Common Human Parasitic Infections

Why This Matters

Understanding human parasitic infections requires more than memorizing a list of organisms and symptoms—you're being tested on your ability to recognize transmission mechanisms, life cycle stages, host-parasite relationships, and pathophysiological processes. These infections demonstrate fundamental parasitological concepts: how vector biology shapes disease distribution, why certain parasites cause tissue-specific damage, and how life cycle complexity determines prevention strategies.

When you encounter exam questions about parasitic infections, you'll need to connect the dots between transmission route, target organ system, and clinical presentation. An FRQ might ask you to compare two waterborne protozoa or explain why certain helminths cause anemia while others cause obstruction. Don't just memorize that hookworms cause anemia—understand why their feeding behavior leads to blood loss. That mechanistic thinking is what separates strong answers from mediocre ones.

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Vector-Borne Protozoan Infections

These parasites depend on arthropod vectors for transmission, creating complex life cycles that involve both vertebrate and invertebrate hosts. The vector determines geographic distribution, while the parasite's target tissue determines pathology.

Malaria (Plasmodium species)

• Transmitted by female Anopheles mosquitoes—sporozoites travel to liver hepatocytes before invading erythrocytes in the blood stage
• Cyclical fevers result from synchronized rupture of infected red blood cells releasing merozoites and triggering cytokine cascades
• Severe falciparum malaria causes cerebral involvement and organ failure due to cytoadherence of parasitized RBCs to vascular endothelium

Leishmaniasis (Leishmania species)

• Sandfly vectors (Phlebotomus/Lutzomyia) transmit promastigotes that transform into amastigotes within host macrophages
• Clinical spectrum ranges from cutaneous ulcers to fatal visceral disease depending on species and host immune response
• Intracellular survival—parasites evade killing by preventing phagolysosome fusion, a key exam concept in immune evasion

Trypanosomiasis (Trypanosoma species)

• African sleeping sickness (T. brucei)—transmitted by tsetse flies; crosses blood-brain barrier causing neurological deterioration
• Chagas disease (T. cruzi)—transmitted by triatomine bugs via fecal contamination; causes chronic cardiomyopathy decades after infection
• Antigenic variation in T. brucei allows immune evasion through continuous switching of variant surface glycoproteins (VSGs)

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Waterborne and Fecal-Oral Protozoa

These parasites spread through contaminated water or food, with cyst stages providing environmental resistance. Cyst formation is the key adaptation allowing fecal-oral transmission and survival outside the host.

Giardiasis (Giardia lamblia)

• Cysts survive chlorination—ingestion of as few as 10 cysts can establish infection in the duodenum and jejunum
• Malabsorptive diarrhea results from villous atrophy and brush border enzyme deficiency, not tissue invasion
• Characteristic trophozoite morphology—binucleate with ventral adhesive disc; often described as having a "face-like" appearance on microscopy

Cryptosporidiosis (Cryptosporidium species)

• Highly chlorine-resistant oocysts—responsible for major waterborne outbreaks; requires filtration for removal
• Self-limiting in immunocompetent hosts but causes severe, potentially fatal chronic diarrhea in AIDS patients
• Intracellular but extracytoplasmic—parasites develop within a parasitophorous vacuole at the microvillus surface

Amoebiasis (Entamoeba histolytica)

• Tissue-invasive protozoan—trophozoites secrete cysteine proteases that lyse colonic epithelium, causing flask-shaped ulcers
• Extraintestinal spread can produce liver abscesses containing "anchovy paste" material; right lobe most commonly affected
• Must distinguish from E. dispar—morphologically identical but nonpathogenic; antigen detection or PCR required for differentiation

Toxoplasmosis (Toxoplasma gondii)

• Definitive host is the cat—oocysts shed in feces; humans acquire infection from undercooked meat (tissue cysts) or cat feces
• Asymptomatic in immunocompetent adults but causes severe congenital defects (chorioretinitis, hydrocephalus, intracranial calcifications) and reactivation encephalitis in AIDS
• Bradyzoites in tissue cysts represent latent infection that persists lifelong; reactivation occurs when cellular immunity wanes

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Soil-Transmitted Helminths (Intestinal Nematodes)

These roundworms share a common transmission pattern through fecal contamination of soil. Eggs require soil maturation, making sanitation and hygiene the primary prevention strategies.

Ascariasis (Ascaris lumbricoides)

• Most common human helminth worldwide—eggs mature in soil; larvae undergo hepatopulmonary migration before establishing in small intestine
• Löffler syndrome occurs during lung migration—eosinophilia, cough, and transient pulmonary infiltrates
• Intestinal obstruction in heavy infections; worms may migrate into bile duct or appendix causing acute surgical emergencies

Hookworm Infection (Ancylostoma duodenale and Necator americanus)

• Percutaneous larval penetration—filariform larvae in soil penetrate bare feet, migrate through lungs, and mature in small intestine
• Iron-deficiency anemia is the hallmark pathology; adult worms attach to mucosa and feed on blood (0.03-0.2 mL/worm/day)
• Ground itch—pruritic papular rash at larval entry site; a diagnostic clue in endemic areas

Trichuriasis (Trichuris trichiura)

• Whipworm—thin anterior end embeds in colonic mucosa while thick posterior remains in lumen
• Rectal prolapse in heavy pediatric infections due to straining and inflammation; associated with Trichuris dysentery syndrome
• No tissue migration phase—eggs hatch in intestine and larvae mature in situ, distinguishing it from Ascaris and hookworm

Enterobiasis (Enterobius vermicularis)

• Pinworm—most common helminth in developed countries—eggs deposited perianally at night cause intense pruritus
• Autoinfection cycle—scratching transfers eggs to fingers and mouth; eggs are immediately infectious (no soil maturation)
• Scotch tape test for diagnosis—adhesive tape applied perianally in morning captures characteristic plano-convex eggs

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Tissue-Invasive Helminths

These worms migrate through or reside in tissues beyond the GI tract, causing organ-specific pathology. Understanding the life cycle explains which organs are affected and why.

Schistosomiasis (Schistosoma species)

• Freshwater snail intermediate host—cercariae penetrate skin during water contact and mature into adult flukes in venous plexuses
• Egg-induced granulomatous inflammation causes pathology; S. mansoni/japonicum affect liver (periportal fibrosis), S. haematobium affects bladder (hematuria, cancer risk)
• Praziquantel is treatment of choice; targets adult worms but eggs already deposited continue causing damage

Taeniasis and Cysticercosis (Taenia species)

• Intestinal tapeworm from undercooked pork (T. solium) or beef (T. saginata)—adult worms cause minimal symptoms
• Neurocysticercosis—T. solium eggs (not meat) cause larval cysts in brain; leading cause of acquired epilepsy in endemic areas
• Critical distinction: eating undercooked pork → intestinal tapeworm; ingesting eggs → cysticercosis. Humans become accidental intermediate hosts.

Filariasis (Wuchereria bancrofti and Brugia malayi)

• Mosquito-transmitted nematodes—microfilariae circulate in blood with nocturnal periodicity matching vector feeding behavior
• Lymphatic obstruction from adult worms and inflammatory response leads to lymphedema and elephantiasis in chronic infection
• Diethylcarbamazine (DEC) kills microfilariae; mass drug administration programs aim for elimination

Onchocerciasis (Onchocerca volvulus)

• Blackfly vector (Simulium)—larvae mature into adults in subcutaneous nodules; microfilariae migrate through skin and eyes
• River blindness—microfilariae in cornea and retina cause progressive vision loss; second leading infectious cause of blindness
• Ivermectin kills microfilariae and reduces transmission; donated through Mectizan program for mass treatment

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Quick Reference Table

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Self-Check Questions

1. Which two waterborne protozoa have chlorine-resistant cyst/oocyst stages, and how do their mechanisms of diarrhea differ (invasive vs. malabsorptive)?

2. Compare the transmission routes of Ascaris and hookworm—why does hookworm cause "ground itch" while Ascaris does not?

3. A patient with AIDS presents with ring-enhancing brain lesions. Which protozoan is most likely responsible, and what life cycle stage causes reactivation disease?

4. Explain why ingesting undercooked pork causes intestinal taeniasis, but ingesting T. solium eggs causes neurocysticercosis. What role does the human play in each scenario?

5. Compare and contrast the pathophysiology of lymphatic filariasis and onchocerciasis—both are filarial infections, so why do they affect different organ systems?