Gram-negativeBacilliEnterobacterales

Salmonella typhi

Facultative intracellular, flagellated Gram-negative bacillus of the family Enterobacteriaceae that causes typhoid (enteric) fever, characterized by sustained bacteremia, fever, and potential intestinal perforation.

Organism Card

DomainMust know
Identity
  • Salmonella enterica serovar Typhi (typhoidal Salmonella) [1][2]
  • G−ve bacillus; facultative anaerobe; Enterobacteriaceae
  • Human-only pathogen (no animal reservoir) — contrast with non-typhoidal Salmonella
  • Other typhoidal serovars: Paratyphi A, B, C
Lab discriminator
  • G−ve bacillus on Gram stain ("bacteria stained in red colour" — past paper clue) [5]
  • Non-lactose fermenter on MacConkey agar
  • H₂S producer on XLD / SS agar (black colonies)
  • Vi (virulence) capsular antigen — distinguishes Typhi from Paratyphi
  • Does NOT produce gas from glucose (vs most other Salmonella spp.)
Reservoir / transmission
  • Faecal-oral via contaminated water/food [1][2]
  • Strictly human reservoir; chronic gallbladder carriers excrete organism
  • Travel-associated: South/Southeast Asia (Bangladesh, India, Pakistan) — classic exam stem [1][5]
  • "Did not drink exclusively from bottled water" — key risk factor in vignette [5]
Key virulence
  • Vi capsule → anti-phagocytic; resists complement-mediated killing
  • Survives & replicates inside macrophages (intracellular pathogen)
  • Invades through Peyer's patches in terminal ileum → bacteraemia
  • IFN-gamma pathway defects (e.g. MSMD/STAT1 deficiency) → susceptibility to Salmonella [3]
Clinical syndromes
  • Enteric (typhoid) fever: stepwise rising fever over 1st week [1][2]
  • Faget sign: relative bradycardia / sphygmothermic dissociation (fever 40°C + pulse 50 bpm) [1][5]
  • Rose spots: faint salmon-coloured macules on trunk/abdomen [1][2]
  • Constipation early → diarrhoea later (classic biphasic GI pattern) [5]
  • Hepatosplenomegaly; RLQ tenderness (Peyer's patches)
  • Complications: GI perforation (ileal, surgical emergency), myocarditis, hepatitis, DIC, osteomyelitis [1][2][5]
Diagnosis
  • Blood culture: positive 40–80% (best in 1st week of fever) [1][2][4]
  • Stool culture: positive 30–40% (often negative early) [1][2][4]
  • Bone marrow aspirate culture: GOLD STANDARD (most sensitive) — usually not done due to invasiveness [4]
  • Widal test (serology): anti-O and anti-H agglutinating antibodies; 4-fold rise in paired sera needed; cannot differentiate Typhi vs Paratyphi; limited utility in endemic areas [1][2][4]
  • Screen for sensitivity to 3rd-gen cephalosporins and fluoroquinolones [4]
Treatment
  • Antibiotics of choice: 3rd-gen cephalosporins (ceftriaxone), azithromycin, fluoroquinolones (if susceptible) [1][6]
  • Fluoroquinolone resistance increasingly common — always check susceptibility [6]
  • ± Steroids in severe/complicated cases [2]
  • Surgical intervention for GI perforation (emergency laparotomy) [5]
Prevention
  • Food and water hygiene — most important prevention measure [1][2][6]
  • Vaccines available (Vi polysaccharide IM; Ty21a oral live attenuated) — but hygiene still paramount [6]
  • Notifiable disease in Hong Kong
  • S. Typhi is an encapsulated organism → post-splenectomy infection risk (OPSI list) [7]
Classic traps
  • Typhi vs non-typhoidal Salmonella: Typhi = enteric fever (systemic, invasive); NTS = gastroenteritis (inflammatory diarrhoea) [8]
  • Widal test trap: single titre meaningless; does NOT distinguish Typhi from Paratyphi [4]
  • Relative bradycardia + rose spots + travel from South Asia → typhoid (not malaria) [5]
  • Malaria also causes fever after travel but expect cyclical fever, anaemia, thrombocytopenia, no rose spots
  • Osteomyelitis in sickle cell disease: Salmonella is the classic pathogen (not S. aureus) [7]
  • Fecal mononuclear WBCs (not neutrophils) on stool exam — distinguishes invasive/typhoidal from inflammatory colitis [8]

Exam Intelligence

On this page

No Headings