Parasitology — Malaria, Intestinal Parasites & Filariasis

🟢 Lite — Quick Review (1h–1d)

Rapid summary for last-minute revision before your exam.

Malaria species and features:

• P. falciparum: Most dangerous; crescents (gametocytes); high parasitemia; causes cerebral malaria, renal failure; chloroquine resistance (Widespread in India/SE Asia)
• P. vivax: Relapsing malaria; dormant hypnozoites in liver; prefer young RBCs → mild parasitemia; Causes spleen enlargement
• P. ovale: Relapsing; similar to vivax; rare in India
• P. malariae: Benign; quartan malaria (72-hour cycles); can cause nephrotic syndrome
• P. knowlesi: Zoonotic (macaques); quotidian (daily) fever; SE Asia

Cerebral malaria: P. falciparum; ring forms in capillaries; malarial retinopathy (white dots, ring hemorrhages); fatality 15–20% despite treatment.

Vivax vs falciparum: P. vivax — Schüffner stippling (red dots) in RBCs; P. falciparum — Maurer clefts (blue dashes); no splenomegaly in falciparum.

⚡ Exam tip: Think malaria for fever + travel to endemic area + no vaccination. Thick and thin smears are gold standard.

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🟡 Standard — Regular Study (2d–2mo)

Standard content for students with a few days to months.

Malaria

Life Cycle

1. Infective stage: Sporozoites in saliva of infected female Anopheles mosquito (transmitted during bite)
2. Liver stage (exo-erythrocytic): Sporozoites → liver → develop into schizonts → release merozoites (P. vivax/P. ovale also leave hypnozoites)
3. Blood stage (erythrocytic): Merozoites invade RBCs → ring forms → trophozoites → schizonts → merozoites → new RBCs (cycle continues)
4. Gametocyte formation: Some merozoites → gametocytes (male microgametocytes, female macrogametocytes) → taken up by mosquito
5. Mosquito stage: Gametocytes → fertilization in mosquito gut → ookinete → oocyst → sporozoites migrate to salivary glands

P. falciparum Specifics

• Infected RBCs express PfEMP1 (adherence ligand) → cytoadherence to endothelial cells → sequestration in deep vascular beds (brain, kidney, placenta)
• Crescent-shaped gametocytes (pathognomonic)
• Can infect RBCs of all ages → high parasitemia
• Cerebral malaria: Sequestration of parasitized RBCs in brain capillaries → endothelial activation → coma
• Blackwater fever: Intravascular hemolysis → hemoglobinuria (classically with quinine)
• Chloroquine resistance: Due to chloroquine resistance transporter (CRT/PfCRT) mutation; widespread in P. falciparum globally

P. vivax Specifics

• Hypnozoites in hepatocytes → dormant forms → cause relapses weeks–months after primary attack
• Infects young RBCs (reticulocytes) → moderate parasitemia
• Enlarged RBCs with Schüffner stippling (eosinophilic dots)
• Causes significant splenomegaly (splenic congestion and immune response)
• Primaquine (15 mg/day × 14 days) required for hypnozoite eradication (test for G6PD deficiency first — causes hemolysis in G6PD-deficient patients)
• Spleen: In P. vivax, the spleen plays a major role in clearing infected RBCs; splenomegaly is pronounced

Diagnosis

• Gold standard: Thick and thin peripheral blood smears (Giemsa stain)
  • Thick smear: Detects presence of malaria (more sensitive)
  • Thin smear: Species identification, parasitemia quantification
• RDTs (rapid diagnostic tests): Detect HRP2 (P. falciparum) or aldolase (pan-malarial)
• PCR: Most sensitive; used for species confirmation and low-level parasitemia
• Fluorescence microscopy (QBC): Acridine orange-stained capillaries — faster but less specific

Treatment of Malaria

Type	Treatment
Uncomplicated P. falciparum (chloroquine-sensitive areas)	Chloroquine
Uncomplicated P. falciparum (chloroquine-resistant)	ACT (Artemisinin-based Combination Therapy): Artemether-Lumefantrine, Artesunate-Amodiaquine
Severe P. falciparum	IV Artesunate (life-saving); quinine if artesunate unavailable
P. vivax/P. ovale (including radical cure)	Chloroquine + Primaquine (for hypnozoites); if G6PD-deficient → primaquine is contraindicated
P. malariae	Chloroquine
P. knowlesi	ACT or Chloroquine

Note: Primaquine destroys hypnozoites of P. vivax and P. ovale; essential for preventing relapses; must test for G6PD deficiency first.

Complications

• Cerebral malaria: Altered consciousness, seizures, coma; P. falciparum
• Severe anemia: Hemolysis; especially P. falciparum
• Renal failure: Acute tubular necrosis, blackwater fever; P. falciparum
• Pulmonary edema/ARDS: P. falciparum
• Hypoglycemia: Especially with quinine/quinidine and in severe malaria
• Metabolic acidosis: Especially in children
• Pregnancy: P. falciparum → placental sequestration → low birth weight, stillbirth, maternal anemia

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Intestinal Parasites

Protozoa

Giardia lamblia (Giardiasis)

• Flagellated protozoan; trophozoite (pear-shaped with falling-leaf motility; 4 flagella, 2 nuclei, suction disc) and cyst (oval, 4 nuclei)
• Transmission: Fecal-oral (contaminated water); cysts survive chlorination; beaver and muskrats are reservoirs
• Clinical: Malabsorption syndrome — bloating, flatulence, steatorrhea (greasy, foul-smelling stools); no dysentery or blood in stool
• Diagnosis: Stool ova and cyst (3 samples); string test (Enterotest); duodenal biopsy
• Treatment: Metronidazole (flagyl); tinidazole (single dose alternative)

Entamoeba histolytica (Amoebiasis)

• Transmission: Fecal-oral (contaminated food/water)
• Intestinal disease: Amoebic dysentery — mucus and blood in stool (invasion of colonic mucosa); flask-shaped ulcers in colon
• Extraintestinal: Amoebic liver abscess (most common); right lobe of liver; “anchovy paste” aspirate; fever, right hypochondrial pain
• Diagnosis: Stool for cysts/trophozoites (must distinguish from non-pathogenic E. dispar); serology (anti-amoebic antibodies); liver abscess → ultrasound/CT
• Treatment: Metronidazole for tissue phase; paromomycin or iodoquinol for luminal phase
• Important: E. histolytica has ingested RBCs in trophozoite (E. dispar does not)

Cryptosporidium parvum

• Apicomplexan protozoan; sporozoites with oocysts (acid-fast positive)
• Transmission: Fecal-oral (contaminated water; highly chlorination-resistant); person-to-person
• Clinical: Watery diarrhea (non-bloody), crampy abdominal pain; severe in immunocompromised (AIDS with CD4 <100 → cholera-like diarrhea)
• Diagnosis: Modified acid-fast stain of stool; stool antigen ELISA; PCR
• Treatment: Nitazoxanide (immunocompetent); optimized ART + nitazoxanide (AIDS patients); paromomycin + azithromycin (severe cases)

Helminths

Ascaris lumbricoides (Ascariasis)

• Nematode (roundworm); largest intestinal nematode (25–35 cm)
• Transmission: Fecal-oral (eggs with embryonated larvae in soil-contaminated food)
• Clinical: Asymptomatic most common; larval migration → pneumonitis (Löffler syndrome = eosinophilic pneumonia, dry cough, wheeze, eosinophilia); intestinal phase → malabsorption, intestinal obstruction (especially children with heavy worm load)
• Complications: Intestinal perforation, biliary colic, cholangitis, appendicitis (worms migrate)
• Diagnosis: Stool eggs (ova are golden-brown, bile-stained, oval with irregular outer coat)
• Treatment: Albendazole (single dose 400 mg) OR mebendazole; pyrantel pamoate

Hookworm (Ancylostoma duodenale & Necator americanus)

• Nematodes; A. duodenale (“老” hookworm, also causes eosinophilic pneumonitis and “ground itch”) and N. americanus (“新” hookworm)
• Transmission: Larvae penetrate skin (barefoot walk on contaminated soil); larvae migrate to lungs → coughed up → swallowed
• Clinical: Iron deficiency anemia (most common complication) — worms suck blood from intestinal mucosa; eosinophilia
• Diagnosis: Stool ova (ova of hookworm have characteristic cleavage at 2–8 cell stage); eosinophilia
• Treatment: Albendazole OR mebendazole; iron supplementation

Enterobius vermicularis (Pinworm)

• Nematode; small (2–13 mm); most common worm infection in children in developed countries
• Transmission: Fecal-oral; eggs also spread via clothing, bedding, fingernails (autoinfection)
• Clinical: Perianal pruritus (itching worse at night due to female worm migrating to anal area to lay eggs); vulvovaginitis in girls; irritability
• Diagnosis: Cellophane/tape test (transparent tape pressed on perianal skin in morning before bathing; eggs adhere; microscopy)
• Treatment: Albendazole OR mebendazole (single dose; repeat after 2 weeks for autoinfection); treat entire family

Taenia saginata (Beef Tapeworm) & Taenia solium (Pork Tapeworm)

• Cestodes; adult worms in human intestine; larvae in cattle (T. saginata) or pigs (T. solium)
• T. solium: More dangerous — can cause cysticercosis (human becomes intermediate host by ingesting eggs from another human with intestinal taeniasis)
• Cysticercosis: Neurocysticercosis (NCC) — most common cause of adult-onset epilepsy in India/Latin America; calcified lesions in brain parenchyma (seizures); racemose form in basal cisterns/ventricles
• Diagnosis: Stool for eggs/proglottids; serology (EITB assay for cysticercosis); CT/MRI brain
• Treatment: Intestinal: Praziquantel (5 mg/kg single dose) OR Niclosamide. Neurocysticercosis: Albendazole + steroids ± praziquantel; surgery for obstructive hydrocephalus

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Filariasis

Lymphatic Filariasis (Elephantiasis)

Causative organisms: Wuchereria bancrofti (#1 cause, 90%), Brugia malayi, Brugia timori

• Transmitted by: Culex mosquito (W. bancrofti), Mansonia (Brugia)
• Endemic in: India (especially UP, Bihar, Kerala, Andhra Pradesh), SE Asia, Africa, Pacific islands
• Life cycle: Microfilariae in mosquito → develop to L3 larvae → transmitted to human during bite → migrate to lymphatics → mature to adult worms → release microfilariae → mosquito picks up

Clinical:

• Asymptomatic (majority) — subclinical lymphatic damage
• Acute filarial lymphangitis: Fever, painful lymphadenopathy, retrograde lymphangitis (red streaking)
• Chronic: Lymphedema (gradual swelling of limb/scrotum), elephantiasis (non-pitting edema with skin thickening), hydrocele
• Tropical pulmonary eosinophilia (TPE): Syndrome of cough, wheeze, low-grade fever, marked eosinophilia (ILS >3000/µL); microfilariae trapped in lungs

Diagnosis:

• Nocturnal periodicity: W. bancrofti microfilariae appear in peripheral blood at night (10 pm–2 am) — night blood sample required; microfilariae in mosquito vector
• Blood smear: Examine at night (10 PM–2 AM) — thick and thin Giemsa-stained smear
• DEC provocation test: DEC causes microfilariae to appear in superficial capillaries
• PCR: Most sensitive; antigen detection (ICT card test for W. bancrofti)
• Ultrasound: “Filarial dance sign” (movement of adult worms in scrotal lymphatics)

Treatment:

• Diethylcarbamazine (DEC): 6 mg/kg/day × 12 days (microfilaricidal and adulticidal)
• ** ivermectin** + albendazole (used in mass drug administration programs)
• Combination: DEC + albendazole > ivermectin + albendazole > DEC alone
• Prevention: Mass Drug Administration (MDA) with DEC + albendazole (annual, for ≥5 years in endemic areas)
• TPE: DEC 6 mg/kg/day × 14 days + corticosteroids

Onchocerciasis (River Blindness)

• Causative: Onchocerca volvulus; vector: Blackfly (Simulium); endemic: West Africa, Yemen
• Clinical: Skin nodules (onchocercomas), skin depigmentation (“leopard skin”), ocular disease (river blindness — keratitis, chorioretinitis, optic atrophy)
• Diagnosis: Skin snip (microfilariae in dermis); Slit-lamp (microfilariae in anterior chamber)
• Treatment: Ivermectin (kills microfilariae, not adult worms); vector control

Key NEET PG Pearls

1. P. falciparum malaria is most dangerous — crescents (gametocytes), high parasitemia, cerebral malaria, chloroquine-resistant; treated with ACT
2. P. vivax has hypnozoites — requires primaquine for radical cure (test G6PD first); Schüffner stippling; spleen significantly enlarged
3. G6PD deficiency + primaquine = hemolytic anemia; always test before prescribing primaquine
4. Giardia: Foul-smelling, greasy stool (malabsorption) but NO blood; no dysentery; treated with metronidazole
5. E. histolytica: Flask-shaped colonic ulcers; amoebic liver abscess (right lobe, anchovy paste aspirate); cysts have 4 nuclei
6. Cryptosporidium: Acid-fast oocysts; severe watery diarrhea in AIDS (CD4 <100); nitazoxanide treatment
7. Ascariasis: Largest roundworm; causes Löffler syndrome (eosinophilic pneumonitis) during larval migration; intestinal obstruction in children
8. Hookworm: Penetrates skin (barefoot = portal entry); iron deficiency anemia; eggs have 2–8 cell cleavage
9. Taenia solium: Intestinal tapeworm from undercooked pork; cysticercosis from ingesting eggs → NCC (most common cause of epilepsy in India)
10. Wuchereria bancrofti: Microfilariae are nocturnal (appear in peripheral blood at night) — sample timing is critical for diagnosis; transmitted by Culex mosquito

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