Yersinia pestis (Plague)
Definitions & Key takeaways
Yersinia pestis is a Gram-negative bacillus that grows well on blood, chocolate, and MacConkey agar. Its virulence factors include capsular antigen F1, which protects it from neutrophils, and Yops, which inactivates macrophages, as well as a siderophore which it uses for iron uptake. It produces a disease called plague, which has three forms - bubonic, septicemic, and pneumonic. Plague is diagnosed by identifying the bacteria in cultures from blood, bubo aspirate, and sputum or in a peripheral blood smear with Gram, Wright-Giemsa, or Wayson staining and also through serological tests and rapid antigen tests. Effective treatment of plague involves aminoglycosides like gentamicin and streptomycin.
Yersinia pestis is a Gram-negative coccobacillus which belongs to a family of bacteria called the Enterobacteriaceae. It causes a disease called plague, which is transmitted by rodents, mainly rats, as well as prairie dogs, and their fleas.
Plague is highly contagious, and there have been three major pandemics in human history - one of them, known as the Black Death, killed up to one-third of the European population.
Yikes! Now, Yersinia pestis has a thin peptidoglycan layer, so it doesn’t retain the crystal violet dye during Gram staining.
Instead, like any other Gram-negative bacteria, it stains pink with safranin dye. On Wright-Giemsa and Wayson staining it has a bipolar staining which means that only the poles of the bacteria stain, and the rest of it remains unstained, so the bacteria look like safety pins under the microscope.
Alright, now Yersinia pestis is non-motile, non-spore forming, facultative anaerobic which means it can survive in both aerobic and anaerobic environments and facultative intracellular which means it can survive both inside and outside the cells.
It’s oxidase and urease negative which means it doesn’t produce these enzymes and catalase positive which means it produces an enzyme called catalase.
Also, it’s indole negative which means it doesn’t convert tryptophan into indole. Yersinia pestis grows well on MacConkey agar, sheep blood agar, and chocolate agar.
MacConkey agar is used to identify if a bacteria ferments lactose or not, and it contains a pH sensitive dye and lactose.
So, if a bacteria ferments lactose, it means that it’s able to ferment lactose and produce acid which causes the pH sensitive dye to turn pink leading to formation of pink colonies.
Non-lactose fermenters, like Yersinia pestis, aren’t able to modify the PH sensitive dye, grow into colorless colonies. Next, on sheep blood agar and chocolate agar, Yersinia pestis forms opaque, yellow colonies that look like fried eggs.
Finally, the triple sugar iron test, or TSI for short can be done to assess hydrogen sulfide production. This medium contains three sugars - lactose, glucose and sucrose, as well as iron and a pH sensitive dye.
If the bacteria produces hydrogen sulfide, that reacts with the iron, and a black precipitate forms in the test tube. Yersinia pestis doesn’t, so no precipitate forms.
Now, the pathogenesis of Yersinia pestis consists of two components - the transmission of bacteria from fleas and the host response to the bacteria.
First, fleas get infected with Yersinia pestis by feeding on a bacteremic host like rats, which then colonizes the flea midgut.
So, when the flea bites a human it regurgitates the bacteria into the bite wound. So, once the bacteria gets inside the host, neutrophils and macrophages come to the wound site to kill the bacteria.
Now, the bacteria has a capsule which consists of a capsular antigen, called F1, with antiphagocytic properties. But, inside the flea gut, it loses this capsule, so neutrophils can easily destroy the bacteria.
Sadly, macrophages are not as efficient in killing the bacteria so, if the bacteria is caught by macrophages it can survive inside them and get carried to lymph nodes where it replicates and cause lymphadenopathy.
Inside macrophages, it starts to use virulence factors to avoid destruction. So, now it starts again to produce it’s capsular antigen F1.
Also, it has a type III secretion system, or T3SS for short, which is a collection of proteins that can dampen the immune response.
So, using T3SS it starts to inject inside the macrophage Yersinia outer proteins, or Yops for short, which block secretion of proinflammatory cytokines such as TNF-alpha and IL-8 and inactivate the macrophages leading to evasion of phagocytosis.
Additionally, it produces a siderophore called yersiniabactin which goes on a hunt for iron and when it captures it, returns to the bacteria.
Iron acquisition is an important step for Yersinia in order to thrive and replicate. Finally, the macrophages burst allowing the bacteria to spread throughout the body, and cause three different forms of the disease: bubonic, septicemic and pneumonic.
Bubonic plague develops when Yersinia pestis spreads to nearby cells in the lymph nodes, making the lymph nodes swell. These swollen lymph nodes are called buboes - hence, bubonic plague.
From the lymph nodes, it can get into the bloodstream, causing septicemic plague - and remember that the bacteria now has its capsular antigen F1 again, so circulating neutrophils can’t destroy them anymore.
Once in the bloodstream, Yersinia pestis secretes endotoxins which lead to an excessive production of thrombin, which creates a pro-coagulant status inside blood vessels, leading to disseminated intravascular coagulation, or DIC.
With DIC, tiny clots form throughout the body, cutting off blood flow in different regions, causing tissue necrosis. the bacteria can travel to any part of the body, which can cause multi organ failure.
If left untreated, septicemic plague can progress to overwhelming sepsis and death. Finally, pneumonic plague develops one of two ways.
One way is when bacteria spread to the lungs from the bloodstream, in which case it’s called secondary pneumonic plague.
Now, when humans with secondary pneumonic plague cough or sneeze, they release respiratory droplets that can cause primary pneumonic plague in individuals who inhale these droplets.
So you can see how this can easily turn into a pandemic situation. Symptoms of bubonic plague include fever, chills, fatigue and on a clinical examination, buboes can be seen, frequently in the inguinal or axillary region.
With septicemic plague, there’s hypotension, malaise, purpuric skin lesions and tissue necrosis which appear as black regions on the limbs.
Finally, with pneumonic plague there’s dyspnea, fever, chest pain, cough and hemoptysis, which is blood in the sputum. Plague can be diagnosed by isolating Yersinia pestis in cultures from blood, bubo aspirate and sputum and also identifying the bacteria in a peripheral blood smear using Gram, Wright-Giemsa or Wayson staining.
Aso, a fourfold increase in antibody titer between serum probes obtained at least 2 weeks apart, done using serological tests, can confirm the diagnosis.
Now, there is a also a rapid antigen test that can be done to identify Yersinia pestis F1 antigen in sputum or serum within 15 minutes.
Finally, a chest X-ray may reveal signs of pneumonic plague, like consolidation which appear as white areas, or cavities which can appear as walled-off, lucent areas within the lung.
Plague can be treated with antibiotics, usually aminoglycosides such as gentamicin and streptomycin. Other antibiotics that can be used are doxycycline, tetracycline, fluoroquinolones and chloramphenicol.
The usual duration of the treatment is 10 to 14 days. Alright, as a quick recap, Yersinia pestis is a Gram-negative bacillus that grows well on blood, chocolate and MacConkey agar.
Its virulence factors include capsular antigen F1, which protects it from neutrophils, and Yops, which inactivate macrophages, as well as a siderophore which it uses for iron uptake.
It produces a disease called plague, which has three forms - bubonic, septicemic and pneumonic. Plague is diagnosed by identifying the bacteria in cultures from blood, bubo aspirate and sputum or in a peripheral blood smear with Gram, Wright-Giemsa or Wayson staining and also through serological tests and rapid antigen test.
Finally, it is treated with aminoglycosides such as gentamicin and streptomycin for a period of 10 to 14 days.
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