Line 7: |
Line 7: |
| | | |
| *Important member of the enterobacteria | | *Important member of the enterobacteria |
− | *Cause disease in humans and animals | + | *Cause disease in humans and animals worldwide |
| *Reservior of infection in poulty, pigs, rodents, cattle, dogs | | *Reservior of infection in poulty, pigs, rodents, cattle, dogs |
| + | *Bacteria may be present in water, soil, animal feed, raw meat |
| *Cause enteritis and systemic infection (septicaemia and abortion) | | *Cause enteritis and systemic infection (septicaemia and abortion) |
| *''Salmonella'' may be carried sub-clinically | | *''Salmonella'' may be carried sub-clinically |
Line 31: |
Line 32: |
| *Single species, ''Salmonella enterica'' | | *Single species, ''Salmonella enterica'' |
| *Over 2400 pathogenic serotypes or serovars identified | | *Over 2400 pathogenic serotypes or serovars identified |
− | *Grouped into 9 groups according to O antigen (lipopolysaccharide) by the Kauffmann-White scheme - determined by slide agglutination of the bacteria with specific antisera | + | *Grouped into 9 groups according to Somatic, O antigen (lipopolysaccharide) by the Kauffmann-White scheme - determined by slide agglutination of the bacteria with specific antisera |
− | *Categorised into serovars depending on and H (flagellar) antigen, e.g. ''Salmonella enterica'' subspecies ''enterica'' serovar Tymphimurium; must also determine phase of H antigen | + | *Categorised into serovars depending on and H (Flagellar) antigen, e.g. ''Salmonella enterica'' subspecies ''enterica'' serovar Tymphimurium; must also determine phase of H antigen (isolates must be in phase 1 to be typed) |
| + | *Most animal and human isolates in Groups B to E |
| | | |
− | ===Pathogenesis=== | + | ===Pathogenicity=== |
| | | |
| *Faecal-oral transmission | | *Faecal-oral transmission |
| + | *Infection frequently transmitted from faeces of rodents and birds |
| + | *Young, immunocompromised animals particularly susceptible |
| *Comparitively large dose required for infection due to gastric acid, normal intestinal flora and local immunity | | *Comparitively large dose required for infection due to gastric acid, normal intestinal flora and local immunity |
| *Enterocolitis: | | *Enterocolitis: |
| **Acute enteritis | | **Acute enteritis |
− | **Bacteria multiply in the intestine and damage epithelial cells | + | **Bacteria adhere to intestinal epithelial cells in the ileum and colon, probably via fimbrae, O antigen and flagellar H antigen |
− | **Cytotoxin may cause epithelial cell damage | + | **Multiply in and destroy epithelial cells |
| + | **Cytotoxin may cause epithelial cell damage by inhibiting protein synthesis and causing calcium escape from cells |
| **Enterotoxin may induce fluid secretion into intestinal lumen | | **Enterotoxin may induce fluid secretion into intestinal lumen |
| **Degeneration of microvilli | | **Degeneration of microvilli |
| *Systemic disease: | | *Systemic disease: |
− | **Bacteria internalised by intestinal epithelial cells | + | **Bacteria invade and replicate in host cells and resist phagocytosis and destruction by complement |
| + | **Bacteria internalised by intestinal epithelial cells by inducing ruffling of cell membranes and uptake into vesicles |
| + | **The organisms replicate within the vesicles and are released from the cells |
| **Stimulate immune response on reaching the lamina propria | | **Stimulate immune response on reaching the lamina propria |
| **Inflammatory response with phagocytosis of bacteria by neutrophils and macrophages | | **Inflammatory response with phagocytosis of bacteria by neutrophils and macrophages |
| **Bacteria either destroyed by the phagocytic cells or survive and multiply in the cells to cause systemic disease | | **Bacteria either destroyed by the phagocytic cells or survive and multiply in the cells to cause systemic disease |
| + | **Resistance to phagocytosis and destruction by complement allows spread within the body |
| + | **LPS O antigens prevent damage to bacterial cell wall by complement |
| + | **LPS also causes endotoxaemia, and may contribute to local inflammatory response damaging intestinal cells to cause diarrhoea |
| + | **Endotoxic shock during septicaemic salmonellosis due to LPS |
| **Intracellular carriage if bacteria no completely removed | | **Intracellular carriage if bacteria no completely removed |
| **Invasive potential of certain strains e.e ''Salmonella'' Dublin associated with carriage of a large plasmid, encoding genes to allow intracellular survival in macrophages and also to allow iron acquisition | | **Invasive potential of certain strains e.e ''Salmonella'' Dublin associated with carriage of a large plasmid, encoding genes to allow intracellular survival in macrophages and also to allow iron acquisition |
Line 58: |
Line 69: |
| **Bacteria can survive intracellularly, avioding the immune system and antimicrobials | | **Bacteria can survive intracellularly, avioding the immune system and antimicrobials |
| **May have latent carriage and intermittent excretion in faeces | | **May have latent carriage and intermittent excretion in faeces |
− | **Stress promotes excretion in carrier animals | + | **Stresses e.g. transportaion, illness, parturition, overcrowding promote excretion in carrier animals |
| **Tortoises, terrapins, snakes and other reptiles ofter carry ''Salmonellae'' | | **Tortoises, terrapins, snakes and other reptiles ofter carry ''Salmonellae'' |
| **Asymptomatic carriage allows faecal spread of infection | | **Asymptomatic carriage allows faecal spread of infection |