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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

Chagas Disease

by Dr. Jaclynn Moskow

Trypanosoma cruzi parasite, 3D illustration. A protozoan that causes Chagas' disease transmitted to humans by the bite of triatomine bug
Trypanosoma cruzi parasite, the etiologic agent of Chagas disease

 

In 1909, Brazilian physician Carlos Chagas learned of a local phenomenon in which blood-sucking insects were biting people on the face during sleep. On April 14, he dissected one such insect and found parasitic euglenoids living inside of it (1). Dr. Chagas named the parasite Trypanosoma cruzi (T. cruzi) and, in this moment, discovered both the causative agent and vector of “Chagas Disease.”

On April 14, 2021, we recognize the second annual World Chagas Disease Day (2). Chagas disease, also known as American Trypanosomiasis, is endemic to Latin America. It can lead to severe cardiac, neurologic, and gastrointestinal disease  – and in some cases is fatal, causing about 12,000 deaths each year (3).

The Chagas disease represents the third-largest tropical disease burden worldwide, after malaria and schistosomiasis (4). It has likely been with us for thousands of years, as T. cruzi DNA has been recovered from ancient mummies and bone fragments (1).

Transmission

Triatomine bugs, also known as “kissing bugs”, “cone-nosed bugs”, or “bloodsuckers”, are the vectors for Chagas disease. They acquire T. cruzi after biting infected animals or humans and transmit the parasite to others through their feces. There are over 150 species of domestic and wild animals that serve as reservoirs for Chagas disease (5), including dogs, cats, pigs, rabbits, raccoons, rats, bats, armadillos, and monkeys.

 

The kissing bug. Blood sucker, infection is known as Chagas disease.
‘Kissing bug’,  vector of Chagas disease

 

Triatomine bugs are commonly found in rural areas, in houses made from materials such as mud, adobe, straw, and palm thatch (6). They feed at night. If they defecate on an individual and T. cruzi gains access to the body via a mucus membrane or break in the skin, the transmission of Chagas disease may occur.

Vertical transmission of Chagas disease is possible during pregnancy. Chagas disease can also be transmitted via blood transfusion and organ transplantation, and there is some evidence that it may be transmitted through sex and in rare instances through consumption of game meat. It can also be acquired by consuming food or water contaminated with insect remains (4).

 

Clinical Presentation

The incubation period for Chagas disease depends upon the mode of transmission. Vectorially transmitted cases usually manifest in one-to-two weeks, while orally transmitted cases may take up to 3 weeks – and transfusion-based cases up to 120 days (5).

Chagas disease has an acute and chronic phase. The acute phase is often asymptomatic or mild in nature and usually resolves spontaneously (5). The acute phase may begin with the development of a “chagoma” – an indurated area of erythema and swelling with local lymph node involvement (7). “Romana’s sign” consists of painless edema of the eyelids and periocular tissues (resulting from conjunctival inoculation) and is usually unilateral. Patients in the acute phase may develop fever, malaise, and anorexia. Generalized lymphadenopathy and mild hepatosplenomegaly may be present. Rarely, meningoencephalitis or severe myocarditis with arrhythmias and heart failure may occur.

10% to 30% of acute infections will progress to chronic disease. Chronic disease may present years or decades after the initial infection. Cardiac manifestations include arrhythmias, thromboembolism, and cardiomyopathy. Arrhythmias may present as episodes of vertigo, syncope, or seizures. Congestive heart failure may develop, leading to death. Cerebral disease can also occur and is characterized by headache, seizures, focal neurological deficits, and evidence of ischemia and infarct. Gastrointestinal manifestations include megaesophagus and megacolon. Dysfunction of the urinary bladder is also reported. Chagas disease has an overall case-fatality rate of 10% (7).

Patients with chronic Chagas disease who become immunosuppressed may experience a reactivation of the infection. In individuals with concurrent HIV/AIDS and Chagas disease, the central nervous system is the most commonly affected site, and space-occupying lesions often occur. (8).

 

Diagnosis and Treatment

Chagas disease may be diagnosed through visualization of protozoa in blood or tissue, serology, xenodiagnosis, or PCR. The anti-parasitic medications Nifurtimox or Benznidazole can be used for treatment. Treatment is curative in approximately 50-80% of acute-phase cases, and 20-60% of chronic phase cases (9). Treatment is curative in greater than 90% of congenital cases when given within the first year of life (10). Treatment of pregnant women is not recommended (11).

Prevalence 

Vector-borne transmission of Chagas disease only occurs in the Americas. Approximately 121 million individuals are at risk in Central and South America and Mexico. If you have a GIDEON account, click here to explore our Chagas disease outbreak map. An estimated 8 million people are currently infected (12).  

Vector-borne transmission of Chagas disease is exceedingly rare in the United States, with 28 cases documented between 1955 and 2015 (13). About 300,000 people are currently living in the United States with Chagas disease that was acquired in Latin America (14). In Europe, the prevalence of T. cruzi infection among Latin American migrants is approximately 6% (4).

In 2007, two notable outbreaks occurred as the result of ingestion of sources contaminated with T. cruzi. 166 cases occurred in Brazil from contaminated food and 128 cases in Venezuela from contaminated juice (4). 

 

Prevention

Vector-control programs centered around the widespread use of insecticides have led to some success in decreasing the prevalence of Chagas disease. This progress, however, has been recently complicated by the emergence of insecticide-resistant vectors.

 

Falling death rates of Chagas disease (Trypanosomiasis – American), 1990 – 2016

 

Trypanosomiasis – American is otherwise known as Chagas disease

 

Individuals living in endemic areas can decrease their risk of contracting the disease by completing home improvement projects aimed at disrupting triatomine bug nests. These nests are commonly found beneath porches, between rocky surfaces, in wood/brush piles, rodent burrows, and chicken coops (15). Individuals traveling to endemic areas can decrease their risk of contracting the disease by applying insect repellent, wearing protective clothing, and using bed nets.

The screening of blood products for Chagas disease is another important prevention strategy. In most endemic countries, all blood donations are tested for T. cruzi antibodies. In countries in which cases are imported, screening strategies vary (16, 17). In the United States, all first-time blood donors are tested. In Canada, the UK, and Spain, only donors considered “at-risk” are tested (such as those who previously lived in, or recently traveled to, Latin America). In Sweden, individuals who lived in endemic countries for more than five years are precluded from donating blood, while in Japan, only individuals with a known history of Chagas disease are excluded. In China, blood donors are not currently screened for Chagas disease.

Recently, a new surveillance system for Chagas disease has been implemented in some countries where malaria is also endemic; microscopy technicians have been trained to identify T. cruzi in malaria films (18).

 

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References 

(1) D. Steverding, “The history of Chagas disease”, Parasites & Vectors, vol. 7, no. 1, p. 317, 2014. Available: 10.1186/1756-3305-7-317

(2) “World Chagas Disease Day: raising awareness of neglected tropical diseases”, World Health Organization, 2019. [Online]. Available: https://www.who.int/neglected_diseases/news/world-Chagas-day-approved/en/

(3) B. Lee, K. Bacon, M. Bottazzi and P. Hotez, “Global economic burden of Chagas disease: a computational simulation model”, The Lancet Infectious Diseases, vol. 13, no. 4, pp. 342-348, 2013. Available: 10.1016/s1473-3099(13)70002-1 

(4) “Trypanosomiasis – American Worldwide Distribution”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/trypanosomiasis-american-12460/worldwide

(5) A. Rassi, A. Rassi and J. Marin-Neto, “Chagas disease”, The Lancet, vol. 375, no. 9723, pp. 1388-1402, 2010. Available: 10.1016/s0140-6736(10)60061-x

(6) “Parasites – American Trypanosomiasis (also known as Chagas Disease): Detailed FAQs”, Centers for Disease Control and Prevention, Global Health, Division of Parasitic Diseases and Malaria, 2021. [Online]. Available: https://www.cdc.gov/parasites/chagas/gen_info/detailed.html#intro

(7) “Trypanosomiasis – American”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/trypanosomiasis-american-12460

(8) A. Vaidian, L. Weiss, and H. Tanowitz, “Chagas’ disease and AIDS”, Kinetoplastid Biol Dis, vol. 3, no. 1, p.2, 2004. Available: 10.1186/1475-9292-3-2

(9) J. Guarner, “Chagas disease as example of a reemerging parasite”, Seminars in Diagnostic Pathology, vol. 36, no. 3, pp. 164-169, 2019. Available: 10.1053/j.semdp.2019.04.008

(10) F. Machado et al., “Chagas Heart Disease”, Cardiology in Review, vol. 20, no. 2, pp. 53-65, 2012. Available: 10.1097/crd.0b013e31823efde2

(11) E. Howard, P. Buekens and Y. Carlier, “Current treatment guidelines for Trypanosoma cruzi infection in pregnant women and infants”, International Journal of Antimicrobial Agents, vol. 39, no. 5, pp. 451-452, 2012. Available: 10.1016/j.ijantimicag.2012.01.014

(12) “Chagas disease (American trypanosomiasis): Epidemiology”, World Health Organization, 2021. [Online]. Available: https://www.who.int/chagas/epidemiology/en/

(13) S. Montgomery, M. Parise, E. Dotson and S. Bialek, “What Do We Know About Chagas Disease in the United States?”, The American Journal of Tropical Medicine and Hygiene, vol. 95, no. 6, pp. 1225-1227, 2016. Available: 10.4269/ajtmh.16-0213

(14) “Parasites – American Trypanosomiasis (also known as Chagas Disease): Epidemiology & Risk Factors”, Centers for Disease Control and Prevention, Global Health, Division of Parasitic Diseases and Malaria, 2019. [Online]. Available: https://www.cdc.gov/parasites/chagas/epi.html

(15) “Parasites – American Trypanosomiasis (also known as Chagas Disease): Triatomine Bug FAQs”, Centers for Disease Control and Prevention, Global Health, Division of Parasitic Diseases and Malaria, 2020. [Online]. Available: https://www.cdc.gov/parasites/chagas/gen_info/vectors/index.html

(16) A. Angheben et al.,”Chagas disease and transfusion medicine: a perspective from non-endemic countries”, Blood Transfus, vol. 13, no. 4, pp. 40-50, 2015. Available: 10.2450/2015.0040-15

(17) V. Mangano, M. Prato, A. Marvelli, G. Moscato and F. Bruschi, “Screening of at‐risk blood donors for Chagas disease in non‐endemic countries: Lessons from a 2‐year experience in Tuscany, Italy”, Transfusion Medicine, vol. 31, no. 1, pp. 63-68, 2020. Available: 10.1111/tme.12741 

(18) “Chagas disease (American trypanosomiasis): Prevention of Chagas Disease”, World Health Organization, 2021. [Online]. Available: https://www.who.int/chagas/disease/prevention/en/

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

World Tuberculosis Day 2021

by Dr. Jaclynn Moskow

Doctor with magnifier looking at bacteria in lungs. Tuberculosis, mycobacterium tuberculosis and world tuberculosis day concept on white background. Bright vibrant violet vector isolated illustration

Each year on March 24th, we recognize “World Tuberculosis Day” in an effort to build global awareness about the ongoing tuberculosis epidemic. Tuberculosis is an infectious disease caused by bacteria of the Mycobacterium tuberculosis complex, including Mycobacterium tuberculosis, Mycobacterium africanum, and Mycobacterium bovis (1). Worldwide, tuberculosis is the leading cause of death from an infectious agent (2).

“World Tuberculosis Day” occurs on March 24th as it was on this date, in 1884, that Dr. Robert Koch announced that he had discovered the causative agent of this disease (3).

 

Transmission

Tuberculosis is generally spread via the inhalation of droplet nuclei expelled by individuals with the active pulmonary or laryngeal disease. Less commonly, humans may also acquire tuberculosis from consuming unpasteurized dairy products. The incubation period of tuberculosis ranges from 4w-12w.

 

Clinical Manifestations

Clinical manifestations of tuberculosis vary depending on the site of mycobacterial proliferation (4). Most infections represent reactivation of a dormant focus in a lung and present with chronic fever, weight loss, nocturnal diaphoresis, and productive cough (5). Approximately 8% of patients with pulmonary tuberculosis will experience hemoptysis (6). Tuberculosis can also cause extrapulmonary disease in sites including the bone, joints, muscles, central nervous system, gastrointestinal system, hepatobiliary system, genitourinary system, eyes, breasts, and skin.

Individuals with latent tuberculosis infection (LTBI) do not experience symptoms but are carriers of the disease. They cannot spread the disease to others unless it becomes reactivated. The lifetime risk of reactivation for a person with documented LTBI is estimated to be 5–10% (7). Immunocompromised individuals are much more likely to experience tuberculosis reactivation.  

 

Diagnosis and Treatment

A definitive diagnosis of tuberculosis is made by the identification of the Mycobacterium tuberculosis complex in a clinical sample. Since the culture of these bacteria can be time-consuming, treatment may be initiated based on clinical suspicion alone. Tuberculosis skin tests and blood tests can be used to identify whether an individual has been infected, but cannot be used to distinguish between active and latent infections. Radiographic and other imaging techniques may also be useful in identifying patients, including those with asymptomatic active disease.

 

Mantoux test, positive result. Author: Grook da Oger.
Mantoux test, positive result. Author: Grook da Oger.

 

Typical pulmonary infection is treated with two months of Isoniazid, Rifampin, and Pyrazinamide (with Ethambutol pending results of susceptibility testing), followed by four months of Isoniazid and Rifampin alone. Treatment of multidrug-resistant tuberculosis generally includes the use of five drugs (including Pyrazinamide and/or Rifampin) for at least 6 months, followed by four drugs for 18-24 months (5).

Patients suspected of having active tuberculosis should be isolated, and healthcare personnel should observe relevant precautions.

The Centers for Disease Control and Prevention recommends treating individuals with latent tuberculosis that are at a high risk of progressing to an active infection. Included in the “high risk” designation are individuals with HIV/AIDS and other diseases that weaken the immune system, individuals who became infected with tuberculosis in the last two years, infants and young children, the elderly, and injecting drug users (8).

 

Prevalence 

In 2018, approximately 1.7 billion individuals were infected with Mycobacterium tuberculosis – roughly 23% of the world’s population (9). In 2019, approximately 10 million individuals experienced symptomatic tuberculosis, and approximately 1.4 million died as a result of the disease (10). Tuberculosis is found worldwide, but over 95% of cases and deaths occur in developing countries (10). Eight countries currently account for two-thirds of new tuberculosis cases: India, Indonesia, China, Philippines, Pakistan, Nigeria, Bangladesh, and South Africa (10). If you have a GIDEON account, click here to explore our tuberculosis outbreak map.

 

Tuberculosis cases and rates Worldwide, 1965 – today

Worldwide Tuberculosis cases and rates, 1965 - today

Vaccination 

Currently, Bacille Calmette-Guerin (BCG) vaccine remains the only licensed vaccine for the prevention of tuberculosis. It provides some protection against childhood tuberculosis but is less effective in preventing adult disease (11). BCG is commonly given to children in countries in which tuberculosis is prevalent, and is estimated to decrease the risk of contracting the disease by 50% (12).

 

Prevention for High-Risk Travelers

The Centers for Disease Control and Prevention recommend that “travelers who anticipate possible prolonged exposure to people with tuberculosis (for example, those who expect to come in contact routinely with clinic, hospital, prison, or homeless shelter populations) should have a skin or blood test before leaving the United States. If the test reaction is negative, they should have a repeat test 8 to 10 weeks after returning to the United States. Additionally, annual testing may be recommended for those who anticipate repeated or prolonged exposure or an extended stay over a period of years.” (8)

 

The Future

In 2014, the World Health Organization announced that they seek to end the global tuberculosis epidemic by 2035. They defined this goal “with targets to reduce tuberculosis deaths by 95% and to cut new cases by 90%, and to ensure that no family is burdened with catastrophic expenses due to tuberculosis.”  WHO called on the cooperation and collaboration of governments, and suggested a strategy that focuses on highly vulnerable populations (such as migrants) (13). 

In 2020, they announced that the COVID-19 pandemic has stalled progress, as a result of resources being reallocated (2). They noted, for example, that many diagnostic testing machines have been used to test for COVID-19 instead of for tuberculosis. Hopefully, robust testing efforts for the disease will resume soon, as the identification of cases is critical to ending the epidemic.

 

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References

(1) M. Rowe and J. Donaghy, “Mycobacterium bovis: the importance of milk and dairy products as a cause of human tuberculosis in the UK. A review of taxonomy and culture methods, with particular reference to artisanal cheeses”, International Journal of Dairy Technology, vol. 61, no. 4, pp. 317-326, 2008. Available: 10.1111/j.1471-0307.2008.00433.x

(2) “Global Tuberculosis Report”, World Health Organization, 2020. [Online]. Available: https://apps.who.int/iris/bitstream/handle/10665/336069/9789240013131-eng.pdf

(3) “The Clock Is Ticking: World TB Day 2021”, World Health Organization, 2021. [Online]. Available: https://www.who.int/campaigns/world-tb-day/world-tb-day-2021

(4) W. Cruz-Knight and L. Blake-Gumbs, “Tuberculosis”, Primary Care: Clinics in Office Practice, vol. 40, no. 3, pp. 743-756, 2013. Available: 10.1016/j.pop.2013.06.003

(5) “Tuberculosis”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/tuberculosis-12470

(6) U. Seedat and F. Seedat, “Post-primary pulmonary TB haemoptysis – When there is more than meets the eye”, Respiratory Medicine Case Reports, vol. 25, pp. 96-99, 2018. Available: 10.1016/j.rmcr.2018.07.006

(7) “Latent tuberculosis infection (LTBI): FAQs”, World Health Organization, 2021. [Online]. Available: https://www.who.int/tb/areas-of-work/preventive-care/ltbi/faqs/en/

(8) “Tuberculosis: Basic TB Facts: TB Prevention”, Centers for Disease Control and Prevention, Division of Tuberculosis Elimination, 2016. [Online]. Available: https://www.cdc.gov/tb/topic/basics/tbprevention.htm

(9) “Global Health: Newsrooms: Global Health Topics: Tuberculosis”, Centers for Disease Control and Prevention, Global Health, 2020. [Online]. Available: https://www.cdc.gov/globalhealth/newsroom/topics/tb/index.html

(10) “Tuberculosis: Key Facts”, World Health Organization, 2020. [Online]. Available: https://www.who.int/news-room/fact-sheets/detail/tuberculosis

(11) S. Fatima, A. Kumari, G. Das, and V. Dwivedi, “Tuberculosis vaccine: A journey from BCG to present”, Life Sciences, vol. 252, p. 117594, 2020. Available: 10.1016/j.lfs.2020.117594

(12) G. Colditz, “Efficacy of BCG Vaccine in the Prevention of Tuberculosis”, JAMA, vol. 271, no. 9, p. 698, 1994. Available: 10.1001/jama.1994.03510330076038

(13) “WHO End TB Strategy”, World Health Organization, 2021. [Online]. Available: https://www.who.int/tb/post2015_strategy/en/

Springtime Diseases: From Spring Fever to Lyme Disease

by Dr. Jaclynn Moskow

March 20th marks the Spring Equinox when the sun crosses the equator and spring officially begins in the Northern Hemisphere. We generally associate spring with melting snow, blooming flowers, and mating animals; but did you know it is also associated with an increase in the incidence of certain diseases?

There are many factors that cause some infectious diseases to follow seasonal patterns. Changes in temperature and precipitation influence biotic and abiotic environments, disease vectors and hosts, and human behavior, including the amount of time spent outdoors (1). On a molecular level, the numbers of circulating lymphocytes and other immune cells have been observed to vary depending on the season. This may occur as a result of the circadian nature of adrenocortical hormones coupled with fluctuating vitamin D and melatonin levels (2). Additionally, temperature, moisture, and UV light can affect the infectivity of pathogens. The disease pathogens themselves, and their animal and plant reservoirs, insect vectors, and other factors ebb and flow with changes in temperature, rainfall, and many other influences. 

Young pretty girl blowing nose in front of blooming tree. Spring allergy concept

 

Spring Fever

There is actually a historical basis to the term “spring fever.” During the 18th century, individuals sometimes became ill during the springtime, experiencing weakness, joint swelling, loose teeth, and poor wound healing: the clinical manifestations of scurvy (3). As societies became more urbanized, those living in cities were faced with a lack of fruits and vegetables during the winter months, leading some to develop vitamin C deficiency.

Today, scurvy is quite rare. When seen, it is usually among alcoholics or individuals following very extreme diets (4), as opposed to city dwellers lacking access to food sources. The term “spring fever” is now used colloquially to describe a feeling of restlessness and excitement that accompanies the start of spring. “Spring fever” is a disease of the past, but other diseases of springtime remain.

 

Seasonal Allergies/Asthma

Allergies occur when the immune system is triggered by a non-pathogenic substance, resulting in signs and symptoms of inflammation. Many of the same substances that can trigger allergies can also trigger asthma.

Trees, grasses, and weeds produce pollen during the springtime that can instigate allergies and asthma. Additionally, certain molds that are allergenic for some people may increase in number during the spring. Individuals with allergies to pet dander may also see an increase in symptoms, as animals shed their winter coats.

Signs and symptoms of seasonal allergies include congestion, sneezing, coughing, sore throat, post-nasal drip, and headache. Eyes may become red, itchy, watery, and/or swollen. Skin rashes may also be present, as may lymphadenopathy. In extreme cases, anaphylaxis may occur. Asthma is characterized by difficulty breathing, tightness in the chest, wheezing and coughing.

It is estimated that 10–30% of the global population are affected by allergic rhinitis (5). Asthma is less common, affecting about 300 million people worldwide (6.) Those suffering from seasonal allergies will find relief by avoiding known triggers. Utilization of a HEPA filter may be of benefit, as may keeping windows and doors closed. Masks can be worn when gardening and mowing the lawn, and taking a shower immediately after these activities may also provide relief. Frequently brushing and grooming pets and vacuuming dander may also help. 

Oral antihistamines and decongestants can be used, and in extreme cases, corticosteroids may be warranted. Allergy shots are also a key option. Asthmatic attacks can be managed with a number of medications, including corticosteroids, leukotriene modifiers, beta-agonists, theophylline, ipratropium, and various immunomodulators.

Woman with a spring allergy or a cold sneezing with tissue

Rhinoviruses

Rhinoviruses are the most common causes of the common cold. Unlike influenza, which peaks in the winter, rhinovirus cases peak during the fall and spring (7). Rhinoviruses are members of the genus Enterovirus of the family Picornaviridae. Rhinovirus infection has an incubation period of 1-9 days (8).

Rhinovirus infection can resemble seasonal allergies, causing congestion, sneezing, coughing, sore throat, and headache. Unlike with seasonal allergies, muscle aches are also common, and low-grade fever may occur. Rhinoviruses can cause ear infection, and bronchiolitis/bronchitis can develop, especially in children. Rarely, pneumonia may occur. Rhinovirus may also instigate asthma attacks.

Rhinovirus infection is generally self-limiting. Patients may obtain symptomatic relief using nasal decongestants, cough suppressants, and NSAIDs. Many of the same strategies being employed to limit the spread of SARS-CoV-2 can also reduce rhinovirus transmission, including frequent hand washing, avoiding contact with those who are ill and isolating patients.

 

Lyme Disease

Lyme disease is caused by Borrelia spp. and transmitted to humans through the bites of infected Ixodes ticks, often referred to as black-legged ticks/deer ticks. Most cases are acquired from immature ticks (nymphs) which are small (less than 2 mm), and difficult to see. They feed during the spring and summer months (9) – the peak season of Lyme disease (10).

The tick Ixodes ricinus crawling on human skin. This kind of animal is a distributor of Borrelia spp, an agent of Lyme disease
Ixodes ricinus tick is a distributor of Borrelia spp., an agent of Lyme disease

 

Lyme disease has an incubation period ranging from 2-180 days, with most cases manifesting within 7 to 14 days. About 25% of patients recall a recent tick bite. Erythema migrans is present in 75% of cases and is usually neither pruritic nor painful. Multiple skin lesions may occur in 20% to 50% of cases. A nodule in the nipple or ear lobe (borrelial lymphocytoma) may be present. Acrodermatitis chronicum atrophicans can also occur, typically seen on the hands and feet (11). 

Neurological manifestations occur in 10-15% of patients (12). The most common of these include lymphocytic meningitis, cranial neuritis, mononeuropathy multiplex, and painful radiculoneuritis. The range of joint involvement includes tendonitis, myositis, and bursitis, which wax and wane. The cardiac disease may be characterized by arrhythmia, heart block, chest pain, and pericarditis or myopericarditis. Rarely, other organs may become involved. 

Doxycycline, Ceftriaxone, Amoxicillin, and Cefuroxime can be used as a treatment, with dosage, route, and duration varying according to patient age and the nature and severity of the disease.

About 30,000 cases of Lyme Disease are reported to the Centers for Disease Control and Prevention (CDC) each year, but they estimate that as many as 476,000 people will actually contract the disease (13). Most cases occur in Pennsylvania, New York, Connecticut, and other states in the Northeastern United States. The disease is also common in Wisconsin and Minnesota. Lyme disease has been reported in Asia: in China, Korea, Japan, Indonesia, Nepal, and eastern Turkey. In Europe, most Lyme disease cases occur in Scandinavian countries, Germany, Austria, and Slovenia (14).

The CDC recommends that individuals spending time in wooded and grassy areas perform daily “tick checks.” By removing a tick within 24 hours, Lyme disease transmission is greatly decreased. It is important to contact a health professional before attempting to remove a tick. When outdoors, covering skin by wearing long clothing can also reduce transmission. 

Stay safe and Happy Spring!

 

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References

(1) M. Martinez, “The calendar of epidemics: Seasonal cycles of infectious diseases”, PLOS Pathogens, vol. 14, no. 11, p. e1007327, 2018. Available: 10.1371/journal.ppat.1007327

(2) A Fares A, “Factors influencing the seasonal patterns of infectious diseases”, Int J Prev Med, vol. 4, no. 2, pp. 128-32, 2013.

(3) P. Janson, “When Spring Fever Was a Real Disease”, Emergency Medicine News, vol. 38, p. 1, 2016. Available: 10.1097/01.eem.0000484361.70086.35

(4) M. Weinstein, P. Babyn and S. Zlotkin, “An Orange a Day Keeps the Doctor Away: Scurvy in the Year 2000”, PEDIATRICS, vol. 108, no. 3, pp. e55-e55, 2001. Available: 10.1542/peds.108.3.e55

(5) C. Schmidt, “Pollen Overload: Seasonal Allergies in a Changing Climate”, Environmental Health Perspectives, vol. 124, no. 4, 2016. Available: 10.1289/ehp.124-a70

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

(7) A. Monto, “The seasonality of rhinovirus infections and its implications for clinical recognition”, Clinical Therapeutics, vol. 24, no. 12, pp. 1987-1997, 2002. Available: 10.1016/s0149-2918(02)80093-5

(8) Lessler, N. Reich, R. Brookmeyer, T. Perl, K. Nelson and D. Cummings, “Incubation periods of acute respiratory viral infections: a systematic review”, The Lancet Infectious Diseases, vol. 9, no. 5, pp. 291-300, 2009. Available: 10.1016/s1473-3099(09)70069-6

(9) “Lyme disease: Transmission”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Vector-Borne Diseases (DVBD), 2020. [Online]. Available: https://www.cdc.gov/lyme/transmission/index.html

(10) S. Moore, R. Eisen, A. Monaghan and P. Mead, “Meteorological Influences on the Seasonality of Lyme Disease in the United States”, The American Journal of Tropical Medicine and Hygiene, vol. 90, no. 3, pp. 486-496, 2014. Available: 10.4269/ajtmh.13-0180

(11) “Lyme disease”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/lyme-disease-11360

(12) J. Halperin, “Neurologic Manifestations of Lyme Disease”, Current Infectious Disease Reports, vol. 13, no. 4, pp. 360-366, 2011. Available: 10.1007/s11908-011-0184-x

(13) “Lyme disease: Data and Surveillance”, Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Vector-Borne Diseases (DVBD), 2021. [Online]. Available: https://www.cdc.gov/lyme/datasurveillance/index.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Flyme%2Fstats%2Findex.html

(14) Meyerhoff, J, “What is the global prevalence of Lyme disease?”, Medscape.com, 2019. [Online]. Available: https://www.medscape.com/answers/330178-101008/what-is-the-global-prevalence-of-lyme-disease

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

Congenital Infections: TORCH

by Dr. Jaclynn Moskow

Pregnant woman cuddling her belly
By obtaining proper prenatal and perinatal care, pregnant women can optimize their chances of preventing, detecting, and treating congenital infections.

 

Congenital infections are caused by pathogens transmitted from a mother to her offspring during pregnancy or delivery. These infections can cause significant fetal and neonatal morbidity and mortality. The mnemonic “TORCH” is often used to refer to common congenital infections:

 

T – Toxoplasma

O – Other (Syphilis, Parvovirus B19, Varicella-Zoster, etc)

R – Rubella

C – CMV

H – Herpes Simplex Virus

 

Congenital Toxoplasmosis

Congenital toxoplasmosis is caused by the parasite Toxoplasma gondii. It can be acquired when a pregnant woman consumes raw or undercooked meat, or contacts contaminated water, soil, or cat feces (generally from outdoor cats that hunt.) The classic triad of congenital toxoplasmosis is 1) chorioretinitis 2) hydrocephalus and 3) cerebral calcifications. 

Symptoms often do not occur until months after birth and may include seizures, cognitive impairment, and cerebellar dysfunction (1). The retinal disease associated with congenital toxoplasmosis is progressive. Other clinical manifestations may include fever, rash, hydrocephalus or microcephaly, sensorineural hearing loss, congenital nephro­sis, hematologic abnormalities, hepatosplenomegaly, various endocrinopathies, and myocarditis. Infection can lead to spontaneous abortion, prematurity, stillbirth, and perinatal death. 

Congenital toxoplasmosis is more severe when acquired in early pregnancy. The incidence is highest in the Eastern Mediterranean and Africa (2). Rates are estimated at 1 per 3000-10000 live births in the United States (3) and 6.7 per 10000 live births in Europe – with 81% of all confirmed cases in the EU/EEA occurring in France (4). Spiramycin can decrease the risk of vertical transmission, but will not treat the fetus if the infection has already occurred. Infants born with this disease may benefit from pyrimethamine, sulfadiazine, and leucovorin. 

To help prevent infection, pregnant women should avoid consuming raw and undercooked meat, wear gloves when gardening, and avoid changing cat litter.

 

Congenital Rubella

Rubella, also known as “German measles,” is caused by the Rubella virus (Togaviridae family). It is most severe when acquired during the first trimester of pregnancy when the maternal infection will lead to fetal demise in 40-90% of cases (5). Congenital rubella can cause cardiac abnormalities, including patent ductus arteriosus and pulmonary artery stenosis. It can also cause ophthalmic abnormalities such as cataracts, glaucoma, retinopathy, and microphthalmia. Sensorineural deafness is common, and microcephaly, cognitive impairment, and meningoencephalitis may occur. Hepatosplenomegaly, hepatitis, hemolytic anemia, and thrombocytopenic purpura may also be observed. 

The incidence of congenital rubella has plummeted in countries that employ widespread vaccination. In recent times, documented cases of rubella in the United States are virtually all imported. Cases and outbreaks continue in Europe but at a very low rate. In 2008, 48% of all cases occurred in Southeast Asia and 38% in Africa (6). There is no effective treatment for congenital rubella.

 

Regional comparison of Congenital Rubella Syndrome prevalence, 1999 – 2019

Congenital infections - Congenital Rubella Syndrome prevalence: comparison between regions worldwide, 1999 - 2019

 

Congenital CMV

Congenital cytomegalovirus (CMV) is the most common congenital viral infection in the developed world. Clinical manifestations include sensorineural hearing loss, visual impairment, cerebral palsy, and cognitive difficulty. It can also cause neonatal cholestasis, pulmonary hypertension, and epilepsy. 10-20% of all hearing impairment in children is caused by congenital CMV (7).

CMV is identified in 5 to 7 per 1000 live births in the USA, Canada, Western Europe, and Australia; and 10-30 per 1000 live births in Latin America, Africa, and most Asian countries (8). Symptomatic infants may benefit from treatment with valganciclovir. It is difficult to prevent the acquisition of CMV, but some have suggested that pregnant women can decrease risk by avoiding contact with the saliva and urine of young children.

 

Congenital HSV

Congenital herpes simplex virus (HSV) most commonly occurs when an infant is exposed to the mother’s genital tract during delivery. Both herpes simplex-1 and herpes simplex-2 can cause congenital HSV. The risk of transmission from mother to infant depends primarily on when the maternal infection was acquired. When a mother is infected close to the time of delivery, the fetal infection rate is estimated at 25-60%. This rate drops to less than 2% when a mother is infected during the first half of pregnancy or earlier (9).

Signs of congenital HSV infection may occur between birth and six weeks of age. Disseminated disease may involve the liver, lung, central nervous system, and skin. “SEM disease” is limited to the skin, eyes, and/or mouth. Congenital HSV may cause a vesicular rash, hypothermia, lethargy, seizures, respiratory distress, hepatosplenomegaly, thrombocytopenia, hepatic dysfunction, cerebrospinal fluid pleocytosis, and sepsis. Congenital HSV is fatal in 50% of cases (10). The incidence of congenital HSV is estimated to be between 1 in 3000-20000 live births. All pregnant women should be tested for HSV, and those who are positive should receive prophylactic acyclovir or a similar drug at the time of delivery. Infected infants should be treated as well.

 

Congenital Syphilis

Congenital syphilis occurs when the bacterium Treponema pallidum is transmitted transplacentally or via the birth canal. The rate of vertical transmission increases as the pregnancy advances and transmission is more likely when the mother is experiencing early disease (11). Congenital syphilis can sometimes be detected by the appearance of nonimmune hydrops fetalis on ultrasound examination.

Congenital syphilis may be divided into two clinical syndromes: early congenital syphilis and late congenital syphilis. The early disease manifests within the first two years of life and is characterized by rash, adenopathy, and hepatosplenomegaly. Mucous patches and condylomata lata may be seen.  The eyes may be affected, and cranial nerve palsy and seizures may occur. Thrombocytopenia with petechiae and purpura are often noted. Other manifestations can include anemia, myocarditis, pancreatitis, nephrotic syndrome, and malabsorption. Osteochondritis is often seen on imaging. 

Late congenital syphilis manifests after two years of age. Dental findings include “Hutchinson’s teeth” and “mulberry molars.” Interstitial keratitis and eighth cranial nerve deafness can occur. Rhagades may be seen. Bone and joint abnormalities may include frontal bossing, saddle nose deformity, protuberant mandible, short maxilla, high palatal arch, sternoclavicular joint thickening (Higouménakis sign), saber shin, and Clutton’s joints. Central nervous system involvement can include cognitive impairment, hydrocephalus, seizures, cranial nerve palsy, paralysis, and optic nerve atrophy.

 

Congenital infections, Syphilis in the United States, 1941 – 2019

 

Graph illustrating the prevalence of congenital infection - Syphilis in the United States, 1941 - 2019

 

The WHO estimates that there were approximately 661,000 total cases of congenital syphilis in 2016, resulting in over 200,000 stillbirths and neonatal deaths (12) – with most cases occurring in South America and Africa. The CDC reports that congenital syphilis is on the rise in the United States, with the number of cases in 2018 being highest since 1998 (13).

All pregnant women should be tested for syphilis at their first prenatal visit. Penicillin is the only known effective antimicrobial agent for the prevention of vertical transmission and treatment of fetal and neonatal infection.

 

Congenital Parvovirus B19

Parvovirus B19 is estimated to infect 1-5% of pregnant women. Most infections are without consequence to the fetus, but in rare cases, serious fetal disease can arise (14). In infected fetuses, ultrasound may show nonimmune hydrops fetalis. 

Congenital parvovirus B19 often causes severe anemia and may also cause thrombocytopenia. Neurological manifestations include hydrocephalus, cerebellar hemorrhage, and polymicrogyria. Cardiac complications can include Ebstein’s anomaly, ventricular septal defect, cardiomyopathy, second‐degree heart block, and myocarditis. Ocular involvement may include corneal opacification, aphakia, and microphthalmia. Gastrointestinal manifestations include meconium peritonitis, fetal liver calcifications, portal tract fibrosis, and hypoplasia of the abdominal muscles. Congenital parvovirus B19 can also cause cleft lip and palate, micrognathia, bifid scrotum, secundum atrial septal defect, and micropenis with perineoscrotal hypospadias.

Intrauterine fetal blood transfusion can be used to treat the severe fetal anemia associated with congenital parvovirus B19 infection. 

 

Congenital Varicella-Zoster

Varicella-zoster congenital infections are caused by the virus that causes chickenpox and shingles. Infection may be characterized by low birth weight, hypoplasia of the extremities, dermal scarring, focal muscular atrophy, encephalitis, cortical atrophy, chorioretinitis, and microcephaly. Neonatal varicella zoster may occur when a mother contracts varicella virus between five days before delivery – to 48 hours after delivery. Neonatal varicella has a fatality rate of up to 30% (15). Congenital Varicella-Zoster virus infection is rare since most women are immune by childbearing age – having either been infected during childhood or vaccinated. Infants born with congenital varicella zoster may improve with acyclovir. 

 

Additional Congenital Infections

Additional viral agents of fetal and neonatal morbidity and mortality include HIV, Hepatitis B and C, measles, enteroviruses, adenovirus, lymphocytic choriomeningitis virus, West Nile virus, Zika virus, and Chikungunya virus. Additional bacterial causes include Group B Streptococcus, Chlamydia trachomatis, Neisseria gonorrhoeae, , Escherichia coli, Mycobacterium tuberculosis, and Coxiella burnetii. A parasite, Plasmodium falciparum (the causative agent of malaria) is also associated with congenital infection. 

By obtaining proper prenatal and perinatal care, pregnant women can optimize their chances of preventing, detecting, and treating congenital infections. 

 

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References

(1) Hampton MM. Congenital Toxoplasmosis: A Review. Neonatal Netw. 2015;34(5):274-8. doi: 10.1891/0730-0832.34.5.274.

(2) Rostami A, Riahi SM, Contopoulos-Ioannidis DG, Gamble HR, Fakhri Y, Shiadeh MN, Foroutan M, Behniafar H, Taghipour A, Maldonado YA, Mokdad AH, Gasser RB. Acute Toxoplasma infection in pregnant women worldwide: A systematic review and meta-analysis. PLoS Negl Trop Dis. 2019 Oct 14;13(10):e0007807. doi: 10.1371/journal.pntd.0007807.

(3) McAuley JB. Congenital Toxoplasmosis. J Pediatric Infect Dis Soc. 2014 Sep;3 Suppl 1(Suppl 1):S30-5. doi: 10.1093/jpids/piu077.

(4) “Congenital toxoplasmosis – Annual Epidemiological Report for 2016”, European Centre for Disease Prevention and Control, 2021. [Online]. Available: https://www.ecdc.europa.eu/en/publications-data/congenital-toxoplasmosis-annual-epidemiological-report-2016. 

(5) Best JM. Rubella. Semin Fetal Neonatal Med. 2007 Jun;12(3):182-92. doi: 10.1016/j.siny.2007.01.017. 

(6) Bouthry E, Picone O, Hamdi G, Grangeot-Keros L, Ayoubi JM, Vauloup-Fellous C. Rubella and pregnancy: diagnosis, management and outcomes. Prenat Diagn. 2014 Dec;34(13):1246-53. doi: 10.1002/pd.4467. 

(7) Goderis J, De Leenheer E, Smets K, Van Hoecke H, Keymeulen A, Dhooge I. Hearing loss and congenital CMV infection: a systematic review. Pediatrics. 2014 Nov;134(5):972-82. doi: 10.1542/peds.2014-1173. 

(8) Fowler KB, Boppana SB. Congenital cytomegalovirus infection. Semin Perinatol. 2018 Apr;42(3):149-154. doi: 10.1053/j.semperi.2018.02.002.

(9) Fernandes ND, Arya K, Ward R. Congenital Herpes Simplex. 2021 Jan 11. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 29939674.

(10) Westhoff GL, Little SE, Caughey AB. Herpes simplex virus and pregnancy: a review of the management of antenatal and peripartum herpes infections. Obstet Gynecol Surv. 2011 Oct;66(10):629-38. doi: 10.1097/OGX.0b013e31823983ec.

(11) Cooper JM, Sánchez PJ. Congenital syphilis. Semin Perinatol. 2018 Apr;42(3):176-184. doi: 10.1053/j.semperi.2018.02.005.

(12) “WHO publishes new estimates on congenital syphilis”, World Health Organization, 2021. [Online]. Available: https://www.who.int/reproductivehealth/congenital-syphilis-estimates/en/.

(13) “STD Facts – Congenital Syphilis”, Cdc.gov, 2021. [Online]. Available: https://www.cdc.gov/std/syphilis/stdfact-congenital-syphilis.htm.

(14) Ornoy A, Ergaz Z. Parvovirus B19 infection during pregnancy and risks to the fetus. Birth Defects Res. 2017 Mar 15;109(5):311-323. doi: 10.1002/bdra.23588. 

(15) “GIDEON”, App.gideononline.com, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/varicella-12550.

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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Pathogen of the month: Chikungunya virus

by Dr. Jaclynn Moskow

 

Chikungunya virus, 3D illustration. Emerging mosquito-borne RNA virus from Togaviridae family that can cause outbreaks of a debilitating arthritis-like disease
3D illustration of the Chikungunya virus

 

Chikungunya refers to an infection caused by the Chikungunya virus, an alphavirus of the Togaviridae family. Like its close relative, the Semliki Forest virus, the Chikungunya virus is transmitted from human to human via mosquito bites. 

Chikungunya is characterized by fever, joint and muscle pain, and rash.  The disease was discovered in Tanzania in 1952, and since that time has been identified in over 60 countries around the world. The word “Chikungunya” means “that which bends up” in the Makonde language, spoken by a group indigenous to Tanzania and Mozambique. It is thought that this term was coined to describe the posture of patients affected with severe disease.

 

Transmission

Mosquito species that carry Chikungunya include Aedes aegypti in the tropics, Aedes albopictus in the tropics and colder areas, and approximately one dozen Aedes species in Africa, including Aedes furcifer and Aedes taylori. Transmission occurs after a mosquito bites someone infected with Chikungunya and then subsequently bites someone else. Mosquitos pick up the Chikungunya virus from human blood, the virus then replicates inside the mosquito and can be transmitted via their salvia. Once a mosquito acquires the virus, it will likely carry it for the rest of its life. There is evidence that some animals, including non-human primates, rodents, and birds, may act as reservoirs for the Chikungunya virus.

Aedes aegypti Mosquito. Close up a Mosquito Mosquito on leaf,Mosquito Vector-borne diseases,Chikungunya.Dengue fever.Rift Valley fever.Yellow fever.Zika virus.
Aedes aegypti mosquito, the vector of Chikungunya

 

Signs and Symptoms

Signs and Symptoms of Chikungunya develop after a 2-12 day incubation period. Cases vary in severity, and asymptomatic infection may occur. The rate of asymptomatic cases is estimated to be between 4% and 28%.

Cases often begin with an abrupt onset of fever. Polyarthralgia occurs in 70% of cases, usually involving small joints. Swelling of joints may also occur, typically without fluid accumulation. In greater than 50% of cases, a maculopapular rash on the palms, soles, limbs, torso, and/or face is present. This rash may progress to desquamation. Fever generally resolves within one week, but joint pain may persist for months. Sometimes, a “saddle-back fever curve” is seen, with fever resolving and then returning. Moderate to severe lymphopenia is often noted. Thrombocytopenia, leukopenia, elevated liver enzymes, anemia, and elevated creatinine may also be observed.

Facial and neck erythema and conjunctival suffusion may be noted. Headache, photophobia, retro-orbital pain, pharyngitis, nausea, and vomiting can occur. Sometimes, pneumonia and dry cough are seen. Pruritus is common. Patients may complain of exhaustion and insomnia. Symptoms of Chikungunya can persist from one week to several months. Residual chronic joint pain may continue in some cases. Chronic disease is more common in older patients and patients with prior rheumatological disease.

Chikungunya can also cause neurological and ophthalmologic complications. Eye involvement may include retinitis, retinal detachment, optic neuritis, uveitis, dendritic lesions, and Fuchs heterocyclic iridocyclitis. Neurological manifestations can include altered mental function, encephalitis, seizures, myelopathy, Guillain-Barré syndrome, bulbar palsy, acute flaccid paralysis, focal neurological deficit, and sudden sensorineural hearing loss.

Additional rare complications of Chikungunya include hemorrhagic syndrome, cardiovascular shock, arrhythmias, myopericarditis, renal failure, rhabdomyolysis, and thrombocytopenic purpura.

Children with Chikungunya are more likely to experience neurological and dermatological symptoms, and less likely to have arthralgia. Transplacental transmission of the virus can occur and may result in neonatal encephalopathy, neonatal respiratory distress, sepsis, necrotizing enterocolitis, and cardiologic complications. Infants who become infected during the perinatal period may experience fever, rash, peripheral edema, lymphopenia, and thrombocytopenia. Congenital and perinatal infections are associated with poor neurodevelopmental outcomes. Transmission of Chikungunya via breastfeeding has not been noted.

Fatalities from Chikungunya are rare, occurring in about 1 per 1,000 cases. Fatalities are more common in newborns and individuals with multiple medical comorbidities. The use of NSAIDs prior to hospitalization is associated with an increase in disease severity. Infection with Chikungunya is likely to protect against future disease. 

 

Diagnosis and Treatment

A diagnosis of Chikungunya should be considered in individuals living in – or having traveled to – areas with known outbreaks presenting with acute onset of fever and joint pain. Dengue fever and Zika virus infection should be considered in a differential diagnosis of Chikungunya, as they are also carried by Aedes species mosquitoes and may present with similar signs and symptoms.

PCR, serology, and viral culture can be used for laboratory confirmation of Chikungunya. Chikungunya is classified as a biosafety level-3 pathogen, and samples should be handled accordingly. Blood-borne transmission from patients to healthcare workers and laboratory personnel has been documented.

Patients with Chikungunya are treated with supportive care, including hydration and pain management. It is important to prevent mosquito bites during the first week of illness, in order to prevent additional transmission.

 

Chikungunya outbreaks

Between 1952 and 2013, Chikungunya virus outbreaks were identified in Africa, Asia, Europe, and the Indian and Pacific Oceans. In 2013, cases were first identified in the Americas and nations of the Caribbean, and today the majority of cases occur in these locations – where populations have no preexisting immunity.

Over the past decade, the countries that reported most cases of Chikungunya have included Haiti, Dominican Republic, Guadeloupe, Martinique, El Salvador, Honduras, Nicaragua, Columbia, Bolivia, Brazil, Ethiopia, Chad, India, Laos, and French Polynesia. If you have a GIDEON account, click to explore Chikungunya Outbreak Map.

Between 2004 and 2006, an outbreak of Chikungunya that began in Kenya resulted in 500,000 cases in countries of the Indian Ocean, including one-third of the population of La Reunion Island. This outbreak spread to India, where almost 1.5 million people were infected. Ongoing outbreaks have been occurring in Brazil since 2014, with over 300,000 cases occurring in 2016. It is thought that a mutation occurred around 2005 that enabled the virus to survive in Aedes albopictus; and that having this additional species as a vector has fueled recent outbreaks.

Local transmission was reported for the first time in Europe in 2007, with 197 cases occurring in north-eastern Italy. The source of this outbreak was traced to a single individual who had returned from India with the infection. A second outbreak occurred in Europe in 2014, centered mainly in France and the UK and resulting in about 1500 cases.

Chikungunya cases in United States, 2006 - 2020, GIDEON graph

 

In 2014, local transmission of the Chikungunya virus was identified in the territories of the United States for the first time, with 4,659 cases occurring between American Samoa, Puerto Rico, the U.S. Virgin Islands, and Florida. Since that time, the rate of local transmission in the United States has decreased each year, with 179 cases occurring in 2016, 8 cases in 2018, and no cases in 2020.

 

Prevention

There is currently no vaccine to prevent Chikungunya. The CDC recommends the use of the Environmental Protection Agency (EPA)-registered insect repellents when traveling to areas with outbreaks. Wearing long sleeves and pants can also reduce transmission, as can sleeping in places with air conditioning and window and door screens. The CDC also recommends using 0.5% permethrin to treat clothing and gear to repel mosquitos.

During outbreaks, measures should be taken to control mosquito populations by reducing both natural and artificial water-filled habitats where they may breed. Any items that may hold water, such as pools, buckets, planters, and trash containers, should be regularly emptied and cleaned.

 

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This blog was written using data from the GIDEON database, CDC, and WHO.

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