Abstract
Fowl cholera caused by Pasteurella multocida exerts a massive economic burden on the poultry industry. Lipopolysaccharide (LPS) is essential for the growth of P. multocida genotype L1 strains in chickens and specific truncations to the full length LPS structure can attenuate bacterial virulence. Here we further dissected the roles of the outer core transferase genes pcgD and hptE in bacterial resistance to duck serum, outer membrane permeability and virulence in ducks. Two P. multocida mutants, ΔpcgD and ΔhptE, were constructed, and silver staining confirmed that they all produced truncated LPS profiles. Inactivation of pcgD or hptE did not affect bacterial susceptibility to duck serum and outer membrane permeability but resulted in attenuated virulence in ducks to some extent. After high-dose inoculation, ΔpcgD showed remarkably reduced colonization levels in the blood and spleen but not in the lung and liver and caused decreased injuries in the spleen and liver compared with the wild-type strain. In contrast, the ΔhptE loads declined only in the blood, and ΔhptE infection caused decreased splenic lesions but also induced severe hepatic lesions. Furthermore, compared with the wild-type strain, ΔpcgD was significantly attenuated upon oral or intramuscular challenge, whereas ΔhptE exhibited reduced virulence only upon oral infection. Therefore, the pcgD deletion caused greater virulence attenuation in ducks, indicating the critical role of pcgD in P. multocida infection establishment and survival.
Highlights
Pasteurella multocida (P. multocida), an encapsulated gram-negative bacterium, can cause endemic and epizootic diseases in a wide range of animal species, including fowl cholera (FC) in domestic and wild birds
The mutants carrying the empty plasmid produced truncated LPS phenotypes, while complementation of each mutation with the appropriate gene provided in trans resulted in the production of a longer LPS molecule compared with the LPS produced by the corresponding mutant (Figure 3), suggesting the production of functional PcgD or HptE protein and formation of the full-length LPS outer core in the complemented strain
FC is one of the most important diseases, leading to massive economic losses to the poultry industry worldwide; the underlying mechanisms of the high mortality and severe tissue damage caused by the causative agent, P. multocida, are still poorly understood [7]
Summary
Pasteurella multocida (P. multocida), an encapsulated gram-negative bacterium, can cause endemic and epizootic diseases in a wide range of animal species, including fowl cholera (FC) in domestic and wild birds. FC manifests as acute or peracute systemic disease or chronic localized infection, leading to a high rate of morbidity and mortality in birds and posing a massive economic burden on the poultry industry worldwide. The clinical course of the disease usually ranges from a few hours to several days with a virulent strain, and death occurs suddenly in peracute cases [7]. Despite the economic importance of the bacterium, P. multocida is still an enigmatic pathogen, and the exact molecular mechanisms responsible for pathogenesis in pasteurellosis remain largely unknown. Only a few virulence factors, such as capsule and LPS [8, 9], and several regulators, including Hfq, Fis, Crp, and PhoP [10,11,12,13], have been shown to have roles in P. multocida virulence
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