Difference between revisions of "Yersinia"
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− | + | * Cause [[Intestines - disease due to pathogens|intestinal disease]] | |
+ | |||
+ | ===Overview=== | ||
+ | |||
+ | *Cause disease in animals and are important zoonoses | ||
+ | *10 species of which ''Y. pestis, Y. pseudotuberculosis and Y. enterocolitica'' are pathogenic to animals and humans; ''Y. pestis'' is the most pathogenic | ||
+ | *Rodents provide a reservoir of ''Y. pestis'', which is the cause of human plague; fleas transmit the infection to other animals and humans | ||
+ | *''Y. pseudotuberculosis and Y. enterocolitica'' reside in the intestine of domestic and wild animals and birds | ||
+ | *Birds may cause mechanical transfer of the organisms | ||
+ | |||
+ | ===Characteristics=== | ||
+ | |||
+ | *Enterobacteria, but grow more slowly and at lower temperatures than other enterobacteria | ||
+ | *Gram negative, non-spore forming, facultative anaerobes - rods or colibacilli | ||
+ | *Non-lactose fermentors | ||
+ | *Facultative intracellular pathogens | ||
+ | *Show bipolar staining in Giemsa-stained smears from animal tissue | ||
+ | *Pathogenic strains identified by serotyping and biotyping | ||
+ | |||
+ | ===Pathogenesis=== | ||
+ | |||
+ | *''Y. enterocolitica and Y. pseudotuberculosis'' enter the intestinal mucosa via M cells of the Peyer's patches | ||
+ | *Engulfed by macrphages in the mucosa | ||
+ | *All three invasive species are facultative intracellular organisms and grow inside macrophages | ||
+ | *Plasmid and chromosomal-encoded virulence factors required for survival and multiplication in macrophages | ||
+ | *Survive in phagolysosomes and do not interfere with degranulation or lysosomal fusion | ||
+ | *Resistant to macrophage killing mechanisms | ||
+ | *Antiphagocytic proteins secreted by the organisms interfere with host neutrophils | ||
+ | *''Y. pestis is more invasive than the other species and also possesses and antiphagocytic capsule and a plasminogen activator which aids systemic spread; endotoxin also contributes to its pathogenicity | ||
+ | *Transport within macrophages to mesenteric lymph nodes | ||
+ | *Replication in lymph nodes and development of necrotic lesions, with neutrophil invasion | ||
+ | *The bacteria destroy the macrophages causing septicaemia | ||
+ | |||
+ | ===Clnical infections=== | ||
+ | |||
+ | ===Diagnosis=== | ||
+ | |||
+ | ===Control=== | ||
+ | |||
+ | ===Treatment=== |
Revision as of 13:11, 9 February 2008
- Cause intestinal disease
Overview
- Cause disease in animals and are important zoonoses
- 10 species of which Y. pestis, Y. pseudotuberculosis and Y. enterocolitica are pathogenic to animals and humans; Y. pestis is the most pathogenic
- Rodents provide a reservoir of Y. pestis, which is the cause of human plague; fleas transmit the infection to other animals and humans
- Y. pseudotuberculosis and Y. enterocolitica reside in the intestine of domestic and wild animals and birds
- Birds may cause mechanical transfer of the organisms
Characteristics
- Enterobacteria, but grow more slowly and at lower temperatures than other enterobacteria
- Gram negative, non-spore forming, facultative anaerobes - rods or colibacilli
- Non-lactose fermentors
- Facultative intracellular pathogens
- Show bipolar staining in Giemsa-stained smears from animal tissue
- Pathogenic strains identified by serotyping and biotyping
Pathogenesis
- Y. enterocolitica and Y. pseudotuberculosis enter the intestinal mucosa via M cells of the Peyer's patches
- Engulfed by macrphages in the mucosa
- All three invasive species are facultative intracellular organisms and grow inside macrophages
- Plasmid and chromosomal-encoded virulence factors required for survival and multiplication in macrophages
- Survive in phagolysosomes and do not interfere with degranulation or lysosomal fusion
- Resistant to macrophage killing mechanisms
- Antiphagocytic proteins secreted by the organisms interfere with host neutrophils
- Y. pestis is more invasive than the other species and also possesses and antiphagocytic capsule and a plasminogen activator which aids systemic spread; endotoxin also contributes to its pathogenicity
- Transport within macrophages to mesenteric lymph nodes
- Replication in lymph nodes and development of necrotic lesions, with neutrophil invasion
- The bacteria destroy the macrophages causing septicaemia