15.2 Parasites

Why parasite life cycles are the scored skill

/practice/nbce-part1Practice questions with detailed explanations

Quick Answer: Protozoa are unicellular (trophozoite ± cyst). Helminths are worms: nematodes (round), cestodes (tape), trematodes (flukes). Ectoparasites live on the surface (lice, scabies mites). Giardia and Entamoeba are fecal–oral cysts. Plasmodium is Anopheles. Toxoplasma is cats and undercooked meat. Enterobius is perianal eggs. Taenia solium eggs cause cysticercosis. Trichinella is undercooked pork muscle. Body lice vector typhus; Sarcoptes burrows in stratum corneum.

Three groups, three body plans

Protozoa are single-celled eukaryotes. Intestinal and some tissue protozoa alternate trophozoite (feeding, motile, labile in the environment) and cyst (infective, hardy). Blood protozoa use vectors and named stages (sporozoite, merozoite, trypomastigote, amastigote). They have no chitin wall and no ergosterol requirement like fungi; metronidazole, artemisinins, and folate-pathway drugs appear as treatment names, but Part I still wants the organism and the cycle.

Helminths are multicellular. Nematodes (roundworms) have cylindrical bodies and separate sexes; intestinal examples are Enterobius, Ascaris, hookworms, Strongyloides, Trichinella. Cestodes (tapeworms) are flat, segmented proglottids with a scolex; humans eating larval cysts get adult worms in the gut; humans eating eggs of Taenia solium or Echinococcus become the intermediate host with tissue cysts. Trematodes (flukes) need snails; cercariae invade skin (Schistosoma) or are eaten in undercooked fish/crab/plants (Clonorchis, Paragonimus, Fasciola). Eosinophilia is a nematode/cestode/trematode blood clue, not a protozoan clue (except sometimes Isospora / Cystoisospora and recovering malaria).

Ectoparasites are arthropods that live on the host: Pediculus (lice), Pthirus pubis, Sarcoptes scabiei. They are not protozoa. Some are vectors of bacteria (Rickettsia prowazekii on the body louse)—a bacteria-chapter crossover (/study-guides/nbce-part1/microbiology-host-pathogens/bacteria).

Giardia duodenalis (lamblia, intestinalis)

The most commonly identified intestinal parasite in the United States. Reservoir: humans and many mammals (beavers give the backpacker story). Infective form: cysts passed in stool; they survive cold water and are relatively chlorine-tolerant, so municipal outbreaks and stream water both appear in stems. Infectious dose is low (tens of cysts). Excystation in the duodenum releases trophozoites: pear-shaped, two nuclei, four pairs of flagella, ventral sucking disk that adheres to the brush border and flattens villi. No invasion of the mucosa, no blood in stool as a rule. Clinical: watery, greasy, foul diarrhea, bloating, flatulence, lactose intolerance, weight loss—a malabsorption picture. IgA deficiency and hypogammaglobulinemia increase severity and persistence. Daycare and oral–anal contact are additional fecal–oral routes. Diagnosis: stool antigen or NAAT; microscopy shows cysts (oval, four nuclei when mature) or trophozoites. Historic string test is not required if antigen is offered. Metronidazole or tinidazole is the usual drug name on a distractor list.

Entamoeba histolytica

Not E. dispar, which looks the same on a poorly collected slide but does not invade. Reservoir: humans. Infective form: quadrinucleate cysts in feces (food, water, hands, sexual fecal–oral contact). Trophozoites exist in the colon but die quickly outside the body—they are not the environmental survivor. Invading trophozoites ingest erythrocytes (a morphology clue) and release cysteine proteases. Flask-shaped ulcers undermine colonic mucosa (cecum and ascending colon favored). Extraintestinal: trophozoites travel via portal blood to the right lobe of the liver and form an anchovy-paste abscess (necrotic, chocolate-brown). Lungs and brain are rarer. Clinical: dysentery with blood and mucus, or a febrile right-upper-quadrant abscess without current diarrhea. Diagnosis: stool antigen/PCR to separate dispar; serology useful for liver abscess when stool is already negative. Treatment logic: a tissue agent (metronidazole) then a luminal cysticidal agent (paromomycin or iodoquinol)—killing trophozoites without clearing cysts leaves the patient infectious.

Plasmodium: Anopheles, liver, then red cells

Malaria is an intraerythrocytic protozoan infection. Vector and definitive host: female Anopheles mosquito (sexual cycle / sporogony in the mosquito). Intermediate host: humans (asexual schizogony). Cycle: mosquito injects sporozoites → hepatocytes (exoerythrocytic schizont) → merozoites flood blood → invade RBCs as rings → trophozoites → schizonts → more merozoites (fever spike when the RBC lyses) → some become gametocytes that the next mosquito drinks.

Hypnozoites of vivax and ovale sleep in hepatocytes and cause relapses months later unless primaquine or tafenoquine is given (check G6PD first). Falciparum does not relapse from hypnozoites; recrudescence is from surviving blood stages. Gold-standard diagnosis: thick smear (sensitivity) and thin smear (speciation). Rapid antigen tests exist; they can miss non-falciparum or low parasitemia. Chloroquine still works in a few regions; artemisinin combination therapy is the falciparum standard in resistant zones—Part I wants species and cycle more than a travel-clinic algorithm.

Cerebral malaria is a falciparum cytoadherence infarct-and-coma picture, not a primary chiropractic headache. Fever periodicity is useful when classic, but falciparum often is not textbook-tertian.

Toxoplasma gondii

An apicomplexan like Plasmodium, but the definitive host is the cat (and other felids): only cats shed oocysts in feces. Oocysts sporulate in 1–5 days in the environment—so daily litter-box changing reduces risk; the freshly passed oocyst is not yet infectious. Intermediate hosts: almost all warm-blooded animals, including humans. Tissue bradyzoite cysts concentrate in brain, heart, and skeletal muscle. Human acquisition: (1) ingestion of sporulated oocysts (cat feces, contaminated water/produce), (2) undercooked meat with bradyzoites (pork, lamb, venison), (3) transplacental tachyzoites during primary maternal infection, (4) organ transplant or blood, rarely.

Immunocompetent adult: often asymptomatic or a heterophile-negative mononucleosis-like illness with cervical nodes. Congenital (primary infection during pregnancy; chronic maternal latency is much lower risk): chorioretinitis, hydrocephalus, intracranial calcifications—the classic triad—plus blueberry-muffin rash, seizures, hearing loss. First-trimester infection: fewer transmissions, worse disease; third trimester: more transmissions, milder neonatal disease. AIDS reactivation: multiple ring-enhancing brain lesions (basal ganglia, corticomedullary), fever, focal neuro deficit, CD4 typically <100 cells/µL. Contrast with primary CNS lymphoma (often single ring lesion, EBV in the tumor). Treatment names: pyrimethamine + sulfadiazine + leucovorin. Serology (IgM/IgG, avidity) dates infection in pregnancy.

Cats are definitive hosts; humans are accidental intermediate hosts. That sentence answers most Toxoplasma items.

Enterobius vermicularis (pinworm)

The most common helminth in U.S. children. Infective form: embryonated eggs (already mature when laid, or within hours). Cycle: fecal–oral, including autoinfection and family/fomite spread (eggs light enough to move on air to bedding and clothing). Gravid females migrate out the anus at night and glue eggs to perianal skin. Clinical: nocturnal perianal pruritus, restless sleep, sometimes vulvovaginitis in girls; no eosinophilia as a rule because there is no tissue-invasive larval migration. Diagnosis: cellulose-tape (Scotch-tape) test on perianal skin in the morning before bathing, not a random stool O&P (eggs are not concentrated in feces). Treat the household; wash linens. Pyrantel or albendazole are the named drugs. This is a contact and fomite nematode, not a pork nematode and not a malaria vector story.

Taenia saginata and Taenia solium

Both are cestodes acquired as adult tapeworms when humans eat cysticerci in undercooked beef (T. saginata) or pork (T. solium). Adults live in the small bowel, shed proglottids and eggs in stool, and may cause mild GI symptoms or passing of segments.

The Part I discriminator is cysticercosis. Only T. solium eggs (from human feces—your own, or a food handler) infect humans as the intermediate host. Larvae encyst in brain, muscle, eye. Neurocysticercosis is a leading cause of adult-onset seizures in endemic regions (Latin America, parts of Asia and Africa). MRI/CT: cysts, scolex, calcifications. T. saginata does not cause human cysticercosis. T. solium scolex has hooks (armed); saginata is unarmed and has more uterine branches in the proglottid (~15–30 vs ~7–13). Eating pork cysticerci → adult intestinal tapeworm. Eating eggs → cysticercosis. Those are opposite cycles; mixing them is the classic trap.

Echinococcus granulosus (hydatid) is a related exam neighbor: dogs are definitive hosts; sheep (and humans) intermediate; liver (then lung) hydatid cysts; rupture → anaphylaxis. Not the pork tapeworm, but the same egg-versus-larva logic.

Trichinella spiralis

Reservoir: pigs, wild boar, bear, walrus, other carnivores. Infective form: encysted larvae in striated muscle of undercooked meat. Cycle: ingested larvae become adults in the small bowel (week 1: GI symptoms) → newborn larvae disseminate hematogenously → encyst in skeletal muscle that is active and well perfused (extraocular, tongue, deltoid, diaphragm, gastrocnemius). Clinical (week 2+): fever, myalgia, periorbital edema, subungual splinter hemorrhages, eosinophilia, elevated muscle enzymes (CK). Severe disease: myocarditis, encephalitis. Diagnosis: serology, sometimes muscle biopsy with coiled larvae in nurse cells. Prevention: cook pork and wild game thoroughly; freezing kills some T. spiralis in pork but not all sylvatic species (T. nativa in bear is freeze-resistant). A patient who presents to a chiropractic office with diffuse myalgia, periorbital puffiness, and a bear-sausage history needs eosinophils and a medical workup, not a lumbar adjustment as the first move.

Other protozoa and helminths worth a table row

These are not the assignment’s named core, but they fill adjacent stems so you do not mis-tag the core organisms.

Ectoparasites: lice and scabies

Pediculus humanus capitis (head louse): nits cemented to hair shafts; school-age spread by head contact and shared hats; not an important typhus vector. Pediculus humanus corporis (body louse): lives in clothing seams, not on hair; associated with crowding and poor hygiene; vector of Rickettsia prowazekii (epidemic typhus), Bartonella quintana (trench fever), and Borrelia recurrentis (louse-borne relapsing fever). Pthirus pubis (crab louse): coarse hair of pubis, axilla, eyelashes; sexual contact. Treatment names: topical permethrin or ivermectin; for body lice, washing clothing and bedding is the control method because the louse is in the cloth.

Sarcoptes scabiei var. hominis: a mite that burrows in stratum corneum. Transmission: prolonged skin-to-skin contact (household, sexual); fomites matter more in crusted (Norwegian) scabies, where mite burden is enormous (thousands to millions vs ~10–15 in classic scabies). Clinical: intense nocturnal pruritus, burrows in finger webs, wrists, elbows, belt line, genitals; face and scalp spared in immunocompetent adults (infants can have face/scalp). Itch is largely type IV hypersensitivity to mite products—so symptoms can lag first infestation by weeks and can persist days after mites are dead. Crusted scabies: immunocompromise, Down syndrome, neuropathy; thick scale, often less itch, highly infectious. Diagnosis: mineral-oil scraping of a burrow. Permethrin 5% from neck down, or oral ivermectin; treat close contacts; bag or wash linens.

Pathogenicity pattern. Protozoa damage by adhesion (Giardia), invasion and lysis (Entamoeba, Plasmodium), or cyst reactivation (Toxoplasma). Helminths damage by mechanical load, inflammation to eggs or larvae, and eosinophil-rich responses. Ectoparasites damage by bite, burrow, and hypersensitivity, plus vectoring bacteria. Resistance in this chapter means cysts that shrug off chlorination (Giardia, Cryptosporidium), hypnozoites that shrug off blood schizonticides, and eggs that survive on fomites (Enterobius)—not MRSA-style mecA.

Parasite items close when you state the infective stage and the next host. Epidemiology in the next section asks how health agencies count and interrupt those same cycles at population scale.