Actinobacillus pleuropneumoniae
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Actinobacillus pleuropneumoniae
The bacterium Actinobacillus pleuropneumoniae (App) consists of at least twelve different serotypes, some of which produce no disease but others cause severe disease. Serotypes vary in different countries. Types 1, 5, 9, 11 and 12 are usually highly virulent and strains 3 and 6 are mild. App is carried in the tonsils and upper respiratory tract
| Kingdom | Bacteria |
|---|---|
| Phylum | Proteobacteria |
| Class | Gammaproteobacteria |
| Order | Pasteurellales |
| Family | Pasteurellaceae |
| Genus | Actinobacillus |
| Species | A. pleuropneumoniae |
| Binomial | Actinobacillus pleuropneumoniae |
Contents |
[edit] Surface Characteristics
Actinobacillus pleuropneumoniae consists of a characteristic lipopolysaccharide [LPS] on its outer surface. It consists of a polysaccharide covalently linked to a lipid component, termed lipid A, which anchors the LPS in the outer membrane. This polysaccharide is divided into the core oligosaccharide (linked to lipid A) and the O-polysaccharide or O-antigen. O chains of LPS of most serotypes were structurally similar, being composed of repeating tetrasaccharide units with identical trisaccharide residues forming a common backbone
[edit] Transmission
APP quickly colonizes the host animal, first by attaching to the epithelial cells of the tonsils and then moving to the lower respiratory tract where it creates the majority of damage.
[edit] Pathogenic Activity
Actinobacillus pleuropneumoniae [APP] causes porcine pleuropneumonia, a highly contagious disease for which there is no effective vaccine. It has high morbidity and mortality rates and can cause severe economic losses to swine producers. APP severely damages the lungs of growing pigs and can linger on as a chronic infection, leading to poor weight gain and serving as a source of future outbreaks. Swine producers must rapidly control APP outbreaks and use preventative measures to control this disease.
[edit] Virulence
As the bacteria multiplies, it releases particles of an outer membrane that contain lipopolysaccharides (LPS) and cytotoxins. Neutrophils arriving as the beginning of an inflammatory response are attracted by the LPS and are then destroyed by the cytotoxins. As the neutrophils are destroyed, lysozymes are released, damaging nearby tissue. The tissue damage can progress rapidly, and some animals that are infected with APP will die within 4-12 hours of exposure. The LPS and cytotoxins not only help the bacteria damage the host cells, they also prevent the bacteria from being destroyed by impairing phagocytosis and complement activity.
[edit] References
Bossé JT, Janson H, Sheehan BJ, Beddek AJ, Rycroft AN, Kroll JS, Langford PR. [2002] Actinobacillus pleuropneumoniae: pathobiology and pathogenesis of infection. Microbes Infect 4(2): 225-35 PMID: 11880056
