Difference between revisions of "Pasteurella multocida"

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''Pasteurella multocida PM70''
''Pasteurella multocida PM70''
It is commonly known as avian cholera.

Revision as of 02:50, 5 June 2007

A Microbial Biorealm page on the genus Pasteurella multocida


Higher order taxa

Bacteria; Proteobacteria; Gammaproteobacteria; Pasteurellales; Pasteurellaceae; Pasteurella


Pasteurella multocida PM70

It is commonly known as avian cholera.

NCBI: Taxonomy

Description and significance

In 1878, Pasteurella multocida was discovered in birds infected with cholera. Then in 1880, Louis Pasteur isolated it. P. multocida is a small, gram-negative bacterium. It is non-motile coccobacillus and penicillin-sensitive. It can cause infections in humans, as a result of cat or dog bites and scratches. Mammals and birds have it as part of their normal respiratory microbiota and display infections. P. multocida live in the upper respiratory tract of many vertebrate hosts. These include cats, dogs, rabbits, cows, pigs, and fowl. The host species provides these bacteria with nutrients, and if the bacteria are present in an external environment, it is only temporary. This bacteria is located in a wide range of environments. Cholera outbreaks are usually reported in the United States in north central California, the MidWest, and the Muleshoe National Refuge in Texas.

Genome structure

Number of nucleotides: 2257487

Number of protein genes: 2015

Number of RNA genes: 77

It has a circular chromosome and a plasmid. The chromosome is 2250 kb long.

Cell structure and metabolism

The P. multocida genome shows 129 lipoproteins that are secreted and located in the outer membrane. Protein H has been found to be the major polypeptide in the outer membrane of the P. multocida. This bacteria has a capsule and lipopolysaccharides. The capsule helps to avoid phagocytosis. Lipopolysaccharides are important for survival of the bacteria in the host. The P. multocida toxin has surface adhesis and iron acquisition proteins for attachment and invasion of host cells and to survive in a hostile environment.


P. Multocida causes disease in both wild and domesticated animals. If released into the environment by dead birds, it can infect healthy birds, so cholera in birds spreads quickly in wetlands. It can be spread through contaminated drinking water and waste. Inhalation is also another means of transmission of the bacteria. Disease outbreaks have been shown to follow bird migration routes, especially the snow geese. Wildlife biologists believe that these bacteria are transmitted by carrier birds or live in contaminated wetlands throughout the whole year.


P. Multocida virulence is caused by a toxin, which is encoded by a bacteriophage. The toxin activates Rho GTPases, which hydrolyze GTP. This is needed for actin stress fiber formation, which aides in endocytosis of P. multocida. The host cell cycles is modulated by this toxin as well. The toxin acts as an intracellular mitogen. It is a facultative anaerobe, so it is oxidase and catalase-positive, and can ferment carbohydrates under anaerobic conditions. P. Multocida lives in a variety of animals and can be passed onto humans through cat scratches and dog bites or by oral and respiratory infections. It can also cross the blood brain barrier and cause meningitis.

Application to Biotechnology

Vaccinations can be derived from P. multocida against the diseases that it can cause. P. multocida produces a 140 kDa protein toxin that activates signal transduction pathways, which activates phospholipase C beta, Rho A, Jun kinase, and ERK.

Current Research

P. multocida mutants are being researched for their ability to cause diseases. In vitro experiments show that the bacteria responds 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. The piglets that were born were inoculated. The piglets who had nonvaccinated mothers developed atrophic rhinitis, and only a few piglets with vaccinated mothers developed the disease.


Al-Hasani, K., Boyce, J., McCarl, VP., Bottomley, S., Wilkie, I., Adler, B. “Identification of novel immunogens in Pasteurella multocida.” Microbial Cell Factories, vol. 6, no. 3.

Basagoudanavar, S.H., Singh, D.K., Varshney, B.C. 2006. “Immunization with outer membrane proteins of Pasteurella multocida (6:B) provides protection in mice.” Journal of Veterinary Medicine, Vol. 53, no. 10. (524-530)

Harper, M., Boyce, J.D., Adler, B. “Pasteurella multocida pathogenesis: 125 years after Pasteur.” FEMS Microbiology Letters, vol. 265, no. 1. (1-10)

Yokose, N., Dan, K. “Pasteurella multocida sepsis, due to a scratch from a pet cat, in a post-chemotherapy neutropenic patient with non-Hodgkin lymphoma.” International Journal of Hematology, vol. 85, no. 2. (146-148)

Edited by Christina Fong student of Rachel Larsen and Kit Pogliano at UCSD.