Species of bacterium
Pasteurella multocida
is a
Gram-negative
, nonmotile,
penicillin
-sensitive
coccobacillus
of the family
Pasteurellaceae
.
[1]
Strains of the species are currently classified into five
serogroups
(A, B, D, E, F) based on
capsular
composition and 16 somatic
serovars
(1?16).
P. multocida
is the cause of a range of diseases in mammals and birds, including
fowl cholera
in
poultry
,
atrophic rhinitis
in pigs, and bovine hemorrhagic
septicemia
in cattle and buffalo. It can also cause a
zoonotic
infection in humans, which typically is a result of bites or scratches from domestic pets. Many mammals (including domestic cats and dogs) and birds harbor it as part of their normal respiratory
microbiota
.
History
[
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]
Pasteurella multocida
was first found in 1878 in cholera-infected birds. However, it was not isolated until 1880, by
Louis Pasteur
, in whose honor
Pasteurella
is named.
[2]
Disease
[
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]
- See:
Pasteurellosis
P. multocida
causes a range of diseases in wild and domesticated animals, as well as humans. The bacterium is found in birds,
cats
, dogs, rabbits, cattle, and pigs. In birds,
P. multocida
causes avian or
fowl cholera
disease; a significant disease present in commercial and domestic poultry flocks worldwide, particularly layer flocks and parent breeder flocks.
P. multocida
strains that cause fowl cholera in poultry typically belong to the serovars 1, 3, and 4. In the wild, fowl cholera has been shown to follow bird migration routes, especially of
snow geese
. The
P. multocida
serotype-1 is most associated with avian cholera in North America, but the bacterium does not linger in
wetlands
for extended periods of time.
[3]
P. multocida
causes atrophic rhinitis in pigs;
[4]
it also can cause
pneumonia
or
bovine respiratory disease
in cattle.
[5]
[6]
It may be responsible for mass mortality in
saiga antelopes
.
[7]
In humans,
P. multocida
is the most common cause of wound infections after dog or cat bites. The infection usually shows as soft tissue inflammation within 24 hours. High
leukocyte
and
neutrophil
counts are typically observed, leading to an inflammatory reaction at the infection site (generally a diffuse, localized
cellulitis
).
[8]
It can also infect other locales, such as the respiratory tract, and is known to cause regional
lymphadenopathy
(swelling of the lymph nodes). In more serious cases, a
bacteremia
can result, causing an
osteomyelitis
or
endocarditis
. Patients with a joint replacement (perhaps notably knee replacement) in place may, in particular, be at risk of secondary infection of that joint during an episode of P multocida cellulitis/bacteraemia. The bacteria may also cross the
blood?brain barrier
and cause
meningitis
.
[9]
Virulence, culturing, and metabolism
[
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]
P. multocida
expresses a range of
virulence factors
including a
polysaccharide
capsule
and the variable
carbohydrate
surface molecule,
lipopolysaccharide
(LPS). The capsule has been shown in strains of serogroups A and B to help resist
phagocytosis
by host
immune cells
and capsule type A has also been shown to help resist complement-mediated
lysis
.
[10]
[11]
The LPS produced by
P. multocida
consists of a hydrophobic lipid A molecule (that anchors the LPS to the outer membrane), an inner core, and an outer core, both consisting of a series of sugars linked in a specific way. There is no
O-antigen
on the LPS and the molecule is similar to LPS produced by
Haemophilus influenzae
and the
lipooligosaccharide
of
Neisseria meningitidis
. A study in a serovar 1 strain showed that a full-length LPS molecule was essential for the bacteria to be fully virulent in chickens.
[12]
Strains that cause atrophic rhinitis in pigs are unique as they also have
P. multocida
toxin (PMT) residing on a
bacteriophage
. PMT is responsible for the twisted snouts observed in pigs infected with the bacteria. This toxin activates
Rho
GTPases
, which bind and hydrolyze
GTP
, and are important in
actin
stress fiber formation. Formation of stress fibers may aid in the
endocytosis
of
P. multocida
. The host cell cycle is also modulated by the toxin, which can act as an intracellular
mitogen
.
[13]
P. multocida
has been observed invading and replicating inside host
amoebae
, causing lysis in the host.
P. multocida
will grow at 37 °C (99 °F) on
blood
or
chocolate agar
,
HS agar
,
[14]
but will not grow on
MacConkey agar
. Colony growth is accompanied by a characteristic "mousy" odor due to
metabolic
products.
A
facultative anaerobe
,
P. multocida
it is
oxidase-positive
and
catalase-positive
. It can also
ferment
a large number of
carbohydrates
in anaerobic conditions.
[9]
The survival of
P. multocida
bacteria has also been shown to be increased by the addition of salt into their environments. Levels of
sucrose
and
pH
also have been shown to have minor effects on bacterial survival.
[15]
Diagnosis and treatment
[
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]
Diagnosis of the bacterium in humans was traditionally based on clinical findings, and culture and
serological
testing, but
false negatives
have been a problem due to easy death of
P. multocida
, and serology cannot differentiate between current infection and previous exposure. The quickest and most accurate method for confirming an active
P. multocida
infection is molecular detection using
polymerase chain reaction
.
[16]
This bacterium can be effectively treated with
β-lactam antibiotics
, which inhibit cell wall synthesis. It can also be treated with
fluoroquinolones
or
tetracyclines
; fluoroquinolones inhibit bacterial
DNA synthesis
and tetracyclines interfere with
protein synthesis
by binding to the bacterial
30S
ribosomal
subunit. Despite poor
in vitro
susceptibility results,
macrolides
(binding to the ribosome) also can be applied, certainly in the case of pulmonary complications. Due to the polymicrobial etiology of
P. multocida
infections, treatment requires the use of antimicrobials targeted at the elimination of both aerobic and anaerobic, Gram-negative bacteria. As a result,
amoxicillin-clavulanate
(a beta-lactamase inhibitor/penicillin combination) is seen as the treatment of choice.
[17]
Current research
[
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]
P. multocida
mutants
are being researched for their ability to cause diseases.
In vitro
experiments show the bacteria respond to low iron. Vaccination against progressive atrophic rhinitis was developed by using a recombinant derivative of
P. multocida
toxin. The vaccination was tested on pregnant gilts (female swine without previous litters). The piglets born to treated gilts were inoculated, while the piglets born to unvaccinated mothers developed atrophic rhinitis.
[18]
Other research is being done on the effects of protein, pH, temperature, sodium chloride (NaCl), and sucrose on
P. multocida
development and survival in water. The research seems to show the bacteria survive better in 18 °C (64 °F) water compared to 2 °C (36 °F) water. The addition of 0.5% NaCl also aided bacterial survival, while the sucrose and pH levels had minor effects, as well.
[19]
Research has also been done on the response of
P. multocida
to the host environment. These tests use DNA microarrays and proteomics techniques.
P. multocida
-directed mutants have been tested for their ability to produce disease. Findings seem to indicate the bacteria occupy host niches that force them to change their gene expression for energy metabolism, uptake of iron, amino acids, and other nutrients.
In vitro
experiments show the responses of the bacteria to low iron and different iron sources, such as
transferrin
and
hemoglobin
.
P. multocida
genes that are upregulated in times of infection are usually involved in nutrient uptake and metabolism. This shows true virulence genes may only be expressed during the early stages of infection.
[20]
Genetic transformation
is the process by which a recipient bacterial cell takes up DNA from a neighboring cell and integrates this DNA into the recipient's
genome
.
P. multocida
DNA contains high frequencies of putative
DNA uptake sequences
(DUSs) identical to those in
Hemophilus influenzae
that promote donor DNA uptake during
transformation
.
[21]
The location of these sequences in
P. multocida
shows a skewed distribution towards genome maintenance genes, such as those involved in
DNA repair
. This finding suggests that
P. multocida
might be competent to undergo transformation under certain conditions, and that genome maintenance genes involved in transforming donor DNA may preferentially replace their damaged counterparts in the DNA of the recipient cell.
[21]
References
[
edit
]
- ^
Kuhnert P; Christensen H, eds. (2008).
Pasteurellaceae: Biology, Genomics and Molecular Aspects
. Caister Academic Press.
ISBN
978-1-904455-34-9
.
- ^
Pasteur, Louis (2011-05-13).
"The Attenuation of the Causal Agent of Fowl Cholera"
.
- ^
Blanchlong, JA. “Persistence of pasteurella multocida in wetlands following avian cholera outbreaks.” Journal of Wildlife diseases, 2006; 42(1):33-39
- ^
Elias B, Hamori D. Data on the aetiology of swine atrophic rhinitis. V. The role of genetic factors. Acta Vet Acad Sci Hung. 1976;26(1):13?19. [PubMed]
- ^
Irsik, M B Bovine respiratory disease associated with Mannheimia Haemolytica or pastuerella multocida. VM 163, University of Florida
- ^
Kokotovic, Branko; Friis, Niels F; Ahrens, Peter (2007).
"Mycoplasma alkalescens demonstrated in bronchoalveolar lavage of cattle in Denmark"
.
Acta Veterinaria Scandinavica
.
49
(1): 2.
doi
:
10.1186/1751-0147-49-2
.
ISSN
1751-0147
.
PMC
1766361
.
PMID
17204146
.
- ^
Richard A. Kock, Mukhit Orynbayev, Sarah Robinson, Steffen Zuther, Navinder J. Singh, Wendy Beauvais, Eric R. Morgan, Aslan Kerimbayev, Sergei Khomenko, Henny M. Martineau, Rashida Rystaeva, Zamira Omarova, Sara Wolfs, Florent Hawotte, Julien Radoux and Eleanor J. Milner-Gulland:
Saigas on the brink: Multidisciplinary analysis of the factors influencing mass mortality events
. Science Advances 17 Jan 2018: Vol. 4, no. 1, eaao2314
DOI: 10.1126/sciadv.aao2314
- ^
Ryan KJ; Ray CG, eds. (2004).
Sherris Medical Microbiology
(4th ed.). McGraw Hill.
ISBN
0-8385-8529-9
.
- ^
a
b
Casolari C, Fabio U. Isolation of Pasteurella multocida from Human Clinical Specimens: First Report in Italy. European Journal of Epidemiology. Sept 1988; 4(3):389-90
- ^
Chung JY, Wilkie I, Boyce JD, Townsend KM, Frost AJ, Ghoddusi M, Adler B: Role of capsule in the pathogenesis of fowl cholera caused by Pasteurella multocida serogroup A. Infect Immun 2001, 69(4):2487-2492.
- ^
Boyce JD, Adler B: The capsule is a virulence determinant in the pathogenesis of Pasteurella multocida M1404 (B:2). Infect Immun 2000, 68(6):3463-3468.
- ^
Harper M, Cox AD, St Michael F, Wilkie IW, Boyce JD, Adler B. A heptosyltransferase mutant of
Pasteurella multocida
produces a truncated
lipopolysaccharide
structure and is attenuated in virulence. Infect. Immun. 2004; 72(6):3436-43.
- ^
Lacerda HM, Lax AJ, Rozenqurt E. Pasteurella multocida toxin, a potent intracellularly acting mitogen, induces p125FAK and paxillin tyrosine phosphorylation, actin stress fiber formation, and focal contact assembly in Swiss 3T3 cells. J Biol Chem. 5 Jan 1996; 271(1):439-45.
- ^
[1]
, by Younginfrontier,
[2]
.
HS agar
, by Laboratorios CONDA,
PDF
.
- ^
Bredy, JP. “The effects of six environmental variables on Pasteurella multocida populations in water.” Journal of Wildlife Diseases, vol. 25, no. 2 (232-239)
- ^
Miflin, J.K. and Balckall, P.J. (2001) Development of a 23 SrRNA-based PCR assay for the identification of Pasteurella multocida. Lett. Appl. Microbiol. 33: 216-221
- ^
Red Book: 2006 Report of the Committee on Infectious Diseases - 27th Ed.
- ^
Nielsen JP Vaccination against progressive atrophic rhinitis with a recombinant “Pasteurella multocida” toxin derivative. Canadian Journal of Veterinary Research, vol.55, no.2 (128-138)
- ^
Bredy, JP. The effects of six environmental variables on
P. multocida
populations in water. “Journal of Wildlife Diseases”, vol. 25, no.2 (232-239)
- ^
Boyce, JD. How does
P. multocida
respond to the host environment? “Current Opinion in Microbiology” vol.9 no.1 (117-122)
- ^
a
b
Davidsen T, Rødland EA, Lagesen K, Seeberg E, Rognes T, Tønjum T (2004).
"Biased distribution of DNA uptake sequences towards genome maintenance genes"
.
Nucleic Acids Res
.
32
(3): 1050?8.
doi
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10.1093/nar/gkh255
.
PMC
373393
.
PMID
14960717
.
External links
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]