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Protozoal Intestinal Infections andTrichomoniasis

Chapter 236 | Part 5: Infectious Diseases · Part 5 – Infectious Diseases: Parasitic · Chapter 236

Key Clinical Points

  1. Giardiasis is diagnosed by detection of parasite antigens in feces, identification of cysts (8–12 μm × 7–10 μm, four nuclei) or trophozoites (pear-shaped, two nuclei), or NAATs.
  2. Cryptosporidium oocysts are small (4–5 μm), acid-fast, and resistant to routine chlorination; they can cause biliary tract complications in AIDS patients.
  3. Cystoisospora belli oocysts are large (~25 μm) and require specific testing as they are not detected by conventional stool O+P.
  4. Cyclospora cayetanensis oocysts are 8–10 μm, variably acid-fast, and fluorescent under UV light; treatment is TMP-SMX.
  5. Microsporidia (E. bieneusi, E. intestinalis) are obligate intracellular protozoa; E. bieneusi is primarily gastrointestinal, while other species may involve the lungs, eyes, or other systems.
  6. Trichomonas vaginalis is diagnosed by wet mount (50–60% sensitivity) or NAAT (high sensitivity); treatment is metronidazole (2g single or 500mg BID x 7 days).
  7. Metronidazole resistance in Trichomonas vaginalis requires higher doses or alternative agents like tinidazole.
  8. Fever, blood, or mucus in stools are uncommon in giardiasis and suggest a different diagnosis or concomitant illness.
  9. Eosinophilia may be detectable in immunocompetent hosts with Cystoisospora infection but is not found in other enteric protozoan infections.
  10. Balantidium coli causes dysentery similar to amebiasis; it is more common where pigs are raised.

1. DEFINITION & OVERVIEW

• Giardiasis: Infection by Giardia duodenalis (also G. lamblia or G. intestinalis); a common cosmopolitan protozoal parasite causing endemic and epidemic intestinal disease and diarrhea. • Cryptosporidiosis: Caused by Cryptosporidium; self-limited in immunocompetent hosts but can be severe in persons with AIDS or other forms of immunodeficiency. • Cystoisosporiasis: Infection caused by Cystoisospora belli via consumption of oocysts. • Cyclosporiasis: Global diarrheal illness caused by Cyclospora cayetanensis. • Microsporidiosis: Infections by obligate intracellular spore-forming protozoa (e.g., Enterocytozoon bieneusi, Encephalitozoon intestinalis); common in AIDS patients. • Balantidiasis: Infection by Balantidium coli, a large ciliated protozoal parasite causing large-intestinal disease analogous to amebiasis. • Blastocystosis: Infection by Blastocystis hominis; pathogenicity is uncertain. • Dientamoebiasis: Infection by Dientamoeba fragilis; unique among intestinal protozoa for having a trophozoite stage but no cyst stage. • Sarcocystosis: Zoonotic infections where humans can be the definitive or dead-end intermediate host. • Trichomoniasis: Infection of the genitourinary tract by Trichomonas vaginalis, a major cause of symptomatic vaginitis.

2. EPIDEMIOLOGY

• Giardiasis: ◦ Prevalence: 20–40% in resource-constrained areas with limited access to sanitation, especially among young children. ◦ Settings: Common in daycare centers (person-to-person) and among travelers/campers (waterborne). • Cryptosporidiosis: ◦ Second most common cause of moderate to severe diarrhea during the first two years of life in resource-constrained areas. ◦ Zoonotic transmission: C. parvum can spread from infected animals to humans. • Cystoisosporiasis: Most common in tropical and subtropical countries. • Cyclosporiasis: Reported globally (USA, Asia, Africa, Latin America, Europe). • Microsporidiosis: Most common among patients with AIDS; less common in other immunocompromised hosts; rare in immunocompetent hosts. • Balantidiasis: More common where pigs are raised. • Trichomoniasis: Prevalence highest among those with multiple sexual partners or other STDs; 2–3 million infections annually in the USA.

3. ETIOLOGY & PATHOPHYSIOLOGY

• Giardia Pathophysiology: ◦ Attachment: Trophozoites adhere to the proximal small bowel mucosa via a ventral sucking disk. ◦ Mechanism: Not invasive; however, they may elicit enterocyte apoptosis, epithelial barrier dysfunction, and malabsorption/secretion. ◦ Clinical Result: Loss of brush-border enzyme activities leads to lactose intolerance; chronic cases may show flattened villi (similar to tropical sprue). • Cryptosporidium Pathophysiology: ◦ Location: Found in intracellular vacuoles in the small bowel. ◦ Complications: In AIDS patients, involvement of the biliary tract can cause papillary stenosis, sclerosing cholangitis, or cholecystitis. • Microsporidia Pathophysiology: ◦ Nature: Obligate intracellular spore-forming protozoa (0.5–2 μm × 1–4 μm). ◦ Replication: Merogony and sporogony in epithelial cells, endothelial cells, or macrophages. ◦ Spread: Spores shed in bodily fluids; E. bieneusi is presumed primarily in the gastrointestinal tract; other species may involve lungs, respiratory tract, eyes, or cause systemic infections (e.g., meningitis, nephritis). • Other Pathogens: ◦ Balantidium coli: Resides/replicates in the large bowel; trophozoites released from ingested cysts. ◦ Dientamoeba fragilis: Trophozoite stage only; transmission mechanism unknown. ◦ Sarcocystis spp.: Zoonotic; humans are definitive or dead-end hosts. ◦ Trichomonas vaginalis: Pear-shaped, motile (10 × 7 μm); replicates by binary fission in the lower genital tract.

4. CLINICAL FEATURES

• Giardiasis: ◦ Spectrum: Asymptomatic carriage to ful1ment diarrhea and malabsorption. ◦ Acute Presentation: Incubation 5–6 days to 1–3 weeks; symptoms include diarrhea, abdominal pain, bloating, belching, flatus, nausea, and vomiting. ◦ Chronic Presentation: May occur with or without acute phase; characterized by increased flatus, loose stools, sulfurous belching, and weight loss (duration >1 week). ◦ Red Flags: Fever, blood, or mucus in stool are uncommon; presence suggests a different diagnosis or concurrent illness. ◦ Extraintestinal: Urticaria, anterior uveitis, and arthritis (causality unclear). ◦ High Risk: Severe in hypogammaglobulinemia or cystic fibrosis; refractory in AIDS patients. • Trichomoniasis: ◦ Women: Malodorous vaginal discharge (often yellow), vulvar erythema/itching, dysuria/frequency (30–50%), dyspareunia. ◦ Men: Asymptomatic or urethritis, epididymitis, prostatitis. ◦ Incubation: 5–28 days.

5. DIFFERENTIAL DIAGNOSIS

• Giardiasis vs. Others: ◦ Absence of blood/mucus: Suggests non-giardiasis etiology. • Trichomoniasis: ◦ Symptoms do not clearly distinguish it from other types of infectious vaginitis. • Sarcocystosis: ◦ Intestinal form is self-limited; diagnosis via stool (though oocysts are rarely seen during the diarrheal phase).

6. INVESTIGATIONS & DIAGNOSIS

  1. Identify Giardiasis: • Antigen detection in feces (often first-line). • Microscopy: Identify cysts (8–12 μm × 7–10 μm, 4 nuclei) or trophozoites (pear-shaped, 2 nuclei, flagella). • NAAT: Highly sensitive.
  2. Identify Cryptosporidiosis: • Modified acid-fast stain (detects 4–5 μm oocysts). • Direct immunofluorescent antibody staining (DFA) (70–90% sensitivity). • NAAT.
  3. Identify Cystoisospora & Cyclospora: • Acid-fast stain (Cystoisospora ~25 μm; Cyclospora 8–10 μm). • Fluorescence under UV light (Cyclospora). • NAAT.
  4. Identify Microsporidiosis: • Special fecal stains, tissue biopsies (histology), or NAAT.
  5. Identify Trichomoniasis: • Wet mount: 50–60% sensitivity; provides immediate diagnosis. • DFA: 70–90% sensitivity. • NAAT: Highly sensitive/specific for urine, endocervical, and vaginal swabs.

Table 236-1 Diagnosis of Intestinal Protozoal Infections

PARASITE STOOL O+P FECAL ACID-FAST STAIN FECAL ANTIGEN IMMUNOASSAYS FECAL NAATS OTHER
Giardia + / ± ± + + DFA
Cryptosporidium ± + + +
Cystoisospora ± + – +
Cyclospora ± + + +
Dientamoeba ± – + +
Balantidium + – – – –
Microsporidia – – – + Special fecal stains, tissue biopsies

6.1 Diagnostic Table Summary

Table 236-1 summarizes the diagnostic utility of various methods: • Giardia: Stool O+P (+/±), Acid-Fast (±), Antigen (+), NAAT (+), Other (DFA). • Cryptosporidium: Stool O+P (±), Acid-Fast (+), Antigen (+), NAAT (+). • Cystoisospora: Stool O+P (±), Acid-Fast (+), Antigen (—), NAAT (+). • Cyclospora: Stool O+P (±), Acid-Fast (+), Antigen (+), NAAT (+). • Dientamoeba: Stool O+P (±), Acid-Fast (—), Antigen (+), NAAT (+). • Balantidium: Stool O+P (+), others (—). • Microsporidia: Stool O+P (—), Acid-Fast (—), Antigen (—), NAAT (+), Other (Special stains, biopsy).

7. MANAGEMENT & TREATMENT

  1. Giardiasis Treatment: • Metronidazole: 250–500 mg TID x 5 days. • Tinidazole: 2 g single dose. • Nitazoxanide: 500 mg BID x 3 days.
  2. Cryptosporidiosis Treatment: • Support: Fluids, electrolytes. • Nitazoxanide: 500 mg BID x 3 days (not for immunocompromised).
  3. Cystoisosporiasis Treatment: • TMP-SMX: 160/800 mg BID x 7–10 days; for HIV patients, continue 3x daily for 3–4 weeks.
  4. Cyclosporiasis Treatment: • TMP-SMX: 160/800 mg BID x 7–10 days.
  5. Microsporidiosis Treatment: • Keratoconjunctivitis: Topical fumagillin suspension. • HIV-infected (E. intestinalis): Albendazole.
  6. Balantidiasis Treatment: • Tetracycline: 500 mg QID x 10 days. • Metronidazole: Alternative agent.
  7. Blastocystosis Treatment: • Metronidazole: 500–750 mg TID x 5–10 days. • Tinidazole: 2 g single dose.
  8. Dientamoebiasis Treatment: • Paromomycin: 25–35 mg/kg per day in three doses for 7 days. • Metronidazole: 500–750 mg TID x 10 days.
  9. Trichomoniasis Treatment: • Metronidazole: 2 g single or 500 mg BID x 7 days. • Tinidazole: 2 g single dose. • Refractory cases: Higher doses or alternative agents like tinidazole. • Concurrent treatment: All sexual partners must be treated concurrently.

8. KEY PEARLS & HIGH-YIELD POINTS

• Giardia Morphology: Cysts (8–12 μm × 7–10 μm, 4 nuclei) vs Trophozoites (pear-shaped, 2 nuclei). • Cryptosporidium Size: Small oocysts (4–5 μm); acid-fast; resistant to chlorine. • Cystoisospora Size: Large oocysts (~25 μm); not seen on standard O+P. • Cyclospora Size: 8–10 μm; acid-fast and UV fluorescent. • Microsporidia: Small (0.5–2 μm × 1–4 μm); intracellular; common in AIDS. • Trichomoniasis Treatment: Metronidazole (2g single or 500mg BID x 7 days) is standard; treat all partners. • Clinical Rule-out: Presence of blood/mucus in stool suggests non-giardiasis infection. • Eosinophilia: Present in Cystoisospora, but not other enteric protozoan infections.

Reference Tables

TABLE 236-1 Diagnosis of Intestinal Protozoal Infections PARASITE Giardia Cryptosporidium Cystoisospora Cyclospora…

Harrison's 22e, p.1805

PARASITE STOOL O+P FECAL ACID-FAST STAIN FECAL ANTIGEN IMMUNOASSAYS FECAL NAATS OTHER
Giardia + + + DFA
± + + +
Cystoisospora ± + +
± + +
Dientamoeba ± + +
+
Microsporidia – + Special fecal stains,
tissue biopsies