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How does Naegleria fowleri reach the CNS?
Contaminated warm freshwater enters the nose. Trophozoites migrate along the olfactory nerves through the cribriform plate, causing primary amebic meningoencephalitis.
What clinical presentation suggests chronic strongyloidiasis?
Intermittent abdominal pain, diarrhea, urticarial or pruritic skin lesions, and eosinophilia, potentially persisting for years after exposure in an endemic region.
What clinical presentation suggests chronic strongyloidiasis?
Intermittent abdominal pain, diarrhea, urticarial or pruritic skin lesions, and eosinophilia, potentially persisting for years after exposure in an endemic region.
What is larva currens in Strongyloides infection?
A rapidly migrating, intensely pruritic, serpiginous or linear eruption, often near the perianal region, buttocks, or trunk, associated with autoinfection.
How do humans acquire Ancylostoma duodenale infection?
Infective filariform larvae penetrate exposed skin after contact with contaminated soil, often during barefoot walking. A. duodenale may also be acquired orally.
Which parasites classically cause cutaneous larva migrans?
Zoonotic hookworms, particularly Ancylostoma braziliense and Ancylostoma caninum, whose larvae migrate through human skin producing pruritic serpiginous tracks.
What is the difference between cutaneous larva migrans and the initial skin lesion of human hookworm infection?
What is the difference between cutaneous larva migrans and the initial skin lesion of human hookworm infection?
What laboratory findings are characteristic of megaloblastic anemia caused by fish tapeworm infection?
Elevated MCV, macro-ovalocytes, hypersegmented neutrophils, and decreased vitamin B12. Neurologic manifestations may include reduced vibration sense or paresthesias.
What exposure suggests Dibothriocephalus latus infection?
Consumption of raw or undercooked freshwater fish containing infective larvae.
What is the mechanism of vitamin B12 deficiency in fish tapeworm infection?
The adult tapeworm competes with the host for intestinal vitamin B12, potentially causing megaloblastic anemia and neurologic dysfunction.
What diagnostic finding is characteristic of Naegleria fowleri infection?
Motile trophozoites may be identified in a fresh CSF wet mount. Diagnosis may also be confirmed by molecular testing.
What is the typical clinical course of primary amebic meningoencephalitis?
Rapidly progressive fever, severe headache, meningismus, altered mental status, and often fatal meningoencephalitis within days.
How does Giardia duodenalis cause malabsorption?
It adheres to the proximal small intestinal mucosa without tissue invasion, disrupting brush-border function and causing villous injury and fat malabsorption.
What are the characteristic clinical findings of giardiasis?
Foul-smelling, greasy diarrhea (steatorrhea), bloating, flatulence, abdominal cramps, and a history of contaminated water exposure.
What is the characteristic morphology of Giardia trophozoites?
Pear-shaped, flagellated trophozoites with two nuclei and four pairs of flagella, giving a face-like appearance.
Pear-shaped, flagellated trophozoites with two nuclei and four pairs of flagella, giving a face-like appearance.
Tinidazole or metronidazole; nitazoxanide is another option.
How is cryptococcal meningitis classically identified in CSF?
India ink can demonstrate encapsulated budding yeast with a clear halo. CSF cryptococcal antigen testing is more sensitive.
What distinguishes Cryptococcus neoformans from many other yeasts?
A thick polysaccharide capsule, narrow-based budding, and urease positivity.
Which stain can demonstrate the polysaccharide capsule of Cryptococcus in tissue?
Mucicarmine stains the capsule red-pink. India ink demonstrates a clear halo in fluid preparations.
What does thermal dimorphism mean in pathogenic fungi?
Growth as mold at approximately 25°C and as tissue-associated yeast at body temperature, with important exceptions such as Coccidioides (spherules).
Which endemic pathogenic fungi are classically thermally dimorphic?
Histoplasma, Blastomyces, Sporothrix, Paracoccidioides, and Coccidioides. Coccidioides forms spherules rather than yeast in human tissue.
What are common manifestations of babesiosis?
Fever, chills, fatigue, hemolytic anemia, jaundice, and sometimes splenomegaly. Severe disease is more likely in asplenic or immunocompromised patients.
What are the characteristic microscopic findings of mucormycosis?
Broad, ribbon-like, pauciseptate hyphae with irregular wide-angle branching, often approaching 90°. Common genera include Rhizopus and Mucor.
What are the major risk factors for invasive mucormycosis?
Diabetic ketoacidosis or poorly controlled diabetes, neutropenia, hematologic malignancy, transplantation, immunosuppression, and iron overload.
What clinical presentation suggests rhinocerebral mucormycosis?
Poorly controlled diabetes with facial pain, headache, periorbital swelling, cranial nerve abnormalities, and a black necrotic eschar involving the nasal turbinates or palate.
Why does mucormycosis cause black necrotic tissue?
The fungi invade blood vessels (angioinvasion), causing thrombosis, impaired blood supply, tissue infarction, and necrosis.
What is the management of invasive mucormycosis?
Urgent surgical debridement plus systemic antifungal treatment, usually liposomal amphotericin B, with correction of underlying predisposing conditions.
How do the hyphae of Aspergillus differ from Mucorales?
Aspergillus: relatively narrow, septate hyphae with acute-angle branching (~45°). Mucorales: broad, pauciseptate hyphae with irregular wide-angle branching.
What is an aspergilloma?
A fungal ball formed by Aspergillus colonization of a preexisting pulmonary cavity, often presenting with hemoptysis.
Which immunodeficiency predisposes to Aspergillus infection due to impaired oxidative killing?
Chronic granulomatous disease, caused by defective NADPH oxidase and impaired respiratory burst.
What are the three major phases of the Plasmodium life cycle in humans and mosquitoes?
1. Hepatic stage: sporozoites infect hepatocytes and produce merozoites. 2. Erythrocytic stage: merozoites infect RBCs, causing clinical malaria. 3. Sexual stage: gametocytes are ingested by mosquitoes and develop into new sporozoites.
What is the developmental sequence of Plasmodium within erythrocytes?
Ring form → trophozoite → schizont → erythrocyte rupture, releasing merozoites that infect additional red blood cells.
Why does malaria cause recurrent episodes of fever, chills, and sweating?
Synchronized rupture of infected erythrocytes releases merozoites and inflammatory parasite products, triggering cytokine-mediated febrile episodes.
Which Plasmodium species produce dormant liver hypnozoites?
Plasmodium vivax and Plasmodium ovale. Hypnozoites can reactivate months or years later, causing relapse.
How are hepatic hypnozoites eliminated in P. vivax or P. ovale infection?
Primaquine or tafenoquine is used for radical cure, when appropriate, after quantitative G6PD testing because these drugs can cause severe hemolysis in G6PD deficiency.
How are hookworm infections diagnosed?
Detection of hookworm eggs in stool by ova and parasite microscopy. Peripheral eosinophilia and iron-deficiency anemia may support the diagnosis.
Which two hookworms commonly infect humans and cause iron-deficiency anemia?
Ancylostoma duodenale and Necator americanus. They attach to intestinal mucosa and cause chronic blood loss.
What is the mechanism of action of praziquantel?
It increases calcium permeability in susceptible cestodes and trematodes, causing sustained muscular contraction, paralysis, and tegument damage.
What tapeworm is associated with vitamin B12 deficiency, and how is it treated?
Dibothriocephalus latus (formerly Diphyllobothrium latum), the fish tapeworm. Praziquantel is generally the treatment of choice.