who are at increased risk for contracting waterborne diseases is people that are immunocompromised, including individuals living with HIV/AIDS. Unfortunately, the HIV epidemic has hit hardest in areas where access to clean water is lacking. 

Countries that have reported recent outbreaks of Cholera include Bangladesh, Haiti, The Democratic Republic of the Congo, Ethiopia, Somalia, and Yemen.[5]  The Democratic Republic of the Congo and Haiti have also reported recent outbreaks of Typhoid fever, as have Uganda and Pakistan.[6]

 

HOW CAN TRAVELERS AVOID WATERBORNE DISEASES?

Tourists are at increased risk for contracting waterborne diseases, in part because they lack prior exposure and immunity. To avoid waterborne illnesses when traveling to an area of concern, the Centers for Disease Control and Prevention (CDC) recommends the following[7]:

  •     Eat only foods that are cooked and served hot
  •     Avoid food that has been sitting on a buffet
  •     Eat raw fruits and vegetables only if you have washed them in clean water or peeled them
  •     Only drink beverages from factory-sealed containers
  •     Avoid ice – which may have been prepared from unclean water
  •     Only drink pasteurized milk
  •     Wash hands often with soap and water for 20 seconds, especially after using the bathroom and before eating
  •     If soap and water are not available, use a hand sanitizer that contains at least 60% alcohol
  •     Keep your hands away from your face and mouth

Travelers can also receive vaccines for some waterborne diseases, namely, Typhoid Fever, Hepatitis A, and Cholera.  Since the efficacy of these vaccines varies, general precautions including avoidance of tap water should still be taken.

Glass of contaminated water on grey background

 

WHAT WATERBORNE DISEASES ARE SEEN IN THE DEVELOPED WORLD?

Sporadic outbreaks of several waterborne diseases are also reported in industrialized countries. A well-known example occurred in 1993 in Milwaukee, Wisconsin when over a two-week period approximately 403,000 individuals experienced a diarrheal illness. The cause was determined to be Cryptosporidium that had contaminated one of the city’s water-treatment plants.[8]  A more recent example occurred in 2019 when over 2000 residents of a small island in Norway became ill as a result of Campylobacter contaminating the local water supply.[9] 

In 2015, 31% of students at a school camp in South Korea became ill as a result of water contaminated with E. coli.[10] There have also been outbreaks of typhoid fever in the United States. Outbreaks of waterborne disease increase after extreme weather events such as flooding caused by heavy rains and snowfall. After Hurricane Katrina, Salmonella enterica, Vibrio cholerae, and Norovirus were detected in individuals in evacuee camps.[11]

 

CONTRACTING WATERBORNE DISEASES WHILE SWIMMING

Waterborne diseases can also be contracted by swimming in pools, lakes, rivers, and oceans. This includes Giardia lamblia, which is one of the most common intestinal parasites worldwide, including in the United States. Giardia lamblia can enter the body in a number of ways, including ingestion of water while swimming. 

Another parasite that can be contracted while swimming is Naegleria fowleri, which is found in freshwater and often referred to in headlines as “the brain-eating amoeba.” Naegleria fowleri invades the body via the nose and travels to the brain by way of the olfactory nerve. Unlike Giardiasis, Primary Amebic Meningoencephalitis caused by Naegleria fowleri is almost always fatal. Fortunately, the condition is exceedingly rare.

Over 250 million persons suffer from Schistosomiasis – in Africa, Asia, and the Americas.  Parasites enter through the skin, usually while swimming, working, or simply walking through freshwater. The parasites travel through the bloodstream, eventually lodging in the liver, urinary system, and other organs with resultant damage to tissues, or even cancer which can develop over many years.

Recreational water areas such as pools, hot tubs, and spas are also at risk of contamination by a variety of pathogens. Between 2000 and 2014, 212 reported outbreaks of Cryptosporidium were associated with recreational water facilities.[12] Adenovirus is also known to cause outbreaks from recreational water, as is Legionella pneumophila. Legionella pneumophila is a unique waterborne pathogen in that it often must be aerosolized to cause infection. The organism is transmitted via hot tubs, showers, humidifiers, and air conditioning systems. Aerosolization allows Legionella pneumophila to enter the lungs and thus, unlike other waterborne pathogens, it can cause respiratory illness. A milder form of the disease caused by Legionella species is known as Pontiac fever, and the more severe form is known as Legionnaires’ Disease.

 

CAN SARS-COV-2 BE TRANSMITTED THROUGH THE WATER SUPPLY?

Fortunately, you cannot contract COVID-19 through contaminated water. Viruses may be classified as either enveloped or non-enveloped. Viruses with envelopes have an outer layer of proteins and lipids that surround their viral capsids. Non-enveloped viruses can survive for relatively long periods outside the body – and in much harsher conditions – than can enveloped viruses. 

Viruses that cause waterborne diseases, such as Hepatovirus A, Norovirus, Rotavirus, and Adenovirus, are all non-enveloped. In contrast, members of the Coronaviridae (such as SARS-CoV-2) are enveloped and thus cannot be spread through the water supply.

 

SARS-CoV-2 structure. Anatomy of the coronavirus

 

Although we cannot contract SARS-CoV-2 from the water supply, inactive SARS-CoV-2 viral material can still be detected in the wastewater from areas with COVID-19 outbreaks. This can be useful in tracking outbreaks. In Switzerland, for example, laboratories were able to determine that a new “British variant” of SARS-CoV-2 had arrived by simply monitoring wastewater.[13]  In fact, monitoring wastewater is an emerging epidemiological tool for tracking many pathogens, including many of the waterborne diseases discussed above.

 

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References:

[1] World Health Organization. 1 in 3 people globally do not have access to safe drinking water – UNICEF, WHO. New York, Geneva: World Health Organization; 18 June 2019. [cited 2021 Jan 10]. Available from: https://www.who.int/news/item/18-06-2019-1-in-3-people-globally-do-not-have-access-to-safe-drinking-water-unicef-who

[2] World Bank. World Development Indicators 2015. Washington, DC: World Bank Publications; 2015. [cited 2021 Jan 10]. Available from: https://openknowledge.worldbank.org/handle/10986/21634

[3] Prüss-Üstün A, et al. Safer water, better health: costs, benefits and sustainability of interventions to protect and promote health. World Health Organization. 2008.

[4] Jong-wook, L. Water, sanitation and hygiene links to health. Geneva: World Health Organization; Nov 2004. [cited 2021 Jan 10.] Available from: https://www.who.int/water_sanitation_health/publications/facts2004/en/

[5] European Centre for Disease Prevention and Control. Cholera worldwide overview. Solna: ECDC; 2021. [cited 2021 Jan 11.] Available from: https://www.ecdc.europa.eu/en/all-topics-z/cholera/surveillance-and-disease-data/cholera-monthly

[6] World Health Organization. Emergencies preparedness, response – Typhoid fever. New York, Geneva: World Health Organization; 2021. [cited 2021 Jan 11]. Available from: https://www.who.int/csr/don/archive/disease/typhoid_fever/en/

[7] Center for Disease Control and Prevention. Travels Health – Disease Directory – Typhoid Fever. Atlanta: CDC; 01 Dec 2020. [cited 2021 Jan 10.] Available from: https://wwwnc.cdc.gov/travel/diseases/typhoid

[8] Mac Kenzie WR, et al. A massive outbreak of Cryptosporidium infection transmitted through the public water supply. N Engl J Med. 1994;331:161-167.

[9] Paruch L, et al. DNA-based faecal source tracking of contaminated drinking water causing a large Campylobacter outbreak in Norway 2019. Int J Hyg Environ Health. 2020 Mar;224:113420.

[10] Park J, et al. A waterborne outbreak of multiple diarrhoeagenic Escherichia coli infections associated with drinking water at a school camp. Int J Infect Dis. 2018

[11] Center for Disease Control and Prevention. Infectious Disease and Dermatologic Conditions in Evacuees and Rescue Workers After Hurricane Katrina – Multiple States, August – September, 2005. Morbidity and Mortality Weekly Report. 30 September, 2005;54(38):961-964.

[12] Hlavsa MC, et al. Outbreaks Associated with Treated Recreational Water – United States, 2000-2014. MMWR Morb Mortal Wkly Rep 2018;67:547–551

[13] Jahn, K. Detection of SARS-CoV-2 variants in Switzerland by genomic analysis of wastewater samples. medRxiv 2021.01.08.21249379; doi: https://doi.org/10.1101/2021.01.08.21249379

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