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Haemophilus parasuis

Introduction

Haemophilus parasuis is a Gram-negative, rod-shaped bacterium that causes Glasser’s disease in pigs. While H. parasuis is often found in swines’ upper respiratory tract (URT) as part of their normal microbiota, stressed and immunocompromised pigs are susceptible to infection and subsequent disease, which is characterized by pneumonia, fibrinous polyserositis, polyarthritis and meningitis. In 1910, Glasser was the first to describe the bacterial infection, and by 1943, it was evident that the causal pathogen was H. parasuis. Since then, worldwide outbreaks of Glasser’s disease are on the rise, and infection afflicts almost every large-scale swine production system. H. parasuis is also implicated in increasing the morbidity and mortality of other viral infections, such as Porcine Reproductive and Respiratory Syndrome Virus.

Disease

H. parasuis is most commonly transmitted via direct contact, but is known to also be transferred via aerosol inhalation. Although not well characterized, H. parasuis is thought to infect the pig when its immune system is compromised or when the host experiences stress. The bacteria first attach to and colonize the mucosa of the nasal cavity. Once inside the bloodstream, H. parasuis targets the epithelial cells lining the chest, abdomen, brain cavity, heart sac, and joints (serosal membranes). Once the bacteria adhere to the epithelial cells, it induces cell death, which in turn releases signaling molecules that induce the host’s immune system. This will then cause inflammation and can lead to severe inflammatory injuries, such as swollen joints and purple extremities. Currently, there have been 21 different serovars, variations of H. parasuis with different surface proteins, classified. The different serovars range in virulence with the most virulent being able to invade endothelial cells. However, this invasion is not required for disease to occur.

H. parasuis can cause three clinical forms of Glasser’s disease—a sporadic form in young pigs, a second form characterized by sub-capsular kidney bleeding and sudden death, and a third form as a secondary agent in infections of Circovirus and virus causing swine Reproductive and Respiratory Syndrome. At the beginning of the acute form, pigs often show symptoms of increased body temperature of above 40 °C, lethargy, coughing, anorexia, and incoordination. If H. parasuis crosses the endothelial cells lining the blood-brain barrier and reaches the central nervous system, it can cause meningitis, which is characterized by inflammation of the sacs that surround the brain. This disturbs the nervous system and can cause neurological clinical signals such as tremors and convulsions. If the disease progresses to chronic form, then chronic arthritis and severe fibrosis can occur and stunt growth rate.

Figure 1: Three months old piglet that died due to Glasser’s Disease. It is exhibiting severe inflammation of the peritoneum (serous membrane lining the cavity of the abdomen and covering the abdominal organs) with accumulation of fluid in the abdominal cavity. (Source: International Journal of Veterinary Sciences and Animal Husbandry, S. Jyoti, R. Nepal, Dr. A. Thapa, Dr. S. Rimal, 2019)  

Epidemiology

H. parasuis infection often occurs when an animal is purchased from an infected herd, thus introducing the bacteria to an unaffected herd (Figure 2). An infected herd is susceptible to an infection by a different serovar of H. parasuis because infection by one serovar does not provide immunity towards another serovar of H. parasuis. Therefore, a herd that was previously infected by one serovar can become infected by a different serovar of H. parasuis. The introduction of the new serovar occurs when a pig infected with the different serovar is brought into the herd. For example, a herd that was infected with serovar 1 does not have immunity towards serovar 2. If a pig infected with serovar 2 is introduced to this herd, then the pigs of the herd can become infected with serovar 2. When infection happens, animals of all ages are susceptible of contracting the disease, possibly leading to an outbreak. During an H. parasuis infections outbreak, infection rate of adults can reach 15% and young pigs 50%. 

Piglets are often the most afflicted with Glasser’s disease as infected mothers can transfer the bacteria through their breast milk. Piglets colonized by pathogenic variants will become carriers of the disease, but are immune. This is because their immune systems are able to develop while receiving immune protection from proteins in the mother’s milk. These animals will later carry the disease, but will not exhibit any observable symptoms. However, piglets that are not colonized by pathogenic serovar are highly susceptible to infection when they stop suckling. Since their developing immune systems have not been exposed to the pathogenic H. parasuis, the piglets are not able to ward off infection, leading to high rates of Glasser’s disease at the age of 5 to 6 weeks.

Figure 2: Illustration showing a possible case of transmission of H. parasuis. Source: J. Dujardin, 2019.

Virulence

During infection, H. parasuis firstly invades the lung epithelium using a variety of virulence factors. As the first step in this process, the bacteria adheres to the host epithelium. This is facilitated by fimbriae, which are adhesion proteins on the bacterial surface. Secondly, H. parasuis must avoid the host’s immune system, which has cells trying to engulf and process the bacteria. For example, alveolar macrophages are innate immune cells located in the lungs’ alveoli and they constantly pick up bacteria to try and identify pathogens. When they find an invading microbe, macrophages will initiate an innate immune response. In order to circumvent these cells, H. parasuis has two virulence factors—a capsule and imitation of host cells’ surfaces. The capsule is a protective cover that is part of its outer membrane and protects the bacteria from most host immune responses, including engulfment by macrophages. All host cells are covered in sialic acid; therefore, H. parasuis mimics this by sialylation of their capsule layer. By having this virulence factor, the bacteria evade digestion. H. parasuis does this in an attempt to delay macrophage activity and, ultimately, the immune response.

If the macrophage is successful in engulfing H. parasuis, the cell still has to kill the bacteria via the release of destructive proteins and molecules. However, H. parasuis’s capsule interferes with the macrophage’s ability to mount this response. Therefore, the bacteria are able to live intracellularly in these immune cells. Once inside the macrophage, the bacteria prevent certain inflammatory messages from being produced as well as modify the surface proteins on the macrophage’s surface. This delays the host’s inflammatory response and gives the bacteria time to spread throughout the body. They can then enter the bloodstream and colonize elsewhere, such as the liver, brain and kidneys. In fact, H. parasuis itself is not what causes death when a pig is infected, it is rather the delayed-onset of systemic inflammation, which sometimes can lead to septic shock.

Overall, much is still unknown and not understood regarding H. parasuis. Further identification of virulence factors and their respective mechanisms will help elucidate aspects of its infection. Many aspects of its infection remain to be associated with and explained by identification of more virulence factors.

Figure 3: Bacterial infection process in the lung alveoli and consequent spreading throughout the body via the bloodstream. By G. Mezentzeff and V. Guay, 2019.

Prevention and Treatment

Good animal hygiene and nutrition as well as animal management are important factors that can help prevent incidence of infection. Most importantly, transport and the raising of animals need to be closely monitored to prevent the spread of disease to new regions and prevent outbreaks. Antibiotics, specifically prophylactic antimicrobials, can also be used as a method of prevention in piglets. This is useful since H. parasuis is able to colonize piglets as early as less than ten days of age. 

Another possible method used to control H. parasuis infection is vaccination, typically through the single dose injection of Parasail HPS injectable vaccine or Ingelvac HP-1 vaccine in the intramuscular space of the animal. Vaccines are administered to both piglets and mothers. The proportion of animals that are infected by H. parasuis is significantly lower in vaccinated than non vaccinated animals. Revaccination should take place right after the piglets stop drinking milk in order to provide the necessary protection against H. parasuis. Idealially, H. parasuis infection is prevented through the combination of vaccination of the sows and piglets and prophylactic antibiotic treatment of newborn piglets.

In the case where an animal is infected with H. parasuis, antibiotics can be used. For example, H. parasuis is successfully treated with synthetic penicillin, which acts to weaken and burst the cell walls of the bacteria. The drugs accomplish this by preventing the bacteria’s peptidoglycan, a cell wall layer, from crosslinking effectively during cell wall synthesis. Enroflox, Excede, and Draxxin, are all injectable over the counter antimicrobial solutions and three of the most effective treatments against H. parasuis. It is recommended to target antibiotic therapy towards the sows, as well as piglets, and to begin treatment immediately after symptoms are observed. The dose administered depends on the severity of the infection: if the disease has spread to the tissues, spinal fluids, or has affected joints, a higher dose is used. 

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References

Brockmeier, Susan L., et al. “Virulence and draft genome sequence overview of multiple strains of the swine pathogen Haemophilus parasuis.” PloS one 9.8 (2014): e103787.

Costa-Hurtado, Mar, et al. “Changes in macrophage phenotype after infection of pigs with Haemophilus parasuis strains with different levels of virulence.” Infection and   immunity 81.7 (2013): 2327-2333.

Iowa State University Haemophilus parasuis (Glasser’s Disease) Iowa State University. (2019). Retrieved November 13, 2019, from Iastate.edu website: https://vetmed.iastate.edu/vdpam/FSVD/swine/index-diseases/glasser-disease

Nedbalcova, K., et al. “Haemophilus parasuis and Glässer’s disease in pigs: a review.” Veterinarni Medicina 51.5 (2006): 168-179.

Oliveira, Simone, and Carlos Pijoan. “Diagnosis of Haemophilus parasuis in affected herds and use of epidemiological data to control disease.” Journal of Swine Health and Production 10.5 (2002): 221-225.

Oliveira, Simone, P. J. Blackall, and Carlos Pijoan. “Characterization of the diversity of Haemophilus parasuis field isolates by use of serotyping and genotyping.” American journal of veterinary research 64.4 (2003): 435-442.

Oh, Y., Han, K., Seo, H. W., Park, C., & Chae, C. (2013). Program of vaccination and antibiotic treatment to control polyserositis caused by Haemophilus parasuis under field conditions. Canadian journal of veterinary research, 77(3), 183-190.

Pipestone Veterinary Sevices (PVS). (2018). Retrieved November 11, 2019, from https://pipevet.com/glassers-disease-in-swine.

Rapp-Gabrielson, V. J. “Haemophilus parasuis. 6 Disease of Swine th. Ed.: 475-481. Straw, B.8 E. et al. eds.” (1999).

Sack, Meike, and Nina Baltes. “Identification of novel potential virulence-associated factors in Haemophilus parasuis.” Veterinary microbiology 136.3-4 (2009): 382-386.

Solano-Aguilar, G. I., et al. “Protective role of maternal antibodies against Haemophilus parasuis infection.” American journal of veterinary research 60.1 (1999): 81-87.

White, Mark. NADIS – National Animal Disease Information Service. 2012, https://www.nadis.org.uk/disease-a-z/pigs/glaessers-disease/.

Bacillus cereus

Introduction

Bacillus cereus is a Gram-negative, spore-forming, rod-shaped bacterium (Figure 1) that causes food poisonings and food infections. This microorganism is a common soil inhabitant and can grow in almost all types of food. B. cereus was first identified as a foodborne pathogen by Hauge (1955) from a case of the diarrheal type of illness due to the consumption of vanilla extract. In 1971, the emetic type of food poisoning was found to be caused by B. cereus in fried rice, which gave its name of “fried rice syndrome”. The heat-resistant spore, a dormant structure of bacteria formed under stressful conditions, helps B. cereus to survive during food processing, thus raises issues of food safety, especially in pre-packed and ready-to-eat foods. 

Figure 1: Microscopic image of B. cereus stained with Gram’s method. Source: Dr. William A. Clark (1977), Public Health Image Library, Center for Disease Control. 

Disease

B. cereus forms resistant spores which protect it from extreme conditions such as temperature, pH, and radiation. The spore helps its persistence and transmission through processed, pasteurized, sterilized, and heat-treated food products, increasing its chance of human ingestion.  Contaminated foods either by B. cereus or the toxins produced by this bacterium food are the primary causes of the diseases (Figure 2). The food infection is caused by the growth of B. cereus in the intestine. Vegetables, meats, and dairy products are common vehicles for the transmission of this type of disease. Symptoms usually include abdominal pain and diarrhea that begin 4-16 hours after eating the contaminated food. On the other hand, the emetic syndrome of B. cereus food poisoning, also called “fried rice syndrome”, is due to the preformed toxin predominantly in starchy foods such as fried rice and pasta. Because the preformed toxins rather than the growth of the bacterium cause this type of illness, the onset of syndromes is more rapid compared to the diarrheal type. Symptoms are characterized by nausea and vomiting, starting in 1-5 hours after the consumption of contaminated foods. Both types of illnesses could be resolved without treatments and symptoms usually disappear within two days. However, individuals with compromised immune system may develop systemic infection due to introduction of the bacteria into the bloodstream.  

 

 

Figure 2: Transmission pathways of B. cereusdemonstrating how it enters the food production, followed by the human digestive system. The bacteria spread through insects, higher trophic animals like cows, or foods, and the ingestion of contaminated foods leads to illnesses. Source: Lina Bendjaballah 

Virulence Factors

B. cereus can form biofilms on abiotic surfaces or even living tissues. Biofilms are communities made up of bacteria and extracellular matrix, conferring B. cereus its adhesiveness and resistance to extreme temperature and pH. This bacterium secretes enormous number of metabolites, enzymes, toxins and generates resistant spores within biofilms. Ingestion of foods containing B. cereus in biofilms can lead to unproductive inflammation, a long-term inflammation that results in tissue death and connective tissue scarring. The biofilm helpB. cereus attach to the intestine tissuesallowing it to persistently trigger immune responses through the release of bacteria or toxins and enzymes it produces.  

B. cereus colonizes, grows and releases toxins in the human small intestine, which can cause food infections. Hemolysin BL (Hbl), non-hemolytic enterotoxin (Nhe), and cytotoxin K (CytK) are the three enterotoxins that B. cereus produces and are responsible for the diarrhoeal syndrome. These enterotoxins kill host cells by forming pores in their cell membranes (Figure 3). Hbl can also weaken immune responses by destroying the immune cells, such as macrophages and dendritic cells, which accelerates the spread of B. cereus and tissue damage. Widespread destruction of epithelial tissue in the intestine leads to ineffective absorption of water and, therefore, diarrhea.  

Figure 3: Illustration showing possible mechanism of Hbl toxin according to description of Shoeni and Wong (2005)As one of the three pore-forming enterotoxins, Hbl could perforate cell membrane through oligomerization (binding of smaller components into a unit) of its 3 components. This leads to massive ions and water loss of the targeted cell, severely disturbing the cell’s normal functions and eventually leading to cell lysis. Source: Xin Yue Liu 

On the other hand, the food poisoning or intoxication is attributed to the toxin called cereulide in the contaminated foods. This toxin is released in the food before it’s ingested. This preformed toxin is resistant to extreme pH, heat, and breakdown of proteins. Thus, cereulide in foods may persist after reheating and stomach acid. This emetic toxin causes mitochondria, the powerhouses of cells, to swell by interfering with the important energy production process called oxidative phosphorylation. This interference will halt energy production in the form of ATP, an organic chemical that provides the energy required in many biological functions such as muscle contraction, protein synthesis, regulation of normal cell functions, etc. In this case, the muscle cells of the gastrointestinal tract with dysfunctional mitochondria cannot survive due to energy deficiency, leading to cell death and inevitably causes damages in the muscle tissue. The progressive degeneration of the muscles leads to gastrointestinal dysmotility and symptoms like vomiting and nausea.

Other various enzymes also contribute to the virulence of B. cereus. Beta-lactamase provides the bacterium resistance to beta-lactam antibiotics such as penicillin and its derivatives. B. cereus also produces collagenase to degrade extracellular matrix (secreted proteins and polysaccharides providing structural and biochemical support to surrounding cells), thus facilitating its invasion of tissues. Protease is another weapon that B. cereus uses to infect host cells by hydrolyzing important proteins such as hemoglobin (carries oxygen in red blood cells) or albumin (regulates the osmotic pressure of the blood).  

Epidemiology

The percentage of foodborne diseases due to B. cereus differs from country to country. During the 1990s, B. cereus was responsible for 47% of the total food poisoning cases in Iceland, 22% in Finland, and 8.5% in The Netherlands. This bacterium is also the primary cause of foodborne diseases in Norway. Other countries reported much lower numbers, such as England and Wales (0.7%), Japan (0.8%), USA (1.3%) and Canada (2.2%). Since most patients with food poisoning recover quickly and few seek medical advice, the number of B. cereus cases might be heavily underestimated. The dominant type of food poisoning caused by B. cereus also varies in different countries. The diarrheal syndrome is more prevalent in many European countries such as Hungary, Finland, Bulgaria, and Norway, whereas more cases of the emetic type have been reported in Japan. 

Foods contaminated by B. cereus or the toxins it produces are the major causes of foodborne illnessesAlthough B. cereus is an uncommon causative agent in the United States, an outbreak of B. cereus gastroenteritis occurred among 140 guests who attended a wedding reception in Napa County due to having contaminated Cornish game hens. Therefore, good hygiene and food handling practices are important in controlling B. cereus intoxication and food infection. 

Treatment and Prevention

Usually no treatment is needed in both the diarrheal and emetic cases since the symptoms are mild and can be resolved on its own. The patients can recover within two days. However, in some severe cases, administration of fluids is required to avoid excessive water loss. Since B. cereus is widely present in the environment, prevention methods thus focus on preventing the germination of spores and minimizing the production of toxins. Foods should be maintained above 60°C or below 4°C, and reheating premade food should ensure that the internal temperature reaches 74°C 

References

Granum PE and Lund T. (1997). Bacillus cereus and its food poisoning toxins. FEMS Microbiology Letters. 157(2): 223–228. 

Griffiths MW and El-Arabi TF. (2013). Bacillus cereus. Foodborne infections and intoxications (fourth edition). 401-407. 

Griffiths MW and Schraft H. (2017). Bacillus cereus Food Poisoning. Foodborne Diseases (third edition). 395-405. 

Kotiranta A, Lounatmaa K, Haapasalob M. (2000). Epidemiology and pathogenesis of Bacillus cereus infections. Microbes and Infections. 2(2): 189-198. 

Majed R, Faille C, Kallassy M, Gohar M. (2016). Bacillus cereus Biofilms-Same, Only Different. Frontiers in Microbiology. 7:1056. 

National Institute of Neurological Disorders and Stroke. (2019). Mitochondrial Myopathy Fact Sheet. NIH Publication No. 15-6449. 

Shoeni JL and Wong ACL. (2005). Bacillus cereus Food Poisoning and its Toxins. Journal of Food Protection. 68(3): 636-648. 

Senesi S and Ghelardi E. (2010). Production, Secretion and Biological Activity of Bacillus cereus Enterotoxins. Toxin. 2(7): 1690–1703. 

Slaten DD, Oropeza RI, Werner S. (1992). An Outbreak of Bacillus cereus Food Poisoning: Are Caterers Supervised Sufficiently. Public Health Reports. 107(4): 477-480. 

Tewari A and Abdullah S. (2015). Bacillus cereus food poisoning: international and Indian perspective. Journal of Food Science and Technology. 52(5): 2500–2511. 

 

Bartonella quintana – Europe (WWI) 1914-1918

By Beatrice Cooney, Jasmine Coulombe & Leah Hiscott

Introduction

Bartonella quintana infection, colloquially known as trench fever, is a vector-borne disease that is primarily transmitted by the human body louse. It was first described during World War I when it infected over 1 million soldiers in Europe. Upon its emergence, military medical officials were baffled by the symptoms arising in the soldiers – the characteristics of the condition were unlike anything they had seen before. Patients were suffering from severe headaches and dizziness; muscle pain and stiffness in the legs (particularly the shins); as well as relapsing fever. Doctors debated whether this was the emergence of a new disease or if it was an older one making a comeback, until it was officially recognized as a novel condition in the summer of 1916.

Trench fever is rarely fatal but it is extremely debilitating, which posed a significant efficiency problem for the armies affected by it. Infection is associated with a variety of clinical conditions such as chronic bacteremia, the presence of bacteria in the bloodstream; endocarditis, an infection of the lining of the heart; lymphadenopathy, a disease of the lymph nodes; and bacillary angiomatosis, which causes lesions on the surfaces of many different organs. Trench fever is thus a gateway to much more serious health concerns.

B. quintana has not since caused an epidemic to the scale of WWI, but it is not eradicated either. Since the 1990’s, B. quintana has reemerged as “urban trench fever” among impoverished and homeless populations that are subjected to unsanitary and crowded conditions that lend itself to the parasites that could transmit the infection. 

B. quintana is a facultative, intracellular, Gram-negative rod with the human body louse, Pediculus humanus corporis, typically acting as its vector. The lice primarily infest clothing and the unhygienic and crowded conditions of the trenches during the war aided in its proliferation. B. quintana multiples in the intestines of the louse and is passed on to humans via the spreading of its feces on damaged skin. The lice also bite their victims, injecting an anesthetic that prompts an allergic reaction that leads to scratching, which only further facilitates B. quintana’s transmission.

Fig.1: Dorsal view of a female body louse, Pediculus humanus var. corporis. Some of the external morphologic features displayed by members of the genus Pediculus include an elongated abdominal region without any processes, and three pairs of legs, which are all equal in length and width. Source: CDC Public Health Image Library.

Fig 2: Example of lesions caused by scratching, allowing a route of transmission for the bacteria to humans through the louse feces in the abrasions. Source: Foucault, C., Brouqui, P., & Raoult, D. (2006). Bartonella quintana Characteristics and Clinical Management. Emerging Infectious Diseases, 12(2), 217-223. https://dx.doi.org/10.3201/eid1202.050874.

Source & cause of the outbreak

With its first appearance during WWI, trench fever was thought to be some type of infection and was typically compared to malaria due to the omnipresence of fever, a cardinal sign of infection. Thanks to careful observation of cases coming into the infirmary, it was correctly postulated that the condition might be carried by a parasite found in the trenches. Physicians named voles or mice as the vector, shedding light on the horrendous conditions in the trenches until body louse was dubbed the culprit of the disease. This was supported by the fact that the disease was especially prevalent in the winter, when flies and mosquitos were absent from the trenches. By the end of 1916, most had agreed that louse transmitted B. quintana, as this was the most common parasite found in the trenches. However, the definitive experimental proof was still lacking. By 1917, two years after its first appearance, both the British and the Americans set up committees dedicated to tracking down the transmissive agent of the disease. The Americans concluded that it was the bite of the louse that transmitted the disease, making it the vector. However, it was the British that demonstrated that it was the transmission of louse excreta into the damaged skin that conveyed the causative agent. It is now known that mature louse can live for up to 30 days.

The infection itself is sudden, persistent and unpleasant. At the time of infection, it is common to experience a fever lasting between 2 to 6 days, accompanied by headaches, back and leg pain, and a fleeting rash. Recovery can take up to two months and relapse, even 15 years later, is common; about five percent of cases become chronic. The bacteria carried by the lice infect the blood, bone marrow, and skin of its patients and can be detected even after treatment and recovery. Today, the disease is treated with antibiotics, typically chlortetracycline, but others options are available as well. 

Ending the outbreak

Despite the slow response to the outbreak containment, treatment ended up being extremely successful. Even before the real causative agent was discovered, trench fever was recognized as a serious issue likely arising from the abhorrent conditions endured by soldiers. After identification, the “Department of Government Circular Memorandum No. 16” was outlined as a reference for better health. Although many of the suggestions were unrealistic for those on the front lines, serious effort was made nonetheless. Regular showers every other week were demanded, and mobile delousing stations moved around base camps in an effort to eradicate the source. The most effective effort, however, came at the end of the war. For fear that the disease might spread to Britain’s general population, strict sanitation regimes were implemented for all soldiers returning home. Thankfully, this was successful and the British population was able to avoid the disease many of their soldiers were due to suffer from for the rest of their days.

Aftermath

Research continued into the root cause of trench fever, despite the fact it was not prevalent in the general population after the outbreak during the war, it did reappear as a small epidemic in the German troops on the Eastern front during World War II. Furthermore, it still appears today in homeless and immunocompromised populations. As B. quintana was not cultured during the outbreak in the first World War, work slowly continued to try and isolate the bacterium causing trench fever. While the disease was putatively linked to louse infestation, the bacterium itself was not isolated until 1961 by J William Vinson of Harvard University and Henry Fuller of Walter Reed Army Institute of Research. As this occurred after WWII, the defensive strategies for the second war focused on preventing louse infestation by providing better hygiene for soldiers, as well as soldiers tended to be more spread out and mobile. After the second World War, antibiotic susceptibility testing and genome sequencing occurred and therefore lead to a better understanding of the transmission of the disease and its treatment.

Conclusion

The outbreak of trench fever posed a significant hurdle for armies during WWI, leading to a loss in soldiers and an increased demand for medical care. The slow response to determine the cause of the disease, due to the lack of knowledge at the time regarding the classification of bacteria, was detrimental to the war effort. However, as the war ended, the disease was well contained and extreme preventative measures halted the spread to the general public. While trench fever is still seen today in niche populations, general understanding, prevention, and treatment of the disease has greatly increased, alleviating the threat of future outbreaks.

References

Anstead, G. M. (2016). The centenary of the discovery of trench fever, an emerging infectious disease of World War 1. The Lancet Infectious Diseases, 16(8). doi: 10.1016/s1473-3099(16)30003-2

Atenstaedt, R. L. (2007). The response to the trench diseases in World War I: A triumph of public health science. Public Health, 121(8), 634. 

Atenstaedt, R. L. (2006). Trench fever: the British medical response in the Great War. Journal of the Royal Society of Medicine, 99(11), 564-568. doi:10.1258/jrsm.99.11.564

European Centre for Disease Prevention and Control. (n.d.). Facts about Bartonella quintana      infection. Retrieved November 15, 2019, from European Centre for Disease Prevention and Control website: https://www.ecdc.europa.eu/en/bartonella-quintana-infection-trench-fever/facts

Foucault, C., Brouqui, P., & Raoult, D. (2006). Bartonella quintana Characteristics and Clinical Management. Emerging Infectious Diseases, 12(2), 217-223. https://dx.doi.org/10.3201/eid1202.050874.

Holmes, F. (2006). Trench Fever in the First World War. Retrieved from University of Kansas Medical Center website: http://www.kumc.edu/wwi/index-of-essays/trench-fever.html

Pennington, H. (2019). The impact of infectious disease in war time: a look back at WW1. Future Microbiology, 14(3), 217–223. https://doi.org/10.2217/fmb-2018-0323

Ruiz, J. (2018). Bartonella quintana, past, present, and future of the scourge of World War I. Apmis, 126(11), 831–837. doi: 10.1111/apm.12895

 

Gonorrhea outbreak in New Brunswick

By Yifan Ding and Thomas MacDougall

Introduction

In April 2019, New Brunswick chief medical officer Dr. Jennifer Russell declared a provincial gonorrhea outbreak due to the steep increase of gonorrhea cases reported in the province. From 2013 to 2017, the average number of gonorrhea cases in New Brunswick was 54 annually. However, the number of cases in 2018 rose to 96; almost two times the average of the past 5 years. In addition to the spike in 2018, another 20 cases were reported in the first quarter of 2019 compared to the  previous 5 year average of 12 reported first quarter cases. Most patients are aged between 20 to 39 and reports of the disease are evenly distributed throughout the province.

Gonorrhea

Gonorrhea is a sexually transmitted infection (STI) caused by a bacterium called Neisseria gonorrhoeae. Not everyone infected with the bacterium will show symptoms, but those who do will commonly experience pain or a burning sensation while urinating. Between the sexes, women are more prone to being asymptomatic than men. Symptoms in women may include vaginal discharge, pelvic pain, and vaginal bleeding outside of regular periods, and men may experience testicular pain and creamy discharge from the penis. Like many other STIs, gonorrhea can be acquired by having vaginal, anal, or oral sex with an infected individual. Men and women aged 20 to 39 report the most instances of the disease of any age group. If not treated, severe cases may lead to infertility, and pregnant women carrying the disease may transfer it to their child at birth.

Figure 1: Visualization of a Neisseria gonorrhoeae cell. Source: Centers of Disease Control and Prevention. Gonorrhea. Last reviewed September 28th, 2017. https://www.cdc.gov/std/gonorrhea/default.htm (accessed 12 November 2019)

Source of the outbreak

Increasing antibiotic resistance in bacteria has played a role in the outbreak. It’s possible that an individual received treatment but the bacterial strain that they carried was resistant to the antibiotics, and without follow-up testing that person may not have confirmed that they were cured. The recent circulating strains of gonorrhea have shown resistance to all of the common antibiotics in Canada, including penicillins, macrolides, quinolones and tetracyclines. This resistance to antibiotics results in ineffective treatment and more difficulty in curing the infection. Ineffective treatments result in more severe infections and increase the transmission of resistant bacteria strains. A lax opinion in sexually active individuals about taking the time to get checked for STIs once a year is likely to have been a driving factor in the spread of the disease throughout the province, as early diagnosis and treatment of the disease is vital in reducing its ability to resist antibiotics.

Figure 2: History of antibiotic use in order to treat Gonorrhea. Source: Centers for Disease Control and Protection. Latest data on Antibiotic Resistant Gonorrhea. 2016.  https://www.cdc.gov/nchhstp/newsroom/2016/data-on-antibiotic-resistant-gonorrhea.html

Cause of the outbreak

The uptick in transmission from the popularity of dating apps will be the cause of the outbreak. In 2017, Cabecinha et al. conducted a research on the relationship between dating apps and STIs, their research showed that using dating apps to find sexual partners was strongly associated with sexual risk, increasing the probability of getting infected. Social media and dating apps are widely used among young adults in New Brunswick and the rest of Canada. These dating apps enable their users to communicate quickly to arrange anonymous sexual encounters. In most cases, individuals are not familiar with their sexual partners and do not know if their sexual partners are healthy or not because many people with gonorrhea may not show any symptoms. With accessible forms of contraception such as birth control or IUDs (intrauterine devices), many sexual encounters happen without protection, enabling the transmission of the disease by individuals not showing symptoms. Partners not knowing and disclosing their sexual health allows the bacteria to spread freely.

Measures taken to end the outbreak

The Office of Public Health has put out advertisements on dating apps and social media  in an attempt to spread awareness about the outbreak and to encourage the use of protection during sex. Practicing safe sex is the most useful way to prevent spreading of sexually transmitted infection like gonorrhea. The easiest and most effective method is to use condoms. Knowing about the health condition of the sexual partners is also important to not get infected by gonorrhea. It is recommended that people should have their regular sexual partners instead of anonymous sexual partners, ensuring that both are safe. People should also talk to their partners about their sexually transmitted infection status and the use of protection.

As not everyone who is infected with gonorrhea shows symptoms, the Chief Medical Officer recommends sexually active individuals to go to see a doctor or a public health office to get tested at least once per year.  A simple urine sample or swab test is helpful in diagnosing the disease. It is important for those concerned they might be infected to consult a doctor for treatment and adhere to any follow-up recommendations, as improper use of antibiotics can accelerate the spread of antibiotic resistance.

Aftermath

As of November 15 2019, the outbreak has yet to have been officially declared over. The persistable nature of gonorrhea makes it very difficult and unlikely for it to be completely eliminated from the province. As there is yet no publicly available vaccine for gonorrhea, the Office of Public Health may only continue to educate and offer treatment to the public in hopes of stemming the spread of the infection and reducing infection rates back to historical averages. 

References:

New Brunswick Office of Public Health. April 26 2019. Gonorrhea on the rise in New Brunswick. https://www2.gnb.ca/content/gnb/en/departments/health/news/news_release.2019.04.0252.html (Accessed 11 November 2019)

Ashleigh R Tuite, Thomas L Gift, Harrell W Chesson, Katherine Hsu, Joshua A Salomon, Yonatan H Grad, Impact of Rapid Susceptibility Testing and Antibiotic Selection Strategy on the Emergence and Spread of Antibiotic Resistance in Gonorrhea, The Journal of Infectious Diseases, Volume 216, Issue 9, 1 November 2017, Pages 1141–1149, https://doi.org/10.1093/infdis/jix450

Choudhri Y, Miller J, Sandhu J, Leon A, Aho J. Gonorrhea in Canada, 2010-2015. Canada Communicable Disease Report, Volume 44, Issue 2, 1 February 2018, Pages 37-42, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5933854/

Mackenzie K, Morgan MD, Catherine F, Decker MD. Gonorrhea. Disease-a-Month, Volume 62, Issue 8, August 2016, Pages 260-268. https://doi.org/10.1016/j.disamonth.2016.03.009

Cabecinha M, Mercer CH, Gravningen K, Aicken C, Johns KG, Tanton C, Wellings K, Sonnenberg P, Field N. Finding sexual partner online: prevalence and associations with sexual behaviour, STI diagnoses and other sexual health outcomes in the British population. 2017. Sexual transmitted infection, Volume 93, Issue 8, 10 April 2017, Pages 572-582. doi: 10.1136/sextrans-2016-052994

 

Legionella pneumophila – Flint, Michigan 2014

by Nicolas Puertas, Misghana Kassa, and Sarah Krnjevic

Introduction

Between 2014 to 2015, Genesee County in Flint, Michigan was subject to an outbreak of Legionnaires’ disease. The county changed its source and treatment of drinking water, and following this switch discovered that the water was contaminated with heavy metals when residents complained about discoloration of tap water and shared symptoms like rashes. Over the course of June 2014 to March 2015, Genesee County reported 88 cases of Legionnaires’ disease and 12 recorded deaths associated with the outbreak. In January 2016, the health departments of the state of Michigan and Genesee County officially announced that 2 clusters of Legionnaires’ disease had occurred in Genesee County between 2014-2015.

Figure 1: Legionella Pneumophila. Source: CDC. This illustration depicts a three-dimensional (3D) computer-generated image of a group of Gram-negative, Legionella pneumophila, bacteria. The artistic recreation was based upon scanning electron microscopic (SEM) imagery [Image]. (2016). Retrieved from https://phil.cdc.gov/Details.aspx?pid=22879

Description of the Disease

Legionnaires’ disease is caused by Legionella pneumophila infection when the immune system is unable to clear the bacteria fast enough. The disease causes pneumonia which induces severe lung damage to the host. The symptoms include: coughing, shortness of breath, fever, muscle aches, headaches, and can also be associated with diarrhea, nausea, and confusion.

L. pneumophila (displayed in Figure 1) is a Gram-negative bacteria that can survive both in the environment and inside of a host. It is a robust bacteria that can live in multiple types of harsh environment for a long period of time. It can withstand temperatures going from 0-68°C and pH from 5-8.5. Legionella species are usually found in biofilms inside of natural and manmade water systems. Biofilms are an aggregation of bacteria with layers of polysaccharides, proteins, and DNA which protect the organism from potentially harmful factors in the environment such as biocides and chlorine.

Source of the Outbreak 

Laboratory tests have demonstrated that L. pneumophila is sensitive to chlorine, which is the case for many bacteria. This chemical oxidizes the bacteria’s cell wall, effectively killing it. For this reason, it is common practice to add chlorine to water in water distribution systems.

The source of the L. pneumophila outbreak was linked to Flint’s new water source, the Flint River, which was contaminated with heavy metals. The water was found to be highly contaminated with lead and iron, which interfered with the water’s disinfection process. When it passed through the water distribution system these metals would react with the chlorine added for disinfection. By occupying the chlorine molecules these metals prevented them from acting as a disinfectant, and more specifically prevented them from killing off any L. pneumophila present in biofilms inside the water system. Additionally, the chlorine induced corrosion when reacting with the metal of the pipes, providing an ideal environment for L. pneumophila growth. These uninhibited biofilms as demonstrated in Figure 2 were the source of the outbreak in 2014.

Figure 2: Pipe cross section with biofilm formation of Legionella. Source: CDC. (2018). What Owners and Managers of Buildings and Healthcare Facilities Need to Know about the Growth and Spread of Legionella  [Image]. Retrieved from https://www.cdc.gov/legionella/wmp/overview/growth-and-spread.html.

Cause of the Outbreak

The outbreak was caused by the change in water source in 2014 from Lake Huron to Flint River. Prior to this change, the number of cases of Legionnaires’ disease was relatively low at 6-12 cases per year in the Flint area. Following the switch, however, the incidence spiked up to 45 cases per year. Residents began complaining about an acrid smell, discoloration of tap water and shared symptoms like rashes. The aspiration of this water highly contaminated with Legionella provided an entry for the bacteria into the lungs of residents of Flint. This would occur if the water was accidentally inhaled from choking or through small droplets sprayed from outdoor fountains or sprinklers. In individuals without a strong immune system, infection and lethal pneumonia would follow, also known as Legionnaires’ disease.

Measures Taken to End the Outbreak

In October 2015, in order to end the outbreak, the county switched back to its original water supply Lake Huron. The incidence of Legionnaires’ disease then decreased to 16 cases in 2016 and 4 cases in 2017. The outbreak ended, although the bacteria has not completely gone from the water system. There are still detectable levels of Legionella in Flint River’s water today (although below the threshold for concern), found in 25 percent of all nationally collected samples in 2018.

Aftermath

This event was recorded as the 3rd largest Legionnaires’ disease outbreak in American history and as a consequence received nation-wide press. Two high ranking Michigan officials belonging to the Department of Health and Human services faced criminal charges for involuntary manslaughter relating to the outbreak of Legionnaires’ disease. The charges stemmed from the delay in alerting the residents of the county about the outbreak. A lapse of communication between stakeholders like public health agencies, water utilities and the general population prevented a swift reaction to the outbreak. Improving communication channels has been identified as a factor in mitigating the spread of future disease. Furthermore, the outbreak highlights problems with aging infrastructure and a lack of corrosive control shared among municipalities across America. After all, it was the lack of corrosion control that triggered the deterioration of the metallic infrastructure which led to the leaching of heavy metals into the water source.  The management of distribution systems and infrastructure upgrades are ultimately central in preventative measures and would benefit from increased funding for public services.

References

Byrne, B.G., McColm, S., McElmurry, S.P., Kilgore, P.E., Sobeck, J., Sadler, R., Love, N.G., Swanson, M.S. 2018. Prevalence of Infection-Competent Serogroup 6 Legionella pneumophila within Premise Plumbing in Southeast Michigan. mBio. 9 (1): e00016-18. doi: 10.1128/mBio.00016-18 

Centers for Disease Control and Prevention (CDC). 2018. Legionella (Legionnaires’ Disease and Pontiac Fever). Retrieved from: https://www.cdc.gov/legionella/about/signs-symptoms.html#legionnaires

Diederen, B. M. W. 2008. Legionella spp. and Legionnaires’ disease. Journal of Infection. 56: 1–12. doi: https://doi.org/10.1016/j.jinf.2007.09.010

Fraser, D. W., et al. 1977. Legionnaires’ disease: description of an epidemic of pneumonia. The New England Journal of Medicine. 297: 1189–1197. doi:10.1056/NEJM197712012972201

Hersher, R. 2018. Lethal Pneumonia Outbreak Caused By Low Chlorine In Flint Water. Retrieved from https://www.npr.org/sections/health-shots/2018/02/05/582482024/lethal-pneumonia-outbreak-caused-by-low-chlorine-in-flint-water.

Marrie, T. J., Garay, J. R. & Weir, E. 2010. Legionellosis: Why should I test and report? Canadian Medical Association Journal. 182(14): 1538–1542. doi:10.1503/cmaj.082030

Peplow, M. 2018. The Flint water crisis: how citizen scientists exposed poisonous politics. Nature. 559(7713): 180-180. doi: 10.1038/d41586-018-05651-7

Rhoads, W.J., Garner, E., Ji, P., Zhu, N., Park, J., Schwake, D.O., Pruden, A., Edwards, M.A. 2017. Distribution System Operational Deficiencies Coincide with Reported Legionnaires’ Disease Clusters in Flint, Michigan. Environmental Science & Technology. 51 (20): 11986-11995. doi: 10.1021/acs.est.7b01589

Zahran, S., McElmurry, S.P., Kilgore, P.E., Mushinski, D., Press, J., Love, N.G., Sadler, R.C., Swanson, M.S. 2018. Assessment of the Legionnaires’ disease outbreak in Flint, Michigan. PNAS. 115 (8): E1730-E1739. doi: https://doi.org/10.1073/pnas.1718679115

 

Bartonella quintana

by Fahima Ahmed, Christina Ghaly, Kathia Farah, and Bailey Jarrett

INTRODUCTION

Bartonella quintana is a pathogenic microorganism that is the causative agent of Trench Fever. Found in clothes and associated with poor hygiene, poverty and cold weather, this bacterium multiplies in the intestine of a louse (a small wingless parasitic insect) and is excreted in its feces. It is then transmitted by blood-suckling lice on the human body (Pediculus humanus). The pathogen is able to grow in red blood cells, and may result in chronic bacteremia if the individual is immunocompetent.

DISEASE

The vector-borne disease is characterized by fever, headaches, shin pain and dizziness, caused by destruction of the red blood cells. Transmission to humans occurs through contact of the excrement with breaks in the skin. The lice inject proteins that induce scratching, making fecal transmission easier. B. quintana adheres to the epithelium and endothelium, which is a tissue made of a single layer of cells that line the heart, blood and lymph vessels, and invades erythrocytes. Clinical manifestations of this disease range from asymptomatic infection to severe illness. The lipopolysaccharide (a large molecule consisting of a lipid and sugar on the surface of Gram-negative bacteria) of this pathogen was shown to down-regulate the action of immune cells and pro-inflammatory cytokines, resulting in the absence of symptoms usually manifested during bacteremia (the presence of bacteria in the blood). However, when the bacterium remains in the blood persistently, years after the initial infection, it results in chronic bacteremia, as well as disruption and inflammation of vascular tissues.

EPIDEMIOLOGY 

Bartonella quintana was first identified as a human pathogen during World War I, when it caused an epidemic of Trench Fever among one million soldiers in Europe. B. quintana is now found worldwide and causes febrile outbreaks (symptoms of a fever), although infected people regularly recover. It is most commonly recognized as a disease among the homeless population in the United States and Europe. This is because poor sanitation, personal hygiene and alcoholism increase its transmission rate. In France, 30% of 71 tested homeless people had a high concentration of antibodies against B. quintana, with 14% that were bacteremic. In Seattle, 20% of low income patients had antibody titers for B. quintana of 1:64 or greater, meaning there is evidence of recent or current infection. A severe form of B. quintana has also been reported in immunocompromised patients, such as those with AIDS. 

VIRULENCE 

Bartonella quintana infects red blood cells in a stepwise fashion as shown below.

Figure 1. Erythrocytic Infection of Bartonella. B. quintana adheres to erythrocytes (1) and invades them (2). The pathogen grows and stays in a vacuolar-compartment inside red blood cells (3). Adapted from: Deng H., Pang Q., Zhao B., Vayssier-Taussat M. (2018) Molecular mechanisms of Bartonella and mammalian erythrocyte interactions: a review. In Frontier Cellular Infection Microbiology, 8, 431-442. doi: 10.3389/fcimb.2018.00431.

B. quintana uses multiple virulence factors to infect red blood cells. The type-IV secretion system (T4SS) is the most important one. T4SS are made up of proteins that form a channel across the membranes of bacteria. Through this channel, bacteria can transfer toxins, DNA plasmids or proteins directly into the cytoplasm of recipient cells. The system mediates intimate contact with host cells. The T4SS of B. quintana, called Trw, is necessary for erythrocyte infection, although its function as a secretion system is not clear. However, the role of the Trw in adhesion of RBCs is well-known. Trw has multiple copies of two surface-exposed subunits, TrwL and TrwJ (seen in Figure 2 (b)). These components help to recognize and bind specifically to erythrocyte receptors on the cellular membrane. The virulence factor is therefore responsible for the specificity of host cells it infects. The Trw initiates attachment to RBCs while other virulence factors are used for further adherence and invasion. For example, variable outer-membrane proteins (VOMPs) bind to the components of the extracellular matrix of the host, such as fibronectin and collagen, and allow entry of the pathogen into RBCs. 

Figure 2. Adherence of Bartonella quintana to a red blood cell using a T4SS Trw (a). A hypothetical structure of T4SS Trw. EX: Extracellular matrix; OM: Outer membrane; PP: Periplasm; IM: Inner membrane; CY: Cytoplasm. The letters represent Trw subunits, including TrwJ and TrwL (b). Source: Deng H., Pang Q., Zhao B., Vayssier-Taussat M. (2018) Molecular mechanisms of Bartonella and mammalian erythrocyte interactions: a review. In Frontier Cellular Infection Microbiology, 8, 431-442. doi: 10.3389/fcimb.2018.00431.

Once in the cytoplasm, the bacteria proliferates inside a vacuole that supports its growth. The pathogen also acquires nutrients from the host by using hemin-binding protein (that bind to hemin found in hemoglobin of human blood) and other proteins involved in amino acid nutrient uptake. B. quintana stays inside for the lifetime of erythrocytes, increasing the likelihood of transmission by blood-sucking vectors.

TREATMENT

The choice of antibiotic therapy for B. quintana infection is problematic. A lot of antibiotics cannot reach intracellular bacteria since they cannot cross the host cell membrane, making them unable to treat the infection effectively.

Randomized trials on affected patients have shown an eradication following a doxycycline and gentamicin treatment, when given together. Doxycycline is capable of intracellular penetration and will stop the growth of the bacteria.

A benefit from aminoglycoside therapy was also suggested following treatment for patients with endocarditis. Patients who received a regimen that included at least 14 days of an aminoglycoside had a greater likelihood of achieving full recovery and surviving the infection, as opposed to those treated only with doxycycline.

REFERENCES

Angelakis, E., Raoult, D. (2014) Bartonellosis, Cat-scratch Disease, Trench Fever, Human Ehrlichiosis. In Manson’s Tropical Infectious Diseases, 23, 385-394.

Brouqui, P., Doudier, B. (2013) Trench Fever. In Hunter’s Tropical Medicine and Emerging Infectious Disease, 9, 561-563.

Brouqui, P., Dolan, M. J., Koehler, J. E., Maguina, C., Raoult, D., Rolain, J. M. (2004) Recommendations for Treatment of Human Infections Caused by Bartonella Species. In Antimicrobial Agents and Chemotherapy, 48(6), 1921-33. doi: 10.1128/AAC.48.6.1921-1933.2004

Brouqui, P., Foucault, C., Raoult, D. (2006) Bartonella quintana Characteristics and Clinical Management. In Emerging Infectious Disease, 12(2), 217-223.

Cohn, J., Mazo, D., Mosepele, M. (2012) Bartonella Infection in Immunocompromised Hosts: Immunology of Vascular Infection and Vasoproliferation. In Clinical and Developmental Immunology 2012, 612809.

Deng H., Pang Q., Zhao B., Vayssier-Taussat M. (2018) Molecular mechanisms of Bartonella and mammalian erythrocyte interactions: a review. In Frontier Cellular Infection Microbiology, 8, 431-442. doi: 10.3389/fcimb.2018.00431.

Harms A., Dehio C. (2012) Intruders below the radar: molecular pathogenesis of Bartonella spp. In Clinical Microbiology Reviews, 25(1) 42-78. doi: 10.1128/CMR.05009-11

Jackson, L. A., Spaeh, D. H., Kippen, D. A., Sugg, N. K., Regnery, R. L., Sayers, M. H., & Stamm, W. E. (1996). Seroprevalence to Bartonella quintana among Patients at a Community Clinic in Downtown Seattle. Journal of Infectious Diseases, 173(4), 1023–1026. doi: 10.1093/infdis/173.4.1023

Malgorzata-Miller, G. et al. (2016) Bartonella quintana lipopolysaccharide (LPS): structure and characteristics of a potent TLR4 antagonist for in-vitro and in-vivo applications. In Sci. Rep. 6, 34221. doi: 10.1038/srep34221

Maurin, M., Raoult, D. (1996) Bartonella (Rochalimaea) quintana infections. In Clinical Microbiology Reviews, 9(3), 273-92.

Maurin, M., & Raoult, D. (2001) Use of aminoglycosides in treatment of infections due to intracellular bacteria. In Antimicrobial agents and chemotherapy, 45(11), 2977–86. doi:10.1128/AAC.45.11.2977-2986.2001

Spach, D. (2019) Clinical features, diagnosis, and treatment of Bartonella quintana Infections. Retrieved from UpToDate.com/  https://www.uptodate.com/contents/clinical-features-diagnosis-and-treatment -of-bartonella-quintana-infections#references

Salmonella enteritidis – Canada 2019

by Gigi de Fort-Menares Lee, Gabriel Pineda, and Victoria Tseng Paepcke

Introduction:

On May 25, 2019, the Public Health Agency of Canada declared a national Salmonella outbreak linked to Compliments Chicken Strips. Currently, there have been 11 reported cases across 7 different provinces between September 2018 and April 2019. One individual has been hospitalized and no deaths have been reported due to this outbreak.  As well, the suspected source has been identified. Unfortunately, there have been a multitude of outbreak investigations associated with frozen raw breaded chicken products and Salmonella since May 2017. 

Description of the Disease:

Salmonella is a genus of Gram-negative, rod-shaped, facultative anaerobic bacterium (See Figure 1). The outbreaks caused by frozen raw breaded chicken are linked to Salmonella enteritidis (S. enteritidis), the most common serotype in Canada. S. enteritidis is an intracellular pathogen which causes the disease salmonellosis. Due to its prevalence, it is one of the most important zoonotic diseases and frequently is transmitted to humans through the consumption of raw animal products such as poultry meat and eggs. Interestingly, these bacteria prefer the intestinal tract of animals as their environment but can persist for a long period of time in other environments by forming biofilms. To clarify, biofilms are generally a mass of bacteria that are held within a gel-like structure. After ingestion, the stomach’s acidity degrades the meat and the pathogen multiplies in the small intestine before establishing infection. 

Figure 1: Salmonella spp. are Gram-negative, rod-shaped, facultative anerobic bacteria.  Public Health Image Library, Center for Disease Control, James Archer (2019).

Symptoms of salmonellosis depend largely on the species and/or serovar of bacterium. For S. enteritidis, symptoms include diarrhea, vomiting, abdominal pain, fever, chills and headache. The onset of symptoms appears 6 to 72 hours after ingestion of the bacteria and illness typically lasts 2 to 7 days. Most cases of salmonellosis are relatively mild and patients will make a full recovery without treatment. However, children and elderly patients are more susceptible to the associated dehydration which can lead to a more serious or even life-threatening illness. Antibiotics are only administered to infants, the elderly, immunocompromised people or if the infection has spread to other parts of the body. Furthermore, antibacterial therapy is not recommended in moderate cases because increased use of antibiotics accelerates the evolution of bacterial strains by allowing these strains to pick up new factors which consequently could lead to drug resistance. Unfortunately, several resistant serotypes of Salmonella have arisen and antibacterial resistance is thus a growing concern. 

Source of the Outbreak:

Several outbreaks of S. enteritidis have occurred in Canada over the years. As mentioned, the most recent outbreak of the bacteria was reported on May 25, 2019.  The outbreak originated from chicken strips sold under the brand “Compliments” from Sofina Foods Inc. The Public Health Agency of Canada reported 11 cases of infection nationwide: 2 in British Columbia, 1 in Alberta, 2 in Ontario, 3 in Quebec, 1 in New Brunswick, 1 in Nova Scotia and 1 in Prince Edward Island. Furthermore, other cases of salmonellosis have arisen in Canada. For instance, in March 2019, 34 cases related to frozen raw breaded chicken were reported with the majority of cases occurring in Ontario (22). The Canadian Food Inspection Agency (CFIA) investigated the sources of outbreaks of S. enteritidis and posted a list of products that had tested positive for the bacteria from outbreaks dating back to 2017. 

*  Table has been modified from the original table compiled by the CFIA. Source: List of recalls of frozen raw breaded chicken products due to Salmonella: from July 2017 to present. 2019. Ottawa (ON): Government of Canada; [accessed 2019 Nov 10]. http://inspection.gc.ca/about-the-cfia/accountability/food-safety-investigations/raw-breaded-chicken-products/eng/1536716947924/1536717030715

Cause of the Outbreak: 

According to the Public Health Agency of Canada, outbreaks of S. enteritidis can be caused by contact with infected animals and surfaces and ingestion of contaminated food (See Figure 2). Interestingly, S. enteritidis infection is especially a problem among poultry, as the bacteria colonize the reproductive tract of hens. Thus, the interior of eggs become colonized prior to shell formation. Furthermore, chickens occasionally ingest either their own or other chickens’ feces that may contain the pathogen promoting transmission. Accordingly, ingestion of contaminated food is the cause of the outbreak under discussion as the frozen raw breaded chicken contained the pathogen. In 2009, Dominguez and Schaffner demonstrated that S. enteritidis is able to survive under freezing conditions (- 20 °C) for almost 16 weeks explaining why frozen food is a source of outbreak. Moreover, infected individuals do not cook the meat properly, allowing the bacteria to survive.  Other causes of contamination include unsanitary distribution management and antibiotic resistance. Antibiotic resistance is partially responsible for S. enteritidis outbreaks as with increased resistance, there are more cases of salmonellosis which consequently increases the risk of an outbreak to occur. Interestingly, in 2018, Nair et al. explained that after the approval and increased usage of fluoroquinolones, serotypes acquired resistance to the antibiotic. In support of this claim, they showed a positive correlation between cases of Salmonella Heidelberg infection in Canada and antibiotic resistance. Overall, several factors contributed to the initiation of the S. enteritidis outbreak.

Figure 2: Possible routes of S. enteritidis transmission to humans. Source: Victoria Tseng Paepcke (2019).

Measures Taken to End Outbreak:

In order to end the outbreak, Compliments Chicken Strips with a best before date of November 24, 2019 were recalled on May 24, 2019.  Although no longer available in stores, this product may be found in freezers of homes or restaurants.  Consequently, the Government of Canada (GC) advises the public not to consume nor sell the recalled product and to seal the product in a plastic bag and either dispose of it or return it to where it was purchased. 

Canadian chicken farms and processing plants must routinely disinfect their facilities in order to prevent S. enteritidis outbreaks from raw breaded chicken, as the facilities may experience contamination from either the live or frozen chickens. Farmers must also routinely check for S. enteritidis within their flock and ensure that birds are handled using sanitary procedures. Actions to eliminate the bacteria at the production level aid in reducing cases among consumers.

If consumers are infected with S. enteritidis, treatment by fluids, electrolytes, anti-diarrheals and antibiotics may be recommended.  Fluids and electrolytes are used to replenish body fluids as infection can cause dehydration.  Anti-diarrheals may be used to relieve symptoms such as cramping and diarrhea.  As previously mentioned, if a person has either a severe case of intestinal infection, bloodstream infection or a compromised immune system, he or she may be prescribed antibiotics.

Aftermath:

S. enteritidis in breaded chicken has a better chance of infecting people because of the golden coating of the nuggets or strips that appears cooked.  Thus, the GC has enforced safe cooking practices in order to reduce potential infections.  For example, the GC suggests that all frozen raw breaded chicken products should be cooked to an internal temperature of 74°C and microwave cooking is not recommended due to uneven heating.  Thus, actions to reduce S. enteritidis cases can be performed by a range of parties, from individual citizens to the GC.

Due to numerous outbreaks like the one discussed, stricter standards have been implemented. Starting April 1, 2019, the CFIA stated that all breaded chicken manufacturers need to reduce S. enteritidis levels to below detectable amounts.  In other words, most chicken products will be pre-cooked. Also, “uncooked products” must be stated clearly on the packaging and cooking instructions must be present on both the box and internal bag. Overall, regulations have been changed with the hope of preventing future S. enteritidis outbreaks.

Sources:

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