Pasteurella multocida
| Pasteurella multocida | |
|---|---|
| |
| Gram-stainedphotomicrograph depicting numerousPasteurella multocidabacteria | |
Scientific classification
| |
| Domain: | Bacteria |
| Phylum: | Pseudomonadota |
| Class: | Gammaproteobacteria |
| Order: | Pasteurellales |
| Family: | Pasteurellaceae |
| Genus: | Pasteurella |
| Species: | P. multocida
|
| Binomial name | |
| Pasteurella multocida Trevisan 1887 (Approved Lists 1980)
| |
Pasteurella multocidais aGram-negative,nonmotile,penicillin-sensitivecoccobacillusof the familyPasteurellaceae.[1]Strains of the species are currently classified into fiveserogroups(A, B, D, E, F) based oncapsularcomposition and 16 somaticserovars(1–16).P. multocidais the cause of a range of diseases in mammals and birds, includingfowl cholerainpoultry,atrophic rhinitisin pigs, and bovine hemorrhagicsepticemiain cattle and buffalo. It can also cause azoonoticinfection 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 respiratorymicrobiota.
History
[edit]Pasteurella multocidawas first found in 1878 in cholera-infected birds. However, it was not isolated until 1880, byLouis Pasteur,in whose honorPasteurellais named.[2]
Disease
[edit]- See:Pasteurellosis
P. multocidacauses 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. multocidacauses avian orfowl choleradisease; a significant disease present in commercial and domestic poultry flocks worldwide, particularly layer flocks and parent breeder flocks.P. multocidastrains 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 ofsnow geese.TheP. multocidaserotype-1 is most associated with avian cholera in North America, but the bacterium does not linger inwetlandsfor extended periods of time.[3]P. multocidacauses atrophic rhinitis in pigs;[4]it also can causepneumoniaorbovine respiratory diseasein cattle.[5][6]It may be responsible for mass mortality insaiga antelopes.[7]
In humans,P. multocidais the most common cause of wound infections after dog or cat bites. The infection usually shows as soft tissue inflammation within 24 hours. Highleukocyteandneutrophilcounts are typically observed, leading to an inflammatory reaction at the infection site (generally a diffuse, localizedcellulitis).[8]It can also infect other locales, such as the respiratory tract, and is known to cause regionallymphadenopathy(swelling of the lymph nodes). In more serious cases, abacteremiacan result, causing anosteomyelitisorendocarditis.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 theblood–brain barrierand causemeningitis.[9]
Virulence, culturing, and metabolism
[edit]P. multocidaexpresses a range ofvirulence factorsincluding apolysaccharidecapsuleand the variablecarbohydratesurface molecule,lipopolysaccharide(LPS). The capsule has been shown in strains of serogroups A and B to help resistphagocytosisby hostimmune cellsand capsule type A has also been shown to help resist complement-mediatedlysis.[10][11]The LPS produced byP. multocidaconsists 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 noO-antigenon the LPS and the molecule is similar to LPS produced byHaemophilus influenzaeand thelipooligosaccharideofNeisseria 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 haveP. multocidatoxin (PMT) residing on abacteriophage.PMT is responsible for the twisted snouts observed in pigs infected with the bacteria. This toxin activatesRhoGTPases,which bind and hydrolyzeGTP,and are important inactinstress fiber formation. Formation of stress fibers may aid in theendocytosisofP. multocida.The host cell cycle is also modulated by the toxin, which can act as an intracellularmitogen.[13]P. multocidahas been observed invading and replicating inside hostamoebae,causing lysis in the host.P. multocidawill grow at 37 °C (99 °F) onbloodorchocolate agar,HS agar,[14]but will not grow onMacConkey agar.Colony growth is accompanied by a characteristic "mousy" odor due tometabolicproducts.
Afacultative anaerobe,P. multocidait isoxidase-positiveandcatalase-positive.It can alsofermenta large number ofcarbohydratesin anaerobic conditions.[9]The survival ofP. multocidabacteria has also been shown to be increased by the addition of salt into their environments. Levels ofsucroseandpHalso have been shown to have minor effects on bacterial survival.[15]
Diagnosis and treatment
[edit]Diagnosis of the bacterium in humans was traditionally based on clinical findings, and culture andserologicaltesting, butfalse negativeshave been a problem due to easy death ofP. multocida,and serology cannot differentiate between current infection and previous exposure. The quickest and most accurate method for confirming an activeP. multocidainfection is molecular detection usingpolymerase chain reaction.[16]
This bacterium can be effectively treated withβ-lactam antibiotics,which inhibit cell wall synthesis. It can also be treated withfluoroquinolonesortetracyclines;fluoroquinolones inhibit bacterialDNA synthesisand tetracyclines interfere withprotein synthesisby binding to the bacterial30Sribosomalsubunit. Despite poorin vitrosusceptibility results,macrolides(binding to the ribosome) also can be applied, certainly in the case of pulmonary complications. Due to the polymicrobial etiology ofP. multocidainfections, 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
[edit]P. multocidamutantsare being researched for their ability to cause diseases.In vitroexperiments show the bacteria respond to low iron. Vaccination against progressive atrophic rhinitis was developed by using a recombinant derivative ofP. multocidatoxin. 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 onP. multocidadevelopment 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 ofP. multocidato 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 vitroexperiments show the responses of the bacteria to low iron and different iron sources, such astransferrinandhemoglobin.P. multocidagenes 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 transformationis the process by which a recipient bacterial cell takes up DNA from a neighboring cell and integrates this DNA into the recipient'sgenome.P. multocidaDNA contains high frequencies of putativeDNA uptake sequences(DUSs) identical to those inHemophilus influenzaethat promote donor DNA uptake duringtransformation.[21]The location of these sequences inP. multocidashows a skewed distribution towards genome maintenance genes, such as those involved inDNA repair.This finding suggests thatP. multocidamight 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.ISBN978-1-904455-34-9.
- ^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
- ^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]
- ^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.ISSN1751-0147.PMC1766361.PMID17204146.
- ^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, eaao2314DOI: 10.1126/sciadv.aao2314
- ^Ryan KJ; Ray CG, eds. (2004).Sherris Medical Microbiology(4th ed.). McGraw Hill.ISBN0-8385-8529-9.
- ^abCasolari 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 ofPasteurella multocidaproduces a truncatedlipopolysaccharidestructure 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 onP. multocidapopulations in water. “Journal of Wildlife Diseases”, vol. 25, no.2 (232-239)
- ^Boyce, JD. How doesP. multocidarespond to the host environment? “Current Opinion in Microbiology” vol.9 no.1 (117-122)
- ^abDavidsen 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:10.1093/nar/gkh255.PMC373393.PMID14960717.
