Pasteurella multocida

Pasteurella
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Pasteurellales
Family: Pasteurellaceae
Genus: Pasteurella
Species

Pasteurella multocida

Pasteurella multocida is a Gram-negative, non-motile coccobacillus that is penicillin-sensitive and belongs to the Pasteurellaceae family [1]. It can cause avian cholera in birds and a zoonotic infection in humans, which typically is a result of bites or scratches from domestic pets. Many mammals and fowl harbor it as part of their normal respiratory microbiota, displaying asymptomatic colonization.

Contents

History

Pasteurella multocida was first found in 1878 in cholera-infected birds. However, it was not isolated until 1880, by Louis Pasteur - the man in whose honor Pasteurella is named.[2]. The bacteria is found in many environments but the associated cholera outbreaks are usually found in central California, the Midwest, and Texas.

Disease

See: Pasteurellosis

P. multocida causes disease in wild and domesticated animals as well as humans. The bacterium can be found in fowl, felines, canines, rabbits, cattle and pigs. In birds, P. multocida causes avian cholera; the disease has been shown to follow 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]. In humans, P. multocida is the most common cause of infection from animal injuries (pneumonia in cattle and pigs, atrophic rhinitis in pigs and goats, and wound infections after dog/cat-bites.) The infection usually shows as soft tissue inflammation within 24 hours. A high leukocyte and neutrophil count is typically observed, leading to an inflammatory reaction at the infection site (generally a diffuse localized cellulitis).[6] 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. The bacteria may also cross the blood-brain barrier and cause meningitis.[7]


Virulence, culturing, and metabolism

A bacteriophage encodes the toxin responsible for most P. multocida virulence factors. 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.[8] P. multocida has been observed invading and replicating inside host amoebae, causing lysis in the host. P. multocida will grow at 37 degrees Celsius on blood or chocolate agar, 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 carbohydrates in anaerobic conditions.[9]. The survival of P. multocida bacteria has also been shown to be increased by the addition of salt into its environment. Levels of sucrose and pH also have been shown to have minor effects on the bacterium’s survival. [10]


Diagnosis and Treatment

Diagnosis of the bacterium was traditionally based on clinical findings, culture and seriological 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 PCR. [11] This bacterium can be effectively treated with beta-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.[12]

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 giltsin (sows without previous litters). The piglets that were born were inoculated, while the piglets born to non-vaccinated mothers developed atrophic rhinitis. [13] Other research is being done on the effects of protein, pH, temperature, NaCl and sucrose on P. multocida development and survival. The research seems to show that the bacteria survive better in waters that are 18 degrees Celsius compared to 2 degrees Celsius. The addition of NaCl by 0.5% also aided the bacterium’s survival, while the sucrose and pH levels had minor effects as well. [14]. Ongoing 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 that 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 transferring and hemoglobin. P. multocida genes that are upregulated in times of infection are usually involved in nutrient uptake and metabolism. This shows that true virulence genes may only be expressed during the early stages of infection. [15]


References

  1. ^ Kuhnert P; Christensen H (editors). (2008). Pasteurellaceae: Biology, Genomics and Molecular Aspects. Caister Academic Press. ISBN 978-1-904455-34-9 . http://www.horizonpress.com/past. 
  2. ^ Pasteur, Louis. "The Attenuation of the Causal Agent of Fowl Cholera". http://www.pasteurbrewing.com/Articles/works-of-louis-pasteur-english/the-attenuation-of-the-causal-agent-of-fowl-cholera.html. 
  3. ^ Blanchlong, JA. “Persistence of pasteurella multocida in wetlands following avian cholera outbreaks.” Journal of Wildlife diseases, vol.42, no.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 withMannheimia Haemolytica or pastuerella multocida. VM 163, University of Florida
  6. ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9. 
  7. ^ 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
  8. ^ [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.
  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. ^ Bredy, JP. “The effects of six environmental variables on Pasteurella multocida populations in water.” Journal of Wildlife Diseases, vol. 25, no. 2 (232-239)
  11. ^ 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
  12. ^ Red Book: 2006 Report of the Committee on Infectious Diseases - 27th Ed.
  13. ^ 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)
  14. ^ Bredy, JP. The effects of six environmental variables on P. multocida populations in water. “Journal of Wildlife Diseases”, vol. 25, no.2 (232-239)
  15. ^ Boyce, JD. How does P. multocida respond to the host environment? “Current Opinion in Microbiology” vol.9 no.1 (117-122)

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