Difference between revisions of "Erysipelothrix rhusiopathiae"
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*Non-motile | *Non-motile | ||
*Catalase negative, oxidase negative, coagulase positive | *Catalase negative, oxidase negative, coagulase positive | ||
| − | |||
| − | |||
*Grow on nutrient agar; growth enhanced by addition of blood or serum | *Grow on nutrient agar; growth enhanced by addition of blood or serum | ||
*Small colonies with incomplete haemolysis in 48 hours | *Small colonies with incomplete haemolysis in 48 hours | ||
| − | *Hydrogen sulphide | + | *Hydrogen sulphide formed as black central line in TSI agar |
*Growth over wide rangs of temperatures and pH | *Growth over wide rangs of temperatures and pH | ||
| + | |||
| + | |||
| + | ===Identification and diagnosis=== | ||
| + | |||
| + | *Isolates from acute infections produce smooth colonies; 1.5mm diamteter, convex and circular with even edges | ||
| + | *Isolates from chronic infections produce rough colonies; larger, flat and opaque colonieswith irregular edges | ||
| + | *Biochemical tests | ||
| + | *Serotypying according to a heat-stable peptidoglycan extracted from the cell wall | ||
| + | *Virulence testing in lab animals | ||
| + | *PCR for detection of virulent isolates | ||
| + | |||
| + | |||
| + | ===Pathogenesis and pathogenicity=== | ||
| + | |||
| + | *Route of infection: ingestion from pig faeces | ||
| + | *Entry via tonsils, skin or mucous membranes | ||
| + | *Capsule prevents phagocytosis | ||
| + | *Adhere to endothelial cells | ||
| + | *Produce neurominidase which enhances cell penetration | ||
| + | *Septicaemia with vascular damage | ||
| + | *Swelling of endothelial cells, monocyte adherence to vascular walls and hyaline microthrombus formation | ||
| + | *Bacteria localise in synovia of joints and on heart valves during bacteraemia and cause chronic lesions | ||
| + | *Host immune response to persistent bacterial antigens causes long-term damage to the joints | ||
| + | |||
| + | |||
| + | ===Clinical infections=== | ||
Revision as of 12:02, 26 May 2008
- Causes arthritis in sheep and arthritis and discospondylitis in pigs
- May be involved in cutaneous lesions
Overview
- Causes erysipelas in pigs and turkeys worldwide
- Occasionally infects sheep and other animals
- Causes erysipeloid, a localised cellulitis in humans
- Found in porcine tonsils - 50% of pigs are thought to be carriers
- Bacteria excreted in faeces and oronasal secretions
- Survive in soil for less than 35 days
- Present on fish
Characteristics
- Gram-positive, small rod (smooth form) or filamentous (rough form)
- Facultative anaerobe
- Non-motile
- Catalase negative, oxidase negative, coagulase positive
- Grow on nutrient agar; growth enhanced by addition of blood or serum
- Small colonies with incomplete haemolysis in 48 hours
- Hydrogen sulphide formed as black central line in TSI agar
- Growth over wide rangs of temperatures and pH
Identification and diagnosis
- Isolates from acute infections produce smooth colonies; 1.5mm diamteter, convex and circular with even edges
- Isolates from chronic infections produce rough colonies; larger, flat and opaque colonieswith irregular edges
- Biochemical tests
- Serotypying according to a heat-stable peptidoglycan extracted from the cell wall
- Virulence testing in lab animals
- PCR for detection of virulent isolates
Pathogenesis and pathogenicity
- Route of infection: ingestion from pig faeces
- Entry via tonsils, skin or mucous membranes
- Capsule prevents phagocytosis
- Adhere to endothelial cells
- Produce neurominidase which enhances cell penetration
- Septicaemia with vascular damage
- Swelling of endothelial cells, monocyte adherence to vascular walls and hyaline microthrombus formation
- Bacteria localise in synovia of joints and on heart valves during bacteraemia and cause chronic lesions
- Host immune response to persistent bacterial antigens causes long-term damage to the joints