Infective Diarrhoea

Infective diarrhoea is among the highest-yield infectious disease topics for NEET PG, mainly through pattern-recognition vignettes: the organism, the stool description, the toxin mechanism, and the drug of choice. The single most rewarding division is secretory (watery, non-inflammatory) versus invasive (inflammatory/dysenteric) diarrhoea, because it instantly predicts the stool findings, the site of involvement, and the management.

Definition and classification

Diarrhoea = passage of ≥3 loose/liquid stools per day (or more frequently than normal for that individual), or stool weight >200 g/day. Infective diarrhoea is acute if it lasts <14 days, persistent if 14–30 days, and chronic if >30 days. Most acute infective diarrhoea is viral and self-limiting.

The two pathophysiological buckets you must master:

Feature	Secretory (non-inflammatory)	Invasive (inflammatory)
Site	Proximal small bowel	Colon / distal ileum
Mechanism	Enterotoxin → ↑cAMP/cGMP → Cl⁻ secretion	Mucosal invasion, cytotoxin
Stool volume	Large, watery	Small, frequent
Blood/mucus	Absent	Present (dysentery)
Fever	Usually absent	Often present
Stool WBC/lactoferrin	Absent	Present
Classic organisms	Vibrio cholerae, ETEC, viruses	Shigella, EIEC, Campylobacter, Salmonella, Entamoeba, C. difficile

High-yield: Faecal leucocytes (stool microscopy showing pus cells) point to an invasive/inflammatory cause; their absence with profuse watery stool points to a toxin-mediated secretory cause. This single test is the commonest "investigation of choice" MCQ in this topic.

Secretory diarrhoea

Vibrio cholerae

A comma-shaped, oxidase-positive, motile (single polar flagellum, "shooting-star/darting" motility on dark-field) Gram-negative bacillus. Grows on TCBS agar as yellow colonies (sucrose fermenter). Serogroups O1 and O139 cause epidemic cholera. O1 has two biotypes — Classical and El Tor (ELTOR) — and three serotypes (Ogawa, Inaba, Hikojima).

• El Tor biotype is responsible for the current 7th pandemic: it is haemolytic, Voges-Proskauer positive, resistant to polymyxin B, and agglutinates chicken RBCs — and causes more carriers/mild infections than the classical biotype.
• Cholera toxin (CT): the B subunit binds GM1 ganglioside; the A subunit ADP-ribosylates the Gsα protein → permanently active adenylate cyclase → ↑cAMP → massive Cl⁻ and water secretion.
• Clinical: sudden painless profuse rice-water stool (flecks of mucus, no faecal odour, "fishy" smell), vomiting, no fever, leading to rapid isotonic dehydration, sunken eyes, washerwoman's hands, hypovolaemic shock, and metabolic acidosis with hypokalaemia.

High-yield: Cholera = rice-water stools + isotonic, hypokalaemic dehydration + no fever + no abdominal pain. The B subunit binds GM1 ganglioside; A subunit raises cAMP.

Management flow: Assess dehydration → aggressive rehydration first (Ringer lactate IV for severe; ORS for mild-moderate) → then antibiotic. Rehydration saves life; antibiotics only shorten illness and shedding.

• Antibiotic of choice (adults): single-dose doxycycline 300 mg. Alternatives: azithromycin (drug of choice in pregnancy and children), ciprofloxacin.
• A single dose of azithromycin is preferred in children/pregnancy.

Enterotoxigenic E. coli (ETEC)

The leading cause of traveller's diarrhoea. Produces heat-labile toxin (LT) — mechanism identical to cholera toxin (↑cAMP) — and heat-stable toxin (ST) which acts via guanylate cyclase → ↑cGMP. Watery diarrhoea, no blood. Management is rehydration; azithromycin or a fluoroquinolone shortens illness.

E. coli pathotype	Disease	Key fact
ETEC	Traveller's diarrhoea, infant watery diarrhoea	LT (cAMP) + ST (cGMP)
EPEC	Infantile watery diarrhoea	"Attaching & effacing", bundle-forming pilus
EIEC	Dysentery (Shigella-like)	Invades colon, no toxin
EHEC (O157:H7)	Bloody diarrhoea → HUS	Shiga-like (verocytotoxin); avoid antibiotics
EAEC	Persistent diarrhoea	"Stacked-brick" aggregative adherence

High-yield: In EHEC O157:H7 (sorbitol-NON-fermenter on sorbitol-MacConkey), antibiotics and antimotility agents are contraindicated because they increase the risk of haemolytic uraemic syndrome (HUS).

Viral causes

Rotavirus is the commonest cause of severe dehydrating diarrhoea in children <2 years; NSP4 acts as a viral enterotoxin. Diagnosis by stool ELISA; prevention by live oral rotavirus vaccine. Norovirus is the commonest cause of epidemic non-bacterial gastroenteritis (cruise ships, hostels) with prominent vomiting.

Invasive / inflammatory diarrhoea

Shigella (bacillary dysentery)

Non-motile, non-lactose-fermenting, Gram-negative; S. dysenteriae type 1 is the most virulent and produces Shiga toxin (inhibits 60S ribosome, 28S rRNA cleavage), which can precipitate HUS. As few as 10–100 organisms cause disease (very low infective dose).

• Clinical: fever, crampy abdominal pain, tenesmus, and scanty blood- and mucus-containing stools (dysentery). Stool microscopy shows abundant pus cells, RBCs and macrophages.
• Complications: HUS, reactive arthritis (HLA-B27), toxic megacolon, seizures in children (febrile/Ekiri syndrome).
• Treatment: ciprofloxacin (or ceftriaxone/azithromycin); rehydrate. Avoid antimotility drugs in dysentery.

High-yield: HUS = microangiopathic haemolytic anaemia + thrombocytopenia + acute kidney injury. Caused by Shiga toxin (S. dysenteriae 1) and Shiga-like toxin (EHEC O157:H7).

Non-typhoidal Salmonella

S. enteritidis / S. typhimurium, classically from poultry and eggs. Inflammatory diarrhoea with fever. It is one of the conditions where antibiotics are usually NOT given in healthy hosts (they prolong the carrier state); reserve antibiotics for extremes of age, immunosuppression, sickle cell disease, or invasive/bacteraemic disease (then ceftriaxone/ciprofloxacin).

Campylobacter jejuni

Gram-negative, comma/S-shaped ("gull-wing"), microaerophilic, grows at 42 °C on Skirrow's/Campy medium. The commonest bacterial cause of diarrhoea in many developed countries; transmitted via poultry and unpasteurised milk.

• Clinical: prodrome of fever/myalgia → bloody diarrhoea, severe abdominal pain that can mimic appendicitis (pseudo-appendicitis).
• Key associations: Guillain–Barré syndrome (molecular mimicry, anti-GM1; commonest preceding infection of GBS) and reactive arthritis.
• Treatment of choice: azithromycin (macrolide); fluoroquinolone resistance is rising.

High-yield: Campylobacter → Guillain–Barré syndrome. Microaerophilic, grows at 42 °C; macrolide (azithromycin) is the drug of choice.

Clostridioides difficile (pseudomembranous colitis)

A Gram-positive, spore-forming anaerobe. Develops after antibiotic use disrupts colonic flora — classically clindamycin, broad-spectrum cephalosporins, and fluoroquinolones. Produces Toxin A (enterotoxin) and Toxin B (cytotoxin).

• Clinical: watery-to-bloody diarrhoea, cramps, fever, leucocytosis (sometimes marked, >15,000); colonoscopy shows raised yellow-white pseudomembranes/plaques.
• Diagnosis: stool NAAT/PCR for toxin genes or GDH antigen + toxin EIA (two-step algorithm). Do not test asymptomatic/formed stools.
• Treatment (current guidance): oral vancomycin or fidaxomicin is now first-line for both initial and recurrent episodes; oral metronidazole is reserved for non-severe disease where the preferred drugs are unavailable. Stop the offending antibiotic. Fulminant disease: high-dose oral vancomycin + IV metronidazole. Recurrent disease: fidaxomicin, bezlotoxumab (anti-toxin B monoclonal), or faecal microbiota transplant.

High-yield: Pseudomembranous colitis follows antibiotics (clindamycin classic). Diagnosis is stool toxin/PCR; first-line treatment has shifted to oral vancomycin or fidaxomicin, not metronidazole.

Entamoeba histolytica (amoebic dysentery)

Faeco-oral, cyst with 4 nuclei is infective. Invades colon → flask-shaped ulcers; stool shows trophozoites with ingested RBCs (erythrophagocytosis) — the classic exam clue. Most common extra-intestinal complication is right-lobe liver abscess ("anchovy-sauce" pus). Treatment: metronidazole/tinidazole followed by a luminal agent (diloxanide furoate / paromomycin) to clear cysts.

Feature	Bacillary (Shigella)	Amoebic (E. histolytica)
Onset	Acute, fever, toxaemia	Gradual, less toxic
Stools	Numerous, scanty, more blood	Fewer, copious, "anchovy/jam"
Microscopy	Pus cells +++	RBC-containing trophozoites
Tenesmus	Marked	Less
Treatment	Ciprofloxacin	Metronidazole + luminal agent

Diagnosis and investigation of choice

Stepwise approach: History (travel, food, antibiotics, day-care, immune status) → assess hydration → decide if inflammatory (blood/fever) vs non-inflammatory → stool microscopy for faecal leucocytes → targeted tests.

• Investigation of choice for the inflammatory vs non-inflammatory split: stool microscopy for pus cells/RBCs.
• Stool culture, multiplex stool PCR panels for outbreaks/persistent/bloody diarrhoea.
• Hanging-drop / dark-field microscopy for V. cholerae darting motility; TCBS for culture.
• C. difficile: stool toxin EIA + GDH, or NAAT.
• Amoebiasis: stool wet mount for trophozoites; serology for invasive/liver abscess.

Oral Rehydration Solution (ORS)

ORS is the most important intervention overall; the glucose–sodium co-transporter (SGLT1) keeps working even in cholera, allowing oral fluid replacement. The WHO/UNICEF low-osmolarity ORS (2003) is the standard.

Component	Low-osmolarity ORS (mmol/L)
Sodium	75
Glucose	75
Potassium	20
Chloride	65
Citrate	10
Total osmolarity	245

High-yield: Low-osmolarity ORS = Na 75, glucose 75, total osmolarity 245 mmol/L. The reduced osmolarity lowers stool output, vomiting, and need for IV fluids compared with the older (311 mmol/L) formula.

Adjuncts: zinc supplementation (20 mg/day for 10–14 days; 10 mg if <6 months) reduces duration and severity of childhood diarrhoea and is strongly recommended by WHO. Continue feeding/breastfeeding.

Mnemonic for invasive (inflammatory) organisms — "Campylobacter, Shigella, Salmonella, EIEC, EHEC, C. difficile, Entamoeba, Yersinia" vs the secretory toxin producers (Vibrio, ETEC, viruses).

Drug-of-choice summary

Pathogen	Drug of choice (when indicated)	Note
V. cholerae	Doxycycline (single dose); azithromycin in pregnancy/children	Fluids first
ETEC (traveller's)	Azithromycin / fluoroquinolone	+ loperamide if no blood/fever
Shigella	Ciprofloxacin / ceftriaxone / azithromycin	Rehydrate
Non-typhoidal Salmonella	Usually none; ceftriaxone if invasive/high-risk	Antibiotics prolong carriage
Campylobacter	Azithromycin	GBS association
EHEC O157:H7	No antibiotics	Risk of HUS
C. difficile	Oral vancomycin / fidaxomicin	Stop culprit antibiotic
E. histolytica	Metronidazole + luminal agent	Liver abscess risk
Giardia	Tinidazole / metronidazole	"Fatty, foul" malabsorptive stool

Complications

• HUS (Shigella, EHEC) — avoid antibiotics in EHEC.
• Severe dehydration, hypovolaemic shock, hypokalaemia, metabolic acidosis (cholera).
• Guillain–Barré syndrome, reactive arthritis (Campylobacter; reactive arthritis also Shigella, Salmonella, Yersinia — HLA-B27).
• Toxic megacolon and perforation (Shigella, C. difficile, amoebic colitis).
• Amoebic liver abscess; enteric fever / bacteraemia with Salmonella.
• Post-infectious irritable bowel syndrome and lactose intolerance.

Key differentials

Non-infective causes that mimic infective diarrhoea: inflammatory bowel disease (UC/Crohn — important mimic of chronic invasive picture), coeliac disease, microscopic colitis, ischaemic colitis, drug-induced (laxatives, metformin, magnesium), and overflow diarrhoea in faecal impaction. Giardia lamblia and Cryptosporidium (commonest in HIV/immunocompromised, acid-fast oocysts) cause persistent watery diarrhoea. Vibrio parahaemolyticus (seafood, Kanagawa phenomenon) causes self-limited diarrhoea.

Recently asked / exam angle

• Stool microscopy: "Trophozoite with ingested RBCs" → E. histolytica; "abundant pus cells, no organism seen" → invasive bacterial (Shigella).
• Mechanism MCQs: Cholera toxin → ADP-ribosylation of Gs → ↑cAMP; ST of ETEC → ↑cGMP. Pertussis toxin (contrast) ribosylates Gi.
• Single-best-drug: Campylobacter → azithromycin; cholera → doxycycline; C. difficile → oral vancomycin/fidaxomicin; EHEC → supportive only.
• ORS composition: Na 75 / glucose 75 / osmolarity 245 — frequently asked exact values; zinc duration 10–14 days.
• Association links: Campylobacter–GBS; Shigella/EHEC–HUS; Salmonella–poultry/eggs and sickle-cell osteomyelitis; reactive arthritis–HLA-B27.
• Microbiology: TCBS yellow colony = V. cholerae; sorbitol-MacConkey non-fermenter = O157:H7; growth at 42 °C microaerophilic = Campylobacter.
• Image-based: colonoscopy pseudomembranes → C. difficile; flask-shaped ulcers → amoebiasis.

Rapid revision

1. Secretory diarrhoea = watery, no pus cells, toxin-mediated (Vibrio, ETEC, viruses); invasive = bloody/mucoid with faecal leucocytes.
2. Cholera toxin B-subunit binds GM1 ganglioside; A-subunit raises cAMP → rice-water stools; treat with fluids first, then doxycycline.
3. El Tor biotype causes the current pandemic — more carriers, polymyxin B resistant, VP positive, haemolytic.
4. ETEC = traveller's diarrhoea: LT acts like cholera (cAMP), ST acts via cGMP.
5. EHEC O157:H7 causes HUS — never give antibiotics or antimotility drugs.
6. Shigella has a very low infective dose; S. dysenteriae 1 makes Shiga toxin → HUS; treat with ciprofloxacin.
7. Campylobacter (microaerophilic, 42 °C) is the classic antecedent of Guillain–Barré syndrome; drug of choice azithromycin.
8. Non-typhoidal Salmonella usually needs no antibiotics — they prolong the carrier state.
9. C. difficile follows antibiotics (clindamycin); diagnose by stool toxin/PCR; treat with oral vancomycin or fidaxomicin and stop the culprit drug.
10. E. histolytica trophozoites show erythrophagocytosis; flask-shaped ulcers; metronidazole + luminal agent; right-lobe liver abscess with anchovy-sauce pus.
11. Low-osmolarity ORS: Na 75, glucose 75, K 20, citrate 10, Cl 65, osmolarity 245; add zinc 20 mg × 10–14 days in children.
12. Faecal leucocytes on stool microscopy is the key first test separating inflammatory from non-inflammatory diarrhoea.