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Archive for the ‘Microbiology’ Category

Dr. Oli prepares medical students for real-life situations

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

 

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

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

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

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

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

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

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

Read the original Times Higher Education article here

 

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The Gut Microbiome and Its Role in Health and Disease

by Dr. Jaclynn Moskow

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

 

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

 

Why Do We Have a Gut Microbiome?

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

 

The Gut Microbiome and COVID-19

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

 

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

 

The Gut Microbiome and Obesity

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

 

The Gut Microbiome and Diabetes 

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

 

The Gut Microbiome, Hypertension, and Cardiovascular Disease

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

 

The Gut Microbiome, Autoimmune Disorders, and Allergies

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

 

The Gut Microbiome and Neuropsychiatric Disorders

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

 

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

 

Fecal Microbiota Transplantation and Clostridium Difficile Colitis

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

 

Optimizing the Microbiome

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

 

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References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Examining Salmonella Typhi and Typhoid Fever

by Dr. Jaclynn Moskow

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

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

Transmission

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

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

Chronic Carriers and the Case of Typhoid Mary

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

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

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

Signs and Symptoms

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

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

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

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

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

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

Illustration of typhoid fever

Diagnosis and Treatment

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

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

Prevalence 

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

Typhoid, estimated cases worldwide 1990 - today

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

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

Prevention

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

Paratyphoid Fever and Typhus

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

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

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References

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

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

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

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

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

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

Pathogen of the Month: Yersinia Pestis

by Dr. Jaclynn Moskow

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

Yersinia pestis illustration
Yersinia pestis – the agent of Plague

Transmission

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

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

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

Yersinia pestis in history

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

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

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

 

 

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

Bubonic Plague

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

 

Bubonic plague transmission - illustration

 

Pneumonic Plague

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

Septicemic Plague

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

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

Diagnosis and treatment

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

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

Prevalence

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

Plague deaths worldwide, GIDEON graph

 

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

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

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

 

Prevention

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

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

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References

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

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

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

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

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

All you need to know about waterborne diseases

by Dr. Jaclynn Moskow

Woman scientist takes a water sample from polluted pond.

 

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

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

Bacteria, virus, and a parasite icon

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

 

WHO IS MOST AFFECTED BY WATERBORNE DISEASES?

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

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

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

Delivery of humanitarian aid and water by military helicopter

 

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

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

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

 

HOW CAN TRAVELERS AVOID WATERBORNE DISEASES?

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

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

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

Glass of contaminated water on grey background

 

WHAT WATERBORNE DISEASES ARE SEEN IN THE DEVELOPED WORLD?

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

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

 

CONTRACTING WATERBORNE DISEASES WHILE SWIMMING

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

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

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

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

 

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

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

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

 

SARS-CoV-2 structure. Anatomy of the coronavirus

 

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

 

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References:

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

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

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

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

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

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

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

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

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

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

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

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

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

Penicillin: the accident that saved many lives

Fleming in his Lab - Photo. Date: 1881 - 1955
Alexander Fleming in his laboratory, 1881 – 1955

 

There have been many happy accidents in science. Several of these were of great benefit to medicine.

For example, in 1895, a German physicist working with a cathode ray tube happened to place his hand in front of the rays and found that he could see his bones in the image projected onto the screen. Soon after that, the first X-ray images were produced.

There have been other instances where serendipity played a role in unearthing effective treatments against diseases. 

 

THE FIND OF THE 20TH CENTURY

The most famous of these happy accidents is the discovery of Penicillin as an antibiotic remedy. 

Alexander Fleming, a Scottish bacteriologist, worked at the inoculations department at St Mary’s Hospital in the early 1900s. 

In September 1928, Fleming had left a pile of bacteria cultures in his laboratory before going on holiday with his family. The cultures he was studying were known to cause septic infections. By accident, he left one of the Petri dishes uncovered.

Fleming returned to find that a bluish-green mold, similar to the mold found on bread, had contaminated the specimen. The area around the mold in the Petri dish was clear of bacteria. 

Fleming observed that the mold seemed to have killed the germs. This mold was identified as a strain of Penicillium. He saw this as a potential treatment for bacterial infections. 

Penicillin culture,1929
Penicillin culture, 1929

 

IMPORTANCE OF SHARED SCIENCE

Fleming was able to further identify that it wasn’t just the mold that killed the bacteria but the ‘juice’ the mold seemed to produce. 

He also discovered that the ‘mold juice‘ was effective against pathogens that are responsible for diseases like Meningitis, Diphtheria and Gonorrhea. 

Fleming’s effort would bear no further fruits. He was not able to produce and purify the ‘mold juice’ in substantial quantities.

However, he named the substance Penicillin and published his findings in the British Journal of Experimental Pathology in 1929. This crucial step allowed others to build on his work.

A decade later, Fleming’s findings piqued the interest of two Oxford scientists: Howard Florey and Ernst Chain. Eventually, they found a way to mass-produce the antibiotic in a form that could kill harmful bacteria without having any toxic effects on the human body.

Vintage vials of Penicillin G
Vintage vials of Penicillin G

 

PENICILLIN’S WARTIME VALUE

During World War I, Alexander Fleming was stationed in France and served in the Army Medical Corps as a captain. He observed that the death of soldiers was not always from wounds inflicted in battle, but rather from bacterial infections.

The principal treatment of such infections consisted of the administration of antiseptics. Fleming noted that these often did more harm than good. He wrote about this, however, his findings were not taken seriously at the time.

During World War I, the death rate from bacterial pneumonia was 18%. In WWII, thanks to Penicillin, the death rate from the same condition fell to less than 1%. This enabled many soldiers to return home in good health.

 

AN EXCEPTIONAL DISCOVERY

The mass production of Penicillin is credited with saving the lives of many thousands of soldiers during World War II. 

Antibiotics of the Penicillin family have been found to cure a wide variety of bacterial infections from mild, moderate upper respiratory tract infections to skin ulcers and urinary tract infections.

In 1944, Alexander Fleming was knighted by King George VI. In 1945, he received a Nobel Prize in Physiology or Medicine, together with Howard Florey and Ernst Boris Chain. 

The praise was well deserved, as infections that were once life-threatening are now only mild inconveniences because of Penicillin’s versatility and efficacy. Penicillin richly deserves its place as one of the most important anti-infective drugs of all time.

Interestingly, Fleming was not the first to observe the antibacterial effect of Penicillium. Between 1868 and 1873, a famous surgeon named Theodor Billroth discovered that it inhibited bacterial growth – but nothing was done about it at the time. He died when Fleming was 13 years old.

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Learn more: GIDEON Guide to Antimicrobial Agents

Leeuwenhoek: scientist who saw ‘animalcules’

Anthony van Leeuwenhoek and animalcules drawings
Antonie van Leeuwenhoek and a drawing of animalcules

 

Some discover their aptitude for science by natural curiosity, which causes them to investigate their surroundings. In doing so they find many hidden secrets that only curiosity like theirs could have revealed. However, an inquisitive nature alone doesn’t make one a scientist. Explorers, adventurers, reporters, and criminal investigators all lead lives based on it too.

Something special happens when curiosity is coupled with an empirical mind. That combination begins to approach the scientific method. The only thing left is to provide a record of findings so that other scientists can attempt to falsify the results.

 

Scientist By Nature

Antonie van Leeuwenhoek did all of this and more. He used the scientific method to unearth the existence of previously unseen organisms, and he was in regular correspondence with the Royal Society in London, discussing his findings.

Leeuwenhoek was a businessman by trade, but a scientist by nature. His skill in grinding glass allowed him to produce single-lens microscopes that could magnify over 200 times. 

On 17th September 1683, Leeuwenhoek was the first to report the existence of bacteria seen through his microscopes. He called them little “animalcules”.

He achieved clearer and brighter images than any of his scientific fellows would achieve for centuries. This led to doubts and questions about the certainty of what he claimed to have seen.

It wasn’t until 1981 that Leeuwenhoek’s original specimens at the Royal Society were successfully photographed. Even this was done using one of his surviving microscopes. This finally dispelled the lingering disbelief that he indeed saw what he claimed. 

 

The Father Of Microbiology

Leeuwenhoek had 112 of his 200 letters published in the journal of the Royal Society. He was one of the journal’s most prolific writers, touching on many aspects of biology and even mineralogy. 

However, Leeuwenhoek’s greatest delights and findings were in the field of microbiology. His discoveries are still informing the discipline and being proven true today, especially his reports on bacteria.

 

The Importance of Bacteria

The world is now very aware of the presence and importance of bacteria. Some bacteria can be harmful, but most are beneficial.

We know that bacteria are used to treat some of the foods we love like yogurt and cheese. We know about the use of bacteria for preserving foods in fermentation and pickling. 

However, we also know bacteria are responsible for food spoilage or poisoning in some cases. Pathogenic bacteria may be transmitted in some foods which can cause food poisoning. For example, the CDC warns that soft cheeses made with unpasteurized milk carry a greater risk of causing a Listeria infection.

The importance of bacteria to humans is also seen in medicine and other industries. Bacterial infections and antibiotic remedies are now well known but bacteria have been put to use for a host of other purposes, such as microbial leaching of precious metals in mining.

 

Real-life data for microbiology studies

Just like Leeuwenhoek, modern students of microbiology can use real-life data. Lecturers like Dr. Monika Oli teach microbiology students using GIDEON because of its vast dataset and a versatile toolkit. She knows it gives meaningful context to their studies.

At the time of writing, the GIDEON database includes 1,766 pathogenic bacteria, 154 mycobacteria, and 130 yeasts and algae. And the database is updated daily! 

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Streptomyces – the smell of life

The Mall in Central Park, New York City in late autumn on rainy day
The Mall in Central Park, New York City in late autumn on a rainy day

 

Did you know that humans can detect the smell of wet soil 200,000 times better than sharks sense blood? [1] It appears our olfactory abilities are not that bad after all, at least when it comes to finding potential sources of food. Petrichor, the term to describe the scent was coined in 1964, by scientists I. Bear and R.G. Thomas, meaning “petros” – stone and “ichor” – the blood of the gods [2] in Greek.

Divine or not, Streptomyces is a genus of over 800 bacterial species and subspecies responsible for the earthy smell of Autumn we know and love. But could it be that our innate senses are drawn to wet dirt for more reasons than farming? 

 

Could eating dirt cure the plague?

That is yet to be tested, but Streptomyces are certainly fit for more purposes than poetic walks after the rain. They are the most important source of antibiotics [3].

What is an antibiotic? By definition, it is a substance produced by one organism that is capable of inhibiting the growth or destroying other organisms  – a direct translation from Greek would be ‘anti-life’. In nature, this yields Streptomyces a competitive advantage. Astonishingly, they are responsible for nearly two-thirds of natural antibiotics [4].

For instance, Streptomyces griseus produces Streptomycin, the first antibiotic against tuberculosis, and a drug of choice against the agent of Plague Yersinia pestis, along with other 28 pathogenic bacteria species [5].  Streptomyces avermitilis helps keep parasites in check with its potent avermectins, and Chloramphenicol – a drug effective against 92 pathogens, is produced by Streptomyces venezuelae.

Streptomyces glaucescens under a microscope
Image of Streptomyces glaucescens. Courtesy of Tobias Kieser, John Innes Centre

 

Mavericks of the Streptomyces family

Although these species are not considered to be important agents of infection, it is worth noting that not all Streptomyces bacteria are friends of humanity, however. Two rebels, Streptomyces somaliensis and Streptomyces sudanensis go against the grain by infecting people’s feet with actinomycotic mycetoma.

First described as ‘Madura foot’ in 1842, the disease is thought to date back to the Byzantine period and typically presents as cutaneous and subcutaneous tissue swelling, thickening, or painless nodule involving feet 80% of the time [6].

Mycetoma global distribution map
Mycetoma global distribution map, GIDEON. Dark blue color indicates recent reports of autochthonous cases.

 

Although bacterial mycetoma is endemic throughout the tropical world, S. somaliensis and S. sudanensis are only found in Eastern Africa, as names indicate. In other parts of the world, S.albus has been known to occasionally rear its head [7] in skin infections, although such occurrences are very rare. 

And here’s the most fascinating fact – a distant ‘cousin’ of these pathogens, Streptomyces cattleya is an effective carbapenem used to treat Streptomyces spp. infections. A family feud in all its glory!

 

Why are bacteria named as fungi?

Streptomyces are about 450 million years old. Despite being a genus of bacteria, they are misleadingly suffixed with ‘-myces’, which stands for ‘fungi’ in Greek. This is because the first known example of the species contained branching filaments [8], a characteristic common to fungi.

Other actinobacteria, such as Mycobacteria and Actinomyces bear similar morphological features and thus carry a badge of mushroom in their names. Mycoplasmata – elusive gram-unidentifiable bacteria called ‘fungus form’, were named so by A. B. Frank in 1889. He thought ‘the “infection threads” of the organism were hyphae, and he knew of no hyphal-forming bacteria’ [9].

 

Want to learn more about Streptomyces? Try GIDEON ebook Guide to Medically Important Bacteria, 20% off on our website.

Interested in Mycetoma? Take a look at Mycetoma: Global Status

 

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References:

[1] H. Campbell, “Geosmin: Why We Like The Smell Of Air After A Storm”, American Council on Science and Health, 2018. [Online]. Available: https://www.acsh.org/news/2018/07/28/geosmin-why-we-smell-air-after-storm-13240. [Accessed: 11- Sep- 2020].

[2] I. BEAR and R. THOMAS, “Nature of Argillaceous Odour”, Nature, vol. 201, no. 4923, pp. 993-995, 1964. Available: 10.1038/201993a0 [Accessed 11 September 2020].

[3] K. Chater, “Streptomyces”, Brenner’s Encyclopedia of Genetics, pp. 565-567, 2013. Available: 10.1016/b978-0-12-374984-0.01483-2 [Accessed 11 September 2020].

[4] A. Hasani, A. Kariminik and K. Issazadeh, “Streptomycetes: Characteristics and Their Antimicrobial Activities”, International Journal of Advanced Biological and Biomedical Research, vol. 2, no. 1, pp. 63-75, 2014. Available: http://www.ijabbr.com/article_7033_7733c8235876d7ba635f6c831a916648.pdf. [Accessed 11 September 2020].

[5] “Streptomycin”, App.gideononline.com, 2020. [Online]. Available: https://app.gideononline.com/explore/drugs/20910. [Accessed: 11- Sep- 2020].

[6] V. Lichon and A. Khachemoune, “Mycetoma”, American Journal of Clinical Dermatology, vol. 7, no. 5, pp. 315-321, 2006. Available: 10.2165/00128071-200607050-00005 [Accessed 11 September 2020].

[7] M. Martin, A. Manteca, M. Castillo, F. Vazquez and F. Mendez, “Streptomyces albus Isolated from a Human Actinomycetoma and Characterized by Molecular Techniques”, Journal of Clinical Microbiology, vol. 42, no. 12, pp. 5957-5960, 2004. Available: 10.1128/jcm.42.12.5957-5960.2004 [Accessed 11 September 2020].

[8] K. Chater, “Streptomycesinside-out: a new perspective on the bacteria that provide us with antibiotics”, Philosophical Transactions of the Royal Society B: Biological Sciences, vol. 361, no. 1469, pp. 761-768, 2006. Available: 10.1098/rstb.2005.1758 [Accessed 12 September 2020].

[9] C. Krass and M. Gardner, “Etymology of the term Mycoplasma”, INTERNATIONAL JOURNAL of SYSTEMATIC BACTERIOLOGY, vol. 23, no. 1, pp. 62-64, 1973. Available: https://www.microbiologyresearch.org/docserver/fulltext/ijsem/23/1/ijs-23-1-62.pdf. [Accessed 12 September 2020].

Varicella vs. Monkeypox

Outbreaks of varicella and monkeypox in Africa are occasionally mistaken for “smallpox”   The following table was generated by an interactive tool in Gideon (www.GideonOnline.com) which allows users to generate custom charts that contrast clinical features, drug spectra or microbial phenotypes.

 

 

 

Outbreaks of Non-tubercuous Mycobacterial Infection in the United States

The following chronology of nosocomial mycobacteriosis outbreaks in the United States is abstracted from Gideon www.GideonOnline.com and the Gideon e-book series. [1,2] Primary references available on request.

1987 – An outbreak (17 cases) of Mycobacterium chelonae otitis media was caused by contaminated water used by an ENT practice in Louisiana.
1988 – An outbreak (8 cases) of foot infections due to Mycobacterium chelonae subspecies abscessus infections were associated with a jet injector used in a podiatric office.
1989 to 1990 – An outbreak (16 cases) of sputum colonization by Mycobacterium fortuitum was reported among patients on an alcoholism rehabilitation ward in Washington, D.C.
1991 (publication year) – An outbreak (6 cases) of Mycobacterium fortuitum infection in Washington was associated with contaminated electromyography needles.
1995 to 1996 – An outbreak (87 cases) of postinjection abscesses due to Mycobacterium abscessus in several states was ascribed to an adrenal cortex extract.
1998 – An outbreak (6 cases) of Mycobacterium mucogenicum bacteremia among bone marrow transplant and oncology patients in Minnesota was related to contaminated water.
1999 – An outbreak (10 cases) of intra- and periarticular Mycobacterium abscessus infection in Texas was caused by contaminated benzalkonium chloride used for injection.
2000 to 2001 – An outbreak (110 cases) of skin infections due to Mycobacterium fortuitum was caused by contaminated footbaths in California nail salons.
2001 – An outbreak of Mycobacterium chelonae keratitis in California was associated with laser in situ keratomileusis (LASIK).
2001 to 2002 – An outbreak of Mycobacterium simiae in a Texas hospital was related to contaminated tap water.
2002 – An outbreak (14 confirmed and 11 suspected cases) of soft tissue infections due to Mycobacterium abscessus followed injections of cosmetic substances administered by unlicensed practitioners in New York City.
2002 – An outbreak (115 cases or more) of cutaneous infection by Mycobacterium fortuitum was associated with a contaminated footbath in a nail salon in California.
2002 (publication year) – An outbreak (34 cases) of Mycobacterium chelonae soft tissue infection in California was associated with liposuction.
2002 to 2003 – An outbreak (4 cases) of Mycobacterium chelonae infection among patients undergoing rhytidectomies in New Jersey was caused by a contaminated methylene blue solution.
2003 – An outbreak (3 cases) of Mycobacterium goodii infection was associated with surgical implants in a Colorado hospital.
2004 – An outbreak (12 cases) among Americans of soft tissue infections caused by Mycobacterium abscessus following cosmetic surgery performed at various clinics in the Dominican Republic.
2004 – An outbreak (143 cases) of mycobacterial skin and soft tissue infection (presumed M. fortuitum) was reported among persons attending nail salons in California.
2008 – An outbreak (4 cases) of Mycobacterium mucogenicum bloodstream infections was reported among patients with sickle cell disease, in North Carolina.
2009 (publication year) – An outbreak (6 cases) of Mycobacterium chelonae infection was associated with a tattoo establishment.
2009 – An outbreak (2 cases, 1 confirmed) of Mycobacterium haemophilum skin infection was associated with a tattoo parlor in Washington State.
2011 (publication year) – An outbreak (3 cases) of Mycobacterium bolletii/M. massiliense furunculosis was associated with a nail salon in North Carolina.
2011 (publication year) – An outbreak of Mycobacterium abscessus infection was associated with outpatient rhytidectomies.
2011 – An outbreak (2 cases) of Mycobacterium haemophilum infection was reported among persons receiving tattoos in the Seattle, Washington region. {m 201108122444}
2011 (publication year) – An outbreak (11 cases) of Mycobacterium porcinum infection in a Texas hospital was related to contamination of drinking water.
2011 to 2012 – An outbreak (19 cases) of Mycobacterium chelonae infection involving multiple states was associated with contaminated ink used in tattoo parlors.
2011 to 2012 – An outbreak (15 cases) of infection by rapidly-growing mycobacteria was reported among pediatric hematopoietic cell transplant in a Minnesota hospital.
2013 – An outbreak (2 cases) of non-tuberculous mycobacterial infection was associated with fractionated CO2 laser resurfacing procedures performed at a clinic in North Carolina.
2013 to 2014 – An outbreak (19 cases) wound infection was reported among Americans who had traveled to the Dominican Republic for cosmetic surgery – including 12 due to Mycobacterium abscessus and 2 Mycobacterium fortuitum
2014 – An outbreak (15 cases, 4 fatal) of Mycobacterium abscessus infection in a South Carolina hospital was associated with contact of equipment with contaminated tap water.

References:
1. Berger SA. Infectious Diseases of the United States, 2014. 1145 pages, 478 graphs, 12,294 references. Gideon e-books, https://www.gideononline.com/ebooks/country/infectious-diseases-of-the-united-states/
2. Berger SA. Non-Tuberculous Mycobacteria: Global Status, 2014. 61 pages, 31 graphs, 584 references. Gideon e-books, https://www.gideononline.com/ebooks/disease/non-tuberculous-mycobacteria-global-status/

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