The cause of plague:
a- Y.enterocolitica.
b- Yersinia pestis***
c- Mycobacterium tuberculosis.
d- Non of the above.
---------------------------
The Yersinia pestis enterobacterium is a facultative anaerobic Gram negative bacillus and primary pathogen, of the genus Yersinia, which produces in the human lung plague, bubonic plague and also septicemic plague, although the latter is very rare.
Etymology:
Originally, this microorganism was called Bacterium pestis until 1900, Bacillus pestis until 1923, Pasteurella pestis, until in 1970 it was named Yersinia pestis in honor of Alexandre Yersin, Franco-Swiss bacteriologist of the Pasteur Institute, co-discoverer of the bacterium in 1894 together to Kitasato Shibasaburō, both independently.
History:
Yersinia pestis is an infectious agent that has been directly responsible for more human deaths than any other infectious disease, except malaria. It has originated various pandemics throughout history, among which the following stand out: the plague of Justinian (541-542 AD), which devastated Asia, North Africa, Arabia and part of Europe; the black plague (1347-1351 AD), which ended the life of a third of the population of Europe; and the Third Pandemic (1855-1918), which began in China and India and ended up spreading throughout the rest of Asia, Africa and America.
When the plague epidemic affected Hong Kong in 1894, the Japanese government and the German Koch Institute sent a scientific mission that included the Japanese doctor and bacteriologist Kitasato Shibasaburō. About the same time, the French-Swiss doctor and bacteriologist Alexandre Yersin was sent by the French government and the Pasteur Institute on a similar mission. Both arrived in Hong Kong in June 1894. Soon the two discovered a new type of bacteria in samples of patients with plague and in the organs of dead rats in the plague area.
Kitasato Shibasaburō was the first to publish, before Yersin, a first description of a crop of Yersinia pestis in a preliminary communication in the medical journal The Lancet. A few days later Yersin published his article where he described more fully than Shibasaburō the same bacteria in Annales de l'Institut Pasteur, and shortly after Shibasaburō published the rest of his findings.
The role of Y. pestis in the black plague has been debated among historians; Some have suggested that the black plague spread very quickly to have been caused by Y. pestis. DNA of Y. pestis has been found in the teeth of those who died of black plague, however, medieval corpses that died of other causes did not test positive for Y. pestis. This suggests that it was a contributing factor to European pests, but probably not the only one. It is possible that the selective pressures induced by the pest may have changed the way in which the pathogen manifests itself in humans, being selected against individuals or populations that were more susceptible.
Microbiology:
The genus Yersinia belongs to the Gamma-proteobacterial bacteria in the enterobacterial order, so it is an optional anaerobic gram-negative with fermentative metabolism, it is positive nitrate reductase, positive catalase and negative oxidase. His IMViC tests are positive for methyl red and Voges Proskauer. It is a bipolar staining cocobacillus similar to other Enterobacteria. Its most antigenic virulence factors such as Ag F1, Ag V and Ag W are expressed at 37 ° C. It also has a toxin that acts on the myocardium and liver cells. During the infectious process it generates antifagocytic viscosity. The organism exhibits motility when it is isolated, but loses this capacity while remaining in the host mammal. It has the ability to prevent phagocytosis, this ability is measured by the type III secretion system. When the bacteria is in contact with phagocytic cells, it produces certain proteins that will prevent phagocytosis, this is a product of the Yop-H Gene, induces cytotoxicity, a product of the Yop E Gene, and produces apoptosis, a product of the Yop J-P gene.
The genome of two of the subspecies has been sequenced: Y. pestis medievalis with 4,600,755 base pairs and Y. pestis orientalis with 4,653,728 base pairs.
a- Y.enterocolitica.
b- Yersinia pestis***
c- Mycobacterium tuberculosis.
d- Non of the above.
---------------------------
The Yersinia pestis enterobacterium is a facultative anaerobic Gram negative bacillus and primary pathogen, of the genus Yersinia, which produces in the human lung plague, bubonic plague and also septicemic plague, although the latter is very rare.
Etymology:
Originally, this microorganism was called Bacterium pestis until 1900, Bacillus pestis until 1923, Pasteurella pestis, until in 1970 it was named Yersinia pestis in honor of Alexandre Yersin, Franco-Swiss bacteriologist of the Pasteur Institute, co-discoverer of the bacterium in 1894 together to Kitasato Shibasaburō, both independently.
History:
Yersinia pestis is an infectious agent that has been directly responsible for more human deaths than any other infectious disease, except malaria. It has originated various pandemics throughout history, among which the following stand out: the plague of Justinian (541-542 AD), which devastated Asia, North Africa, Arabia and part of Europe; the black plague (1347-1351 AD), which ended the life of a third of the population of Europe; and the Third Pandemic (1855-1918), which began in China and India and ended up spreading throughout the rest of Asia, Africa and America.
When the plague epidemic affected Hong Kong in 1894, the Japanese government and the German Koch Institute sent a scientific mission that included the Japanese doctor and bacteriologist Kitasato Shibasaburō. About the same time, the French-Swiss doctor and bacteriologist Alexandre Yersin was sent by the French government and the Pasteur Institute on a similar mission. Both arrived in Hong Kong in June 1894. Soon the two discovered a new type of bacteria in samples of patients with plague and in the organs of dead rats in the plague area.
Kitasato Shibasaburō was the first to publish, before Yersin, a first description of a crop of Yersinia pestis in a preliminary communication in the medical journal The Lancet. A few days later Yersin published his article where he described more fully than Shibasaburō the same bacteria in Annales de l'Institut Pasteur, and shortly after Shibasaburō published the rest of his findings.
The role of Y. pestis in the black plague has been debated among historians; Some have suggested that the black plague spread very quickly to have been caused by Y. pestis. DNA of Y. pestis has been found in the teeth of those who died of black plague, however, medieval corpses that died of other causes did not test positive for Y. pestis. This suggests that it was a contributing factor to European pests, but probably not the only one. It is possible that the selective pressures induced by the pest may have changed the way in which the pathogen manifests itself in humans, being selected against individuals or populations that were more susceptible.
Microbiology:
The genus Yersinia belongs to the Gamma-proteobacterial bacteria in the enterobacterial order, so it is an optional anaerobic gram-negative with fermentative metabolism, it is positive nitrate reductase, positive catalase and negative oxidase. His IMViC tests are positive for methyl red and Voges Proskauer. It is a bipolar staining cocobacillus similar to other Enterobacteria. Its most antigenic virulence factors such as Ag F1, Ag V and Ag W are expressed at 37 ° C. It also has a toxin that acts on the myocardium and liver cells. During the infectious process it generates antifagocytic viscosity. The organism exhibits motility when it is isolated, but loses this capacity while remaining in the host mammal. It has the ability to prevent phagocytosis, this ability is measured by the type III secretion system. When the bacteria is in contact with phagocytic cells, it produces certain proteins that will prevent phagocytosis, this is a product of the Yop-H Gene, induces cytotoxicity, a product of the Yop E Gene, and produces apoptosis, a product of the Yop J-P gene.
The genome of two of the subspecies has been sequenced: Y. pestis medievalis with 4,600,755 base pairs and Y. pestis orientalis with 4,653,728 base pairs.
Transmission and infection:
Plague is a natural disease of rodents, with rats being the main reservoir of the disease. After being infected, most rats die, but a small percentage survive, remaining as a source of Y. pestis.
Rats are infected through a vector, which in this case is the rat flea (Xenopsylla cheopis). The flea sucks the blood of an infected animal and ingests Yersinia pestis bacteria, which multiply in the flea's intestine and will be transmitted to another rat in the next flea bite.
The disease will spread so that mortality among rats becomes so high that the flea is looking for new hosts, among which is man.
On May 1, 2015, the first case of Yersinia pestis infection in Atlanta (USA) from a dog to a human was reported.
Pathogeny:
Y. pestis cells produce certain antigenic molecules that contribute more or less to the disease process.
- In the bacterial wall are protein-lipoprotein complexes, called VW and F1 antigens, whose function is to prevent phagocytosis by macrophages and other phagocytic cells.
- Virulent strains of Y. pestis produce and secrete an exotoxin called murine toxin (due to its extreme toxicity to the mouse), whose mode of action is based on inhibiting cellular respiration, blocking electron transport reactions in mitochondria, at the level of coenzyme Q. Although it is not clear that the murine toxin is involved in the pathogenesis of human plague, the symptoms it produces in the mouse are similar to those produced in humans.
- Y. pestis also produces a highly immunogenic endotoxin that can lead to a potent immune response in humans.
Clinical pictures:
Bubonic Plague:
It is the most common type of infection. Once the bacteria have been introduced by biting a flea into a human being, In a short time, peripheral lymph nodes are invaded by secondary buboes, until they break and the cells pass back into the bloodstream, but now in a much higher number, which causes a generalized sepsis.
In this state, multiple hemorrhages occur that lead to black spots on the skin, gangrene processes at the distal extremities of the extremities, severe pain in lymph nodes, prostration, shock and delirium. If the plague is not treated before the septicemic state, death occurs after 3-5 days.
Pneumonic plague:
This type of infection occurs when Y. pestis cells are directly inhaled, or they reach the lungs during bubonic plague. The infection usually passes without symptoms until the last two days of the infectious process, in which large numbers of sputum are emitted with blood. In the absence of treatment death occurs in 2-3 days.
Septicemic plague:
This infection involves a rapid dispersion of Y. pestis throughout the body, through the bloodstream, with no time for buboes to form. Death usually occurs in one day, so it usually does not give time to be diagnosed until autopsy.
Diagnosis:
Blood samples are collected, sputum (in the case of pneumonic plague) or nodal aspirate (in the case of bubonic plague). Direct immunofluorescence (IFD) techniques are used and cultures are performed in a blood-agar medium at 28 ° C and blood culture.
Treatment:
Y. pestis has natural resistance to penicillin, but most strains are sensitive to streptomycin, chloramphenicol and tetracyclines. There is currently some evidence of the sensitivity of Y. pestis to gentamicin and doxycycline.
If treatment is started quickly, the mortality of bubonic plague can be reduced to 1-5% of those infected. Pneumonic and septicemic plague can also be treated, but they usually progress so quickly that antibiotics are always late.
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