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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