Yersinia pestis

Yersinia pestis (formerly Pasteurella pestis) is a gram-negative,

non-motile, rod-shaped, coccobacillus bacterium, with no spores. Yersinia pestis
It is a facultative anaerobic organism that can infect humans via
the Oriental rat flea (Xenopsylla cheopis).[1] It causes the disease
plague, which takes three main forms: pneumonic, septicemic, and
bubonic.[1][2]

All three forms have been responsible for high-mortality

epidemics throughout human history, including the Plague of
Justinian in the sixth century; the Black Death, which accounted
for the death of at least one-third of the European population
between 1347 and 1353; and the Third Pandemic, sometimes A scanning electron micrograph
referred to as the Modern Plague, which began in the late 19th depicting a mass of Yersinia pestis
century in China and spread by rats on steamships, claiming close
bacteria in the foregut of an infected
to 10 million lives.[3][4][5][6]
flea
Those plagues may have originated in Central Asia or China and Scientific classification
were transmitted west via trade routes.[7][6][8] However, research
in 2018 found evidence of the pathogen in an ancient Swedish Domain: Bacteria
tomb, which may have been the cause of what has been described Phylum: Proteobacteria
as the Neolithic decline around 3000 BC, in which European
populations declined significantly.[9] This would suggest that Y. Class: Gammaproteobacteria
pestis may have originated in Europe in the Cucuteni–Trypillia Order: Enterobacterales
culture instead of Asia.[10]
Family: Yersiniaceae
Y. pestis was discovered in 1894 by Alexandre Yersin, a
Genus: Yersinia
Swiss/French physician and bacteriologist from the Pasteur
Institute, during an epidemic of the plague in Hong Kong.[11] Species: Y. pestis
Yersin was a member of the Pasteur school of thought. Kitasato
Binomial name
Shibasaburō, a German-trained Japanese bacteriologist who
practised Koch's methodology, was also engaged at the time in Yersinia pestis
finding the causative agent of the plague.[12] However, Yersin (Lehmann & Neumann, 1896)
actually linked plague with Y. pestis. Formerly named Pasteurella
van Loghem, 1944
pestis, the organism was renamed Yersinia pestis in 1944.
Synonyms
Every year, thousands of cases of the plague are still reported to
the World Health Organization, although with proper treatment,
Bacillus
the prognosis for victims is now much better. A five- to six-fold
increase in cases occurred in Asia during the time of the Vietnam
Bacille de la peste
War, possibly due to the disruption of ecosystems and closer
proximity between people and animals. The plague is now Yersin, 1894
commonly found in sub-Saharan Africa and Madagascar, areas Bacterium pestis
that now account for over 95% of reported cases. The plague also
Lehmann & Neumann, 1896
has a detrimental effect on nonhuman mammals.[13] In the United
States, mammals such as the black-tailed prairie dog and the Pasteurella pestis
endangered black-footed ferret are under threat. (Lehmann & Neumann, 1896) The
 Netherlands, 1920

Contents
General characteristics
Genome
Small noncoding RNA
Pathogenesis and immunity
In reservoir hosts
Vector
In humans and other susceptible hosts
Immunity
Isolation and identification
Ancient DNA evidence
Recent events
References
External links

General characteristics
Y. pestis is a nonmotile, stick-shaped, facultative anaerobic bacterium with bipolar staining (giving it a safety
pin appearance) that produces an antiphagocytic slime layer.[14] Similar to other Yersinia species, it tests
negative for urease, lactose fermentation, and indole.[15] Its closest relative is the gastrointestinal pathogen
Yersinia pseudotuberculosis, and more distantly Yersinia enterocolitica.

Genome

A complete genomic sequence is available for two of the three subspecies of Y. pestis: strain KIM (of biovar
Y. p. medievalis),[16] and strain CO92 (of biovar Y. p. orientalis, obtained from a clinical isolate in the
United States).[17] As of 2006, the genomic sequence of a strain of biovar Antiqua has been recently
completed.[18] Similar to the other pathogenic strains, signs exist of loss of function mutations. 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 Y. pseudotuberculosis and Y. enterocolitica, Y. pestis is host to the plasmid pCD1. It also
hosts two other plasmids, pPCP1 (also called pPla or pPst) and pMT1 (also called pFra) that are not carried
by the other Yersinia species. pFra codes for a phospholipase D that is important for the ability of Y. pestis to
be transmitted by fleas.[19] pPla codes for a protease, Pla, that activates plasmin in human hosts and is a very
important virulence factor for pneumonic plague.[20] Together, these plasmids, and a pathogenicity island
called HPI, encode several proteins that 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 in the host cell (via a type-III secretion system), and acquisition and binding of iron
harvested from red blood cells (by siderophores). Y. pestis is thought to be descended from Y.
pseudotuberculosis, differing only in the presence of specific virulence plasmids.

A comprehensive and comparative proteomics analysis of Y. pestis strain KIM was performed in 2006.[21]
The analysis focused on the transition to a growth condition mimicking growth in host cells.
Small noncoding RNA

Numerous bacterial small noncoding RNAs have been identified to play regulatory functions. Some can
regulate the virulence genes. Some 63 novel putative sRNAs were identified through deep sequencing of the
Y. pestis sRNA-ome. Among them was Yersinia-specific (also present in Y. pseudotuberculosis and Y.
enterocolitica) Ysr141 (Yersinia small RNA 141). Ysr141 sRNA was shown to regulate the synthesis of the
type III secretion system (T3SS) effector protein YopJ.[22] The Yop-Ysc T3SS is a critical component of
virulence for Yersinia species.[23] Many novel sRNAs were identified from Y. pestis grown in vitro and in
the infected lungs of mice suggesting they play role in bacterial physiology or pathogenesis. Among them
sR035 predicted to pair with SD region and transcription initiation site of a thermo-sensitive regulator
ymoA, and sR084 predicted to pair with fur, ferric uptake regulator.[24]

Pathogenesis and immunity

In the urban and sylvatic (forest) cycles of Y. pestis, most of the
spreading occurs between rodents and fleas. In the sylvatic cycle, the
rodent is wild, but in the urban cycle, the rodent is primarily the
brown rat (Rattus norvegicus). In addition, Y. pestis can spread from
the urban environment and back. Transmission to humans is usually
through the bite of infected fleas. If the disease has progressed to the
pneumonic form, humans can spread the bacterium to others by
coughing, vomiting, and possibly sneezing.

Oriental rat flea (Xenopsylla

In reservoir hosts cheopis) infected with the Y. pestis
bacterium, which appears as a dark
Several species of rodents serve as the main reservoir for Y. pestis in mass in the gut: The foregut
the environment. In the steppes, the natural reservoir is believed to (proventriculus) of this flea is
be principally the marmot. In the western United States, several blocked by a Y. pestis biofilm; when
species of rodents are thought to maintain Y. pestis. However, the the flea attempts to feed on an
expected disease dynamics have not been found in any rodent. uninfected host, Y. pestis is
Several species of rodents are known to have a variable resistance, regurgitated into the wound, causing
infection.
which could lead to an asymptomatic carrier status.[25] Evidence
indicates fleas from other mammals have a role in human plague
outbreaks.[26]

The 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 in a massive effect on prairie food webs.[27] However, the transmission dynamics within prairie
dogs do not follow the dynamics of blocked fleas; carcasses, unblocked fleas, or another vector could
possibly be important, instead.[28]

In other regions of the world, the reservoir of the infection is not clearly identified, which complicates
prevention and early-warning programs. One such example was seen in a 2003 outbreak in Algeria.[29]

Vector

The transmission of Y. pestis by fleas is well characterized.[30] 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 system and Yersinia murine toxin (Ymt).
Although Ymt is highly toxic to rodents and was once thought to be produced to ensure reinfection of new
hosts, it is important for the survival of Y. pestis in fleas.[19]

The hemin storage system plays an important role in the transmission of Y. pestis back to a mammalian
host.[31] While in the insect vector, proteins encoded by hemin storage system genetic loci induce biofilm
formation in the proventriculus, a valve connecting the midgut to the esophagus.[32] Aggregation in the
biofilm inhibits feeding, as a mass of clotted blood and bacteria forms (referred to as "Bacot's block" after
entomologist A.W. Bacot, the first to describe this phenomenon).[33] 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 lodged in the proventriculus, which is regurgitated back into the host circulatory system.[33]

In humans and other susceptible hosts

Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors, including an ability of
these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody
production. Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses a plasmin activator
that is an important virulence factor for pneumonic plague and that might degrade on blood clots to facilitate
systematic invasion.[20] Many of the bacteria's virulence factors are antiphagocytic in nature. Two important
antiphagocytic antigens, named F1 (fraction 1) and V or LcrV, are both important for virulence.[14] These
antigens are produced by the bacterium at normal human body temperature. Furthermore, Y. pestis survives
and produces F1 and V antigens while it is residing within white blood cells such as monocytes, but not in
neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies
against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils.[34]

In addition, the type-III secretion system (T3SS) allows Y. pestis to inject proteins into macrophages and
other immune cells. These T3SS-injected proteins, called Yersinia outer proteins (Yops), include Yop B/D,
which form pores in the host cell membrane and have been linked to cytolysis. The YopO, YopH, YopM,
YopT, YopJ, and YopE are injected into the cytoplasm of host cells by T3SS into the pore created in part by
YopB and YopD.[35] The injected Yops limit phagocytosis and cell signaling pathways important in the
innate immune system, as discussed below. In addition, some Y. pestis strains are capable of interfering with
immune signaling (e.g., by preventing the release of some cytokines).

Y. pestis proliferates inside lymph nodes, where it is able to avoid destruction by cells of the immune system
such as macrophages. The ability of Y. pestis to inhibit phagocytosis allows it to grow in lymph nodes and
cause lymphadenopathy. YopH is a protein tyrosine phosphatase that contributes to the ability of Y. pestis to
evade immune system cells.[36] In macrophages, YopH has been shown to dephosphorylate p130Cas, Fyb
(Fyn binding protein) SKAP-HOM and Pyk, a tyrosine kinase homologous to FAK. YopH also binds the p85
subunit of phosphoinositide 3-kinase, the Gab1, the Gab2 adapter proteins, and the Vav guanine nucleotide
exchange factor.

YopE functions as a GTPase-activating protein for members of the Rho family of GTPases such as RAC1.
YopT is a cysteine protease that inhibits RhoA by removing the isoprenyl group, which is important for
localizing the protein to the cell membrane. YopE and YopT has been proposed to function to limit YopB/D-
induced cytolysis.[37] This might limit the function of YopB/D to create the pores used for Yop insertion into
host cells and prevent YopB/D-induced rupture of host cells and release of cell contents that would attract
and stimulate immune system responses.

YopJ is an acetyltransferase that binds to a conserved α-helix of MAPK kinases.[38] YopJ acetylates MAPK
kinases at serines and threonines that are normally phosphorylated during activation of the MAP kinase
cascade.[39][40] YopJ is activated in eukaryotic cells by interaction with target cell phytic acid (IP6).[41] This
disruption of host cell protein kinase activity causes apoptosis of macrophages, and this is proposed to be
important for the establishment of infection and for evasion of the host immune response. YopO is a protein
kinase also known as Yersinia protein kinase A (YpkA). YopO is a potent inducer of human macrophage
apoptosis.[42]

Depending on which form of the plague with which the individual becomes infected, the plague develops a
different illness; however, the plague overall affects the host cell’s ability to communicate with the immune
system, hindering the body to bring phagocytic cells to the area of infection.

Y. pestis is a versatile killer. In addition to rodents and humans, it is known to have killed camels, chickens,
and pigs.[43] Domestic dogs and cats are susceptible to plague, as well, but cats are more likely to develop
illness when infected. In either, the symptoms are similar to those experienced by humans, and can be
deadly to the animal. People can be exposed by coming into contact with an infected animal (dead or alive),
or inhaling infectious droplets that a sick dog or cat has coughed into the air. [44] [45]

Immunity

A formalin-inactivated vaccine was in the past available in the United States for adults at high risk of
contracting the plague until removal from the market by the Food and Drug Administration. It was of
limited effectiveness and could 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 such that vaccines composed of these antigens
may not be fully protective.[46] The United States Army Medical Research Institute of Infectious Diseases
has found that an experimental F1/V antigen-based vaccine protects crab-eating macaques, but fails to
protect African green monkey species.[47] A systematic review by the Cochrane Collaboration found no
studies of sufficient quality to make any statement on the efficacy of the vaccine.[48]

Isolation and identification

In 1894, two bacteriologists, Alexandre Yersin of Switzerland and Kitasato Shibasaburō of Japan,
independently isolated in Hong Kong the bacterium responsible for the Third Pandemic. Though both
investigators reported their findings, a series of confusing and contradictory statements by Kitasato
eventually led to the acceptance of Yersin as the primary discoverer of the organism. Yersin named it
Pasteurella pestis in honor of the Pasteur Institute, where he worked. In 1967, it was moved to a new genus
and renamed Yersinia pestis in his honor. Yersin also noted that rats were affected by plague not only during
plague epidemics, but also often preceding such epidemics in humans and that plague was regarded by many
locals as a disease of rats; villagers in China and India asserted that when large numbers of rats were found
dead, plague outbreaks soon followed.

In 1898, French scientist Paul-Louis Simond (who had also come to China to battle the Third Pandemic)
discovered the rat–flea vector that drives the disease. He had noted that persons who became ill did not have
to be in close contact with each other to acquire the disease. In Yunnan, China, inhabitants would flee from
their homes as soon as they saw dead rats, and on the island of Formosa (Taiwan), residents considered the
handling of dead rats heightened the risks of developing plague. These observations led him to suspect that
the flea might be an intermediary factor in the transmission of plague, since people acquired plague only if
they were in contact with rats that had died less than 24 hours before. In a now classic experiment, Simond
demonstrated how a healthy rat died of the plague after infected fleas had jumped to it from a rat that had
recently died of the plague.[49] The outbreak spread to Chinatown, San Francisco, from 1900 to 1904 and
then to Oakland and the East Bay from 1907 to 1909.[50] It has been present in the rodents of western North
America ever since, as fear of the consequences of the outbreak on trade caused authorities to hide the dead
of the Chinatown residents long enough for the disease to be passed to widespread species of native rodents
in outlying areas.[51]
Ancient DNA evidence
In 2018, the emergence and spread of the pathogen during the
Neolithic decline (as far back as 6,000 years ago) was published.[52]
A site in Sweden was the source of the DNA evidence and trade
networks were proposed as the likely avenue of spread rather than
migrations of populations.

DNA evidence published in 2015 indicates Y. pestis infected humans

5,000 years ago in Bronze Age Eurasia,[53] but genetic changes that
made it highly virulent did not occur until about 4,000 years ago.[54]
The highly virulent version capable of transmission by fleas through
rodents, humans, and other mammals was found in two individuals
associated with the Srubnaya culture from the Samara region in
Russia from around 3,800 years ago and an Iron Age individual from
Kapan, Armenia from around 2,900 years ago.[54][53] This indicates
that at least two lineages of Y. pestis were circulating during the
Bronze Age in Eurasia.[54] The Y. pestis bacterium has a relatively
large number of nonfunctioning genes and three "ungainly"
plasmids, suggesting an origin less than 20,000 years ago.[43]
Y. pestis isolated by Ricardo Jorge
during the 1899 Porto plague
Three main strains are recognised: Y. p. antiqua, which caused a
outbreak
plague pandemic in the sixth century; Y. p. medievalis, which caused
the Black Death and subsequent epidemics during the second
pandemic wave; and Y. p. orientalis, which is responsible for current
plague outbreaks.[55]

Plague causes a blockage in the proventriculus of the flea by forming a biofilm.[56] The biofilm formation is
induced by the ingestion of blood. The presence of a biofilm seems likely to be required for stable infection
of the flea.[57] It has been suggested that a bacteriophage – Ypφ – may have been responsible for increasing
the virulence of this organism.[58]

Recent events
In 2008, the plague was commonly found in sub-Saharan Africa and Madagascar, areas that accounted for
over 95% of the reported cases.[13]

In September 2009, the death of Malcolm Casadaban, a molecular genetics professor at the University of
Chicago, was linked to his work on a weakened laboratory strain of Y. pestis.[59] Hemochromatosis was
hypothesised to be a predisposing factor in Casadaban's death from this attenuated strain used for
research.[60]

In 2010, researchers in Germany definitely established, using PCR evidence from samples obtained from
Black Death victims, that Y. pestis was the cause of the medieval Black Death.[61]

In 2011, the first genome of Y. pestis isolated from Black Death victims was published, and concluded that
this medieval strain was ancestral to most modern forms of Y. pestis. [62]

In 2015, Cell published results from a study of ancient graves.[63] Plasmids of Y. pestis were detected in
archaeological samples of the teeth of seven Bronze Age individuals, in the Afanasievo culture in Siberia,
the Corded Ware culture in Estonia, the Sintashta culture in Russia, the Unetice culture in Poland, and the
Andronovo culture in Siberia.[64]

On September 8, 2016, the Y. pestis bacterium was identified from DNA in teeth found at a Crossrail
building site in London. The human remains were found to be victims of the Great Plague of London, which
lasted from 1665 to 1666.[65]

On January 15, 2018, researchers at the University of Oslo and the University of Ferrara suggested that
humans and their parasites were the biggest carriers of the plague.[66][67]

Two cases of pneumonic plague were diagnosed at a hospital in Beijing's Chaoyang district on 13 November
2019, prompting fears of an outbreak. Doctors diagnosed a middle-aged man with fever, who had
complained of difficulty breathing for some ten days, accompanied by his wife with similar symptoms.[68]
Police quarantined the emergency room at the hospital and controls were placed on Chinese news
aggregators.[68] On the 18th, a third case was reported in a 55-year-old male from Xilingol League, one of
the twelve Mongolic autonomous regions in Northern China. The patient received treatment and 28
symptomless contacts were placed in quarantine. [69]

Officials have increased precautions after a case of bubonic plague was confirmed in Bayannur, a city in
China's Inner Mongolia autonomous region. The patient is in quarantine and being treated. According to
China's Global Times, a second suspected case is also being investigated, and a level 3 alert, which forbids
hunting and eating of animals that could carry plague and calls on the public to report suspected cases, is in
effect until the end of the year.[70]

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External links
Yersinia pestis (http://www.bacteriamuseum.org/index.php/bacterial-species-files/136-yersinia-
pestis). Virtual Museum of Bacteria.
A list of variant strains and information on synonyms (and much more) is available through the
NCBI taxonomy browser (https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=63
2).
CDC's Home page for Plague (https://www.cdc.gov/plague/)
IDSA's resource page on Plague (https://web.archive.org/web/20130927190638/http://www.ids
ociety.org/Plague/): Current, comprehensive information on pathogenesis, microbiology,
epidemiology, diagnosis, and treatment
Plague (Yersinia Pestis) (https://www.drugs.com/health-guide/plague-yersinia-pestis.html)
Wyndham Lathem speaking on "From Mild to Murderous: How Yersinia pestis Evolved to
Cause Pneumonic Plague." (https://www.youtube.com/watch?v=fbeAcPRJPpA)

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