Yersinia pestis

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Yersinia pestis
Yersinia pestis

Yersinia pestis

Systematics
Department : Proteobacteria
Class : Gammaproteobacteria
Order : Enterobacterales
Family : Enterobacteriaceae
Genre : Yersinia
Type : Yersinia pestis
Scientific name
Yersinia pestis
( Lehmann & Neumann 1896) van Loghem 1944

Yersinia pestis - also known as the plague bacterium and plague bacillus - is a gram-negative , uncultivated , sporeless , facultatively anaerobic rod- shaped bacterium . It is one of the enterobacteria and is the causative agent of pulmonary and bubonic plague .

Yersinia pestis was discovered by Alexandre Émile Jean Yersin in 1894. Since 1944, the bacterium previously assigned to the genus Pasteurella has been placed in the genus Yersinia named after Yersin .

virulence

The virulence of Yersinia pestis arises from exotoxin , endotoxin and bacterial capsule formation .

In 1980, Dan Cavanaugh and James Williams discovered that the virulence of the bacterium is temperature dependent. The body temperature of the flea is 24 ° C, that of humans 37 ° C and that of the rat 1.5 ° C higher. The temperature difference between flea and rat can increase the virulence of the bacterium during transmission by almost 50 times. This is due to the ability of the bacterium to develop protective mechanisms against phagocytosis , a component of the human immune system , at higher temperatures . At temperatures such as those prevailing in the flea's body, this protection is not built up and the bacteria are destroyed by leukocytes and monocytes . But 3 hours after entering a body at 37 ° C, the protective mechanism against leukocytes and shortly after that against the monocytes has been established.

Of the hundreds of known bacterial strains, only a few are virulent. The 40–50 strains of Yersinia pestis have a wide range of doses at which half of the test animals die ( LD 50 ), from less than 3 to 100 million in mice .

If the pathogen breaks into the bloodstream, which happens in 50–90% of untreated cases, the plague sepsis develops, i.e. it spreads into the bloodstream. Practically all organs can be affected in this way. Among other things, it comes to pneumonic plague. The danger of reproduction within humans arises from the development of various pathogenicity factors at an ambient temperature of 37 ° C, i.e. body temperature. At this temperature, Yersinia pestis forms an anti- phagocytic capsule, which is designated as fraction 1 (F1), and two other antiphagocytic antigens , the virulence antigens V and W. With regard to the virulence of the pathogen, this means that in the case of Pulmonary plague can be transmitted from person to person if there is contact with highly infectious sputum of a person suffering from pulmonary plague. In this case, primary pulmonary plague can develop within hours.

Systematics and expansion

In 1951, R. Devignat divided the plague bacteria into 3 main variants according to the strong biochemical differences: Variant 1 (later called "Orientalis") is said to have originated in India , Burma and southern China . It is said to be responsible for the pandemic of 1890 and spread over the whole world in a few years. Variant 2 (called "Antiqua"), which he considered to be the oldest, is said to have originated in Central Asia and spread across Central Africa and caused the Justinian plague in the sixth century. The third variant ("Medievalis") also comes from Central Asia, is said to have spread towards Crimea and the vicinity of the Caspian Sea and then triggered the Black Death in Europe and the subsequent epidemics . For a long time, this model was the basis for explaining the pathways of propagation. Later it turned out that both main variants "Medievalis" and "Antiqua" occurred in Kenya and "Orientalis" and "Medievalis" were found together in Turkey .

In their 1999 studies, Mark Achtmann et al. Came to the conclusion that Yersinia pestis is a mutated clone of its close relative Yersinia pseudotuberculosis , a relatively harmless bacterium that can cause stomach problems and is only extremely rarely fatal. The two species have more than 90% of the genetic material in common and, according to taxonomic rules, would be referred to as variants of the same species if they did not have to be clearly distinguished for clinical reasons. The authors said that this variant could be no more than 20,000 years old, but the more uncertain minimum age is probably 1000 years.

In 1997, a strain of plague bacteria was described that was multi-resistant to antibiotics . Since it was not found in older samples, it seems, according to the researchers' statements, to have emerged in 1995.

The first comprehensive look at around 1000 isolates of Y. pestis supported by genome analysis was obtained by Morelli and others in 2010 in a study that showed that the oldest pathogenic strains must have originated in China or Russia. Further connections were found in the expansion of the tribes with trade over the Silk Road , the expeditions of Zheng He and the third pandemic of 1894.

Finally, in 2011, Bos, Schuenemann and others had the opportunity to study the genome of plague bacteria that could be isolated from the teeth of medieval London corpses. A comparison with other known tribes showed that they were tribes that must be most closely related to the oldest tribes from China. This means, for example, that the medieval epidemic actually originated in Asia. Surprisingly, it also means that if there really were earlier plague epidemics, their strains became extinct, since all of the strains known today are descendants of the medieval variant.

Mutations

In Yersinia there are probably 2 plasmids that are characteristic of pestis and make it dangerous. It has already been assumed that a sudden and comprehensive change in virulence may have been a background factor in the fact that a plague epidemic suddenly broke out and then disappeared again across the centuries. In viruses and bacteria in particular, an instability of the genetic material can be observed, which leads to many mutations . In the meantime, the entire genome of Yersinia pestis has been deciphered and mapped . The researchers found that the bacterium has genetic characteristics that indicate frequent “intragenomic recombinations ”, ie that it can take up genes from other pathogenic organisms to a large extent. They said the plague bacteria had characteristics that indicated constant change. A year later, another research group deciphered a different bacterial strain and confirmed this assessment. Annie Guiyoule and Bruno Rasoamanana examined the areas in Madagascar with particularly high plague activity in recent decades. They isolated 187 different strains from 1926 to 1996.

lifespan

At moderate temperatures, Yersinia pestis survives on the mouthparts of fleas for around 3 hours. As early as 1944 it was established that plague bacteria can survive outside a host animal and be virulent in saline solution and a temperature of around 25 ° C for up to 2 weeks, at 2–4 ° C even up to two years. Experiments in the first half of the 20th century also showed that sunlight kills bacteria quickly, but that the lifespan depends heavily on the environment of the bacteria, especially on their support. In a thin lye on glass, the bacteria die within 1 hour, with a thick layer of bacteria the life span quadrupled and on fabric made of hemp they lived up to 14 hours. While temperatures at 55 ° C are deadly, low temperatures do them no harm. In Manchuria , virulent bacteria have even been found in frozen plague corpses. The bacteria were also able to survive for almost a month in grain dust that was contaminated with infectious excretions. Plague bacteria can infect people at room temperature and normal humidity for a period of more than 5 days.

transmission

Fleas , especially the rat flea Xenopsylla cheopis, can transmit the plague pathogen. But Nosopsyllus fasciatus and the human flea Pulex irritans are also discussed, since Xenopsylla cheopis is dependent on tropical temperatures and cannot survive in Europe. Fleas are blood-sucking parasites that can infect their host directly with Yersinia pestis . If the rat flea changes from an infected rodent - for example the brown rat or the house rat - after its death to another host, such as pets or humans, it is able to infect them with the plague bacterium. The plague can be just as deadly for humans as it is for rats.

Symptoms of illness

A local infection occurs at the site of the bite , which is characterized by the formation of a pustule and which leads to what is known as bubonic plague.

The septic (blood-poisoning) form does not always develop a plague bump. The patient dies quickly without any particular external symptoms, but with a high concentration of bacteria in the blood. When these plague bacteria attack the lungs, this form is known as "secondary pulmonary plague", which is the most dangerous form with the fastest course. In addition to a high fever, bloody sputum is one of the few external symptoms.

The blood-poisoning effect is triggered when the bacteria complete their normal life cycle and die. Large amounts of toxic secretions are released directly into the bloodstream; The kidneys and liver can become necrotic trying to clear toxins from the system . In the end, the victim succumbs to a toxic shock .

Reporting requirement

In Germany, direct or indirect evidence of Yersinia pestis must be reported by name in accordance with Section 7 of the Infection Protection Act (IfSG) if the evidence indicates an acute infection. This reporting obligation for the pathogen primarily concerns the lines of laboratories ( § 8 IfSG).

In Switzerland, the positive and negative laboratory analysis findings to be Yersinia pestis laboratory reportable namely after the Epidemics Act (EpG) in connection with the epidemic Regulation and Annex 3 of the Regulation of EDI on the reporting of observations of communicable diseases of man .

literature

  • Kirsten I. Bos u. a .: A draft genome of Yersinia pestis from victims of the Black Death . In: Nature . tape 478 , no. 7370 , 2011, pp. 506-510 , doi : 10.1038 / nature10549 .
  • Herbert Hof, Rüdiger Dörries: Medical microbiology . With the collaboration of Gernot Geginat (=  dual series ). 4th edition. Thieme, Stuttgart 2009, ISBN 978-3-13-125314-9 .
  • A. Rakin: Yersinia pestis - A Threat to Humanity . In: Bundesgesundheitsbl - Health Research - Health Protection . tape 46 , no. 11 , 2003, p. 949-955 , doi : 10.1007 / s00103-003-0713-3 .
  • Verena J. Schuenemann u. a .: Targeted enrichment of ancient pathogens yielding the pPCP1 plasmid of Yersinia pestis from victims of the Black Death . In: Proceedings of the National Academy of Sciences . tape 108 , no. 38 , 2011, p. E746-E752 , doi : 10.1073 / pnas.1105107108 .

Web links

Commons : Yersinia pestis  - album with pictures, videos and audio files

Individual evidence

  1. ↑ JJ van Loghem: The classification of the plague-bacillus. In: Antonie van Leeuwenhoek. Volume 10, 1944, pp. 15-16.
  2. ^ Dan C. Cavanaugh, James E. Williams: Plague: Some Ecological Interrelationships. In: R. Traub, H. Starcke (eds.) Fleas, Proceedings of the International Conference on Fleas . Ashton Wold, Peterborough, UK, June 21-25, 1977. Rotterdam 1980, pp. 245-256, 251.
  3. ^ RD Perry, JD Fetherston: Yersinia pestis — etiologic agent of plague . In: Clinical Microbiology Reviews . tape 10 , no. 1 , January 1, 1997, p. 35–66, here 35–66, 41 .
  4. ↑ R. Devignat: Variétés de l'espèce Pasteurella pestis . In: Bulletin of the World Health Organization . tape 4 , no. 2 , 1951, p. 247-263 , PMC 2554099 (free full text).
  5. ↑ A. Guiyoule, F. Grimont, I. Iteman, PA Grimont, M. Lefèvre, E. Carniel: Plague pandemics investigated by ribotyping of Yersinia pestis strains. In: Journal of Clinical Microbiology . tape 32 , no. 3 , January 3, 1994, pp. 634-641 .
  6. ↑ Mark Achtman, Kerstin Zurth, Giovanna Morelli, Gabriela Torrea, Annie Guiyoule, Elisabeth Carniel: Yersinia pestis, the cause of plague, is a recently emerged clone of Yersinia pseudotuberculosis . In: Proceedings of the National Academy of Sciences . tape 96 , no. 24 , November 23, 1999, pp. 14043-14048 , doi : 10.1073 / pnas.96.24.14043 .
  7. ↑ March Galimand, Annie Guiyoule u. a .: Multidrug Resistance in Yersinia pestis Mediated by a Transferable Plasmid. In: The New England Journal of Medicine . 327, No. 10, 1997, pp. 677-680.
  8. ^ G. Morelli, Y. Song et al. a .: Yersinia pestis genome sequencing identifies patterns of global phylogenetic diversity. In: Nature genetics . Volume 42, Number 12, December 2010, pp. 1140-1143. doi: 10.1038 / ng.705 . PMID 21037571 . PMC 2999892 (free full text).
  9. ↑ Kirsten I. Bos, Verena J. Schuenemann a. a .: A draft genome of Yersinia pestis from victims of the Black Death. In: Nature. Volume 478, 2011, pp. 506-510, doi: 10.1038 / nature10549 .
  10. ^ RD Perry, JD Fetherston: Yersinia pestis — etiologic agent of plague . In: Clinical Microbiology Reviews . tape 10 , no. 1 , January 1, 1997, p. 35–66, here 38–40 .
  11. ↑ a b J. Parkhill, BW Wren and 33 other researchers: Genome sequence of Yersinia pestis, the causative agent of plague . In: Nature . tape 413 , no. 6855 , October 4, 2001, p. 523-527 , doi : 10.1038 / 35097083 .
  12. ↑ Wen Deng et al: Genome Sequence of Yersinia pestis KIM . In: Journal of Bacteriology . tape 184 , no. 16 , August 15, 2002, p. 4601-4611 , doi : 10.1128 / JB.184.16.4601-4611.2002 .
  13. ↑ A. Guiyoule, B. Rasoamanana, C. Buchrieser, P. Michel, S. Chanteau, E. Carniel: Recent emergence of new variants of Yersinia pestis in Madagascar. In: Journal of Clinical Microbiology . tape 35 , no. 11 , January 11, 1997, p. 2826-2833 .
  14. ↑ VA Bibikova: Contemporary Views on the Inter Relationships Between Fleas and the pathogen of Human and Animal Diseases . In: Annual Review of Entomology . tape 22 , no. 1 , 1977, pp. 23-32 , doi : 10.1146 / annurev.en.22.010177.000323 .
  15. ↑ Georges Girard: Hémoculture et bactérémie dans l'infection pesteuese. In: Bulletin of the Exotic Pathology Society. 37, 228.
  16. ^ Robert Pollitzer: Plague . WHO, Geneva 1954, pp. 104-105.
  17. ^ Robert Pollitzer, Karl F. Meyer: The Ecology of Plague. In: Jaques M. May (Ed.): Studies in Disease Ecology. (= Studies in Medical Geography, Vol. 2), New York 1961, pp. 433-590.
  18. ↑ Laura J. Rose, Rodney Donlan, Shailen N. Banerjee, Matthew J. Arduino: Survival of Yersinia pestis on Environmental Surfaces . In: Applied and Environmental Microbiology . tape 69 , no. 4 , January 4, 2003, p. 2166–2171 , doi : 10.1128 / AEM.69.4.2166-2171.2003 .