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YersiniaThe genus Yersinia is named in honor of the French bacteriologist Alexandre Yersin (1863-1943), who discovered the bacillus of bubonic plague in 1894 and prepared a serum to combat the disease. They are nutritionally fastidious, Gram-negative, non-sporeforming, rod-shaped bacteria. There are 3 pathogenic species in the genus; Y. pestis is the causative agent of plague, while Y. enterocolitica and Y. pseudotuberculosis cause Yersiniosis (gastroenteritis). The symptoms of Yersiniosis vary depending on the age of the person infected. Children are infected more
often than adults, and in young children common symptoms are fever, abdominal pain, and diarrhea, which is
often bloody. In older children and adults, right-sided abdominal pain and fever are hallmark symptoms,
resulting in misdiagnosis as appendicitis. The bacteria may also cause infections of other sites, such as
wounds, joints and the urinary tract. In rare cases complications such as skin rash, joint pains, or
septicemia can occur. Only a few strains of Y. enterocolitica cause illness in humans, and the major animal reservoir for Y. enterocolitica strains that cause human illness are pigs. To date, no foodborne outbreaks caused by Y. pseudotuberculosis have been reported in the United States, but human infections transmitted via contaminated water and foods have been reported in Japan. Yersinia pseudotuberculosis is a primary pathogen of wild and domestic animals. In humans, Y. pseudotuberculosis infections are not frequent, although outbreaks associated with consumption of water or food supplies contaminated with animal feces have been reported. Other Yersinia species lack classical virulence factors and are generally considered nonpathogenic to humans, but some have been found to possess novel virulence mechanisms, and some of them have been associated with human disease. In addition to its interest as an enteropathogen in its own right, Y. pseudotuberculosis is now known to be the immediate ancestor of Yersinia pestis, with the divergence as recent as 1.5 to 20 thousand years ago. Unlike the other pathogenic Yersiniae, and the other bacteria covered by ERIC, Yersinia pestis does not cause a gastroenteric disease. Rather, it is the causative agent of bubonic and pneumonic plague - the disease that has come to stand, in the public imagination, as the exemplar of infectious diseases. Rodents are the main reservoir of Y. pestis, but other animals and humans can also serve as hosts. It is transmitted between hosts by fleas, being contracted from the bite of an infected flea or by scratching the flea's feces present at the bite wound. Although pathogenesis in mammals does not involve the gastrointestinal system, transmission via the flea vector does involve a gastroenteric disease of sorts: in the infected flea the digestive tract is partially obstructed by masses of Y. pestis. As a consequence, the flea is effectively starving, causing it to bite more frequently and regurgitate infected material into the bite wounds. In chronically infected fleas the digestive tract is not obstructed, but Y. pestis is present in their feces. From the bite site the bacteria are carried to the regional lymph nodes where they are taken up by macrophages. The intracellular environment induces transformation of the bacteria to an encapsulated form which elaborates a number of virulence factors. The now fully virulent bacteria break out of the phagocytes and infect the lymph nodes producing the characteristic enlarged 'buboes' of bubonic plague. The bacteria are subsequently released into the bloodstream from necrotic lymph nodes, causing a stage called septicemic plague. Endotoxin release results in shock and disseminated intravascular coagulation (DIC); the mortality rate for persons with untreated bubonic plague is between 50% and 80%. However, if detected in the early stages, plague can be treated successfully with antibiotics. Infection of the lung from the bloodstream also can occur, resulting in secondary pneumonic plague. The bacteria can be transmitted via aerosol from an infected person or animal with the pneumonic form of the disease, in which case they are already fully virulent and highly contagious. Pneumonic plague progresses rapidly, and is nearly always fatal within days. Virulence factors of Y. pestis are encoded both on three plasmids and chromosomally. A small 9.6 kb plasmid (pPCP1) encodes the Pla protease, which activates plasminogen - causing blood clots at the bite wound to dissolve and allowing the initial dissemination of the bacteria to the lymph nodes. A 70 kb plasmid (pCD1; also present in Y.pseudotuberculosis, where it is called pIB1) encodes the Yop system, a type III secretion system essential for virulence. A 100 to 110 kb plasmid (pMT1 or pFra) encodes the murine toxin Ymt and the F1 capsular protein. Three distinct biovars of Y. pestis (Antiqua, Mediaevalis, and Orientalis) have been described,
and were once thought to correspond to the three historically recognized pandemics.
They are phylogenetically distinct, as shown by analysis of DNA restriction fragment polymorphisms and ribotyping.
While extensive research has been conducted on Y. pestis, Y. pseudotuberculosis, and Y. enterocolitica, the remaining 8 currently recognized Yersinia species (Y. frederiksenii, Y. intermedia, Y. kristensenii, Y. bercovieri, Y. mollaretii, Y. rohdei, Y. ruckeri, and Y. aldovae -- once collectively called "Y. enterocolitica-like" or atypical Y. enterocolitica strains) have been only moderately studied. They had previously not been clearly recognized as human pathogens, but at least some of them can on rare occasion cause enterocolitis in humans, and draft sequences are available for four strains.
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