Overview
- Important member of the enterobacteria
- Cause disease in humans and animals worldwide
- 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)
- Salmonella may be carried sub-clinically
- Some human strains cause enteric fever (S. Typhi causes typhoid), also gastroenteritis, septicaemia or bacteraemia
Characteristics
- Gram negative bacilli
- Facultative intracellular pathogens
- Non-lactose fermentors, oxidase negative
- Do not produce urease or indole from tryptophan
- Utilise citrate as a carbon source
- Reduce nitrates to nitrites
- Grow on MacConkey
- Red colonies on brilliant green agar indicating alkalinity
- Ferment glucose to produce acid and gas
- Usually produce hydrogen sulphide - red colinies with black centre on XLD agar
- Most motile with flagellae (H antigen)
- H antigen can be in phase 1 or phase 2, depending on a genetic switch allowing for one of the H antigen genes to be transcribed at any one time
Classification
- Single species, Salmonella enterica
- Over 2400 pathogenic serotypes or serovars identified
- 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 (isolates must be in phase 1 to be typed)
- Most animal and human isolates in Groups B to E
Pathogenicity
- 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
- Enterocolitis:
- Acute enteritis
- Bacteria adhere to intestinal epithelial cells in the ileum and colon, probably via fimbrae, O antigen and flagellar H antigen
- 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
- Degeneration of microvilli
- Systemic disease:
- 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
- Acute inflammation, possibly with ulceration; prostaglandin and cytokine production by epithelial cells; enterotoxin production damaging mucosa
- 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
- Resistance to phagocytosis and destruction by complement allows spread within the body - bacteraemia and septicaemia
- 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
- 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
- Salmonellae are facultative intracellular organisms, allowing them to move from the gut in macrophages and cause a bacteraemia and lesions throughout the body
- Possession of Pathogenicity Islands associated with virulence
- Carriage:
- Salmonellae can persist in the gut or gall bladder
- Excreted in faeces after clinical signs disappeared - active carriage
- Bacteria can survive intracellularly, avoiding the immune system and antimicrobials
- May have latent carriage and intermittent excretion in faeces
- Stresses e.g. transportaion, illness, parturition, overcrowding promote excretion in carrier animals and may cause clinical signs to be shown
- Tortoises, terrapins, snakes and other reptiles ofter carry Salmonellae
- Asymptomatic carriage allows faecal spread of infection
Clinical infections
- Zoonotic
- Outbreaks from contaminated imported meat and bone meal
- Some serotypes are host-specific, some infect a wide range of species
- Healthy adult carnivores are resistant to salmonellosis
- Clinical outcome depends on number of bacteria ingested, virulence of serotype, susceptibility of host
- Young and debilitated animals susceptible
- Salmonella serotypes:
- S. Tymphimurium infects many species; causes severe diarrhoea; non-invasive; causes of food poisoning in humans, e.g. from infected poultry
- S. enteritidis: non species-specific; losses in young birds; causes food poisoning in humans
- S. Dublin: invasive serovar; infects cattle
- S. Cholerae-Suis: primarily infects pigs; also causes severe human disease
- S. Pullorum: infects poultry; egg-transmitted; causes bacillary white diarrhoea, known as pullorum disease
- S. Gallinarum: infectes older birds; known as fowl typhoid
- S. Abortis-ovis: infects sheep
- S. Abortus-equi: infects horses outside of the UK
- S. Typhi, S. Paratyphi: infect humans
- Most human infections contracted from animals, especially poulty and cattle
- Enteric salmonellosis:
- Enterocolitis occurs in most farm animal species affecting all ages
- ulcerative enteritis
- Fever, depression, anorexia, foul-smelling diarrhoea containing blood, mucus and epithelial casts
- Dehydration and weight loss
- Abortion
- Fatal within days in severely young animals
- Milder syndrome where endemic on farms, possibly due to acquired immunity
- Chronic enterocolitis can occur in surviving pigs, cattle, horses, causing intermittent fever, soft faeces and gradual weight loss
- Septicaemic salmonellosis:
- Most common in calves, neonatal foals, pigs under one month
- Sudden onset fever, depression, recumbency
- Die within 48 hours if not treated
- Persistent diarrhoea, meningitis, arthritis or pneumonia may occur in surviving animals
- Found in arthritis of horses
- Can cause haemorrhagic disease by secondary thrombocytopenic disease
- S. Cholerae-Suis in pigs causes blue discoloration of ears and snout; co-infection with viruses causes severe clinical forms of disease
- Bovine Salmonellosis:
- Syndrome of fever and diarrhoea (with dysentery), often fatal, in calves and adult cattle
- May cause abortion of pregnant cattle in absence of other signs
- Septicaemia in neonates; accute enteritis in older calves
- Caused by infection with various Salmonella serotypes, e.g. S. Dublin and S. Typhimurium
- An important zoonosis and reportable
- Carrier animals important for spread
- Salmonella Dublin:
- Causes enterocolitis with blood-stained, foul-smelling diarrhoea containing mucus and epithelial cells
- Can cause fatal septicaemia - fever, depression, drop in milk yield; calves may develope arthritis, meningitis, pneumonia
- Abortion with no other clinical signs
- Chronic infections with S. Dublin in calves cause dry gangrene of extremities due to disseminated intravascular coagulation
- Can cause Osteomyelitis in young animals
- Most survivors become subclinical excretors
- May become latent carriers with no excretion
- Salmonellosis in poultry:
- S. Pullorum and S. Gallinarum now rare in UK due to eradication programs including the Pullorum test (whole blood slide agglutination to detect antibody to both S. Pullorum and S Gallinarum)
- These Salmonellae can infect the ovaries of hens and be transmitted via eggs
- Pullorum disease infects young chickens and turkeys (under 3 weeks); high mortality rates; anorexia, depression, white diarrhoea; white nodules throughout lungs; focal necrosis of liver and spleen
- Fowl typhoid causes similar lesions to pullorum disease in young birds; septicaemic condition in adult birds with sudden death (enlarged, friable, bole-stained liver and enlarged spleen)
- Paratyphoid caused by non host-specific Salmonella serotypes, e.g. S. Enteritidis and S. Typhimurium; often subclinical infections
Diagnosis
- History of previous outbreaks; clinical signs
- Post mortem: enterocolitis; blood-stained intestinal contents; enlarged mesenteric lymph nodes
- Laboratory confirmation by detection in faeces and blood from live animals; intestinal contents and tissue samples from dead animals
- Isolation from blood or tissues confirms septicaemic salmonellosis
- Heavy growth on plates innoculated with faeces or intestinal contents from infected animals suggests Salmonella as cause
- Light growth may suggest carrier state
- Culture specimens on BG and XLD agar; also add to enrichment broth such as selinite or tetrathionate broth; incubate plates and broth under aerobic conditions at 37 degrees centigrade for 48 hours; subculture from enrichment broth at 24 and 48 hours
- Suspicious colonies should be identified biochemically by reactions in TSI agar and lysine decarboxylase
- Slide agglutination using antisera for O and H antigens confirm the serotype
- The antigens in both phases of the H antigen must be identified
- Phage typing is used for epidemiological studies of isolates
- A rising antibody titre using paired serum samples in ELISA indicates active infection
Treatment
- Intravenous antibiotics used to treat septicaemic salmonellosis
- Effective antimicrobials include tetracyclines, chloramphenicol, trimethoprim-sulphonamides, ampicillin, amoxicillin, 3rd generation cephalosporins, fluoroquinolones, but depend on the susceptiblity of individual isolate
- Fluid and electrolyte replacent to prevent dehydration and shock
Control
- Reduce exposure of young animals from fomites, food, water, infected animals
- Avoid stresses e.g. overcrowding
- Purchase animals from reliable sources and isolate incoming animals
- Separate animals according to age
- Rodent control, good hygiene, pasture rotation
- Avoid grazing animals on pasture fertilised by slurry for at least 2 months after spreading
- Attenuated live S. Typhimurium and S. Dublin vaccines used in cattle
- Avoid oral prophylactic antimicrobials