GI Infections: Parasitic and Viral Diarrheas

0:00Welcome to Board Pearls. This is episode four of five of the GI Infections chapter, in the Special Populations and Acute or Supportive Care module. In this episode we cover the parasitic and viral diarrheal infections: the parasites from Giardia to Entamoeba histolytica to Strongyloides hyperinfection in steroids, and the viral gastroenteritis differential led by norovirus.

0:23The last episode handled the bacterial and toxin diarrheas by acquisition pattern. The parasites separate the same way, with exposure history the dominant clue, so move to them now.

0:35Parasitic infection is suspected by exposure, by persistence beyond seven to fourteen days, or by specific clinical patterns. Untreated water suggests Giardia. Daycare suggests Giardia or Cryptosporidium. Recent travel to endemic regions suggests Entamoeba histolytica. Prior endemic-area residence in a patient about to start steroids suggests Strongyloides. Peripheral eosinophilia suggests Strongyloides or Cystoisospora. Workup goes by suspected pathogen rather than by a generic ova-and-parasite alone, because antigen tests and PCR have replaced microscopy as the most sensitive modality.

1:13Giardia is the most common diagnosed enteric protozoal infection in the United States. Risk factors are untreated surface water, daycare, men who have sex with men, freshwater swimming, and IgA deficiency or common variable immunodeficiency. The symptom set is foul-smelling fatty diarrhea, bloating, flatulence, abdominal cramping, weight loss, and fatigue. Lactose intolerance often persists for weeks after eradication, and that post-eradication lactose intolerance is the usual explanation for apparent treatment failure.

1:46Diagnosis is stool antigen enzyme immunoassay or stool PCR. Both have sensitivity above ninety percent. Ova-and-parasite microscopy is fifty to seventy percent sensitive on a single specimen, because cyst shedding is intermittent. Treatment is tinidazole two grams as a single oral dose, preferred over metronidazole because tinidazole's longer half-life sustains drug exposure across the giardial life cycle from a single dose. Metronidazole requires repeated dosing and accumulates GI and neurologic side effects. Nitazoxanide five hundred milligrams twice daily for three days is the FDA-approved alternative that also covers Cryptosporidium. Paromomycin is the choice in pregnancy because it is poorly absorbed from the gut lumen, so systemic fetal exposure is negligible while the drug still reaches colonic Giardia. Recurrent giardiasis with sinopulmonary infections should trigger evaluation for common variable immunodeficiency.

2:43Cryptosporidium is acquired from contaminated water, daycare, calves and lambs, and recreational water, and it resists chlorine. In immunocompetent hosts the illness is self-limited over one to two weeks. In HIV at CD4 below one hundred to two hundred, Cryptosporidium produces voluminous chronic watery diarrhea with weight loss and is the leading pathogen in AIDS cholangiopathy. Nitazoxanide has limited efficacy in immunocompromised hosts, and the dominant therapy in HIV is antiretroviral therapy, because immune reconstitution clears the infection where antiparasitic therapy alone fails.

3:22Entamoeba histolytica deserves a careful look, because the treatment rule is two-stage and the reasoning sticks once you see why. The spectrum runs from asymptomatic luminal infection to bloody dysentery to amebic liver abscess, classically right-lobe with anchovy-paste aspirate. The classic colonic ulcer is flask-shaped on histology. Stool antigen enzyme immunoassay distinguishes pathogenic histolytica from non-pathogenic Entamoeba dispar, which microscopy cannot.

3:50Treatment is sequential because amebiasis exists in two anatomic compartments. Metronidazole and tinidazole are well-absorbed and reach tissue at therapeutic concentration, so they kill the invasive trophozoites that cause symptoms. The same systemic absorption means they reach the colonic lumen at low concentration and leave luminal cysts alive. Paromomycin, iodoquinol, or diloxanide furoate are non-absorbed and act in the lumen, killing the cysts that would otherwise excyst and relapse the infection. The regimen is therefore metronidazole or tinidazole first, followed by paromomycin. Amebic liver abscess responds to medical therapy alone in most cases, because trophozoites are tissue-invasive and metronidazole reaches them. Drainage is reserved for large abscesses, peripheral abscesses at risk of rupture, or treatment failure.

4:41Strongyloides is the steroid scenario, and it is the screening decision the boards test most reliably. The organism is acquired from soil contact in tropical and subtropical regions and persists for decades through autoinfection. Endemic exposure includes Latin America, sub-Saharan Africa, Southeast Asia, the Caribbean, and parts of rural southeastern United States including Appalachia. Chronic infection can present with peripheral eosinophilia, intermittent abdominal pain, intermittent diarrhea, and the migratory serpiginous larva currens rash on trunk and perianal skin.

5:14The screening rule is Strongyloides serology by enzyme immunoassay before any planned glucocorticoid course, anti-tumor necrosis factor agent, organ transplant immunosuppression, or chemotherapy in any patient with prior endemic exposure. Stool ova-and-parasite is insensitive because larval shedding is intermittent and low-burden, which is why serology is the screen.

5:38The reason the screen matters is hyperinfection. Steroids and other cellular-immunity blockers tip a chronic carrier into massive autoinfective expansion. Filariform larvae penetrate the bowel wall, drag enteric flora with them, and produce gram-negative bacteremia or meningitis with disseminated strongyloidiasis. Mortality runs as high as seventy percent. When serology returns positive and immunosuppression is urgent, empiric ivermectin is sometimes given before confirmatory testing, because missing chronic infection before steroids is catastrophic.

6:12Treatment of chronic Strongyloides is ivermectin two hundred micrograms per kilogram daily for one to two days, with longer courses for hyperinfection. Ivermectin is preferred over albendazole, because ivermectin paralyzes adult Strongyloides through glutamate-gated chloride channels that mammals lack. Albendazole acts on tubulin and is more active against tissue-stage helminths than against the autoinfective filariform larvae that drive the chronic Strongyloides cycle. Hookworm is the contrast. A single dose of albendazole four hundred milligrams cures hookworm, because hookworm adults live in the gut lumen with no autoinfective cycle to repeat-treat. Strongyloides has autoinfection, which is why the regimens differ.

6:55Anisakiasis is the one-line stem worth keeping in mind. Severe epigastric pain hours after raw fish in a patient who had sushi, sashimi, ceviche, or pickled herring. Endoscopy shows the Anisakis larva embedded in the gastric or duodenal wall, and endoscopic removal is both diagnostic and therapeutic. No antihelminthic reliably treats Anisakis. The cure is mechanical larval removal.

7:23That closes the parasitic block. Move to viral gastroenteritis, where norovirus dominates and the recognition cue is the outbreak pattern.

7:32Norovirus is the leading cause of acute community-acquired and outbreak gastroenteritis in the United States and globally, year-round with a cold-weather peak. The clinical pattern is abrupt onset of vomiting and non-bloody watery diarrhea lasting one to two days, with rapid onset twelve to forty-eight hours after exposure, low-grade fever, and vomiting prominent over diarrhea.

7:53The features that drive the epidemic pattern are mechanical. The infectious dose is about twenty viral particles. Shedding begins before symptoms and continues for weeks after they resolve. The virus persists on surfaces and in food and drinking water across a wide temperature range. There is no cross-protective immunity across many circulating strains, which allows repeat infections in the same person. The classic stems are cruise ships, daycare centers, nursing homes, hospitals, cafeterias, and raw oyster exposures.

8:24The clinical contrast with bacterial enterocolitis is the recognition tool. Vomiting plus a brief illness with low-grade fever points to norovirus. Bloody or mucoid stool with higher fever and longer course points to an invasive bacterial pathogen. The "vomiting plus brief illness" stem on the boards almost always lands on norovirus.

8:45Treatment is supportive with oral rehydration, intravenous fluids if dehydration is severe, and a bland diet as tolerated. There is no specific antiviral. Outbreak control runs on the same physical persistence that drives outbreaks. Alcohol-based hand sanitizers are less effective against norovirus than against most other viruses, so soap-and-water hand hygiene is the right answer at the bedside. Surface disinfection requires bleach-based agents at one thousand to five thousand parts per million. Symptomatic staff are excluded for at least forty-eight hours after symptom resolution. In transplant recipients, chronic norovirus can persist for months, and mycophenolate dose reduction often allows immune-mediated clearance because mycophenolate suppresses T-cell function more than tacrolimus.

9:34Rotavirus historically caused severe pediatric diarrhea, and routine pediatric vaccination with RotaTeq or Rotarix has reduced severe rotavirus disease by about eighty-five percent in vaccinated populations. Rotavirus still matters in unvaccinated and immunocompromised populations. Adenovirus, sapovirus, and astrovirus complete the differential in the multiplex stool PCR era and are typically self-limited.

10:01Pull the parasitic and viral half together. The parasites separate by exposure, with Giardia from water and its tinidazole single dose, Entamoeba histolytica from endemic travel with the two-stage tissue-then-luminal therapy, and Strongyloides as the pre-steroid serology question that prevents seventy-percent-mortality hyperinfection, with Anisakis the raw-fish larva cured by endoscopic removal. Norovirus closes the differential with vomiting, short course, outbreak pattern, and the soap-and-water and bleach answers that follow from its environmental physiology.

10:34The next episode picks up the immunocompromised-host enteric infections, where advanced cellular immunodeficiency opens the differential to organisms the immunocompetent gut contains. We cover CMV colitis with histologic owl-eye inclusions and intravenous ganciclovir treatment. MAC enterocolitis follows with macrolide-containing regimens and the PAS-positive acid-fast-positive macrophage that separates it from Whipple disease. Microsporidia comes in with itraconazole or albendazole chosen by species-level tubulin pharmacology. Cyclospora closes the differential with trimethoprim-sulfamethoxazole, because the coccidian folate pathway has no salvage.

11:15For the full chapter, the practice vignettes, and the topic-tagged question bank, head to board pearls dot com. You'll find the rest of the series on Apple Podcasts, Spotify, or wherever you listen to podcasts. That brings us to the end of episode four of five of chapter thirty three, and I'll see you in the next one.