Pasteurella

multocida

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.
 Pasteurella multocida

Gram-stained photomicrograph depicting

numerous Pasteurella multocida bacteria

Scientific classification

Domain: Bacteria

Phylum: Pseudomonadota

Class: Gammaproteobacteria

Order: Pasteurellales

Family: Pasteurellaceae

Genus: Pasteurella

Binomial name

Pasteurella multocida
 Trevisan 1887 (Approved Lists 1980)

History
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
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][10]
Virulence, culturing, and
metabolism
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.[11][12] 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.[13] 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.[14]
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,[15] but
will not grow on MacConkey agar.
Colony growth is accompanied by
a characteristic "mousy" odor due
to metabolic products.

Being a facultative anaerobe, it is

oxidase-positive and catalase-
positive, and 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.[16]

Diagnosis and treatment

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.[17]

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.[18]

Current research
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.[19] 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.[20]
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.[21]

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.[22] 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.[22]

References
1. Kuhnert P; Christensen H, eds. (2008).
Pasteurellaceae: Biology, Genomics and
Molecular Aspects (http://www.horizonpr
ess.com/past) . Caister Academic Press.
ISBN 978-1-904455-34-9.
2. Pasteur, Louis (2011-05-13). "The
Attenuation of the Causal Agent of Fowl
Cholera" (http://www.pasteurbrewing.co
m/the-attenuation-of-the-causal-agent-of-
fowl-cholera/) .
3. Blanchlong, JA. “Persistence of
pasteurella multocida in wetlands
following avian cholera outbreaks.”
Journal of Wildlife diseases, 2006;
42(1):33-39
4. Eliás B, Hámori 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]
5. Irsik, M B Bovine respiratory disease
associated with Mannheimia Haemolytica
or pastuerella multocida. VM 163,
University of Florida
6. Kokotovic, Branko; Friis, Niels F; Ahrens,
Peter (2007). "Mycoplasma alkalescens
demonstrated in bronchoalveolar lavage
of cattle in Denmark" (https://www.ncbi.nl
m.nih.gov/pmc/articles/PMC1766361) .
Acta Veterinaria Scandinavica. 49 (1): 2.
doi:10.1186/1751-0147-49-2 (https://doi.
org/10.1186%2F1751-0147-49-2) .
ISSN 1751-0147 (https://www.worldcat.or
g/issn/1751-0147) . PMC 1766361 (http
s://www.ncbi.nlm.nih.gov/pmc/articles/P
MC1766361) . PMID 17204146 (https://p
ubmed.ncbi.nlm.nih.gov/17204146) .
7. 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 (http
s://www.science.org/doi/10.1126/sciadv.
aao2314) . Science Advances 17 Jan
2018: Vol. 4, no. 1, eaao2314 DOI:
10.1126/sciadv.aao2314
8. Ryan KJ; Ray CG, eds. (2004). Sherris
Medical Microbiology (4th ed.). McGraw
Hill. ISBN 0-8385-8529-9.
9. 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
10. Rissardo, JamirPitton; Caprara, AnaLetícia
Fornari (2018). "Pasteurella multocida
meningitis following mastoidectomy: A
case report and literature review" (http://
www.ijamhrjournal.org/text.asp?2018/5/
2/78/249068) . International Journal of
Advanced Medical and Health Research.
5 (2): 78.
doi:10.4103/IJAMR.IJAMR_35_18 (http
s://doi.org/10.4103%2FIJAMR.IJAMR_35
_18) . ISSN 2349-4220 (https://www.worl
dcat.org/issn/2349-4220) .
S2CID 59546957 (https://api.semanticsc
holar.org/CorpusID:59546957) .
11. 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.
12. 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.
13. 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.
14. 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.
15. [1] (https://www.younginfrontier.com/@/h
s-agar) , by Younginfrontier, [2] (https://w
ww.younginfrontier.com/web/content/16
2038?unique=cf984919c2c9473df168ca
0ab7e50de8ade7b6e9&download=true) .
HS agar (https://www.condalab.com/prod
ucts/search/?tx_condalabproducts_busqu
eda%5BproductoCod%5D=1809&tx_cond
alabproducts_busqueda%5Bcat1%5D=&tx
_condalabproducts_busqueda%5Bcat2%5
D=&tx_condalabproducts_busqueda%5Bc
at3%5D=&tx_condalabproducts_busqued
a%5Baction%5D=show&tx_condalabprod
ucts_busqueda%5Bcontroller%5D=Catego
ria&cHash=1a2f2c758b5ba27747b0b6ab
0ac3cc45) , by Laboratorios CONDA, PDF
(https://www.condalab.com/pdf/1809.pd
f) .
16. Bredy, JP. “The effects of six
environmental variables on Pasteurella
multocida populations in water.” Journal
of Wildlife Diseases, vol. 25, no. 2 (232-
239)
17. 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
18. Red Book: 2006 Report of the Committee
on Infectious Diseases - 27th Ed.
19. 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)
20. Bredy, JP. The effects of six
environmental variables on P. multocida
populations in water. “Journal of Wildlife
Diseases”, vol. 25, no.2 (232-239)
21. Boyce, JD. How does P. multocida
respond to the host environment?
“Current Opinion in Microbiology” vol.9
no.1 (117-122)
22. Davidsen T, Rødland EA, Lagesen K,
Seeberg E, Rognes T, Tønjum T (2004).
"Biased distribution of DNA uptake
sequences towards genome maintenance
genes" (https://www.ncbi.nlm.nih.gov/pm
c/articles/PMC373393) . Nucleic Acids
Res. 32 (3): 1050–8.
doi:10.1093/nar/gkh255 (https://doi.org/
10.1093%2Fnar%2Fgkh255) .
PMC 373393 (https://www.ncbi.nlm.nih.g
ov/pmc/articles/PMC373393) .
PMID 14960717 (https://pubmed.ncbi.nl
m.nih.gov/14960717) .

External links
Animal bite infections
(healthAtoZ.com) (https://web.archive.
org/web/20070226145037/http://ww
 w.healthatoz.com/healthatoz/Atoz/co
mmon/standard/transform.jsp?reques
tURI=%2Fhealthatoz%2FAtoz%2Fenc
y%2Fanimal_bite_infections.jsp)
Genome Projects (https://gold.jgi.doe.
gov/organisms?setColumns=yes&Orga
nism.Organism+Name=multocida&Org
anism.Domain=) from Genomes
OnLine Database
Type strain of Pasteurella multocida at
BacDive - the Bacterial Diversity
Metadatabase (https://bacdive.dsmz.d
e/strain/11729)

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