Chapter 33, Ep 5 of 5: Immunocompromised-Host Enteric Infections episode artwork

EPISODE · Jul 16, 2026 · 18 MIN

Chapter 33, Ep 5 of 5: Immunocompromised-Host Enteric Infections

from Dr GI Joe · host Board Pearls

The immunocompromised gut expands the pathogen list, and the organizing move is that each organism lives behind a specific cue that names the therapy: name the host, the stain, and the histology, and you name the drug. CMV gives the owl-eye inclusion at the ulcer base treated with ganciclovir, with foscarnet as salvage when UL97 mutations break the prodrug pathway. MAC gives the PAS-positive, acid-fast-positive macrophage treated with a macrolide plus ethambutol, microsporidia turn on beta-tubulin pharmacology, and the coccidians answer to trimethoprim-sulfamethoxazole. The unifying thread is that antimicrobials hold the line while immune reconstitution provides durable clearance.   Topics covered CMV colitis hosts and presentation Biopsy from the ulcer base CMV resistance and foscarnet salvage MAC enterocolitis and combination therapy MAC versus Whipple on acid-fast staining Microsporidia and beta-tubulin pharmacology Cyclospora and coccidian folate biology Cystoisospora and its stem-level fingerprint   Key decisions In acute severe ulcerative colitis refractory to intravenous corticosteroids, look for CMV first, since it is found in roughly a third of these cases and shifts management from biologic escalation to antiviral therapy. Biopsy the ulcer base rather than the edge or normal mucosa for CMV, add immunohistochemistry because hematoxylin and eosin has sensitivity below fifty percent, and treat with intravenous ganciclovir. Switch to foscarnet when ganciclovir fails from UL97 mutations, because foscarnet inhibits UL54 polymerase directly and does not require viral phosphorylation. Treat disseminated MAC with a macrolide plus ethambutol, adding rifabutin in advanced disease, because macrolide monotherapy rapidly selects resistance. Separate MAC from Whipple on the acid-fast stain: MAC-laden macrophages are PAS-positive and acid-fast positive, while Whipple macrophages are PAS-positive and acid-fast negative. Treat Encephalitozoon intestinalis microsporidia with albendazole but use fumagillin for Enterocytozoon bieneusi, whose tubulin variant resists albendazole binding. Treat Cyclospora and Cystoisospora with trimethoprim-sulfamethoxazole, because coccidian folate biology has no salvage pathway, and continue prophylaxis while CD4 stays below two hundred.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: [email protected].

Episode metadata supplied by the publisher feed · Published Jul 16, 2026

The immunocompromised gut expands the pathogen list, and the organizing move is that each organism lives behind a specific cue that names the therapy: name the host, the stain, and the histology, and you name the drug. CMV gives the owl-eye inclusion at the ulcer base treated with ganciclovir, with foscarnet as salvage when UL97 mutations break the prodrug pathway. MAC gives the PAS-positive, acid-fast-positive macrophage treated with a macrolide plus ethambutol, microsporidia turn on beta-tubulin pharmacology, and the coccidians answer to trimethoprim-sulfamethoxazole. The unifying thread is that antimicrobials hold the line while immune reconstitution provides durable clearance.   Topics covered CMV colitis hosts and presentation Biopsy from the ulcer base CMV resistance and foscarnet salvage MAC enterocolitis and combination therapy MAC versus Whipple on acid-fast staining Microsporidia and beta-tubulin pharmacology Cyclospora and coccidian folate biology Cystoisospora and its stem-level fingerprint   Key decisions In acute severe ulcerative colitis refractory to intravenous corticosteroids, look for CMV first, since it is found in roughly a third of these cases and shifts management from biologic escalation to antiviral therapy. Biopsy the ulcer base rather than the edge or normal mucosa for CMV, add immunohistochemistry because hematoxylin and eosin has sensitivity below fifty percent, and treat with intravenous ganciclovir. Switch to foscarnet when ganciclovir fails from UL97 mutations, because foscarnet inhibits UL54 polymerase directly and does not require viral phosphorylation. Treat disseminated MAC with a macrolide plus ethambutol, adding rifabutin in advanced disease, because macrolide monotherapy rapidly selects resistance. Separate MAC from Whipple on the acid-fast stain: MAC-laden macrophages are PAS-positive and acid-fast positive, while Whipple macrophages are PAS-positive and acid-fast negative. Treat Encephalitozoon intestinalis microsporidia with albendazole but use fumagillin for Enterocytozoon bieneusi, whose tubulin variant resists albendazole binding. Treat Cyclospora and Cystoisospora with trimethoprim-sulfamethoxazole, because coccidian folate biology has no salvage pathway, and continue prophylaxis while CD4 stays below two hundred.   For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: [email protected].

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Chapter 33, Ep 5 of 5: Immunocompromised-Host Enteric Infections

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The immunocompromised gut expands the pathogen list, and the organizing move is that each organism lives behind a specific cue that names the therapy: name the host, the stain, and the histology, and you name the drug. CMV gives the owl-eye...

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