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Yellow Fever: Past and Present

1942, Innoculating eggs with yellow fever vaccine. USPHS (United States Public Health Service) Rocky Mountain Laboratory, Hamilton, Montana
Inoculating eggs with yellow fever vaccine, 1942. USPHS (the United States Public Health Service) Rocky Mountain Laboratory, Hamilton, Montana. Photographer: John Vachon

 

written by Dr. Jaclynn Moskow

What is Yellow Fever?

The yellow fever virus, a flavivirus, is transmitted via the bites of various mosquito species. The disease has an average incubation period of 3 to 6 days. The clinical presentation of yellow fever can vary greatly, ranging from a self-limited flu-like illness to overwhelming hemorrhagic fever – with a case fatality rate of 50%. Approximately 55% of yellow fever infections are asymptomatic, 33% are categorized as mild, and 12% severe (1).

Diagram of Symptoms of Yellow fever patient

Yellow fever generally manifests with the acute onset of fever, headache, backache, myalgia, and vomiting. Conjunctival infection may be seen, accompanied by facial flushing, relative bradycardia (Faget’s sign), and leukopenia. In some cases, fever and other symptoms may remit for a few hours to several days. Upon return of symptoms, icteric hepatitis and a hemorrhagic diathesis may follow with epistaxis, bleeding from the gums and gastrointestinal tract, and petechial and purpuric hemorrhages. Weakness, prostration, protracted vomiting, and albuminuria may also be noted. At this stage, patients will experience renal failure, myocardial dysfunction, necro-hemorrhagic pancreatitis, and seizures.

Yellow fever has a case fatality rate of 10 to 60% within 7 days of disease onset (1).

 

 

The Origin and Spread of Yellow Fever

Phylogenetic analyses indicate that yellow fever originated in Africa within the last 1,500 years. Its spread to the Americas coincided with the trans-Atlantic slave trade that began during the 16th century. It is likely that mosquitoes carrying yellow fever were imported into the Americas via slave ships (2). Significant outbreaks followed as the virus was introduced into populations with no pre-existing immunity. During the 18th and 19th centuries, approximately 25 major outbreaks claimed the lives of hundreds of thousands in New York City, Philadelphia, Baltimore, and New Orleans (3). Yellow fever also arrived in Europe during this time, with notable outbreaks occurring at Spanish, Portuguese, French, and British seaports (4).

It is estimated that for every soldier who died in battle during the Spanish-American War, 13 died of yellow fever (5). Yellow fever also killed many thousands during the construction of the Panama Canal. 

William C. Gorgas (1854-1920), on the site of Panama Canal construction.
William C. Gorgas (1854-1920), on the site of Panama Canal construction. As a U.S. Army surgeon during the Spanish American War, he established methods for eradicating mosquitoes hence reducing yellow fever and malaria among soldiers in Cuba. In 1904 he applied these techniques to control disease among the Panama Canal workers. Ca. 1910.

 

 

Development of a Vaccine for Yellow Fever

USA - CIRCA 1940: A stamp printed in USA shows portrait of Dr. Walter Reed, series Scientists, circa 1940

Early attempts to develop a vaccine for yellow fever resulted in the deaths of several test subjects and researchers. In 1900, a team led by Major Walter Reed traveled to Cuba to study the disease. At this point, the medical community was largely dismissive of the theory that mosquitos were the vectors of transmission for yellow fever. Working under the assumption that the mosquito theory was indeed incorrect, Reed’s team began experimenting with mosquitos and volunteers. After receiving criticism about using human test subjects, some team members decided to instead experiment on themselves. Unfortunately, this resulted in the death of physician-scientist Dr. Jesse Lazear – but with his death, the mosquito theory began to gain acceptance (6). 

Despite the death of Dr. Lazear, yellow fever research on human test subjects continued. The Reed team conducted a second and third set of mosquito experiments, offering financial compensation in the form of gold to study participants (6). After learning that none of these latest Reed study participants had died, Cuban physician Dr. John Guiteras began his own experiments. Unfortunately, three of his 42 test subjects succumbed to the illness, and with this, yellow fever research in Cuba came to a halt (7).

Subsequent efforts to control yellow fever centered on reducing mosquito populations as opposed to vaccine development, until 1918 when the Rockefeller Foundation began conducting yellow fever research. Within a year, Japanese scientist Dr. Hideyo Noguchi, who was working with the Foundation, announced that he had successfully developed a vaccine. Individuals in the United States, Latin America, and the French African colonies began receiving his vaccine, but the legitimacy of the studies leading to its development were soon called into question, and ultimately the vaccine was pulled (7).

The Rockefeller Foundation continued its efforts, and in 1925, they sent investigators to Lagos to determine if the African and South American diseases were caused by the same pathogen. Unfortunately, this trip resulted in three more investigators contracting and dying from yellow fever, including Dr. Noguchi. Nonetheless, the Rockefeller Foundation persisted, and a few years later, another candidate vaccine was developed – this time from efforts led by Dr. Max Theiler (7).

Despite the history of physician deaths related to yellow fever experimentation, Brazilian physician Dr. Bruce Wilson volunteered to receive the first dose of the Theiler vaccine. It was designated a success, and mass production began. Soon after, the Pasteur Institute developed their own vaccine, and for the next several years, the Rockefeller Foundation vaccine was used in the West as well as in England, and the Pasteur Institute vaccine used in France and its African colonies (7).

During World War II, the Rockefeller Foundation vaccine was given to almost all US soldiers. Unfortunately, the vaccine contained blood serum, and vaccination efforts resulted in approximately 330,000 soldiers contracting hepatitis B virus infection (8). Blood serum was subsequently removed as a component of the vaccine, and in 1953 a yellow fever vaccine was licensed for civilian use in the US (9). Use of the Pasteur Institute vaccine eventually ceased due to cases of postvaccinal encephalitis, but a variant of the Rockefeller foundation vaccine is still used today. Dr. Theiler received the Nobel Prize in Physiology or Medicine for his critical role in its development.

 

Yellow Fever in 2021

Yellow fever vaccination est. coverage 1980 - 2019

Today, the Centers for Disease Control and Prevention (CDC) recommends vaccination against yellow fever for individuals 9 months and older and who are traveling to or living in areas at risk in Africa and South America (10). It is a live attenuated vaccine, and thus contraindicated in patients who are immunocompromised. The vaccine is highly effective, with a median seroconversion rate of 99% (range 81–100%) in clinical trials (11).

Yellow fever is currently estimated to affect 200,000 people each year, resulting in 30,000 deaths, with 90% of cases occurring in Africa (12). Recent outbreaks have occurred in Brazil, Angola, Nigeria, and the Democratic Rep. of Congo. If you have a GIDEON account, click here to explore the Yellow Fever outbreak map. There are ongoing efforts to expand accessibility to the vaccine in these regions, as well as to implement additional vector control programs. 

The last outbreak of Yellow Fever in the United States occurred in 1905 (13). Yellow fever outbreaks ceased in Europe after World War II, when, for unknown reasons, the Aedes aegypti mosquito disappeared (14).

The absence of yellow fever in Asia is not fully understood. Some have speculated that differences in mosquito species may play a role. Another theory is that there may be a cross-immunity between yellow fever and other flaviviruses endemic to Asia, such as dengue fever. A third theory is that yellow fever has simply never been introduced into Asia (2).

 

 

 

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References

(1) “Yellow fever”, GIDEON Informatics, Inc, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/yellow-fever-12650

(2) Cathey and J. Marr, “Yellow fever, Asia and the East African slave trade”, Transactions of the Royal Society of Tropical Medicine and Hygiene, vol. 108, no. 5, pp. 252-257, 2014. Available: 10.1093/trstmh/tru043 

(3) F. Douam and A. Ploss, “Yellow Fever Virus: Knowledge Gaps Impeding the Fight Against an Old Foe”, Trends in Microbiology, vol. 26, no. 11, pp. 913-928, 2018. Available: 10.1016/j.tim.2018.05.012 

(4) M. Morillon, B. Marfart, and T. Matton, “Yellow fever in Europe in 19th Century”, Ecological Aspects of Past Settlement in Europe. P. Bennike, pp. 211-222, 2002.

(5) Staples, “Yellow Fever: 100 Years of Discovery”, JAMA, vol. 300, no. 8, p. 960, 2008. Available: 10.1001/jama.300.8.960 

(6) “Politics of Participation: Walter Reed’s Yellow-Fever Experiments”, AMA Journal of Ethics, vol. 11, no. 4, pp. 326-330, 2009. Available: 10.1001/virtualmentor.2009.11.4.mhst1-0904

(7) J. Frierson. “The yellow fever vaccine: a history”, Yale J Biol Med, vol. 83, no. 2, pp. 77-85, 2010

(8) M. Furmanski. “Unlicensed vaccines and bioweapon defense in World War II”, JAMA, vol. 282, no. 9, p. 822, 1999

(9) “Historic Dates and Events Related to Vaccines and Immunization”, Immunize.org, 2021. [Online]. Available: https://www.immunize.org/timeline/

(10)”Yellow Fever Vaccine Recommendations”, 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/yellowfever/vaccine/vaccine-recommendations.html

(11) J. Staples, A. Barrett, A. Wilder-Smith and J. Hombach, “Review of data and knowledge gaps regarding yellow fever vaccine-induced immunity and duration of protection”, npj Vaccines, vol. 5, no. 1, 2020. Available: 10.1038/s41541-020-0205-6 

(12) “Yellow Fever”, Centers for Disease Control and Prevention, Global Health, 2018. [Online]. Available: https://www.cdc.gov/globalhealth/newsroom/topics/yellowfever/index.html

(13) K. Patterson, “Yellow fever epidemics and mortality in the United States, 1693–1905”, Social Science & Medicine, vol. 34, no. 8, pp. 855-865, 1992. Available: 10.1016/0277-9536(92)90255-o 

(14) “Facts about yellow fever”, European Centre for Disease Prevention and Control, 2021. [Online]. Available: https://www.ecdc.europa.eu/en/yellow-fever/facts

 

 

How Vaccines Work

Development and manufacture process of a new vaccine. Final production of filled vials of Covid-19 vaccine. Bio science 3D illustration.

 

You may know they save lives, but have you ever wondered how vaccines work? As mass vaccination programs in response to the COVID-19 pandemic are underway, there is a heightened interest in understanding vaccines and their mechanism of action.

Vaccines stimulate the immune system to recognize and respond to specific pathogens. Differing vaccines accomplish this through a variety of mechanisms. Vaccines can be divided into five basic categories: live attenuated vaccines, inactivated vaccines, subunit vaccines including toxoids, mRNA vaccines, and viral vector vaccines.

 

Live Attenuated Vaccines

Live attenuated vaccines contain live viruses or bacteria that have been weakened to reduce virulence. Following ingestion or injection, the body mounts an immune response that is similar to what would occur if it were to encounter the natural disease. Since the pathogens used in live attenuated vaccines have been weakened, they cause only mild symptoms – or no symptoms at all. Live attenuated vaccines generally provide the longest-lasting immunity of any vaccine type.

Examples of live attenuated viral preparations include measles, mumps, rubella, varicella, rotavirus, yellow fever, oral polio vaccine, and intranasal influenza vaccine. Live attenuated bacterial vaccines include the BCG vaccine for tuberculosis and the oral cholera vaccine. In general, viral vaccines have greater efficacy than bacterial vaccines.

The eradication of smallpox was accomplished through a live attenuated vaccine, which contained a related virus (vaccinia). In the veterinary world, widespread use of a live attenuated vaccine led to the eradication of Rinderpest, also known as ‘cattle plague’, caused by a morbillivirus of the family Paramyxoviridae. 

Live attenuated vaccines are generally contraindicated in pregnant women and immunocompromised patients, such as those receiving immunosuppressive therapy or living with HIV/AIDS or congenital immunodeficiency. 

It is extremely rare for a live attenuated vaccine virus to mutate into a more virulent form and cause disease. Cases of this phenomenon have been documented with oral polio vaccine, at a reported rate of one case per 750,000 children receiving their first dose (1). As a result of these rare instances, in many countries (including the United States), the oral polio vaccine is no longer used and has been replaced by inactivated preparations.

 

How inactivated vaccines work

Inactivated vaccines, also known as killed vaccines, prime the immune system with bacteria or viruses that have been inactivated to remove all virulence. They cannot cause the disease they protect against and are generally considered safe for immunocompromised and pregnant patients. The protection provided by inactivated vaccines does not usually last as long as that provided by live attenuated vaccines, and booster doses are often recommended. 

Examples of inactivated vaccines include hepatitis A, rabies, intramuscular influenza, intramuscular polio, and variants of the pertussis vaccine. Several inactivated SARS-CoV-2 vaccines have been developed, including China’s “Sinovac”, India’s “Covaxin”, and Russia’s “CoviVac”.

 

How vaccines work: inactivated vaccine
Inactivated vaccine mechanism of action

 

How subunit vaccines work

Subunit vaccines contain fragments of a pathogen (i.e., a polypeptide or polysaccharide) often bound to other molecules. As with inactivated vaccines, these cannot produce the disease itself and are generally considered safe for immunocompromised and pregnant patients. Booster doses are often required.

Examples of subunit vaccines include hepatitis B, human papillomavirus (HPV), Haemophilus influenzae type B (HiB), herpes zoster, meningococcus B, pneumococcal, and one variant of the pertussis vaccine. Occasionally, the subunit used in these vaccines is an attenuated toxin (toxoid).  Examples of toxoid vaccines include tetanus and diphtheria.

There are several subunit vaccines for SARS-CoV-2 in various stages of clinical trials around the world.

 

Messenger RNA (mRNA) – a new type of vaccine

mRNA vaccines are a new type of vaccine and contain fragments of mRNA that encode a piece of protein from the pathogen of interest. After being vaccinated with such a vaccine, the body’s own cells incorporate the mRNA and produce the protein, which the immune system then recognizes as foreign. The Pfizer-BioNTech and Moderna COVID-19 vaccines are both mRNA vaccines. There are several additional mRNA vaccines currently in development. 

 

How vaccines work: mRNA vaccine schematic illustration
mRNA vaccine mechanism of action

 

How viral vector vaccines work

Viral vector vaccines use modified versions of viruses as “vectors” to deliver a nucleic acid of the pathogen of interest into the cell. Once inside the cell, the DNA is transcribed into mRNA, and the mRNA is translated into protein. The body then recognizes this protein as foreign and mounts an immune response, similar to that which occurs with mRNA vaccines. The Johnson & Johnson COVID-19 vaccine works in this manner.

 

How vaccines work: viral vector vaccine
Viral vector vaccine mechanism of action

 

 

Dr. Steve Berger on Vaccines

GIDEON co-founder Dr. Steve Berger, reflects on vaccines: “Vaccines continue to save millions of lives and have prevented untold misery to the human species. Although the effectiveness of individual vaccines may vary, and most may cause occasional side effects, the cost of non-vaccination – in both death and suffering – will always be much higher.”

 

Optimizing Immunity

Proper nutrition, exercise, ample sleep, and adequate levels of Vitamin D have been shown to enhance the efficacy of vaccines as well as strengthen the immune system as a whole. This is discussed in more detail in our blog: Strengthen Your Immune System! Your Guide to the Ultimate 2021 New Years Resolution

 

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References:

(1) “Poliomyelitis Prevention in the United States: Introduction of A Sequential Vaccination Schedule of Inactivated PoliovirusVaccine Followed by Oral Poliovirus Vaccine; Recommendations of the Advisory Committee on Immunization Practices (ACIP)”, Cdc.gov, 1997. [Online]. Available: https://www.cdc.gov/mmwr/preview/mmwrhtml/00046568.htm.

Pathogen of the month: Staphylococcus aureus

by Dr. Jaclynn Moskow

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

 

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

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

 

Staphylococcus Aureus Skin infections

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

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

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

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

 

Staphylococcus Aureus Pneumonia 

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

 

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

 

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

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

 

Food Poisoning From Staphylococcus Aureus 

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

 

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

Toxic Shock Syndrome From Staphylococcus Aureus

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

 

Staphylococcus Aureus Endocarditis

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

 

Other Infections Caused By Staphylococcus Aureus

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

 

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References 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

What to Do When Faced With a Fungal Infection at Home

Woman looking at black mold (fungal infection) on the ceiling

written exclusively for gideononline.com by Jennifer Birch

 

Fungal infections are a rampant problem in America. According to the Center for Disease Control and Prevention (CDC), there were over 75,000 hospitalizations for fungal disease in 2017. However, this figure is most likely an underrepresentation, given that fungal infections go largely undiagnosed. Regardless, some of them can cause illness and even death if left untreated. Individuals should be aware of the signs, treatment options, and prevention methods for fungal infections.

 

What is a fungal infection?

Fungi cause fungal infections. Most relate this type of microorganism to mushrooms, but they also come in the form of mold, mildew, and yeast. When a harmful fungus comes into contact with your skin, especially through an open wound, it can cause an infection. Some types of fungi also release tiny spores into the air as a means of reproduction. Inhaling these spores can also cause a fungal infection to spread in your lungs.

Given that there are multiple types of fungi, it follows that there are also many different diseases that stem from the initial infection. One example is Candidiasis, which is caused by yeast – the most common cause of fungal infections worldwide. Other fungal diseases include dermatophytosis, endemic mycoses, and a whole slew of mold-based illnesses.

Regardless of the cause, fungal infections are usually characterized by redness, itching, irritation, and even swelling of the skin. It can be very uncomfortable for anyone who experiences it and must be treated immediately.

 

What are the treatment options?

Most fungal infections will go away with the use of over-the-counter treatments. These include antifungal creams, gels, sprays, and ointments.

However, if it doesn’t improve even after medication, it’s best to seek medical assistance. When visiting your local clinic, you will likely be attended to by a nurse knowledgeable in this area. Most specialist nurses have completed an RN to BSN program, which qualifies them as primary care professionals who can diagnose various conditions, including superficial fungal infections. Note down recommendations made by your nurse regarding treatment and future techniques for prevention against fungal infections.

However, if  infection becomes more serious, prepare to be directed to a dermatologist or an Infectious Disease specialist. After evaluating the area of infection, they will likely prescribe a more potent antifungal cream than you can’t get over the counter. For fungal infections that have begun to spread throughout your body, they might administer an antifungal injection and prescribe oral medication. Make sure to keep in touch with your doctor throughout the treatment process to ensure that the infection isn’t getting worse.

 

Prevention is better than cure

Plenty of fungi thrive in hot and humid weather, especially mold. So, to prevent more fungal infections in the future, you need to ensure your home is clean and dry. Properly ventilate rooms, so moisture doesn’t build up inside. It’s also worth investing in air conditioning units and dehumidifiers to further improve air quality at home. Finally, should you find any mold or mildew growing in your house and deal with it immediately, so it doesn’t propagate further.

In addition to keeping your home clean, you should also practice good personal hygiene. This simply means wearing clean clothes and taking baths regularly. At the end of the day, protecting your home against fungus and keeping your body clean is the surest way to prevent fungal diseases.

Would you like to learn more? Check out our in-depth review of fungal infections by Dr. Moskow here.

 

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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

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