Everything about Yersinia Pestis totally explained
Yersinia pestis (
Pasteurella pestis) is a
Gram-negative bacillus bacterium belonging to the family
Enterobacteriaceae. It is a
facultative anaerobic bipolar-staining cell (giving it a
safety pin appearance).
Human
Y. pestis infection have three main forms, the well-known is
bubonic,
pneumonic, and
septicemic plague. All three forms have been responsible for high mortality rates in
epidemics throughout human history, including the
Black Death that accounted for the death of approximately one-third of the
European population in
1347 to
1353. The
genus Yersinia is
Gram-negative, bipolar staining
coccobacilli, and, similarly to other
Enterobacteriaceae. The closest relative is the gastrointestinal pathogen
Yersinia pseudotuberculosis, and more distantly
Yersinia enterocolitica.
Recently
Yersinia pestis has gained attention as a possible biological warfare agent and the CDC as classified
Y. pestis as
category A pathogen requiring preparation for a possible terrorist attack.
Discovery
Y. pestis was discovered in
1894 by a
Swiss/
French physician and
bacteriologist from the
Pasteur Institute,
Alexandre Yersin, during an
epidemic of plague in
Hong Kong. Yersin was a member of the
Pasteur school of thought.
Shibasaburo Kitasato, a
German-trained
Japanese bacteriologist who practiced
Koch's methodology was also engaged at the time in finding the causative agent of plague. However, it was Yersin who actually linked plague with
Yersinia pestis. Originally named
Pasteurella pestis, the organism was renamed in 1967.
Three
biovars of
Y. pestis are known, each thought to correspond to one of the
historical pandemics of bubonic plague. Biovar
Antiqua is thought to correspond to the
Plague of Justinian; it isn't known whether this biovar also corresponds to
earlier, smaller epidemics of bubonic plague, or whether these were even truly bubonic plague. Biovar
Medievalis is thought to correspond to the
Black Death. Biovar
Orientalis is thought to correspond to the
Third Pandemic and the majority of modern outbreaks of plague.
Y. pestis was carried on rats' fleas.
General characteristics
Y. pestis is similar to other
Yersinia members test negative for the
urease,
lactose-fermentation, and
indole tests.
Genome
The complete
genomic sequence is available for two of the three sub-species of
Y. pestis: strain KIM (of biovar Medievalis), and strain CO92 (of biovar Orientalis, obtained from a clinical isolate in the United States); as of
2006, the genomic sequence of a strain of biovar Antiqua has been recently completed. Similar to the other pathogenic strains, there are signs of the loss of function as adaptive lost. The
chromosome of strain KIM is 4,600,755 base pairs long; the chromosome of strain CO92 is 4,653,728 base pairs long. Like its cousins
Y. pseudotuberculosis and
Y. enterocolitica,
Y. pestis is host to the
plasmid pCD1. In addition, it also hosts two other plasmids, pPCP1 and pMT1 which are not carried by the other
Yersinia species. Together, these plasmids, and a
pathogenicity island called HPI, encode several proteins which cause the pathogenesis for which
Y. pestis is famous. Among other things, these
virulence factors are required for bacterial adhesion and injection of proteins into the host cell, invasion of bacteria into the host cell, and acquisition and binding of iron harvested from red blood cells.
Y. pestis is thought to be descendant from
Y. pseudotuberculosis, differing only in the presence of specific virulence plasmids.
A recent comprehensive and comparative
proteomics analysis of
Y. pestis: strain KIM was recently performed, this analysis focused on the transition to a growth condition mimicking growth in host cells.
Pathogenics and immunity
In reservoir host
The reservoir commonly associated with
Y. pestis are several species of rodents. In the
steppes the
reservoir species are principally believed to be
marmots. While in the United States, several species of
rodents are thought maintain
Y. pestis. However, the case isn't very clear because the expected disease dynamics have not been found in any rodent species. It is known that some individuals in a rodent population will have a different resistance, which could lead to a carrier status. There is some evidence that fleas from other mammals have a role in human plague outbreaks.
This lack of knowledge of the dynamics of plague in mammal species is also true among susceptible rodents such as the black-tailed prairie dog (
Cynomys ludovicianus), in which plague can cause colony collapse resulting a massive effect on prairie food webs. However, the transmission dynamics within prairie dogs doesn't follow the dynamics of blocked fleas; this study's authors believe that carcasses, unblocked fleas, or another vector might be important.
In other regions of the world the reservoir of the infection isn't clearly identified, which complicates prevention and early warning programs. One such is example was the 2003 outbreak in Algeria.
In vector
The transmission of
Y. pestis by
fleas is well characterized. Initial acquisition of
Y. pestis by the vector occurs during feeding on an infected animal. Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage (Hms) system and
Yersinia murine toxin (Ymt).
Although Ymt is highly toxic to rodents and was once thought to be produced to insure reinfection of new hosts, it has been demonstrated that murine toxin is important for the survival of
Y. pestis in fleas.
The Hms system plays an important role in the transmission of
Y. pestis back to a mammalian host. The proteins encoded by Hms genetic loci aggregate in the esophagus and proventriculus of the flea, which is a structure that ruptures blood cells. Aggregation of Hms proteins inhibits feeding and causes the flea to feel hungry. Transmission of
Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges bacteria growing there and is regurgitated back into the host circulatory system.
In humans and other susceptible hosts
Pathogenesis of Y. pestis in mammalian host is due to several factors, which predominately focus on the initial immune response. Flea bite allow for the bacteria through the skin,
Y. pestis also expresses the yadBC gene, which is similar to Invasin in other Yersinia species, allowing for adherence and invasion of epithelium. There are reports that isolates from the pneumatic plague patients have a plasminogen activator, which can remove clots in order for systematic invasion. The majority of the
Y. pestis 's virulence factors are anti-phagocytic in nature. Two important anti-phagocytic
antigens, named F1 (Fraction 1) and V, both important for
virulence.
Additionally the
Type III secretion system injects into macrophage and other immune cells six different effectors collective call YOP(Yersinia Outercoat Proteins) YopO, YopH, YopM, YopT, YopJ, and YopE. These proteins are injected via a long syringe into a pore created in part by YopB and YopD. The next of the effects of these proteins to the limit phagocytosis by targeting [actin] and other cell singling pathway important in the innate immune system
Immunity
A
formalin-inactivated
vaccine once was available for adults at high risk of contracting the plague until removal from the market by the
FDA. It was of limited effectiveness and may cause severe
inflammation. Experiments with
genetic engineering of a vaccine based on F1 and V antigens are underway and show promise; however, bacteria lacking antigen F1 are still virulent, and the V antigens are sufficiently variable, that vaccines composed of these antigens may not be fully protective.
Clinical aspects
Symptoms and disease progression
- Bubonic plague
- Incubation period of 2-6 days, when the bacteria is actively replicating in lymph nodes
- Universally a general lack of energy
- Fever
- Headache and chills occur suddenly at the end of the incubation period. From this point the infection is resolved or lethal.
- Swelling of lymph nodes resulting of buboes, this is the classic sign of bubonic plague
Septicemic plague
Pneumonic plague
- Fever
- Chills
- Cough
- Chest pain
- Dyspnea
- Hemoptysis
- Lethargy
- Hypotension
- Shock
- Symptoms of bubonic or septicemic plague, not always present
From "Harrison's Principles of Internal Medicine 16th Edition"
If this occurs with the classic buboes, this is considered primary, while in secondary occurs after symptoms of bubonic or pneumonic infection. With the bacteria located in the blood, several organs can be affected including the spleen, and brain. With the delocalized infection, an immunologic cascade occurs, this can be seen by the occurrence of DIC, which in turn results in bleeding and narcotized skin and tissue. These widespread infections increase mortality to 22%.
Finally, Pneumonic plague can be from direct aerosol infection in which it's considered primary. While Bubonic, and to a lesser degree, Septicemic plague can gain pneumatic characteristic. As with the other forms of plague after the incubation period of a few hours to days there's sudden onset coughing, elevated temperature, and lack of energy. From this point the infection increases in severity in pneumonia. Due to the high replication rates, death with treated plague is roughly 50%, and almost universally fatal without treatment.
The initial symptoms of plague is very similar to other bacterial diseases, as well as some viral. image (http://www.cdc.gov/ncidod/dvbid/plague/p1.htm) with the exception of the buboes. make diagnosis difficult.
This is the ICD-9 codes for the diseases caused by Y. pestis
020.0 Bubonic plague
020.2 Septicemic plague
020.5 Unspecified pneumonic plague
020.3 Primary pneumonic plague
020.4 Secondary pneumonic plague
Clinical determination
Grams stains can confirm the presence of gram negative rods, and in some cases the identification of the double curved shape. More definitive test is a Anti-F1 serology test, which can differentiate between different species of Yersinia.
Treatment
The traditional first line treatment for Y. pestis has been streptomycin, chloramphenicol, tetracycline, and fluoroquinolones. There is also good evidence to support the use of doxycycline or gentamicin.
It should be noted that strains resistant to one or two agents specified above have been isolated: treatment should be guided by antibiotic sensitivities where available. Antibiotic treatment alone is insufficient for some patients, who may also require circulatory, ventilator, or renal support.
In an emergency department setting, Harrison's principles of internal medicine outlines the following treatment course. Antibiotics within the first 24 hours is very beneficial, with intravenous being preferred in pulmonary or advance cases. streptomycin or gentamicin as the first-line drugs, with chloramphenicol for critical ill patients, or rarely for suspected neuro-involvement.
Historical impact
The role of Y. pestis in the Black Death is debated among historians; some have suggested that the Black Death spread far too rapidly to be caused by Y. pestis. DNA from Y. pestis is alleged to have been found in the teeth of an individual who supposedly died from the Black Death, however, and medieval corpses who died from other causes did test positive for Y. pestis. This suggests that Y. pestis was, at the very least, a contributing factor in some (though possibly not all) of the European plagues. It is possible that the selective pressures induced by the plague might have changed how the pathogen manifests in humans, selecting against the individuals or populations which were the most susceptible.
Further Information
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