Mannheimia haemolytica

Abstract

Mannheimia haemolytica serotype S1 is considered the predominant cause of bovine pneumonic pasteurellosis, or shipping fever. Various virulence factors allow M haemolytica to colonize the lungs and establish infection. These virulence factors include leukotoxin (LKT), lipopolysaccharide, adhesins, capsule, outer membrane proteins, and various proteases. The effects of LKT are species specific for ruminants, which stem from its unique interaction with the bovine b2 integrin receptor present on leukocytes. At low concentration, LKT can activate bovine leukocytes to undergo respiratory burst and degranulation and stimulate cytokine release from macrophages and histamine release from mast cells. At higher concentration, LKT induces formation of transmembrane pores and subsequent oncotic cell necrosis. The interaction of LKT with leukocytes is followed by activation of these leukocytes to undergo oxidative burst and release proinflammatory cytokines such as interleukins 1, 6, and 8 and tumor necrosis factor a. Tumor necrosis factor a and other proinflammatory cytokines contribute to the accumulation of leukocytes in the lung. Formation of transmembrane pores and subsequent cytolysis of activated leukocytes possibly cause leakage of products of respiratory burst and other inflammatory mediators into the surrounding pulmonary parenchyma and so give rise to fibrinous and necrotizing lobar pneumonia. The effects of LKT are enhanced by lipopolysaccharide, which is associated with the release of proinflammatory cytokines from the leukocytes, activation of complement and coagulation cascade, and cell cytolysis. Similarly, adhesins, capsule, outer membrane proteins, and proteases assist in pulmonary colonization, evasion of immune response, and establishment of the infection. This review focuses on the roles of these virulence factors in the pathogenesis of shipping fever.

Genomic signatures of Mannheimia haemolytica that associate with the lungs of cattle with respiratory disease, an integrative conjugative element, and antibiotic resistance genes

“…Typing of M. haemolytica strains based on capsular phenotypes and pulsed-field gel electrophoresis (PFGE) have both indicated that M. haemolytica is comprised of distinct sub-species, or strain types, that do not all equally associate with BRD [10]. Strains with either A2 or A4 capsular serotypes have been more frequently isolated from the upper respiratory tracts of cattle without signs of respiratory disease, while strains with A1 or A6 serotypes have been more frequently isolated from the lungs and nasopharynx of diseased animals [3, 10–12]. Similarly, a dendrogram of PFGE profiles from M. haemolytica strains isolated from the nasopharynx of cattle with or without signs of respiratory disease was found to have two major clusters that disproportionately represented isolates from animals with and without signs of BRD, respectively [13].…”

Pasteurella organism: Its isolation and identification from pneumonic lungs of goats in Ethiopia

“…Various M. haemolytica virulence factors influence the outcome of bacterial-host interactions (Singh et al, 2011). Capsular serotyping provides the primary basis for the classification of strains and epidemiological typing of M. haemolytica (Peterson et al, 2001).…”

Genome Sequence of a Spontaneous Nonhemolytic Mutant of Mannheimia haemolytica 16041065 GH

“…An exotoxin, leukotoxin, is considered the most important virulence factor associated with M. haemolytica (6). Leukotoxin is responsible for M. haemolytica hemolysis on blood agar and causes leukocyte necrosis and apoptosis in vivo , thus allowing the bacterium to escape phagocytosis and killing by neutrophils and macrophages (7, 8). …”