14.4 GI Microbiology, Nutrition & Malabsorption

14.4 GI Microbiology, Nutrition & Malabsorption

Quick Answer: Secretory toxins (cholera, ETEC) vs Shiga (EHEC/Shigella) vs C. diff cytotoxins vs preformed emetic toxins. Invasive enterics cause inflammatory diarrhea. Giardia, Entamoeba, Cryptosporidium, rotavirus, and norovirus complete the micro set. Vitamins A D E K B1 B3 B6 B12 C folate each own a syndrome. Separate bile-salt, pancreatic, and brush-border malabsorption; know marasmus vs kwashiorkor.

Microbiology and nutrition questions are high-yield because they are discrete and table-friendly. Build organism cards and vitamin cards, then connect both to malabsorption geography.

Enteric Pathogens by Mechanism

Secretory toxin–mediated watery diarrhea

Vibrio cholerae: AB toxin; A subunit ADP-ribosylates Gs → ↑cAMP → CFTR Cl− secretion and inhibited Na absorption → voluminous rice-water stool; fecal–oral, contaminated water; no invasion/fecal leukocytes.

ETEC (enterotoxigenic E. coli): traveler’s diarrhea; heat-labile toxin (LT) like cholera (cAMP); heat-stable toxin (ST) raises cGMP; watery diarrhea without invasion.

Shiga and related cytotoxins

EHEC / STEC (e.g., O157:H7): Shiga-like toxin (Stx) inhibits 60S ribosome → epithelial death; bloody diarrhea without intense fever sometimes; undercooked beef, petting zoos; HUS (microangiopathic hemolytic anemia, thrombocytopenia, acute kidney injury) especially in children; antibiotics may increase toxin release—avoid in classic teaching.

Shigella: very low inoculum; invades M cells/colonic epithelium; Shiga toxin in some species (S. dysenteriae type 1); bloody mucoid diarrhea, tenesmus; HUS risk with toxin-producing strains; human-to-human, daycare.

Antibiotic-associated colitis

Clostridioides difficile: spores survive; toxins TcdA and TcdB glucosylate Rho GTPases → cytoskeletal disruption, apoptosis, intense inflammation → pseudomembranous colitis; watery or bloody diarrhea, leukocytosis after antibiotics (clindamycin, fluoroquinolones, cephalosporins classic). NAP1/BI/027 hypervirulent strains appear in outbreak lore.

Invasive / inflammatory enterics

Salmonella enterica (nontyphoidal): poultry/eggs; invades ileum/colon; inflammatory diarrhea; can seed (osteomyelitis in sickle cell—typhoidal and nontyphoidal teaching). S. typhi: human-only, rose spots, relative bradycardia, constipation or diarrhea, marrow/reticuloendothelial infection, chronic gallbladder carriage.

Campylobacter jejuni: poultry; bloody diarrhea, fever; Guillain–Barré and reactive arthritis post-infectious associations.

Yersinia enterocolitica: pseudoappendicitis (mesenteric adenitis), cold enrichment, blood products, iron overload growth; reactive arthritis, erythema nodosum.

Vibrio parahaemolyticus / vulnificus: raw shellfish; vulnificus—bullous skin, septicemia in liver disease/hemochromatosis.

Preformed toxin food poisoning (short incubation)

Late onset (invasive or in vivo toxin) often 12–72 hours with more diarrhea ± fever (Salmonella, Campylobacter, EHEC, etc.).

Parasites and viruses

Giardia lamblia: cysts in water; campers/daycares; foul fatty stools, bloating, brush-border damage/malabsorption; binucleate trophozoites, antigen tests.

Entamoeba histolytica: flask-shaped colonic ulcers; bloody dysentery; anchovy-paste liver abscess (right lobe); flask histology classic.

Cryptosporidium: acid-fast oocysts; watery diarrhea; self-limited in immunocompetent; severe chronic in AIDS (CD4 low); recreational water outbreaks (chlorine tolerant).

Rotavirus: segmented dsRNA; children; winter; villous blunting, watery diarrhea, vaccine-preventable.

Norovirus: calicivirus; cruise ships, closed settings; vomiting and diarrhea; short immunity; very low inoculum.

Vitamin Deficiencies: Mechanisms and Signs

Fat-soluble (A, D, E, K) fail together in cholestasis, pancreatic insufficiency, bile-salt deficiency, celiac, and abetalipoproteinemia.

• Vitamin A: rhodopsin; night blindness, xerophthalmia, Bitot spots, keratinization, immune dysfunction; excess → teratogenesis, idiopathic intracranial hypertension.
• Vitamin D: 1,25-(OH)2D increases gut Ca/PO4 absorption; deficiency → rickets (kids), osteomalacia (adults), hypocalcemia patterns.
• Vitamin E: antioxidant protecting RBCs and neurons; deficiency → hemolytic anemia, spinocerebellar and proprioceptive loss (mimics Friedreich-like findings).
• Vitamin K: γ-carboxylation of factors II, VII, IX, X and proteins C/S; deficiency → ↑PT/INR early, bleeding; newborns, fat malabsorption, warfarin antagonism.

Water-soluble high-yield:

• B1 (thiamine): cofactor for PDH, α-KGDH, transketolase; dry beriberi (neuropathy), wet beriberi (high-output HF), Wernicke (confusion, ataxia, ophthalmoplegia), Korsakoff (confabulation); alcohol/malnutrition—give B1 before glucose conceptually.
• B3 (niacin): NAD/NADP; pellagra—diarrhea, dementia, dermatitis (Casal necklace); Hartnup and carcinoid (tryptophan diversion) associations.
• B6 (pyridoxine): transamination, heme synthesis; deficiency → sideroblastic anemia, convulsions, neuropathy; isoniazid depletes B6.
• B12 (cobalamin): methionine synthase and methylmalonyl-CoA mutase; needs IF and terminal ileum; deficiency → megaloblastic anemia + subacute combined degeneration (dorsal columns + corticospinal); ↑MMA and homocysteine; pernicious anemia, vegan diet, ileal Crohn/resection, diphyllobothrium.
• Folate: one-carbon transfers; megaloblastic anemia without SCD; ↑homocysteine, normal MMA; short body stores—alcohol, poor diet, pregnancy demand, methotrexate/phenytoin.
• Vitamin C: collagen hydroxylation; scurvy—bleeding gums, corkscrew hairs, poor wound healing, perifollicular hemorrhages.

Protein-Energy Malnutrition and Malabsorption Patterns

Marasmus: total calorie deficiency; loss of subcutaneous fat and muscle; wasting, old-man facies; no prominent edema.

Kwashiorkor: protein deficiency dominant (often with some calorie intake from starch); edema (↓ oncotic pressure), fatty liver (↓ apolipoprotein synthesis), flaky-paint skin, irritability, pot belly; more infection risk from immune compromise.

Mixed pictures are common clinically; exam contrasts edema/fatty liver (kwashiorkor) vs pure wasting (marasmus).

Malabsorption pattern recognition

Bile-salt deficiency (cholestasis, ileal resection, bacterial deconjugation in SIBO): long-chain fat and ADEK malabsorption; steatorrhea; oxalate kidney stones after ileal disease.

Pancreatic exocrine insufficiency (chronic pancreatitis, CF, resection): fat and protein maldigestion; neutral fat in stool; response to enzyme replacement; A, D, E, K deficiency; B12 can be affected (protease role in haptocorrin processing) but fat is dominant teaching point.

Brush-border enzyme defects (lactase deficiency most common): osmotic diarrhea after specific sugar; normal fat absorption; hydrogen breath test conceptually; acquired lactase loss with age or after mucosal injury (giardia, celiac, rotavirus).

Mucosal disease (celiac, Whipple, tropical sprue): broad nutrient failure depending on extent—iron/folate (proximal), B12 (ileum if involved).

Lymphatic obstruction / abetalipoproteinemia: fat and fat-soluble vitamins fail despite enzymes and bile; chylous problems or missing chylomicrons.

Exam strategy: match the missing step—emulsification, enzymatic digestion, brush-border hydrolysis, enterocyte processing, or lymphatic export—then predict which nutrients fall. Combine with micro: post-infectious lactase deficiency after viral gastroenteritis, or bile-salt deconjugation in SIBO after MMC failure, links physiology to this section’s pathogens and nutrition outcomes.

Close the GI system loop: hormones and motility (14.1) explain colonization resistance and enzyme timing; luminal pathology (14.2) creates the anatomic substrate for malabsorption; hepatobiliary-pancreatic disease (14.3) removes bile and enzymes; microbes and vitamins (14.4) produce the discrete syndromes CBSE loves to test in isolation or as complications.