Yersinia pestis
Ridhima Melwaney

Plague, the age-old deadly disease that has made its way into the modern era, has been known to cause large- scale epidemics. Originating in Africa where it killed over 100 million people, plague destroyed nearly one fourth of Europe’s population in the Middle age. In the late 18th century, a outbreak occurred in China, spread to Hong Kong and was then spread by rats that were being transported on ships to Africa, Asia, California and several other countries. The most recent outbreak of plague occurred in India in the early twentieth century.

While the disease is mostly transmitted to humans by infected rat flea bites human-to-human transmission may occur during epidemics of pneumonic plague. The cause of the plague is a bacterium called Yersinia pestis. The microorganism was first discovered by Swiss physician Alexandre Yersin who linked Y.pestis to the Black Death epidemic in Europe. The human Y. pestis infection is known to take on three main forms: pneumonic, septicemic and bubonic plagues.

Belonging to the Enterobactericeae family, Yersinia pestis is a gram- negative rod-shaped bacterium. It is a facultative anaerobe that produces and consumes hydrogen for gas. It is also covered by a slime envelope that is heat labile. This bacterium is only motile when it is isolated. Y. pestis has three species of which the complete genomic sequence is known for two. Strain KIM is and strain C092. It also hosts three plasmids, pCD1, pPCP1 and pMT1. These plasmids together with a pathogenicity island called HPI, encode several proteins that give Y. pestsis its pathogenicity.  These virulence factors are fundamental for bacterial adhesion, injection of proteins into host cell and invasion of bacteria into host cell.

Pathology and Prevention

The pathogenesis of Yersinia pestis in mammalian hosts is due to several factors which are mostly related to initial immune response. Disease are caused primarily by flea bites but can also be transmitted by air. These fleas become infected by taking the blood of other infected animals. The coagulase of the bacteria cause blood clots within which the bacilli can multiply. The fleas then deliver thousands of these infected bacilli into the host cell whilst feeding for blood. The bacilli then migrate to regional lymph nodes, are phagocytosed (by polymorphonuclear cells and mononuclear phagocytes) and multiply intracellularly. In the lymph nodes, dense concentrations of plague bacilli, destruction of normal architecture and necrosis is observable. More severe cases may lead to the invasion of distant organs.

Whilst the most important transmission factor of plague is the rat flea, plague can also be spread from one human to another via air. Like other plagues, the contraction results in a sudden onset of coughing, high fevers, fatigue and even swelling of lymph glands. Due to high replication rates, it is very important for these infections to be diagnosed quickly. Death from the pneumonic plague has been proven fatal in roughly 50% of the cases with medical treatment and almost always fatal without.

The major resistance is the development of specific anti-envelope (F1) antibodies, serving as opsonins for virulent organisms allowing their rapid phagocytosis and destruction. Immunologically, this defense mechanism of this disease involves both humoral and cellular factors and is extremely complex as the host is immune to virulent rechallenge. Vaccinations of killed Y. pestis offer some basic host protection but are relatively ineffective.

Treatment and Clinical Approaches

The identification of Y. pestis can be done by gram stains. A more definitive test is the Anti- F1 serology test which allows the differentiation between different species.

The most common treatment against Y. pestis involves the uptake of antibiotics within the first 24 hours. In more advance cases, an intravenous supply of antibiotics is preferred. The first line drugs are streptomycin, gentamicin. Critically ill patients are often given chllorampheniol.

Current Research

Yersinia Pestis was detected on set of 400 year old teeth which was then used as a sample to carry out research due to the lack of adequate infected material which prevented the direct discovery of the plague. Bodies of people who died from the plague in Europe were used and led to the observation that PCR’s including ancient DNA extracts and primers specific for the human beta-goblin gene demonstrated the absence of inhibitors. The incorporation of primers and recognized virulence-associated pla resulted in nucleotide sequences identical to that of present day isolates of the organism. Thus, using nucleic acid-base confirmation, researchers were able to confirm that the Y. pestis infection was present during early years.  Furthermore, after a recent plague surveillance in Madagascar, new variants of Y. pestis have been observed.

Works Cited.

"Black Death." Ilovebacteria. 22 Feb. 2009 <http://ilovebacteria.com/black.htm>.
"Plague." EMedicine. 21 Feb. 2009 <http://emedicine.medscape.com/article/235627overview>.
"Yersinia pestis." MedTv. 25 Oct. 2008. 21 Feb. 2008 <http://plague.emedtv.com/yersinia pestis/yersinia-pestis.html>.
"Yersinia pestis." Microbewiki. 30 July 2007. 21 Feb. 2009 <http://microbewiki.kenyon.edu/index.php/Yersinia_pestis>.

"Yersinia pestis." Wikipedia. 19 Feb. 2008. 21 Feb. 2008 <http://en.wikipedia.org/wiki/Yersinia_pestis>.

 

 

*Disclaimer - This report was written by a student participaring in a microbiology course at the Missouri University of Science and Technology. The accuracy of the contents of this report is not guaranteed and it is recommended that you seek additional sources of information to verify the contents.

 

Return to Missouri S&T Microbiology HomePage Go to DJW's HomePage