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Gonorrhea outbreak in New Brunswick

By Yifan Ding and Thomas MacDougall


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 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. (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.

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.


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. 


New Brunswick Office of Public Health. April 26 2019. Gonorrhea on the rise in New Brunswick. (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,

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,

Mackenzie K, Morgan MD, Catherine F, Decker MD. Gonorrhea. Disease-a-Month, Volume 62, Issue 8, August 2016, Pages 260-268.

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


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

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

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.


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.


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:

Diederen, B. M. W. 2008. Legionella spp. and Legionnaires’ disease. Journal of Infection. 56: 1–12. doi:

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

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:


Bartonella quintana

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


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.


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.


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. 


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.


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.


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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 -of-bartonella-quintana-infections#references

Salmonella enteritidis – Canada 2019

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


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].

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.


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.


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The Ticking Bomb: the effects of climate change on Lyme disease

By: Bérénice Saget, Jess and Emilia

This article is to go further after the bacterial pathogen Borrelia burgdorferi post, go check it out!

Climate change is a recurring theme in today’s media. We hear and read about how our planet is warming, how the climate is becoming more unpredictable, and how this is negatively impacting our lives. Amidst all of this, there is a tiny organism that is greatly benefiting. Meet Ixodes scapularis, better known as the black-legged tick, and its friend, Borrelia burgdorferi, a pathogenic bacterium it can carry. These names might be familiar to you in the context of Lyme disease, which has been on the rise in the Northern hemisphere in recent years.

Lyme Disease

Lyme disease is caused by an infection with the pathogenic bacterium, B. burgdorferi. When a tick attaches and bites through an individual’s skin, the pathogen can be transmitted with the tick’s saliva.

Signs & Symptoms

The first characteristic sign is the “bull’s eye”, also known as erythema migrans rash. This will appear at the site of the tick bite. In the early stages of the disease, a wide variety of symptoms may manifest including but not limited to: 

  • severe headaches
  • facial paralysis
  • muscle & bone aches
  • heart disorders
  • memory loss
  • nerve pain
  • arthritis

The disease is said to be in the early localized stages in the first month post-exposure as the infection stays confined in the skin at the site of the bite. In the early disseminated stage, the bacterium has migrated to the bloodstream and colonized other sites of the body. The disease is classified as at a later stage when the symptoms have persisted for several months to years. It is unclear why symptoms persist after the infection has been cleared. However, it has been proposed that lasting symptoms are caused by the antibodies created during infection that attack the body’s cells that resemble the bacterium’s antigens, leading to an autoimmune disease. Symptoms can become more severe if the infection is left untreated. In rare cases, Lyme disease can lead to death from complications if the heart becomes infected.

Interaction between B. burgdorferi and its vector

Borrelia burgdorferi is a Gram-negative bacterium that grows very slowly. Many different B. burgdorferi strains are associated with Lyme disease and their vector. 

The Borrelia genus is very vast and the different species are hard to differentiate without sequencing the genome. The bacteria within a species also have high variability meaning many different B. burgdorferi strains are associated with Lyme disease. 

This genus is quite unique in the way its metabolism functions. It has evolved to use manganese instead of iron in all of its metabolic pathways. This allows the bacteria to grow in our blood, where the iron is bound to heme and other proteins, without having to synthesize iron-acquiring complexes. The bacteria waste less energy and can focus on escaping the immune system. 

Borrelia spp. uses different techniques to hide in its host and evade the immune system. This allows it to survive longer and gives it a better chance to spread by being transported to another host by a tick. 

The environmental biology of this pathogen is complex since it has a broad spectrum of mammals, birds, and reptiles it can infect. It is vehiculated between hosts by various tick vectors. Many ticks can carry Borrelia spp., and are perfect vectors due to the long-lasting blood meals their bodies can sustain and the enzymes of their saliva preventing inflammation and blood clotting at the infection site. To evade our immune system, the bacteria will increase production of those salivary proteins in infected ticks and bind them.

Coevolution of the ticks and their bacterial guests made them tolerant to one another. The immune system of the tick does not kill the bacteria entirely, it only keeps it in check. Once inside a tick, Borrelia increases the amount of its OspA surface proteins to mediate adhesion to the tick’s gut. There, it remains attached and grows using the nutrients from the tick’s blood meal. Once the tick has digested the blood, Borrelia will change OspA for OspC, which permits its migration to the tick’s vascular system. It will then travel to the salivary glands to be secreted into the tick’s new host. 

The bacteria has adapted very well to the tick, using its nutrients and body as a means of transport without disturbing it.

The tick’s life cycle being complex, the bacteria need to adapt quickly to survive during molting and the passage from tick to mammal. This change of host is sensed by the temperature increase and causes changes in the gene expression of Borrelia to adapt to the change in environments. 

Effect of Climate Change on the Tick Vector

For years, scientists have been warning the public that the Earth is warming and that this could have detrimental environmental and economic effects on life as we know it. Worldwide, there has been an alarming increase in temperature, precipitation patterns, and extreme weather events that are all associated with climate change. The local ecology has not been impervious to these effects either. In Canada alone, there has been documented evidence that increases in temperature have influenced ticks. Hotter temperatures have promoted better conditions for ticks to survive and accelerate their lifecycle, leading to faster propagation.

The Tick’s life cycle

The tick’s life cycle involves 4 stages: eggs, larva, nymph, and adult (Figure 1). Nymphal and adult stages are the infective ones to humans although every stage requires a blood meal from different hosts. Every blood meal gives the pathogen a chance to be transmitted, resulting in spreading of the bacterium as well as the molting or mating of the tick. Humans, however, do not permit the reproduction of the ticks nor B. burgdorferi.

Figure 1. Life cycle of I. scapularis, the vector of Lyme disease. Source: Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Vector-Borne Diseases (DVBD).

Hotter temperatures result in a faster developmental cycle, increased egg production and thus, an increased population. Once larvae have molted into the nymphal stage, the cold winter forces them to remain dormant until spring. However, with warmer winters, these ticks no longer need to hibernate and can become active on warmer days. Warmer winters also affect the tick’s reservoir, especially the white-footed mouse. The mice reproduce in the spring and summer, meaning that shorter winters will also yield higher rates of the tick’s host.

All these changes are permitting the tick population to grow along with its reservoirs and increases their activity even during the winter. Milder temperatures are enabling them to spread to more northern latitudes. Additionally, longer spring and fall seasons have led to humans spending more time outdoors and wearing summer clothing for longer, which also increases the likelihood of tick exposures and therefore, Lyme disease. 

According to the CDC, the number of confirmed cases of Lyme disease has risen from 12,801 cases in 1997 to 29,513 in 2017. A similar trend is observed in Canada (Figure 2). As Lyme disease is becoming more prevalent, it has been receiving increased media coverage and attention from public health agencies. Through education about the disease and its route of transmission, we can promote increased vigilance when outdoors and catch infections early. While climate change threatens to increase the prevalence of the disease, prevention of Lyme disease by education and vaccination will promote better outcomes.

Figure 2. Number of Lyme disease cases by month of onset per year, 2009-2012. Source: Government of Canada, National Lyme Disease Surveillance, 2009-2012.

Vaccines & Prevention

Even though the bacteria show signs of resistance to erythromycin, they are still susceptible to most antibiotics. However, this may change in the future. The more the bacteria is exposed to antibiotics and courses of antibiotic treatment are not completed, the higher the chances of developing antimicrobial resistance (AMR).

In an effort to use fewer antibiotics, a vaccine was created in the US to decrease prevalence of Lyme using the surface Osp A protein as a template to create antibodies. While the vaccine proved to be effective, an unfounded uproar from the public caused widespread disapproval of the vaccine, which was consequently discontinued. A new vaccine VLA15 based on six different variations of the same Osp A protein is currently in the second phase of clinical trials and shows promising results according to the FDA.

The current best practices to prevent the spread of Lyme disease is avoidance of tick-infested areas. If these areas must be visited, skin should be covered by long pants and sleeves; wearing light colors is helpful in spotting the insect. Insect repellents containing DEET are also useful.


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Bouchard, C., Dibernardo, A., Koffi, J., Wood, H., Leighton, P., & Lindsay, L. (2019). Increased risk of tick-borne diseases with climate and environmental changes. Canada Communicable Disease Report = Releve Des Maladies Transmissibles Au Canada, 45(4), 83-89. doi:10.14745/ccdr.v45i04a02

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Comstedt, P., Schüler, W., Meinke, A., & Lundberg, U. (2017). The novel Lyme borreliosis vaccine vla15 shows broad protection against Borrelia species expressing six different ospA serotypes. Plos One, 12(9), 0184357. doi:10.1371/journal.pone.0184357

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Jackson, C., Boylan, J., Frye, J., & Gherardini, F. (2007). Evidence of a conjugal erythromycin resistance element in the Lyme disease spirochete Borrelia burgdorferi. International Journal of Antimicrobial Agents, 30(6), 496-504. doi:10.1016/j.ijantimicag.2007.07.013

Jewett, M., Lawrence, K., Bestor, A., Tilly, K., Grimm, D., Shaw, P., VanRaden, M., Gherardini, F., Rosa, P. (2007). The critical role of the linear plasmid lp36 in the infectious cycle of Borrelia burgdorferi. Molecular Microbiology, 64(5), 1358-74.

Nigrovic, L.E., Thompson, K.M. (2007). The Lyme vaccine: A cautionary tale. Epidemiology and Infection, 135(1), 1-8.

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Bordetella bronchiseptica

By Manon Desjardins et Paloma Jacquet


Bordetella bronchiseptica is a gram-negative, rod-shaped commensal (and possible pathogen) in many wild and domestic animals (figure 1). It colonizes the respiratory tract and is associated with various lung-related infections. Although many B. bronchiseptica strains possess toxins with the potential to destroy tissue, diseases produced by B. bronchiseptica alone are not always severe. Some diseases can however lead to life-threatening pneumonia. Moreover, infection often predisposes an individual to other infections, some of which can have severe clinical consequences. Although it mainly infects animals, there has been infections in immunocompromised humans and the bacteria is considered zoonotic.

Figure 1: Electron microscopy of B. bronchiseptica biofilm on a glass surface. Source: Nicholson, T.L., Conover, M.S., Deora, R., (2012, November 12). Transcriptome Profiling Reveals Stage-Specific Production and Requirements of Flagella during Biofilm Development in Bordetella bronchiseptica (photograph).


The main route of transmission for B. bronchiseptica is oral-nasal via direct aerosol droplets (mainly coughing). Infection is initiated by the attachment of B. bronchiseptica to the ciliated cells of the lungs (figure 2A). Inside the lungs, it is able to evade the immune system and create ciliary dysfunction. Ciliated cells have hair-like structure on their surface and are responsible for moving inhaled debris and other pathogens away from the lower respiratory tract. By paralyzing the cilia, Bbronchiseptica increases its chance for colonization and allows for other bacteria to colonize as well. Oftentimes, animals infected with B. bronchiseptica are infected with another bacteria or virus at the same time.

B. bronchiseptica infects a broad range of mammals and gives rise to a wide spectrum of diseases. It is a major cause of “kennel cough” in dogs, which is characterized by persistent, forceful cough, and bronchopneumonia in cats. It is commonly associated with atrophic rhinitis in pigs and snuffles in rabbits. Human disease is rare, but has occurred in individuals that are immunocompromised and occasionally occurs following contact with sick animals. Diseases in this case include pneumonia, sinusitis, and nosocomial tracheobronchitis.

Host symptoms varies depending on the species affected and may include coughing, sneezing, nasal discharge, swelling of the lymph nodes in the neck, lethargy, fever, and difficulty breathing. In severe cases, B. bronchiseptica can be life threatening.


B. bronchisepticais present and affects animals worldwide. Infections are most commonly found where animals are often in proximity such as animal hospitals, shelters, pet stores and boarding facilities. It is also regularly found in agricultural settings (i.e. commercial rabbiteries) where rapid spread and persistent infection make it difficult to control. Consequent respiratory diseases, which most commonly affects dogs, results in low mortality but morbidity is high. In addition, puppies are much more susceptible than adult dogs because they have yet to develop a strong immune system.

In some situations, the bacteria is present in up to 50% of cat’s nasal swabs from shelters. A European study found that when more cats cohabitate together, more bacteria was isolated from these animals. Another study found that almost 50% of household dogs were carriers of B. bronchiseptica and most of them originated from breeders and pet stores.

Virulence factors

All of B. bronchiseptica s genes for virulence mechanisms are encoded at the bvgAS location in the genome (the genetic material in an organism). Organisms alternate between virulent or non virulent states by turning on or off the bvgAS genes in response to various environmental conditions. Virulence is achieved by causing disfunction in the respiratory tract and the ability to evade the immune system.

Adherence to host cells:

B. bronchiseptica is able to attach to the cells of the upper respiratory system by producing fimbrial adhesins on its surface (figure 2A). They are sticky hair-like structures that allow adherence to host cells and begin infection.

Airway colonization:

The mechanism of ciliated cells paralysis involves the tracheal cytotoxin (TCT) produced by B. bronchiseptica. Ciliated cells in the airways are usually responsible for trapping foreign molecules in a mucus layer and they forcing them out of the body by coughing. TCT targets mitochondria, which produces energy required for the cell’s normal functions. Therefore, it induces ciliostasis meaning it prevents the movement of the cilia. It also causes the extrusion of these cells. Thus, when ciliated cells are paralyzed/killed by this toxin, mucus accumulates in the airways (figure 2B).

Figure 2: Colonization of the ciliated cells by B. bronchiseptica. A) Attachment to the cilia. B) Destruction and paralysis of ciliated cells. Note the mucus that is accumulating in the respiratory tract. Source: Manon Desjardins.

Escape from the immune system:

During a normal immune response, specialized cells such as macrophages and neutrophils migrate to the site of infection and engulf bacteria during a process called phagocytosis (figure 3A) . One of the gene from the bvgAS location encodes for a toxin called adenylate cyclase toxin. The toxin enters the macrophage and/or neutrophil and induces the production of a  molecule called cAMP (figure 3B). High cAMP concentration causes metabolic disturbances and the cell is not able to respond to external signals. Therefore, the macrophage/neutrophil cannot phagocytose the bacteria .

B. bronchiseptica also has a type III secretion system. It allows to deliver toxic components from the bacteria directly into host cells by means of a needle-like structure (figure 3C). These molecules, which are called effectors, induce the host cell to commit apoptosis (cell death). Because the molecules are directly deposited into host cells, they avoid being exposed to antibody mediated immune response or to immune cells, hence why this mechanism is important for bacterial survival inside the host.

Figure 3: Schematic representation of B. bronchiseptica’s virulence factors. A) Normal mechanism of phagocytosis by neutrophils/macrophages. B) Secretion of Adenylate Cyclase Toxin by the bacteria and inhibition of phagocytosis resulting from elevated cAMP in the cell. C) Direct delivery of toxic components into the host cells with the type III secretion system. Source: Manon Desjardins.


In mild cases, the infection can be self-limiting with supportive care. In more severe cases and to treat secondary infections often associated with B. bronchiseptica, antibiotic treatments may be necessary.

Vaccines are available for dogs, cats and swine. Young puppies and kittens may be vaccinated by intranasal, injectable or oral methods. The composition of vaccines depend on the administration method and range from inactivated antigens in injectable vaccines to attenuated avirulent bacteria in intranasal and oral vaccines.


Coote, J. G. (2001).  Environmental Sensing Mechanisms in BordetellaAdvances in Microbial Physiology, 44, 141-181. Retrieved from

Ford, R. B. (2014). Vital Vaccination Series: Kennel Cough Revisited. Today’s Veterinary Practice. Retrieved from

Huebner, E. S., Christman, B., Dummer, S., Tang, Y.-W., & Goodman, S. (2006). Hospital-Acquired Bordetella bronchiseptica Infection following Hematopoietic Stem Cell Transplantation. Journal of Clinical Microbiology44(7), 2581–2583.

Mattoo, S and Cherry, J. D. (2005). Molecular Pathogenesis, Epidemiology, and Clinical Manifestations of Respiratory Infections Due to Bordetella pertussis and Other Bordetella Subspecies. Clinical Microbiology Reviews, 18(2), 326-382. Retrieved from

Nafe, (2014). Diagnostic and Therapeutic Approach: Dogs Infected with Bordetella bronchiseptica & Canine Influenza  Virus (H3N8). Today’s Veterinary Practice. 4(4). Retrieved from

Nicholson, T.L., Conover M.S., Deora, R., (2012, November 12). Transcriptome Profiling Reveals Stage-Specific Production and Requirement of Flagella during Biofilm Development in Bordetella bronchiseptica (photograph). Retrieved from

Sykes, J. E. (2013). Bordetellosis. Canine and Feline Infectious Diseases (pp. 372-379). Retrieved from

Treponema pallidum

by Julia Messina-Pacheco and Lara Montaruli


Within the past three decades, an important reemergence of Treponema pallidum infections has been observed worldwide. This infection manifests itself as syphilis and other treponemal diseases such as bejel, pinta and yaws. Most often acquired through close sexual contact, this helically coiled bacterium belongs to the spirochete phylum, which is distinguished by a double membrane. Despite T. pallidum being one of the first successful antibiotic-treated infections, discussion still surrounds the most effective treatment, mainly due to the inability to culture it in vitro and thus study its antimicrobial susceptibility.


Syphilis is caused by T. pallidum subspecies pallidum, and is divided into four stages of disease progression (primary, secondary, latent and tertiary). The primary stage symptoms are sores at the site of infection, generally around the genitals, anus or mouth and are usually firm, round and painless. Secondary syphilis causes skin rashes, swollen lymph nodes and fever. Once the latent stage is reached, there are no signs or symptoms, as the infection lays ‘dormant’ for multiple years. If left untreated, the disease progresses to the tertiary stage wherein inflammation, apathy, seizures, general paralysis with dementia, and aneurysm formation occur. T. pallidum is generally transmitted through sexual contact, primarily in homosexual men (see Figure 1). It can also be transmitted by transplacental passage during the later stages of pregnancy, giving rise to congenital syphilis. It is highly transmissible as approximately 30% to 60% of those exposed to primary or secondary syphilis will become infected. However, chances of transmission during sex are reduced through the use of condoms to protect the infected area or site of potential exposure.

Figure 1: Number of early syphilis cases by sexual transmission routes between 1992-2008 in Norway. The primary route of transmission overall is by men having sex with men. Source: Biomed Central, BMC Infectious Diseases, Jakopanec et al. (2010)


Syphilis rates steadily decreased with the introduction of penicillin in 1947. However, it was not until the 1980s when the trend reversed in concurrence with increased use of intravenous drugs, the exchange of sex for drugs, anonymous sex, and people with multiple sexual partners, reaching its peak of 53.8 cases per 100,000 population in 1990. Still, syphilis rates continue to increase, for example, in the United States, the number of confirmed primary and secondary syphilis cases almost doubled, jumping from 8 724 to 16 663 between the years 2005 and 2013.

The disease primarily affects individuals between 15 and 40 years of age as there is a direct correlation between incidence of T. pallidum infection and increased sexual activity.  Furthermore, there is a noticeable difference in syphilis rates between men and women: males affected with primary and secondary syphilis outweigh females 10 to 1. On an international level, syphilis is distributed worldwide but remains prevalent in developing countries with rates being highest in the Western Pacific region and Southeast Asia.

Virulence Factors

Although T. pallidum may not exhibit the ‘classical’ virulence factors produced by most pathogens, it successfully attaches to, disseminates through and invades host tissues. These bacteria attach to a variety of host cell types by interacting with different host membrane components. In addition, its spiral shape (see Figure 2) allows it to enter through breaches in the skin and easily swim through gel-like substances, such as mucous membranes, to gain access to host blood and lymph systems. Thus, it propels itself by rotating in a corkscrew-like motion. Unlike most motile bacteria whose flagella are extracellular, in this case, the flagella is located in the space between the cytoplasmic and outer membranes, hidden from the host defenses. One of the major components of the host immune system is the generation of specific proteins, called antibodies, that recognize invading pathogens by binding to molecules on their surface. These immunogenic surface molecules are called ‘antigens’ and can be proteins, carbohydrates, or lipids. As such, the flagella of motile bacteria are composed of protein subunits called flagellin, which constitute a group of proteins called the H antigens. The outer membrane thus forms a barrier between the host defenses and T. pallidum‘s flagellum, preventing the binding of host antibodies to H antigens. In addition, T. pallidum is referred to as the ‘stealth pathogen’ due to the sparsity of immunogenic molecules presented on its outer surface, allowing it to avoid triggering an immune response. However, the few proteins that are presented on its surface are highly variable between individual bacteria of the same species. Thus, pathogens such as T. pallidum that can switch the molecular composition of their surface antigens are said to undergo ‘antigenic variation’. This makes it very difficult for the host to identify the bacterial molecules and subsequently raise an appropriate immune response. All in all, this bacterial pathogen effectively bypasses recognition by the host immune system by altering its surface components and by hiding its flagellum, two potential sources of antigenic molecules.

Figure 2: A photomicrograph showing the spiral, corkscrew-like shape of Treponema pallidum. The periplasmic flagella allows for the dissemination of the pathogen through host tissues and viscous substances, while preventing recognition by the host defenses. Source: Public Health Image Library, Center for Disease Control, Susan Lindsley (1972).


     To date, there is no vaccine available against T. pallidum due to the sparsity and variability of its surface antigens. Thus, in order to successfully treat syphilis, early detection is crucial and followed by antibiotic treatment of syphilis-infected individuals and their partners. Both the CDC and WHO recommend a 10-day course of penicillin for early syphilis, with longer courses of treatment for those with late syphilis. In fact, penicillin is the only antibiotic shown to be effective in treating syphilis in pregnant women, as macrolides do not cross the placental barrier. However, individuals with penicillin allergies should be given doxycycline (cannot be taken during pregnancy) or ceftriaxone. The commonly used antibiotic azithromycin is not recommended, as resistance has emerged in strains of T. pallidum.


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Yersinia pestis

by Tongzhu Meng and Luyang Yuan


Yersinia pestis, also used to be named as Bacterium pestisBacillus pestis and Pasteurella pestis, is the causative agent of plague, which is a disease primarily affecting rodents via their associated fleas and is able to transmit to humans through infectious fleabites. Y. pestis was thought to be responsible for three devastating pandemics throughout human history, including the Justinian’s plague during the 6th century, the Black Death in Europe and Modern plague in China in the later 19th century. The bacterium was discovered during the epidemic of the plague in Hong Kong and had been used as a biological weapon during the 20th century. Y. pestis can be found exclusively in mammalian hosts and arthropod vectors, such as fleas.


Plague is a serious infectious disease that has three major clinical forms: bubonic plague, septicemic plague and pneumonic plague. If the patient is bitten by an infected flea, Y. pestis bypasses the skin barrier, enters the bloodstream and multiplies inside the lymph nodes. In healthy individuals, macrophages are guards of the immune system that are able to digest invading bacteria. Y. pestis inhibits macrophages from clearing bacteria and causes patients to have fever and one or more swollen lymph nodes. Y. pestis prevents local immune cells from eliminating bacteria and communicating with other remote immune cells that are able to help controlling the infection.

Septicemic plague can exist as the first symptom of plague or as secondary symptom of untreated bubonic plague. This form is the result of infectious fleabites or handling tissues or fluids of an infected animal. Under this kind of scenario, patients’ fingers, toes, the nose and other tissues might get black, due to reduced blood flow. They are also susceptible to develop bleeding into the skin and inner organs. Pneumonic plague is the result of inhaling infectious droplets in the air or from untreated bubonic or septicemic plague after the bacteria have spread to the lungs.  It is the most serious form of the plague and is the only form of the disease that can be spread from person to person through infectious droplets. Infections of lung may lead to pneumonia and cause chest pain, respiratory failure and shock.

Figure 1: Summary of transmission process of Yersinia pestis to human. (by Tongzhu Meng)


From 2010 to 2015, WHO reported 3248 cases worldwide, including 584 deaths. Plague epidemics have occurred in Africa, Asia and South America, but since 1990s, most human cases reported were occurred in Africa. Nowadays, the three most vulnerable countries in the world are Democratic Republic of the Congo, Madagascar and Peru. Bubonic plague has a mortality rate of 30% to 60% while pneumonic plague is always fatal unless treatment started within 20 hours of symptom onset.

Over 80% of cases reported in United States were in bubonic form and there was an average of seven human plague cases reported each year for the past decades. These reported human cases covered people in all ages and in both sexes. Moreover, according to the cases reported in the last 20 years, people living in small towns and villages or agricultural areas are more susceptible than those living in larger towns and cities or urban areas.

Virulence Factor:  

Y. pestis gets into the body by flea bites or by contaminated fluid or by infectious droplets in the air. Phagocytes, such as macrophages, are a type of cell that circulates in the body, which can engulf and digest bacteria and other non-self material. In healthy individuals, these cells would recognize bacteria and then engulf it by a process called phagocytosis. This leads to the formation of a bag of bacteria in the phagocyte, which is called phagosome. Then the enzymes located in the phagocytes are pumped into phagosomes to destroy the bacteria.

However, Y. pestis is resistant to phagocytosis. There are two important virulence factors contributing to this property named F1 (Fraction 1) and LcrV. LcrV may also play a role in suppressing the immune response in an individual, it could inhibit production of signal molecules released by immune cells that would lead to the silence of normal immune response. The bacteria are able to move in the circulation and travel to local lymph nodes. It is resistant to be digested by macrophage and it can replicate within the lymph nodes rapidly, which causes swelling and enlargement of the lymph nodes.

Y. pestis has a needle-like structure (Figure 2), which is necessary to infect the host cells. It injects secretory proteins produced by Yersinia into macrophages and other immune cells. Some of these secreted proteins form pores on the host cell membrane and lead to the destruction of the host cells. Those pores created by the secretory proteins serve as gates for the other secretory proteins to get into the cells. Some of these secretory proteins limit the ability of immune cells to engulf the bacteria and other non-self materials and affect the signaling pathway of the immune system. Moreover, some of them could get into the host cells and lead to the killing of the host.

To sum up, Y. pestis is resistant to phagocytosis. It causes the death of host cells and affects the signals between the immune cells in the host that leads to suppression of normal immune responses.

Figure 2: The needle like structure used by Y. pestis to inject virulence factors into host cells.


Contact with dead or infected animals, especially rodents, should be avoided.


Commonly prescribed antibiotics for enterobacteria can be used to treat Y. pestis infections. CDC recommends that the treatment should begin as soon as plague is suspected. The earlier the treatment starts, the greater chance for patients to survive. Gentamicin and streptomycin are often prescribed as first line treatments due to their ability to stop the bacteria from making proteins it requires and to induce bacterial death. However, patients should not maintain on streptomycin for more than full 10 days in order to avoid the risk of developing endotoxic shock. They should gradually change to other antibiotics to continue the treatment. Treatments can be adjusted depending on the patient’s age, medical history and underlying health conditions as well.

WHO does not recommend vaccination against Y. pestis infections for general populations. However, for those who are often exposed to the risk of contamination and for health care workers, vaccinations should be considered.


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Acinetobacter baumannii

by Caitlin Deseve and Jessika Marquis-Hrabe


Acinetobacter baumannii (see Figure 1) is a multi-drug resistant pathogen that has become of great concern to medical facilities around the world. It causes various infections of the blood, brain, lungs, urinary tracts, and open wounds. The species was first identified in 1911 in soil samples, but became prevalent among returning soldiers who were treated in field hospitals of Iraq – thus earning it the common name ‘Iraqibacter’. Its natural habitat is still unknown.

Figure 1: Computer-generated image of Acinetobacter baumanii based on scanning electron microscopy. Source: Public Health Image Library, Center for Disease Control, James Archer, U.S. Centers for Disease Control and Prevention 2013.


Acinetobacter baumannii is a nosocomial bacterial pathogen, meaning it originates from hospital settings. The pathogen is capable of growing at various temperatures and pH conditions, which permits A. baumannii to persist in diverse environments. It causes a range of symptoms once it breaches the skin – from skin infections to pneumonia. It is most common in intensive care units, and in patients in hospital stays longer than 90 days with open wounds and invasive devices.

The most common symptoms of A. baumannii are ventilator-associated pneumonia (VAP) and bloodstream infections. VAP develops when pathogens transmit from external equipment and colonize the patient’s airways. Mortality rates due to A. baumannii-associated pneumonia range from 30 to 75%, with VAP responsible for the higher end. The most reported infections are encountered in the respiratory tract, wounds and catheter insertion sites.


The United States has suffered several outbreaks, mostly associated with the return of military placed in Iraq and Afghanistan. The pathogen is often transmitted by contact to inanimate surface in field hospitals. Improper isolation and disinfecting treatments permitted the transfer of A. baumannii to US hospitals.  In 2004, 83% A. baumannii bloodstream infections were identified in the casualties injured. Infections in military personnel have also been reported in Canada and the United Kingdom.

Additionally, A. baumannii outbreaks have been identified in Europe since the 1980s. In most instances, transmission was caused by transfer of infected patients between hospitals; only one or two epidemic strains were recorded in hospitals. However, the outbreaks were not only limited to the hospitals, but spread internationally through airline travel.

The pathogens` prolonged survival in clinical settings contributes to its continuing outbreaks. Furthermore,  A. baumannii mortality rates are suspected to be associated with warmer temperature conditions, as pathogen colonization appears to be higher in tropical regions.

Virulence Factors

A. baumannii is highly capable of adhering to surfaces using hair-like appendages called pili. Specifically, A. baumannii employs Type IV pili on its surface, which function not only in adherence, but also in motility by extending and retracting. It has become of great concern due to its potential to produce biofilms. Communities of A. baumanni form by sticking together in a slimy extracellular matrix on both skin and hospital equipment. Formation of biofilms (see Figure 2) is a key virulence factor that provides resistance to antibiotics and allows persistence in unfavourable environmental conditions, such as low nutrient availability and desiccation.

Figure 2: Biofilm formation on a surface by Acinetobacter baumannii. 1, Attachment of free cells; 2, cell-cell adhesion in extracellular matrix; 3, dividing cells (proliferation) and cell growth; 4, cells spread and colonize new surfaces.

The presence of competence genes comFECB and comQLONM allow A. baumannii to uptake DNA from the environment and integrate it into its genome through a process called transformation. This factor enables A. baumannii to develop new traits rapidly, such as developing lower susceptibility to antibiotics. Moreover, the pathogen can produce antimicrobial-inactivating enzymes, such as Beta-lactamases. These enzymes destroy antibiotics like penicillins, to render them ineffective.  Finally, A. baumannii has a capsule that surrounds the outer membrane of the bacteria to serve as a protective barrier. Its presence helps the pathogen to evade the human immune response, ultimately making it more persistent in infection sites.


A. baumannii is resistant to disinfectants and known antibiotics. Therefore, sufficient control is the current aim in hospitals. To prevent infection, environmental samples, especially from medical equipment, should be cultured and sources of contamination discarded. Additionally, hygiene control could prevent contamination between surface contact or direct person-person interaction. Should patients be infected, they should be isolated until infection has passed. Antibiotic selection is strenuous due to varying strains acquiring different antibiotic resistance. Discerning application of antibiotics in hospitalized patients is important to minimize drug resistance through pathogen evolution. Therefore, the treatment considered should be determined case-by-case.


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Proteus mirabilis

by Rhea Suvarna


Proteus mirabilis is commonly the causative agent of complicated urinary tract infections (UTIs), UTIs associated with components that compromises the urinary tract or host defense, especially in individuals with functional or structural abnormalities or with long-term catheterization for patients whose bladders will not empty fully or empty at inappropriate times. This bacterium is frequently found in soil and water, and is also part of the normal bacterial community residing in the human gastrointestinal tract.


P. mirabilis causes symptomatic infections of the urinary tract by either ascending from the gastrointestinal tract or by person-to-person transmission usually in healthcare settings.

Individuals with P. mirabilis infection may present with urethritis, cystitis, prostatitis, or pyelonephritis. A history of frequent renal stones can be an indication of chronic P. mirabilis infection. Symptoms of urethritis include painful urination, urine containing white blood cells, and increased frequency of urination. In males, symptoms are usually mild and could include urethral discharge. The symptoms of cystitis are more prominent than urethritis. They include painful urination, increased frequency and urgency of urination, small volume urine, dark urine, urine containing red blood cells, suprapubic pain, and back pain. Prostatitis affects men more acutely than cystitis with the same set of symptoms, though sometimes along with fever and chills. Pyelonephritis results from a complication of either of the conditions mentioned above and therefore, the patient presents symptoms of urethritis or cystitis along with flank pain, costovertebral angle tenderness, nausea and vomiting, fever, and sometimes an enlarged kidney.

The interaction between the bacterium and the host immune system determines the level of infection. Adherence followed by colonization is the basis of UTI pathogenesis. P. mirabilis UTIs occur in an ascending manner. The bacteria first contaminate the tissues surrounding the urethra, then enter the bladder through the urethra and form an initial colony. Following initial colonization, P. mirabilis ascends the ureters thanks to its swarming ability and interacts with epithelial cells of the renal pelvis, allowing for colonization of the kidney. Occasionally, the bacteria break through the renal tubular epithelial barrier and enter the bloodstream.


P. mirabilis causes 1-10% of all UTIs. More specifically, this bacterium accounts for 1-2% of all UTIs in healthy women and in the case of hospital-acquired UTIs and complicated UTIs, P. mirabilis is responsible for 5% and 20-45%, respectively. Recent studies suggest that this species causes 4% of almost 3,000 UTIs in North America.

Factors that may increase the risk for acquiring P. mirabilis UTIs include female sex, longer duration of catheterization, inadequate catheter cleaning or care, underlying illness, and lack of availability of systemic antibiotics.

Virulence Factors

P. mirabilis utilizes a variety of virulence factors that allow it to access and colonize the host urinary tract, including fimbriae and other adhesions, urease and stone formation, iron and zinc acquisition, proteases and toxins, swarming growth, biofilm formation, and regulation of pathogenesis through DNA binding proteins.

The activity of the tiny projections on the bacterium surface, termed fimbriae (or pili), mediate the attachment of the bacterium to host tissue. The tips of these fimbriae contain specific compounds and polysaccharides that permit the bacterium to attach to specific sites in the host. Successful attachment initiates a cascade of events that leads to release of compounds that promote an alkaline pH, making it a suitable environment for survival and propagation. Alkaline pH in the

Urease facilitates virulence via the production of urinary stones. This enzymatic activity results in an increase in local pH, producing an alkaline environment in the urinary tract. The alkaline environment causes the formation of crystalline biofilms and the precipitation of calcium and magnesium ions to form urinary stones. These cause tissue damage and can block urinary flow.

During swarming, the expression of several virulence genes is increased and allows the bacterium to move through ascending urinary tract. The swarming ability of P. mirabilis is especially applicable to catheterized patients, as this bacterium is able to swarm across catheters made of silicon (see Figure 1) or latex. The flagella of P. mirabilis are responsible for the bacterium’s swarming motility, which is fueled by the proton motive force (See Figure 2). Flagellin, the structural component of flagella, is sensed by the host immune system through Toll and NOD-like receptors, which elicits a pro-inflammatory response. However, P. mirabilis flagella encode two flagellins, which allows for antigenic variation. This means that the bacterium is capable of altering its surface proteins to escape recognition by the host immune response.

Figure 1: Episcopic differential interference contrast (EDIC) microscopic image of 24-hour exposure showing multi-layered appearance and highly reflective, motile P. mirabilis (‘grey lines’) on silicone catheter section. Source: PLoS ONE, Wilks et al. (2015).à

Figure 2: Suggested model for the energy metabolism of P. mirabilis during swarming. The proton gradient is generated by membrane respiration to oxidize NADH to NAD+, which powers flagellum rotation and oxidative phosphorylation. Source: mBio, Alteri et. al (2012).


Patients diagnosed with uncomplicated P. mirabilis UTI, patients that are otherwise healthy and have no structural or neurological urinary tract abnormalities, are treated with antibiotics of either a 3-day course of trimethoprim/sulfamethoxazole (TMP/SMZ) or an oral fluoroquinolone. Acute, uncomplicated pyelonephritis may be treated with fluoroquinolone for 7-14 days or a one-time dose of ceftriaxone or gentamycin after either TMP/SMZ, an oral fluoroquinolone, or cephalosporin for 7-14 days. Antibiotic therapy is suggested for patients with more severe P. mirabilis infections.

Those suffering from a complicated P. mirabilis UTI can be treated with oral antibiotics for 10-21 days along with necessary follow-up.


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Umpiérrez, A., Scavone, P., Romanin, D., Marqués, J.M., Chabalgoity, J.A., Rumbo, M., and Zunino, P. 2013. Innate immune responses to Proteus mirabilis flagellin in the urinary tract. Microbes Infect. 15(10–11): 688–696. doi:10.1016/j.micinf.2013.06.007.

Wilks, S.A., Fader, M.J., and Keevil, C.W. 2015. Novel Insights into the Proteus mirabilis Crystalline Biofilm Using Real-Time Imaging. PLoS One 10(10): e0141711. Public Library of Science. doi:10.1371/journal.pone.0141711.