Pasteurella multocida

Pasteurella multocida is a Gram-negative, nonmotile, penicillin-sensitive coccobacillus belonging to the Pasteurellaceae family. Strains belonging to 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 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. P. multocida causes a range of diseases in wild and domesticated animals, as well as humans. The bacterium can be 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. P. multocida causes atrophic rhinitis in pigs; it also can cause pneumonia or bovine respiratory disease in cattle. It may be responsible for mass mortality in saiga antelopes. 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). 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. 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 belonging to 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. 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. 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. 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, 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. 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. 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. 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.