Yersinia pestis
Yersinia pestis is G- bacteria and a major pathogen causing plague pandemics. It was first isolated by Alexander Yersin in 1894 in Hong Kong. Plague is associated with high mortality without antibacterial therapy. In the wild, Yersinia pestis was found in several rodent species. However, Yersinia pestis circulates through flea bites, in humans it is a rat flea bite. Bacteria get into the wound. Human-to-human transmission can occur via aerosol particles or droplet infection and a primary plague infection arise. Plague is rare at this time, occurring in Africa, India, Southeast Asia, Mexico, and the western United States.[1]
Morphology[edit | edit source]
Yersinia pestis is a pleomorphic rod-shaped bacterium with a capsule. It is a stationary stick. Other yersinias are mobile. A common feature of Y. pseudotuberculosis and Y. enterocolitica is that it stains polar. This rod, like all Enterobacteriaceae, is characterized by the ability to grow on simple laboratory soils. Their undemanding growth ranges from 0 to 40°C with a temperature optimum around 30°C.[2]
Antigenic structure[edit | edit source]
On its surface is a localized F1 protein complex, which is a protective antigen. O-specific side chains are not present. Virulent strains form V and W proteins, the production of which is linked to plasmids.
Pathogenicity[edit | edit source]
The pathogenicity of Yersinia pestis is determined by a complex of chromosome and plasmid-linked factors. Surface factors that block phagocytosis are important. Virulent strains of this bacterium are facultatively intracellular parasites that multiply in macrophages. During infection, Yersinia pestis, an facultative intracellular bacterium, exhibits the ability to first invade cells and then thwart phagocytosis of the host cell. During these two distinct phases, the invasion phase and the anti-phagocytic factor phase, the bacteria in manipulating the host cell help to complete each of these functions, but the mechanism by which Yersinia regulates these functions during each step remains unclear. In addition to macrophages, the bacterium is also able to penetrate epithelial cells. During the invasion at the site of injury, a hemorrhagic pustule is formed, from where the infection is further distributed to the descending lymph nodes, in which the subsequent enlargement produces smoke (bubonic form of the plague). Later, bacteremia and sepsis develop. A secondary disease, Pneumonia, may develop, causing Yersinia pestis to spread to the surrounding area by coughing up, and the infected person will develop primary pneumonia – a pulmonary form of the plague. When a patient manages to overcome the disease, he develops good immunity.
Diagnosis and therapy[edit | edit source]
Bacteria are diagnosed from the contents of the pustules, lymph nodes, blood culture, bone marrow, and sputum. Cultivation is possible on blood agar. Bacteria stain according to Gram negative. When testing Yersinia pestis for antibiotic susceptibility, the bacteria were found to be susceptible to chloramphenicol, streptomycin, kanamycin, tetracycline, quinolones. However, plague vaccines produced by Yersinia pestis are in clinical development. Streptomycin can be used in endemic areas. We can induce short-term immunity when a dead vaccine with a protective antigen is given. A live vaccine with live attenuated strains is more effective, but the use of this vaccine is only approved in some parts of the world. There is currently no licensed vaccine to prevent plague in Western Europe.
Links[edit | edit source]
Related articles[edit | edit source]
External links[edit | edit source]
References[edit | edit source]
- JULÁK, Jaroslav. Úvod do lékařské bakteriologie. 1. edition. 2006. ISBN 8024612704.
