Microbiology chapters
Salmonella, E. coli, Pseudomonas and Acinetobacter
The Gram-negative bacilli the exam asks about: Salmonella Typhi and typhoid fever (pathogenesis, the week-by-week diagnostic tests, carriers, XDR typhoid, vaccines), non-typhoidal Salmonella, the diarrhoeagenic E. coli types and E. coli in UTI and neonatal meningitis, and the hospital pathogens Pseudomonas aeruginosa and Acinetobacter baumannii.
In 30 seconds
- Salmonella Typhi (non-lactose fermenter, H₂S +, Vi capsule) spreads by the faecal-oral route from cases and chronic carriers (bacteria in the gallbladder), invades through Peyer patches, multiplies in macrophages and causes enteric fever: step-ladder fever, relative bradycardia, rose spots, splenomegaly, constipation or diarrhoea, and in week 3 intestinal perforation and haemorrhage; diagnosis: blood culture in week 1 (best), bone marrow culture (most sensitive, even after antibiotics), stool and urine culture from week 2–3, Widal (rising O and H titres, poor specificity); Pakistan's XDR typhoid (since 2016) needs azithromycin or carbapenems, and the typhoid conjugate vaccine is in the EPI.
- E. coli: commonest cause of UTI (P fimbriae) and of Gram-negative sepsis, neonatal meningitis (K1 capsule); diarrhoeal types: ETEC (travellers' diarrhoea, LT/ST toxins), EPEC (infant diarrhoea), EHEC O157:H7 (bloody diarrhoea, Shiga-like toxin → haemolytic uraemic syndrome; avoid antibiotics), EIEC (dysentery), EAEC.
- Pseudomonas aeruginosa (oxidase +, non-lactose fermenter, obligate aerobe, blue-green pyocyanin, grape smell) infects burns, cystic fibrosis lungs, ventilated patients, eyes and ears (malignant otitis externa in diabetics), and is often multidrug-resistant; Acinetobacter baumannii causes ICU ventilator pneumonia and wound infections, often carbapenem-resistant (colistin).
On this page
Salmonella
Classification
- S. enterica serovar Typhi and Paratyphi A, B, C: enteric (typhoid) fever; only in humans.
- Non-typhoidal serovars (S. Enteritidis, S. Typhimurium): gastroenteritis; animal reservoirs (poultry, eggs).
Motile (unlike Shigella), non-lactose fermenting, H₂S positive (except Paratyphi A).
Typhoid fever: pathogenesis
- Faecal-oral spread via contaminated water and food; sources are patients and chronic carriers (often food handlers: "Typhoid Mary"). A fairly large dose is needed (stomach acid protects; antacids increase risk).
- Bacteria cross the small-bowel mucosa through M cells of Peyer patches (terminal ileum).
- Taken up by macrophages, carried to mesenteric nodes, then a primary bacteraemia seeds the liver, spleen and bone marrow (reticuloendothelial system), where they multiply (incubation about 1–3 weeks).
- Secondary bacteraemia → symptoms; bacteria reach the gallbladder (bile) and re-enter the gut, inflaming Peyer patches (ulceration).
- Vi capsule resists phagocytosis and complement.
Clinical features
- Week 1: gradually rising (step-ladder) fever, headache, malaise, dry cough, relative bradycardia (pulse slower than expected for the fever), constipation (diarrhoea in children and HIV), coated tongue.
- Week 2: rose spots (faint pink macules on the trunk, fade on pressure), splenomegaly, hepatomegaly, abdominal tenderness, toxaemia, delirium ("typhoid state").
- Week 3: complications: intestinal perforation and haemorrhage (terminal ileal ulcers along the long axis of the gut), encephalopathy, myocarditis, hepatitis, cholecystitis, osteomyelitis.
- Blood: leucopenia with relative lymphocytosis, mild anaemia, raised liver enzymes.
- Relapse in some cases; chronic carrier state (excretion for more than a year) in a small proportion, especially women with gallstones: bacteria persist in the gallbladder.
Laboratory diagnosis by week
| Test | Best time | Notes |
|---|---|---|
| Blood culture | Week 1 (positive in most untreated cases) | Best early test; also gives antibiotic sensitivity; less sensitive after antibiotics |
| Bone marrow culture | Any time | Most sensitive; stays positive after antibiotics have started |
| Stool culture | Weeks 2–3 onward (also for carriers) | Enrichment in selenite F broth; plated on DCA, XLD, Wilson-Blair (black colonies) |
| Urine culture | Weeks 2–3 | Lower yield |
| Widal test (tube agglutination for O and H antibodies) | From the end of week 1; best as a rising titre (4-fold rise in paired sera) | Poor sensitivity and specificity: false positives from previous infection, vaccination, cross-reacting infections and anamnestic responses in endemic countries like Pakistan; false negatives early or after antibiotics. O antibodies rise earlier and fall sooner (recent infection); H antibodies persist (past infection or vaccination) |
| Typhidot and other rapid antibody tests | Week 1–2 | Variable accuracy |
| Vi antibody | Chronic carriers | Screening food handlers |
| Duodenal string test / bile culture | Carriers | (none commonly tested) |
High-yield
Typhoid diagnosis by week: "BASU": Blood culture (week 1), Antibodies (Widal, week 2), Stool (week 3), Urine (week 3–4). Bone marrow culture is the most sensitive at any stage.
Treatment and prevention
- XDR typhoid (outbreak since 2016, starting in Hyderabad, Sindh): resistant to ampicillin, chloramphenicol, co-trimoxazole, fluoroquinolones and third-generation cephalosporins. Uncomplicated: azithromycin; severe or complicated: meropenem (± azithromycin). Follow current national guidance and blood culture sensitivities.
- Sensitive strains: ceftriaxone or azithromycin; fluoroquinolone resistance is widespread.
- Carriers: prolonged antibiotics; cholecystectomy if gallstones.
- Prevention: safe water, sanitation, handwashing, food hygiene, treating carriers among food handlers.
- Vaccines:
- Typhoid conjugate vaccine (Typbar-TCV): Vi polysaccharide conjugated to tetanus toxoid; works from 6 months of age; given in Pakistan's EPI at 9 months (with measles) since 2019, after catch-up campaigns.
- Vi polysaccharide vaccine (IM; over 2 years; boosters every 3 years).
- Ty21a (oral live attenuated).
Non-typhoidal Salmonella
- Gastroenteritis (food poisoning) from poultry, eggs, meat, unpasteurised milk, pet reptiles: fever, vomiting, diarrhoea 12–72 hours after eating; self-limiting; antibiotics usually not needed (prolong carriage) except in infants, the elderly, immunocompromised.
- Bacteraemia and focal infections in HIV, infants and the elderly; infected aortic aneurysms.
- Osteomyelitis in sickle cell disease (Salmonella is a classic cause).
Shigella (brief)
Non-motile, non-lactose fermenting, no H₂S; very low infectious dose (10–100 organisms); invades colonic epithelium → bacillary dysentery (bloody mucoid stools, tenesmus, fever). S. dysenteriae type 1 makes Shiga toxin (HUS). Spread person to person (the "4 Fs": fingers, flies, food, faeces).
Escherichia coli
Normal gut flora; lactose fermenter (pink on MacConkey, green metallic sheen on EMB), indole positive, motile.
Extraintestinal disease
- Urinary tract infection: the commonest cause of community and hospital UTIs (uropathogenic E. coli: P fimbriae bind uroepithelium); cystitis, pyelonephritis.
- Neonatal meningitis (with group B streptococcus): K1 capsule.
- Gram-negative sepsis (commonest cause), endotoxic shock.
- Intra-abdominal infections (peritonitis, cholangitis, appendicitis abscess), hospital pneumonia, wound infections.
- ESBL-producing E. coli are common: carbapenems may be needed.
Diarrhoeagenic E. coli
| Type | Mechanism | Disease |
|---|---|---|
| ETEC (enterotoxigenic) | LT (like cholera toxin: ↑ cAMP) and ST (↑ cGMP); plasmid-encoded; colonisation factors | Travellers' diarrhoea, watery diarrhoea in children in developing countries |
| EPEC (enteropathogenic) | Attaching and effacing lesions (destroys microvilli); no toxin | Infant diarrhoea, nurseries |
| EHEC (enterohaemorrhagic), mainly O157:H7 | Shiga-like toxin (verotoxin) (phage-encoded) inactivates 60S ribosomes; attaching-effacing lesions | Haemorrhagic colitis (bloody diarrhoea, no fever), haemolytic uraemic syndrome (children): microangiopathic haemolytic anaemia (schistocytes), thrombocytopenia, acute kidney injury. Source: undercooked beef, unpasteurised milk, contaminated vegetables. Does not ferment sorbitol (sorbitol MacConkey). Antibiotics may raise HUS risk: supportive care |
| EIEC (enteroinvasive) | Invades colonic cells like Shigella | Dysentery |
| EAEC (enteroaggregative) | Stacked-brick adherence; biofilm | Persistent diarrhoea in children, HIV |
High-yield
ETEC = travellers (watery, toxins). EHEC O157:H7 = bloody diarrhoea + HUS, sorbitol-negative, avoid antibiotics.
Klebsiella and Proteus (brief)
- Klebsiella pneumoniae: large mucoid capsule, non-motile, lactose fermenter; lobar pneumonia in alcoholics and diabetics ("currant jelly" sputum, upper lobe, cavitation, abscess), hospital UTI, sepsis, liver abscess; frequent ESBL and carbapenemase (KPC, NDM) producer.
- Proteus mirabilis: swarming motility, urease + → alkaline urine → struvite (staghorn) stones; UTI; fishy smell.
Pseudomonas aeruginosa
| Feature | Details |
|---|---|
| Microbiology | Gram-negative bacillus, non-lactose fermenter, oxidase-positive, strictly aerobic, motile (polar flagellum); grows almost anywhere, including disinfectants, sinks, humidifiers, eye drops; grows at 42 °C |
| Pigments | Pyocyanin (blue-green; generates reactive oxygen), fluorescein (pyoverdin) (yellow-green, fluoresces under UV); grape-like (sweet) odour; metallic sheen |
| Virulence | Exotoxin A (ADP-ribosylates EF-2), endotoxin, elastase, phospholipase C, alginate biofilm (cystic fibrosis), pili, exoenzyme S |
| Diseases | Burn wound infection (blue-green pus), cystic fibrosis lung infection (mucoid strains, chronic), ventilator-associated pneumonia, catheter UTI, sepsis in neutropenia, malignant (necrotising) otitis externa in diabetics, swimmer's ear, corneal ulcers (contact lenses), hot tub folliculitis, osteomyelitis after a nail puncture through a trainer, osteomyelitis in IV drug users, ecthyma gangrenosum (necrotic skin lesions in neutropenic sepsis) |
| Treatment | Often multidrug-resistant (porins, efflux pumps, β-lactamases). Anti-pseudomonal drugs: piperacillin-tazobactam, ceftazidime, cefepime, carbapenems (not ertapenem), ciprofloxacin (only oral option), aminoglycosides, aztreonam, colistin for resistant strains; combinations in serious infection |
High-yield
Pseudomonas: oxidase +, blue-green pyocyanin, grape smell; burns, cystic fibrosis, ventilators, diabetics' ears, hot tubs, nail puncture.
Acinetobacter baumannii
- Gram-negative coccobacillus, oxidase-negative, strictly aerobic, non-fermenter; survives for long periods on dry surfaces and equipment.
- Hospital (ICU) pathogen: ventilator-associated pneumonia, bloodstream (line) infections, wound and burn infections (including war wounds), UTIs, post-neurosurgical meningitis.
- Often multidrug- or carbapenem-resistant (OXA carbapenemases); treated with colistin, tigecycline, sulbactam-containing regimens, newer agents per sensitivity.
- Control: strict hand hygiene, environmental cleaning, contact precautions, antibiotic stewardship.
Exam focus
Expect: lactose and oxidase reactions, typhoid pathogenesis (Peyer patches, Vi antigen, gallbladder), clinical features by week (relative bradycardia, rose spots, perforation), diagnostic tests by week (blood culture, bone marrow, Widal pitfalls, stool and urine), carriers, XDR typhoid and its treatment, typhoid conjugate vaccine, non-typhoidal Salmonella and sickle cell osteomyelitis, E. coli in UTI and neonatal meningitis, ETEC vs EHEC (HUS, sorbitol), Klebsiella currant jelly sputum, Proteus and struvite, Pseudomonas features, pigments and classic infections, Acinetobacter in ICU and carbapenem resistance.
Quick revision
- Lactose fermenters: E. coli, Klebsiella. Non-fermenters: Salmonella, Shigella, Proteus, Pseudomonas (oxidase +).
- Typhoid: Peyer patches, Vi capsule; relative bradycardia, rose spots; week 3 perforation.
- Diagnosis: blood culture week 1; bone marrow most sensitive; stool/urine weeks 2–3; Widal needs rising titres.
- Carrier: gallbladder. XDR typhoid (Sindh 2016): azithromycin or meropenem. TCV at 9 months in EPI.
- E. coli: commonest UTI, Gram-negative sepsis; K1 neonatal meningitis.
- ETEC travellers' diarrhoea; EHEC O157:H7 → HUS, avoid antibiotics.
- Pseudomonas: pyocyanin, burns, CF, ventilators, malignant otitis externa, hot tubs.
- Acinetobacter: ICU, ventilator pneumonia, carbapenem-resistant (colistin).
Written by The House Job from standard microbiology references (Levinson's Review of Medical Microbiology and Immunology).
FAQ
Which test is best for diagnosing typhoid in the first week?
Blood culture; bone marrow culture is even more sensitive and stays positive after antibiotics.
Where do chronic typhoid carriers harbour Salmonella Typhi?
In the gallbladder, especially when gallstones are present.
Which E. coli causes haemolytic uraemic syndrome?
Enterohaemorrhagic E. coli, especially O157:H7, through its Shiga-like toxin.
Which organism infects burns and cystic fibrosis lungs and makes a blue-green pigment?
Pseudomonas aeruginosa, which produces pyocyanin.