MI4.1-9 | Gastrointestinal & Hepatobiliary Infections — Glossary

IgM antibody to HBV core antigen; marker of acute HBV infection; only marker detectable during the window period.

Antibody against HBsAg; indicates immunity — from vaccination (anti-HBs alone) or natural recovery (anti-HBs + anti-HBc IgG).

Enzyme-linked immunosorbent assay for anti-HCV antibodies; first-line screening test; positive results confirmed by HCV RNA PCR.

The most potent biological toxin; produced by C. botulinum; a metalloprotease that cleaves SNARE proteins, blocking ACh exocytosis at NMJ → flaccid paralysis.

H. pylori virulence factor injected via type IV secretion into epithelial cells; activates Ras–ERK signalling; associated with peptic ulcer and gastric cancer.

Heat-stable, cyclic peptide emetic toxin produced by B. cereus emetic strains in fried rice; survives cooking temperatures.

AB5 enterotoxin of V. cholerae that ADP-ribosylates Gs-alpha, causing persistent adenylate cyclase activation and massive cAMP-driven Cl⁻ secretion.

70–85% of acute HCV infections progress to chronic hepatitis; driven by HCV's ability to evade innate immune responses via NS3/4A protease cleavage of MAVS/TRIF.

Campylobacter-Like Organism test; antral biopsy placed in urea medium → H. pylori urease splits urea → NH₃ → pH ↑ → colour change to pink; rapid diagnosis of H. pylori.

Coccidian parasite causing watery diarrhoea; particularly severe and prolonged in HIV/immunocompromised individuals; oocysts detected by modified ZN stain.

The dormant, environmentally resistant, infective form of protozoa (e.g., Entamoeba, Giardia); transmitted faeco-orally.

Passage of ≥3 loose or liquid stools per 24 hours, reflecting impaired intestinal water absorption or enhanced secretion.

Oral antiviral drugs targeting HCV NS5B RNA polymerase, NS3/4A protease, and NS5A; achieve >95% sustained virological response (cure) in 8–12 weeks.

Inflammatory diarrhoea characterised by blood and mucus in stool, tenesmus, and usually fever, indicating mucosal invasion.

Ingestion of red blood cells by Entamoeba histolytica trophozoites; pathognomonic for this species vs. non-pathogenic Entamoeba.

Enterotoxigenic Escherichia coli; major cause of traveller's diarrhoea; secretes heat-labile (LT) and heat-stable (ST) enterotoxins.

Illness caused by ingesting food contaminated with microorganisms or their preformed toxins, often affecting multiple persons from a common source.

Severe acute liver failure (coagulopathy, encephalopathy) within 8 weeks of jaundice onset; may complicate HAV (<1%), HEV in pregnancy, HBV–HDV co-infection.

Flagellated binucleate protozoan causing malabsorptive, non-bloody diarrhoea; cysts oval with 4 nuclei and axostyle; treated with metronidazole.

Soluble secreted form of HBV core antigen; marker of active viral replication and high infectivity; its clearance (seroconversion to anti-HBe) indicates declining replication.

Passive immunisation product containing high-titre anti-HBs; used for post-exposure prophylaxis (needlestick, neonate of HBsAg-positive mother) within 12–24 hours.

Outer envelope protein of HBV; detected in serum in active infection (acute or chronic); forms the basis of the HBV vaccine.

Gold-standard quantitative marker of HBV replication; measured by PCR; guides initiation and monitoring of antiviral therapy.

Circular ssRNA defective virus requiring HBV HBsAg as its outer envelope; cannot infect or replicate without HBV co-infection.

Family of partially double-stranded DNA viruses; includes HBV; encode a reverse transcriptase and integrate into host DNA in chronic infection.

HEV genotype 1 infection during the third trimester carries a 20–25% case fatality rate; mechanism involves immune dysregulation and high viral load in pregnancy.

Chronic HBV state: HBsAg positive, HBeAg negative, anti-HBe positive, low HBV DNA, normal liver enzymes — minimal liver damage.

Type of food poisoning caused by ingestion of preformed microbial toxin in food; short incubation, no fever, no live pathogen in host.

Small-volume bloody/mucoid diarrhoea resulting from pathogen invasion and destruction of intestinal mucosa (e.g., Shigella, Entamoeba).

Beta-haemolysis of human erythrocytes on Wagatsuma agar by Vibrio parahaemolyticus; mediated by TDH; marker of pathogenic strains.

Presence of PMNs in stool microscopy, indicating invasive pathology; absent in secretory (cholera) or toxin-mediated diarrhoea.

Selective-differential medium containing bile salts and crystal violet; lactose fermenters turn pink (E. coli); NLF organisms pale (Shigella, Salmonella).

Requiring reduced oxygen tension (5–10% O₂) for growth; characteristic of H. pylori and Campylobacter jejuni.

Gold standard for detecting botulinum toxin; patient serum/food extract injected intraperitoneally into mice; flaccid paralysis confirms toxin; neutralised by specific antitoxin.

Non-enveloped ssRNA calicivirus; commonest cause of epidemic gastroenteritis outbreaks in adults; characterised by projectile vomiting.

Non-structural protein 4 of rotavirus; acts as a viral enterotoxin, elevating intracellular Ca²⁺ and triggering Cl⁻ secretion.

Subunit vaccine containing yeast-expressed HBsAg; generates only anti-HBs (no anti-HBc); the world's first cancer-preventing vaccine.

dsRNA, non-enveloped virus with triple-layered wheel-like capsid; leading cause of severe dehydrating diarrhoea in Indian children <5 years.

Large-volume, watery diarrhoea due to excessive intestinal secretion, without mucosal damage (e.g., cholera).

AB5 cytotoxin of Shigella dysenteriae type 1 (and STEC); inhibits 28S rRNA elongation factor → protein synthesis arrest → cell death.

Heat-stable super-antigen protein (SE A–E) produced by S. aureus in food; SE A is most common in outbreaks; triggers vomiting via vagal stimulation.

Thiosulphate–citrate–bile salts–sucrose agar; selective medium for Vibrio; V. cholerae forms yellow colonies (sucrose fermenter).

Painful, persistent desire to defaecate with little or no stool output; a hallmark of colonic or rectal mucosal inflammation.

Oral nucleoside/nucleotide reverse transcriptase inhibitors; first-line antivirals for chronic HBV; suppress HBV DNA to undetectable levels.

Key virulence factor of Vibrio parahaemolyticus; correlates with the Kanagawa phenomenon (beta-haemolysis on Wagatsuma agar); associated with pathogenicity.

Food poisoning where ingested organisms multiply in the gut and produce toxin in vivo; intermediate incubation (8–16 h).

First-line H. pylori eradication regimen: PPI + clarithromycin + amoxicillin for 14 days; effective where clarithromycin resistance <20%.

The active, motile, feeding form of protozoa; the pathogenic form responsible for tissue invasion in amoebiasis.

Non-invasive test: patient ingests ¹³C-labelled urea → H. pylori urease produces ¹³CO₂ → detected in exhaled breath; gold standard for post-eradication confirmation.

Enzyme produced by H. pylori that splits urea into NH₃ and CO₂; neutralises local acid to enable survival in stomach; basis of CLO test and UBT.

H. pylori pore-forming toxin that induces vacuolation and apoptosis in gastric epithelial cells, contributing to mucosal damage.

Polymorphic gene encoding vacuolating cytotoxin of H. pylori; s1m1 allele combination is most virulent; associated with peptic ulcer and gastric adenocarcinoma.

The interval in acute HBV when HBsAg has cleared but anti-HBs has not yet appeared; anti-HBc IgM is the sole diagnostic marker.

Xylose-lysine deoxycholate agar; selective-differential medium; Salmonella forms black colonies (H₂S), Shigella forms red/colourless colonies.