| Pasteurella multocida | |
|---|---|
 | |
| Gram-stained photomicrograph depicting numerousPasteurella multocida bacteria | |
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Pseudomonadati |
| Phylum: | Pseudomonadota |
| Class: | Gammaproteobacteria |
| Order: | Pasteurellales |
| Family: | Pasteurellaceae |
| Genus: | Pasteurella |
| Species: | P. multocida |
| Binomial name | |
| Pasteurella multocida Trevisan 1887 (Approved Lists 1980) | |
Pasteurella multocida is aGram-negative, nonmotile,penicillin-sensitivecoccobacillus from the familyPasteurellaceae.[1] Strains of the species are currently classified into fiveserogroups (A, B, D, E, F) based oncapsular composition and 16 somaticserovars (1–16).P. multocida is the cause of a range of diseases in mammals and birds, includingfowl cholera inpoultry,atrophic rhinitis in pigs, and bovine hemorrhagicsepticemia in cattle and buffalo. It can also cause azoonotic 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 respiratorymicrobiota.
Pasteurella multocida was first found in 1878 in cholera-infected birds. However, it was not isolated until 1880, byLouis Pasteur, in whose honorPasteurella is named.[2]
Pasteurella 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 orfowl 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 ofsnow geese. TheP. multocida serotype-1 is most associated with avian cholera in North America, but the bacterium does not linger inwetlands for extended periods of time.[3]P. multocida causes atrophic rhinitis in pigs;[4] it also can causepneumonia orbovine respiratory disease in cattle.[5][6] It may be responsible for mass mortality insaiga 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. Highleukocyte andneutrophil counts 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, abacteremia can result, causing anosteomyelitis orendocarditis. 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 barrier and causemeningitis.[9]
Pasteurella. multocida expresses a range ofvirulence factors including apolysaccharidecapsule and the variablecarbohydrate surface molecule,lipopolysaccharide (LPS). The capsule has been shown in strains of serogroups A and B to help resistphagocytosis by hostimmune cells and capsule type A has also been shown to help resist complement-mediatedlysis.[10][11] The LPS produced byP. 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 noO-antigen on the LPS and the molecule is similar to LPS produced byHaemophilus influenzae and thelipooligosaccharide ofNeisseria 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. multocida toxin (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 inactin stress fiber formation. Formation of stress fibers may aid in theendocytosis ofP. multocida. The host cell cycle is also modulated by the toxin, which can act as an intracellularmitogen.[13]P. multocida has been observed invading and replicating inside hostamoebae, causing lysis in the host.P. multocida will grow at 37 °C (99 °F) onblood orchocolate agar,HS agar,[14] but will not grow onMacConkey agar. Colony growth is accompanied by a characteristic "mousy" odor due tometabolic products.
Afacultative anaerobe,P. multocida it isoxidase-positive andcatalase-positive. It can alsoferment a large number ofcarbohydrates in anaerobic conditions.[9] The survival ofP. multocida bacteria has also been shown to be increased by the addition of salt into their environments. Levels ofsucrose andpH also have been shown to have minor effects on bacterial survival.[15]
Diagnosis of the bacterium in humans was traditionally based on clinical findings, and culture andserological testing, butfalse negatives have 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. multocida infection 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 withfluoroquinolones ortetracyclines; fluoroquinolones inhibit bacterialDNA synthesis and tetracyclines interfere withprotein synthesis by binding to the bacterial30Sribosomal subunit. Despite poorin vitro susceptibility results,macrolides (binding to the ribosome) also can be applied, certainly in the case of pulmonary complications. Due to the polymicrobial etiology ofP. 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]
Pasteurella multocidamutants 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 ofP. 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 onP. 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 ofP. 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 astransferrin andhemoglobin.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'sgenome.P. multocida DNA contains high frequencies of putativeDNA uptake sequences (DUSs) identical to those inHemophilus influenzae that promote donor DNA uptake duringtransformation.[21] The location of these sequences inP. multocida shows a skewed distribution towards genome maintenance genes, such as those involved inDNA repair. This finding suggests thatP. 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]