BSCI 424 — PATHOGENIC MICROBIOLOGY — Fall 2000

Salmonella Summary

Morphology & Physiology:

  Small Gram-negative bacillus

  Antigens:

  Usually motile (H antigen)

  Possess polysaccharide capsule (K antigen on most Salmonella spp. or Vi antigen of Salmonella typhi and Salmonella paratyphi)

  Specific O antigens

  H₂S produced from inorganic sulfur

  Acid and gas produced from glucose

  Note: S. typhi is a non-gas producer and produces minimal H₂S

  Salmonella spp. are relatively resistant to bile acids and this trait is utilized for selective isolation media

Taxonomy:

  Family Enterobacteriaceae:

  All Enterobacteriaciae:

1. ferment glucose

2. reduce nitrates (NO₃ to NO₂ or all the way to N₂)
   

3. are oxidase negative

  The genus Salmonella contains over 2,000 sero-species and is one of the most important pathogens in the family Enterobacteriaceae

   Taxonomically, all strains of Salmonella fall within one species, S. enterica, but this nomenclature has not caught on and the genus continues to be recognized by the popular species names, many named on the basis of serotyping and outbreaks

  Salmonella enteritidis (enteritis)

  Salmonella typhimurium (enteritis)

  Salmonella cholerasuis (septicemia)

  Salmonella typhi (enteric fever; asymptomatic carriage)

  Salmonella paratyphi (enteric fever; asymptomatic carriage)

  The majority of medically important isolates are found in only a few sero-species

Clinical Syndromes:

  Enteritis (acute gastroenteritis): nausea, vomiting, nonbloody diarrhea, fever (see clinical progression described below in Pathogenesis & Immunity section)

  Enteric fever: prototype is typhoid fever and less severe paratyphoid fever (see clinical progression described below in Pathogenesis & Immunity section)

  Septicemia (particularly S. choleraesuis)

  Prolonged state with fever, chills, anorexia, and anemia

  Lesions in other tissues

  Asymptomatic carriage: gall bladder is the reservoir for S. typhi

Epidemiology:

  Enteritis

  Members of this genus are ubiquitous in the environment and are found in association with both warm and cold blooded animals

  High infectious dose (10⁸ CFU)

  Foodborne disease: poultry, eggs, dairy products, cross-contaminated foods

 6-48h incubation

  Enteric fevers

  Infectious dose (10⁶ CFU)

  Transmission via fecal-oral route = person-to-person spread by chronic carrier through fecally-contaminated food or water

 10-14 day incubation to signs of sepsis; sustained fever (delirium) for one to several weeks before abdominal pain and gastrointestinal symptoms

Pathogenesis & Immunity:

  Exposure to the O and H antigens stimulates the production of specific antibodies

  Natural infection provides limited protection

Enteritis and Septicemia:

  Surface antigens: play a role in attachment and intracellular survival

  Invasiveness

  Penetrate mucus, adhere to and invade into epithelial layer (enterocytes) of terminal small intestine (ileum) and further into subepithelial tissue

  Bacterial cells are internalized in endocytic vacuoles in which the organisms multiply

 PMN's confine infection to gastrointestinal (GI) tract, but organisms may spread hematogenously (through blood, i.e., septicemia) to other body sites

  Inflammatory response mediates release of prostaglandins, stimulating cAMP and active fluid secretion with loose diarrheal stools

 Epithelial destruction occurs during late stage of disease

  Exotoxins

  Several Salmonella serotypes produce enterotoxins similar to both the heat-labile (LT) and heat-stable enterotoxins (ST) , but their effect has not been identified

  A distinct cytotoxin is also produced and may be involved in invasion and cell destruction

Enteric Fevers:

  Surface antigens: play a role in attachment and intracellular survival

  Vi antigen (capsular polysaccharide) of S. typhi and S. paratyphi

  Smooth and rough variants

  Invasiveness

  Pass through intestinal epithelial cells in ileocecal region and infect the regional lymphatic system, invade the bloodstream, and infect other parts of the reticuloendothelial system

  Organisms are phagocytosed by macrophages and monocytes, but survive, multiply and are transported to the liver, spleen, and bone marrow where they continue to replicate

 During the second week, the organisms reenter the bloodstream and cause prolonged bacteremia; biliary tree and other organs are infected; gradually increasing and sustained fever most likely from endotoxemia

   During the second to third week, the bacteria colonize the gall bladder and reinfect the intestinal tract with diarrheal symptoms and possible necrosis of the Peyer's patches

  Endotoxin: could be responsible for the fever or the enteric lesions seen in typhoid fever

Laboratory Identification:

  Stool specimens and rectal swabs should be cultured soon after collection or placed in appropriate transport medium (e.g., Cary-Blair medium)

  Readily isolated on selective/differential agar media (e.g., XLD, XLT-4, SS, or brilliant green agar supplemented with novobiocin)

  Lactose nonfermenter

  Suspect colonies are further analyzed using various biochemicals

  Further identification should be pursued by serotyping and molecular diagnostic methodology

Treatment, Prevention & Control:

  Enteritis: Supportive therapy, dehydration prevention, balancing electrolytes; Avoid antibiotics in gastroenteritis to prevent prolonged carrier state

  Enteric fever or septicemia: ampicillin or chloramphenicol; resistant isolates occur

  S. typhi carried in gall bladder; surgically remove and treat with ampicillin; 85% cure of carrier state

  Observe water standards

  Cook and store foods properly

  Treat carriers, special precautions with food handlers

  Vaccines for typhoid fever

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