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247 Cards in this Set
- Front
- Back
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Chronic Gramulomatous Disease (CGD)
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Mutations of phagosomal NADPH oxidase required for effective respiratory burst
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Chediak-Higashi Syndrome (CHS)
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Mutation of CHS1 gene that encodes cytoplasmic protein involved in intracellular vacuole and granule fusion. Pathogen killing impaired.
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Leukocyte Adhesion Deficiency Type 1 (LAD-1)
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B2-integrins impaired -- neutrophils cannot leave circulation and extravasate into sites of infection/injury
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What genus causes Malaria? What 4 infect humans?
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Plasmodium. P. falciparum, P. vivax, P. ovale, P. malariae
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What transmits malaria to humans?
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Female anopheline mosquitoes
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Malaria Life Cycle
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- Female anopholine mosquito takes blood meal and injects sporozoites
- Sporozoites infect hepatocytes - Parasite undergoes asexual mult - After 6-18d 10k merozoites rupture - Each merozoite infects RBC - Asexual repr in RBC produces 25 merozoites which rupture and infect more RBCs - Occ merozoite differentiates into m/f gametocyte - Another mosquito takes up gametocyte during blood meal - In gut of mosquito gametocytes fuse to ookinete, which attaches to gut wall and develops into sporozoite that migrates to salivary glands |
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What causes the clinical signs of malaria?
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Asexual erythroytic stage parasites
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What is the clinical course of malaria?
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Acute febrile illness that is periodic at either 48 or 72h intervals with 4-8h paroxysms
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What are the clinical stages of a malaria paroxysm?
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Cold stage - vigorous shivering and chills despite elevated temp
Hot stage - Intense heat, headache, fatigue, dizziness, anorexia, myalgia, nausea Sweating - fever starts to decline, feels exausted, sleep |
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Cerebral Malaria
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P. falciparum
diffuse encephalopathy w/LOC. Unresponsive to pain, visual, verbal stimuli. Sequestration in cerebral microvasc. Present with severe headache, followed by drowsiness, confusion, coma |
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Dx of malaria
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Hx endemic area
Sx: fever, chills, headache, malaise Splenomegaly, anemia Blood smear, antigen detection |
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Tx for acute malarial infection
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Fast-acting blood schiontocide (act upon parasite within RBC)
Chloroquine--well tolerated, side effects of pruritus, nausea, agitation. Primaquine--effective against liver stage and prevents future relapses. Chloroquine + Primaquine = radical cure |
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Tx for severe falciparum malaria
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Parenteral administration of either chloroquine, quinine, quinidine, artemisinin until p/o.
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Alternative malaria tx for chloroquine resistance
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mefloquine, quinine + doxycycline, Fansidar (pyrimethamine + sulfadoxine)
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What transmits leishmaniasis?
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Female phlebotomine sandflies
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What causes leishmaniasis?
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Protozoa -- genus leishmania
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What are the 3 forms of leishmaniasis?
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Cutaneous - Old & New world
Visceral (kala-azar) - liver, spleen, bone marrow (L. donovani, L. chagasi, L. infantum) Mucocutaneous (L. braziliensis) |
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Life cycle of leishmania
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- Infected female sandflies inject promastigotes from proboscis during blood meal
- Promastigotes that reach puncture wound phagocytized by macrophages and other mononuclear phagocytic cells - Promastigotes transform in these cells into tissue stage of parasite, amastigotes, which divide and infect other cells - Sandflies ingest infected cells during blood meal - Amastigotes transform into promastigotes, develop in gut, migrate to proboscis |
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Incubation for leishmaniasis
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2-6 mos +
Relapse may occur 10yrs after first episode |
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Clinical signs and sx of visceral leishmaniasis
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Prolonged fever, splenomegaly, anemia, leukopenia, hypergammaglobulinemia.
Cutaneous nodule may or may not appear at site of bite within several days of inoculation. Fever often rises and falls 2x/day. Fatigue, weight loss, dizziness, cough, diarrhea. Lymphadenopathy, hyperpigmentation or lesion of forehead, abdomen, hands, feet. Signs of bleeding, jaundice, progressive wasting. |
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Tx leishmaniasis
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Miltefosine 100mg/day for 4wks p/o.
Sodium Stibogluconate (not FDA approved) Second Line -- amphotericin B, L-ampho, pentamidine, aminosidine |
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What transmits Aftrican trypanosomiasis ("sleeping sickness")?
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Tsetse Fly (Glossinia sp.)
Also, zoonotic infection |
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Trypanosome life cycle
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- Epimastigotes grow/reproduce in vector's gut or salivary glands
- Epimastigotes infect host and transform into trypomastigotes - Parasite grows as trypomastigote in blood of infected vertebrate host - Vector ingests trypomastigotes during blood meal, which transform into epimastigotes |
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Clinical signs and sx of African trypanosomiasis
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Invade CNS and result in fever, lethargy, coma
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Tx for African trypanosomiasis
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Melarsoprol
Pentamidine Suramin Difluromethylornithine (DFMO) (all suboptimal, better pre-CNS dis) |
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What causes American Trypanosomiasis (Chagas' disease)? What does it do?
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Trypanosoma cruzi. Damages neural plexi that control gut motility (dysmotility and dialation), damages conduction system of heart (dialated cardiomyopathy)
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What causes Amoebiasis?
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Entamoeba histolytica
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Life cycle for amoebiasis
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Fecal-oral (same as Giardia)
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Where are amoeba found in body?
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Trophozoites live in gut lumen, gut wall, or extra-GI (liver and lung).
In gut, found in colon. Produce dysentery (flask shaped ulcers), amoeboma, liver abcesses |
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Tx amoebiasis
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Metronidazole does not effectively treat asymptomatic carriage of luminal organisms -- use diiodohydroxyquin, diloxinade, furoate, or paramomyosin in addition.
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Life cycle of Giardia
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- People ingest cysts which develop into trophozoites in duodenum
- Some trophozoites encyst and pass out with feces (infect another person or beaver as resevoir) - Infection never spreads past intestine and not invasive |
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Sx Giardia
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Watery diarrhea, malabsorption, systemic toxicity.
Relapsing course. |
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Tx Giardia
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Quinacrine, metronidazole, furazolidone, tinidazole
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Protozoa
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Malaria, Leshmania, trypanosomes, ameobia, giardia, toxoplasma, trichomonas
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What cells are responsible for humoral immunity (antibody-mediated)?
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B Cells (Lymphocytes)
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What cells are responsible for cell-mediated immunity?
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T Cells (Lymphocytes)
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What are the MHC class I loci?
Where are they found? Who do they present to? What is the structure of MHC class I molecule? What type of protein do they present? |
HLA-A, HLA-B, HLA-C
Found on all nucleated cells. CD8+ (CTLs). Binding groove closed at both ends, so can fit 8-11aa. Single transmembrane polypeptide with 3 extracellular domains (a1, a2, a3) noncovalently associated with b2m -- a3 binds CD8. Present endogenous antigens |
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What are the MHC class II loci?
Where are they found? Who do they present to? What is the structure of MHC class II molecule? What type of protein do they present? |
HLA-DP, HLA-DQ, HLA-DR
Found on APCs. CD4+ (T helper cells). Binding groove open at both ends, so can fit 10-30aa. Two transmembrane polypeptide chains (a1, b1) -- b2 domain binds CD4. Present exogenous antigens. |
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Features of IgG
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Monomers.
4 subtypes (IgG1, IgG2a, IgG2b, IgG3, IgG4). Most versatile Ig b/c carries out all functions of Ig molecules -- essential in humoral responses. Major Ig in serum and extra vasc. sp. Only class of Ig that crosses placenta. Fixes complement & binds to cells. |
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Features of IgM
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Usually pentamer (can be monomer).
All heavy chains same and light same. First made by fetus & produced during primary immune response. Binds Fc receptors. |
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Features of IgA
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Serum IgA monomer, in secretions is dimer.
Associated with protein (secretory component) in secretions. Major class of Ig in secretions. Important in local immunity. |
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Features of IgE
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Very low levels in serum.
Mediates allergic rxns. May defend against parasites so helps diagnose parasitic infections. |
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Name the luminal nematodes.
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ascaris
hookworm strongyloides pin worm whip worm |
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Name the tissue nematodes.
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filaria
loa loa onchocerciasis trichinosis |
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Name the luminal cestodes.
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tapeworms
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Name the tissue cestodes.
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cysticercosis
hydatid disease |
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Name the trematodes.
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schistosomes
clonorchis sinensis fasciola hepatica paragonimus |
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What is the path of ascariasis infection?
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People ingest eggs --> hatch into larvae --> penetrate sm. int --> liver --> r. heart --> lungs --> through alveolar space --> crawl up trachea --> swallowed --> develop into adults in sm. int
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What are the sx of ascariasis infection?
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Pneumonitis, eosinophilia, fever.
Vague GI complaints or obstruction |
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What is tx for ascariasis?
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Mebendazole or albendazole.
Thiabendazole (visceral larva migrans from dog or cat) |
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What are the 2 genus of hookworm?
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Necator americanus
Ancylostoma duodenal |
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How does hookworm get in body?
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Penetrate skin (hair follicles on feet) or are swallowed -- migrate like ascaris
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Sx of hookworm.
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Pneumonitis, eosinophilia, fever.
Iron deficiency anemia and protein-losing enteropathy (edema) (adults attach to villi and suck blood) |
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Tx for hookworm.
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Mebendazole or albendazole.
Thiabendazole (Cutaneous larva migrans from dog and cat) |
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Life cycle of strongyloidiasis.
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Worms reproduce in soil.
Larvae penetrate skin at hair follicles and migrate like ascaris. |
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Sx of strongyloidiasis.
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Pneumonitis, eosinophilia, fever, gram negative bacteremia.
Chronic disease: watery diarrhea and malabsorption. Immunocompromised people hyperinfected w/high mortality |
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Tx of strongyloidiasis.
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Thiabendazol
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Where do pin worm (enterobius vermicularis) and whip worm (tricuris tricuria) reside in humans? How are they transmitted?
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Lumen (never penetrate).
Fecal-oral |
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Sx of pin worm.
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Peri-rectal itching
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Sx of whip worm.
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Rectal prolapse
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Tx for pin or whip worm.
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Mebandazole or albendazole
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What causes lymphatic filariasis?
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Wuchereria bancrofti and brugia malayi
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How is lymphatic filariasis transmitted?
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Culex mosquitos deposit larvae on skin and larvae enter bite.
Adults mature in lymph vessels and release microfilariae w/ temporal periodicity. |
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Sx of lymphatic filariasis.
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Tropical eosinophilia, recurrent laryngitis, elaphantiasis, megascrotum.
Little mortality, lots of morbidity. |
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Tx for lymphatic filariasis.
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DEC
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How is loa loa trasmitted?
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Deer flies (chrysops) transmit larvae
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Life cycle of loa loa.
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Larvae transmitted to human and develop into adult in subcutaneous tissue. Adults wander in subcut tissue releasing microfilaria with diurnal periodicity that peaks at noon. Occasionally cross subconjunctival region.
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Sx of loa loa.
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Dramatic eosinophilia, calabar swelling (patches of localized subcut. edema) over bony prominences.
Travelers have more serious lymphangitis, cardiomyopathy, nephropathy. |
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Tx of loa loa.
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DEC
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What transmits onchocerciasis?
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Female black fly (simulium) transmits larvae into skin.
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Life cycle of onchocerciasis.
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Larvae develop into adults in subcut. tissue.
Males & females coil up and form fibrotic nodules. Release microfilariae into skin. |
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Sx of onchocerciasis.
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Nodules (Thighs/lower back in Africa, head/neck in C. Amer).
Eosinophilia, pruritus, loss of pigment, atrophy of skin. Inflammation of eye --> blindness. |
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Tx of onchocerciasis.
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Ivermectin
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How is trichinella spiralis transmitted?
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Ingestion of undercooked pork/bear that contain larvae
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Life cycle of trichinella spiralis.
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Larvae ingested.
3rd stage larvae hatch and develop into adults in sm. bowel. Adults copulate and release 1st stage larvae which penetrate gut wall and migrate via blood and lymph to striated muscle. In muscle the larvae molt into infective 3rd stage larvae and encyst. Adults in lumen expelled in few weeks. |
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Sx of trichinella spiralis.
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GI sx, eosinophilia, myalgia, cardiomyopathy, CNS disturbances
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Tx for trichinella spiralis.
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Supportive w/ salicylates and steroids.
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Types of luminal cestodes (tapeworms)
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Taenia solium (pork)
Taenia saginata (beef) Diphyllobothrium latum (fish) Hymenolepis nana (human) |
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Life cycle of tapeworms.
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People ingest scolex in raw meet.
Worm matures in sm. intestine. Proglottid passes out w/ feces to infect animal host. Eggs hatch into larvae and migrate to all tissues to form scolices. |
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Sx of tapeworm.
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Little disease.
Diphyllobothrium latum - B12 deficiency |
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Tx of tapeworm.
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Niclosamide or praziquantel
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How is cysticercosis acquired?
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Human ingests gravid proglottid (eggs) from taenia solium.
Scolices disseminated throughout body. Does not occur from eating raw meat. |
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Sx cysticercosis.
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Subcutaneous cysts, seizures, paralysis, hydrocephalus
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Tx cysticercosis.
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Praziquantel and steroids
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What causes hydatid disease?
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Echinococcus multilocularis
Echinococcus granulosus (dog tapeworms w/ sheep intermediate) |
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Life cycle of hydatid disease.
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Humans ingest eggs from dog feces.
Eggs hatch in sm. intestine into larvae which penetrate gut and go to liver, lung, or brain to form cysts containing scolices. |
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Sx of hydatid disease.
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Cysts of Echinococcus multilocularis are multiple, unencapsulated, difficult to remove.
Cysts of Echinococcus granulosus are single, encapsulated, resectable. Don't aspirate or will desseminate scolices. |
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Tx hydatid disease.
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Albendazole and surgery
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Types of Schistosomes.
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Schistosoma hematobium
Schistosoma japonicum Schistosoma mansoni |
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Life cycle of schistosomes.
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Cercaria shed from fresh water snails and penetrate skin to become a schistosomula.
Schistosomula migrates through lungs and develop into adults in either portal or bladder veins. Adults lay eggs which pass out with feces/urine to hatch in fresh water into miracidium which infect snails. |
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Sx of schistosomes.
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Fever, chills, hepatosplenomegaly, lymphadenopathy, eosinophilia.
Chronic infection: hepatosplenomegaly, portal hypertension, urothelial carcinoma |
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Tx schistosomes.
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Praziquantel
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How is Clonorchis sinensis contracted? Where does it live? What are sx? What is tx?
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Contracted by eating raw fish.
Adults live in bile ducts. Sx are bile duct obstruction and cholangiocarcinoma. Tx is praziquantel. |
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How is Fasciola hepatica contracted? Where does it live? What is tx?
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Contracted from contaminated water plants (watercress).
Adults live in bile ducts and liver. Tx is praziquantel. |
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How is Paragonimus westermani contracted? Where does it live? Differential? What is tx?
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Contracted from raw infected crab.
Adults live in lung - pass eggs in sputum and feces. Confused w/ TB. Tx is praziquantel. |
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Prototype type I (immediate) hypersensitivity diseases
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hayfever (allergic rhinitis)
bronchial (allergic) asthma hives (urticaria anaphylaxix "wheal and flare" skin reaction |
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Prototype type II (antibody-mediated or cytotoxic) hypersensitivity diseases
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transfusion reaction
hemolytic anemia thrombocytopenia & leukopenia erythroblastosis fetalis goodpasture syndrome myasthenia gravis graves disease |
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Prototype type III (immune complex) hypersensitivity diseases
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systemic lupus erythematosis (SLE)
serum sickness localized arthus (skin) reaction post-streptococcal glomerulonephritis |
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Prototype type IV (cell-mediated or delayed) hypersensitivity diseases
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contact dermatitis and TB skin test
viral hepatitis |
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Sx of major transfusion reaction.
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fever
chills hemoglobinuria hypotension renal failure |
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Cause of major transfusion reaction.
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Direct cell lysis due to ABO mismatch.
IgM or IgG antibodies react with antigen on cell surface, causing complement activation and assembly of MAC. |
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What is the mechanism of RhoGam? How is it administered?
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IV human immune globulin containing antibodies against Rh+ RBCs that destroys RH+ RBCs before the maternal bloodstream can react by producing its own anti-RH antibodies.
Administer within 72h after delivery. |
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What happens in hemolytic anemia, leukopenia, and thrombocytopenia?
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Individuals produce antibodies to own blood cells, which are destroyed.
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What is Anti-glomerular basement membrane nephritis (goodpasture syndrome)? Who does it typically affect?
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Autoimmune disease.
Antibodies directed against type IV collagen, a normal component of GBM proper. Rapidly progressive renal failure due to glomerular nephritis. When antibodies cross-react with other BMs, such as lung, inflammation results in lung lesions. Autoantibodies deposited in linear array along BM, outlining capillary loops. Typically affects men in twenties. |
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What is the mechanism of autoimmune thyroiditis (Hashimoto's thyroditis)?
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Antibody-dependent cellular cytotoxicity (ADCC)
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What is the mechanism of myasthenia gravis?
Tx? |
Antibody blocking of ACh receptor in motor end plates of skeletal muscle leads to muscle weakness.
Tx options are ACh-esterase inhibitors, immunosuppression, thymectomy. |
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What is the mechanism of graves disease (hyperthyroidism)?
Sx? |
Antibody to TSH receptor stimulates receptor --> stimulates thyroid acinar cells.
Sx include exophthalmos, heat intolerance, anxiety |
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Serum Sickness is prototype disease for what?
Sx? Cause? |
Prototype disease for systemic immune complex disorders.
Sx occur ~10d after injection and are joint inflammation, skin rash (uricaria), fever, glomerulonephritis. Caused by deposition of antigen-antibody complexes. |
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What is systemic lupus erythematosis (SLE)? Who does it affect? What is its course?
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Chronic autoimmune microvascular inflammatory disease that can affect every organ of body.
Most prevalent in women 16-64y.o. Waxing and waning course. |
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What is the mechanism of systemic lupus erythematosis (SLE)?
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Production of autoantibodies to various nuclear antigens (antibodies to dsDNA).
Immune complex-induced vasculitis (microvasculature in BM of skin and kidneys). |
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Sx of systemic lupus erythematosis (SLE)?
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"Butteryfly rash"
Arthritis Glomerulonephritis Hemolytic anemia Thrombocytopenia CNS involvement |
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Contrast glomerulonephritis in SLE vs. goodpasture.
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SLE - course, granular deposition of immune complexes.
Goodpasture - Linear deposition of immune complexes. |
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What are the types of post-infectious glomerulonephritis?
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Post-streptococcal GN
Polyarteritis nodosa |
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How does rheumatic heart disease occur? Who does it affect?
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1-5wks after infection with group A strep.
Occurs secondary to host anti-strep antibodies that are cross-reactive to cardiac antigens. Occurs mainly in ages 5-15yrs |
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What is the "arthus reaction"?
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Localized immune complex disease initiated by injecting antigen into skin of previously immunized person that has preformed antibodies against the antigen already in circulation.
Results in local formation of immune complexes with localized area of tissue necrosis due to acute immune complex vasculitis. |
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What is the time course of the "arthus reaction"? What is an example?
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Evolve over a few hrs and peak 4-10hrs after injection.
Local reaction to tetanus booster is ex. |
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Contrast "Wheal and Flare" and "Arthus reaction".
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"Wheal and Flare" is type 1 reaction that is IgE-mediated local release of histamine - appears immediately and usually subsides within hrs.
"Arthus reaction" is type III reaction that is IC-mediated - develops over hrs - localized area of tissue necrosis from acute IC vasculitis - area of visible edema with severe hemhorrage and ulceration. |
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What is the host response to tuberculosis infection?
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Macrophages phagocytize and try to kill organisms - but mycobacterium bacteria can replicate in phagosomes and macrophages overwhelmed.
Macrophages process and present antigen on their surfaces with MHC class II to recruit T helper cells. Produce IL-12 which drives CD4 cells to become Th1-cytokine producing cells. |
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What kind of hypersensitivity reaction is involved with TB?
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Type IV hypersensitivity reaction (delayed or cell-mediated)
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What does a "Positive PPD" mean?
What is the cause? What does it look like? Tx? |
Person has been exposed to TB at some point and mounted an antigen-specific Th1 reaction. Does not mean person has active TB if nl CXR and no sx. May be at risk of re-activation of TB at later time unless tx.
Caused by accumulation of CD4 T lymphs around small veins and inc microvascular permeability. 8-12h reddening & induration begin. Peaks at 24-72h and subsides. Tx is 9 mos course daily Isoniazid. |
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Why is a "two-step PPD" administered?
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To detect a waning reaction to earlier exposure.
Usually initial neg ppd in elderly person who was exposed to TB as child. Initial neg due to waning Th1 response, but repeat 1-3wks later may be pos because of memory response to previously activated Th1 cells. |
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How are TB granulomas formed?
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Persistent antigens cause the initial perivascular lymph infiltrate to be replaced by macrophages over 2-3wks.
Accumulated macrophages undergo morphologic transformation to epitheliod cells surrounded by collar of lymphs. |
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What type of hypersensitivity reaction is contact dermatits (ex poison ivy)?
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Type IV hypersensitivity reaction: delayed type
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Why does contact dermatitis not cause a reaction upon first exposure?
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It is a cell-mediated reaction to the antigen and takes time to mount Th1 response.
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What is the antigen of poison ivy?
What are other haptens that cause contact dermatitis? |
Antigen is urshiol, a hapten (only capable of becoming full antigen when reacts with skin proteins).
Other haptens are poison oak, metals (nickel), acetylates, chem in rubber |
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When and why does cell-mediated cytotoxicity (a type IV hypersensitivity reaction) occur?
Examples? |
CD8+ cells (CTLs) kill cells with antigens on MHC class I molecules.
CTL response to viral infection can lead to tissue injury by killing infected cells even if virus has no cytopathic effects. Examples are resistance to viral infections, graft rejection, tumor immunity. In Viral hepatitis, HBV replication isn't injurious to host cell but host immune response to viral antigens displayed on infected hepatocytes results in liver injury. |
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what are the enveloped DNA viruses?
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Herpesviridae
Poxviridae Hepadnaviridae (HBV) |
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Structure of Herpesviridae.
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Large and complex.
Linear dsDNA. Envelope with glycoprotein spikes. Icosahedral capsid. Can establish latency. |
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Structure of Poxviridae.
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Largest, most genetically complex.
Oval to brick-shaped morphology. DNA virus - replicate in CYTOPLASM. Encodes all proteins necessary. Assembled in Guarnieri's bodies. |
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Types of Poxviridae.
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Variola (smallpox)
Mulluscum contagiosum Monkeypox Cowpox Vaccinia Orf Virus |
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Why was smallpox able to be eradicated in 1980?
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Humans are only host.
Does not remain latent in host. Cases of variola easy to identify. Vaccine stable and easily transported. Time, money, effort invested. |
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Spread of smallpox within body.
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Virus enters and replicates in resp. tract without causing sx.
Infects macrophages --> enter lymph and carry virus to lymph nodes. Virus replicates and initiates viremia --> infection spreads to spleen, bone marrow, lymph nodes, liver, organs, skin. Secondary viremia causes additional lesions followed by death or recovery. |
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What immune response does smallpox infection trigger?
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Stimulates cytotoxic T-cells, neutralizing antibodies, production of interferon.
Lead to lasting immunity in those who recover. |
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What are the non-enveloped DNA viruses?
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Adenoviridae
Papovaviridae (Papillomaviruses, Polyomaviruses) Parvoviridae |
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Structure of Adenoviruses.
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Non-enveloped DNA virus.
Serotype is mainly a result of differences in penton base and fiber protein, which determine nature of tissues tropism and disease. Among most common causes of viral disease. |
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Spread of Adenoviruses.
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Virions resist drying detergents, GI secretions.
Spread by respiratory, close contact, fecal-oral. Causes lytic, latent, or oncogenic transformation in target cells. |
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Structure of Papovaviridae
(Papillomaviruses - HPV) (Polyomaviruses - JC/BK, SV-40) |
Small icosahedral capsid virion.
Non-enveloped, circular dsDNA. Lytic infections and benign or malignant tumors. |
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Structure of Papillomaviruses.
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8kb circular dsDNA.
Major and minor capsid proteins L1, L2. Encodes early genes (E1-7) E6 & E7 - immortalization and transformation (oncoproteins) |
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How is Papillomavirus acquired?
What does it infect? What can it cause? |
Acquired by direct contact.
Infects epithelial cells of skin or mucous membrane. Promotes outgrowth of basal layer, increasing # of prickle cells --> hyperkeratosis and cell prolif. Warts, dysplasia. |
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What kinds of cutaneous warts are associated with HPV infection?
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Common (fingers, hands)
Plantar (sole of foot) Flat (arms, face, knee) |
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What are the mucosal infections of HPV?
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STIs -->
Anogenital warts (condyloma acuminata): HPV-6 and 11. Cervical neoplasia and cancer: HPV 16, 18, 31, 45. |
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Structure of Paroviridae.
Types and diseases caused. |
Small, un-enveloped DNA virus.
B19 --> Fifth disease (erythema infectionosum) mild febrile exanthematous disease in children. In adults associated with acute polyarthritis. Requires rapidly dividing cells to replicate (RBCs). |
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Facts about Negative stranded RNA viruses.
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All enveloped, nucleocapsid is helical.
Virion contains RNA-dependent RNA transcriptase to synthesize mRNA. Genomic neg-strand not infectious. First step is synthesis of mRNA. Segmented or non-segmented genome. Replicate in cytoplasm (Influenza in nucleus) |
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How does Influenza A differ from Influenza B? (Orthomyxoviridae)
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Both infect humans.
Type A has animal reservoir and divided into subtypes (H1N1, H2N2, H3N2). |
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How is influenza virus (orthomyxoviridae) spread?
What is the incubation time? What is the titer like? What does it infect? |
Spread via person-person through small particle aerosols that enter respiratory tract.
Incubation is short: 18-72hrs. High titers. Infects epithelial cells of respiratory tract. |
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What drugs can be used for prophalactic and theraputic tx of influenza A?
What are other useful antivirals? |
Amantadine & Rimantadine.
Zanamivir (Relenza) & Osteltamivir (Tamiflu). |
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Structure of Influenza virus.
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Enveloped, pleomorphic, segmented, neg-stranded RNA genome.
HA protein involved in attachment of virus to sialic acid residues on host cell surfaces, as well as membrane fusion of endosomes. NA protein digests sialic acid. |
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What are the nucleocapsid contents of orthomyxoviridae?
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8 segments of neg stranded RNA.
4 proteins: NP (major nucleocapsid pr), PA, PB1, PB2 (RNAp components). Matrix (M) proteins: M1 (assembly & budding), M2 (pH activated ion channels for uncoating) --> Amantadine and rimantadine target M2. |
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What are the nucleocapsid contents of orthomyxoviridae?
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8 segments of neg stranded RNA.
4 proteins: NP (major nucleocapsid pr), PA, PB1, PB2 (RNAp components). Matrix (M) proteins: M1 (assembly & budding), M2 (pH activated ion channels for uncoating) --> Amantadine and rimantadine target M2. |
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Orthomyxoviridae replication.
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HA binds to sialic acid receptors on cell surface --> endocytosis.
Nucleic acid released to cytosol and transported to nucleus (unique for RNA since lack 5' capping ability). "Snatch" newly synthesized caps from eukaryotic mRNA's. |
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Antigenic Drift vs Antigenic Shift.
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Antigenic drift - mutations arise in HA & NA genes. Occurs slowly. Slight variations in influenza viruses from year to year. Occurs in A, B, C.
Antigenic shift - cell is doubly infected with >1 type of influenza virus. Genomes reassort. Leads to viruses never seen by immune system. Flu pandemics. Type A. Occurs infrequently. |
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Which type of influenza has an animal reservoir?
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Influenza A.
Also exhibits drift AND shift. |
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Structure of Paramyxoviridae.
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Spherical, enveloped, non-segmented negative-strand RNA genome.
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What are the 2 subfamilies of Paramyxoviridae?
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Paramyxovirinae (Human Parainfluenza Virus 1-4, Mumps, Measles, Nipa/Hendra).
Pneumovirinae (RSV) |
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What glycoproteins are contained in the envelope of Paramyxoviridae?
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Fusion (F) Protein (must be activated by proteolytic cleavage)
HN, H, or G protein (HN in parainfluenza and mumps, H in measles, G in RSV). |
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Characterization of mumps.
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Nonpurulent inflammation of salivary glands, especially the parotids.
Severe manifestations: pancreatitis, meningitis and encephalitis, hearing loss/deafness, orchitis/oophoritis. |
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Pathogenesis of mumps.
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Virus enters respiratory tract.
Grows in salivary glands and local lymph. Spreads to spleen and distant lymph (7-10d). Viremia. spreads to testes, ovary, pancreas, thyroid, salivary glands. |
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How is measles transmitted?
What is measles infection like? |
Person to person via respiratory secretions.
Systemic infection, disseminated by viremia, with acute disease manifestations involving the lymph and respiratory systems, skin, brain. |
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How do measles persist?
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May persist silently for years (constant replication of ribonucleoprotein at low levels) and occasionally cause subacute sclerosing panencephalitis (SSPE) and autoimmune chronic hepatitis.
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Pathogenesis of measles.
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Virus enters through oropharynx.
Local multiplication in resp tract and lymph nodes. Primary viremia. Secondary viremia 5-7d later disseminates virus to mucosa of resp, GI, urinary tracts to skin and CNS. |
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Characteristic signs of measles.
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Maculopapular measles rash caused by immune T cells targeted to infected endothelial cells lining small blood vessels. Lifelong immunity established.
Koplik's spots (red spots with bluish-white specs in centers) appear in oral mucosa. Rash appears 1-2d later, first on head then spreading down body and limbs, including palms and soles. Fever highest on day rash appears. Uncomplicated illness lasts 7-10d. |
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What receptor does measles virus use?
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CD46. (NOT sialic acid)
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Structure of Rhabdoviridae.
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Bullet-shaped with helical nucleocapsid.
Neg-strand RNA. |
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What are the 2 genera of Rhabdoviridae?
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Lyssavirus (rabies).
Visiculovirus (vesicular stomatitis virus - infects horses and cows). |
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Pathogenesis of rabies.
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Following inoculation, virus may replicate locally. Then enters PNS where it travels to CNS.
Diffuse encephalitis. From brain can travel along autonomic nerves leading to infection of cornea, skin, salivary glands. |
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Diagnosis of rabies.
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Hx of exposure and sx common to rabies, but difficult.
Negri bodies in brain diagnostic postmortem. |
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Structure of Picornaviridae.
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Pos-strand RNA virus, non-enveloped, icosahedral capsid.
Contains RNA genome and 4 structural proteins (VP1-VP4). |
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What receptor does coxsackievirus and most rhinoviruses bind to?
What receptor does poliovirus bind to? |
Coxsackievirus and most rhinoviruses bind to ICAM-1.
Poliovirus binds to CD155. |
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What distinguishes enteroviruses from rhinoviruses?
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Enteroviruses can be distinguished from rhinoviruses by stability of capsid at pH3, optimum temp for growth, mode of transmission, diseases.
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What does pos-strand RNA have instead of methylated cap?
What is attached to the 5' end of RNA? |
"Ribosome landing pad" or IRES.
VPg covalently attached to 5' end of RNA to prime for RNA-dependent RNA polymerase. |
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What pH is optimal for enteroviruses?
What temp is optimal for enteroviruses? Transmission? Sx and signs? Immunity? |
pH 3 to pH 9 (can survive gastric acid).
37deg C. Also at room temp. Fecal-oral. Aseptic meningitis, rash. Immunity is type specific. |
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4 subgroups of enteroviruses.
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Poliovirus serotypes 1,2,3.
Echovirus. Coxsackievirus A and B. Unspecified enteroviruses 68-71. |
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Sx of echovirus.
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Aseptic meningitis, rashes, generalized infections in newborn.
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Sx of coxsackievirus.
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Coxsackievirus A - vesicular lesions (herpangina, hand-foot-and-mouth disease).
Coxsackievirus B - (body) myocarditis and pleurodynia. These viruses can also cause polio-like paralytic disease, but usually mild upper resp infection. |
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Sx of unspecified enteroviruses 68-71.
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Enterovirus 70 - hemorrhagic conjunctivitis.
Enterovirus 71 - hand-foot-and-mouth disease, herpangina, encephalitis, acute flaccid paralysis resembling poliomyelitis. |
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Pathogenesis of Picornoviridae.
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Virus enters via upper RT, oropharynx, intestinal mucosa.
Virus shed into feces often for mos. after primary infection. Virus is cytolytic, so viral not immune effects responsible for disease sx. Infection often asymptomatic or mild, flulike or upper RT disease. In sm children often cause of febrile illness. Antibody major protective immune response to enteroviruses. |
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How is poliovirus transmitted?
Pathogenesis of poliovirus. |
Fecal-oral, contaminated food/water.
Virus multiplies in throat and intestinal tract, travels through bloodstream where it infects brain and spinal cord. Most infections asymptomatic. |
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What are possible outcomes for individuals unvaccinated for poliovirus?
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Asymptomatic illness.
Abortive Poliomyelitis (non-spec febrile) Nonparalytic Poliomyelitis Paralytic Polio (major illness)(0.1-2%) - acute flaccid paralysis, usually lower limbs. Affects anterior horn cells of cord and motor cortex of brain. |
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Live-attenuated (Sabin) vs. killed (Salk) vaccine for poliomyelitis.
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Sabin (live) - GI tract + systemic immunity. Vaccine virus shed by vaccinees, so immunizes people that didn't receive it directly. Administered orally. Inexpensive. Risk of paralytic disease in both contacts and recipients if immunocompromised.
Salk (killed) - Humoral immunity. No risk of disease in recipients or contacts. No sig GI immunity. Requires boosters. More expensive. Injection. |
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Structure of Coronaviruses.
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Largest pos-strand RNA virus.
Enveloped, helical nucleocapsid. Lg sz + lack of proof reading = high mutation frequency. Glycoproteins on surface of envelope appear as club- or petal-shaped projections that form crown around virus. |
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What type of virus was SARS?
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Coronavirus.
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Pathogenesis of Coronaviruses.
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Virus replicates in epithelial cells of RT.
Rather unstable (unlike unenveloped rhinoviruses). Transmission by transfer of nasal secretions. Infections usually local but can spread - middle ear, pneumonias, myocarditis. |
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Structure of Caliciviridae.
Transmission? What does it cause? Types? |
Pos-strand RNA.
Non-enveloped, icosahedral capsid. Resistant to environmental pressure. Transmitted fecal-oral in contaminated water, food, shellfish. Common cause of non-bacterial gastroenteritis, resolves after 48h. Norovirus, Sapovirus. |
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Structure of Reoviruses.
What does Rotavirus cause? |
dsRNA genome in 10-12 segments.
Nonenveloped with double-layered protein capsids. Rotavirus is most common cause of dehydrating diarrhea in infants and kids. 25% travelers diarrhea. Not invasive - infects and kills cells via lysis of mature villus tips in sm intestine. |
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Structure of Herpesviruses.
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dsDNA with envelope from host cell membrane.
Surface glycoproteins distinct for each virus. |
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Tissue tropism for herpesviruses.
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HSV-1& 2, VZV - mucocutaneous disease and establish latency in sensory neurons.
CMV, EBV, HHV6-8 - systemic illness, prefer lymphocytes. |
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How do herpesviruses maintain lifelong latency?
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Viral genomes maintained extra-chromosomally, with limited transcription (except HHV-6).
Inhibit apoptosis and immune avoidance. |
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Which herpesviruses can be transmitted vertically?
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All herpesviruses can be transmitted vertically.
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Epidemiology of HSV-1 & 2
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HSV-1 prevalence modified by living conditions.
HSV-2 antibodies appear in puberty and correlate w/ sexual activity. Oral-oral, oral-genital, genital-genital spread occurs. HSV-1 tends to be oral, HSV-2 tends to be genital. |
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Sx of HSV-1 & 2.
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Gingivo-stomatitis & genital herpes.
Herpetic whitlow. Keratoconjunctivitis. Encephalitis. Neonatal infection. |
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Describe Gingivo-stomatitis and Genital Herpes.
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Can be primary or reactivation.
Crops of vesicles and ulcers, inside mouth and gums and in genital area. Painful. Adenopathy. Primary infections often more severe. |
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Describe Herpetic whitlow.
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Viral paronychia. Can occur around fingernails when skin abraded (nail biting). Appears similar to staph with less purulence.
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Where do HSV-1 & 2 remain latent?
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Sensory neurons.
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What type of vaccine is VZV?
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Live virus - should not be given to severely immunocompromised or pregnant.
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Sx of Varicella (chicken pox).
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Primary infection.
2d fever followed by rash with vesicles on erythematous base ("dewdrop on rosepetal"). Vesicles eventually crust, are quite pruritic, can be secondarily infected. Start on face and trunk and spread centripetally. At any time there are lesions present at varying stages of development (distinction from small pox). More severe sx include pneumonia and CNS complications. |
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Sx of Zoster (shingles).
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Reactivation.
Painful eruption of vesicles following a dermatome UNILATERALLY. Usually thoracic but can also be facial. |
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Transmission of Cytomegalovirus (CMV).
Where does CMV stay latent? |
Mother-to-child, breast milk, oral-oral, sexual, transfusion, transplantation.
Latent in PMNs and lymphocytes. |
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Clinical features of CMV.
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CMV mononucleosis - fever, lymphadenopathy, lymphocytosis. Heterophile antibody (mono spot) will be negative.
CMV most common Herpes virus transmitted in utero. |
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Transmission of EBV.
Incubation period of EBV? Where does EBV stay latent? |
Oral-oral, sexual, transfusion.
Incubation period is 30-50d and shedding can occur for mos after infection. Remains latent in lymphocytes. |
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Major clinical syndrome associated with EBV?
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Infectious mononucleosis. Fever, exudative pharyngitis, lymphadenopathy, splenomegaly. Rash may be present. Fatigue. Peripheral lymphocytes atypical appearing.
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Epidemiology of Human Herpesvirus 6 (HHV-6).
Clinical features of HHV-6. Latency. |
Extremely common.
Primary route of infection is from maternal saliva. Roseola infantum (exanthem sibitum/sixth disease), with 3-5d high fever, upper resp sx, lymphadenopathy. When fever resolves, fine maculopapular rash develops. Latent in T-lymph, monocytes, macrophages, megakaryocytes, neuro tissue |
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Epidemiology of HHV-7.
Clinical features of HHV-7. Latency. |
Virtually everyone infected by age 5.
Salivary shedding common/freq. Roseola infantum (like HHV-6), rarely hepatitis and encephalitis. Latent in CD4+ lymphocytes. |
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Epidemiology of HHV-8.
Clinical features of HHV-8. |
Virtually all Kaposi's sarcoma patients seropositive for HHV-8.
Kaposi's sarcoma, primary effusion lymphoma, castleman's disease. |
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Sx of Herpes B virus.
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Hemorrhagic encephalomyelitis in humans.
Benign infection in monkeys. |
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What is pharyngitis?
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Infection of oropharynx.
Discomfort in throat, esp during swallowing. Viruses more common than bacteria. Viral can not be distinguished from bacterial clinically - strep culture. |
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What are sx of nasopharynx infection?
What often causes it? |
Common cold sx.
Most are viral - rhinoviruses (then coronavirus). |
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What is croup?
What causes it? What is its course? Tx? |
Obstruction of upper airway with sudden onset of barking cough, difficulty breathing, and inspiratory stridor.
Usually caused by parainfluenza. Usually preceded by 1-3d nasal discharge and dry cough. Resolves 3-7d. Tx supportive: oral corticosteroids, inhaled epinephrine. |
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Tx of influenza.
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Amantidine & Rimantidine (A only)
Neuraminidase inhibitors: Zanamivir (inhaled), Oseltamivir (oral) (A&B) All for prophylaxis and tx. |
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What is bronchiolitis?
What often causes it? |
Airway obstruction with wheezing and air trapping.
Usually RSV. |
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Pathogenesis of RSV.
Tx of RSV. Prevention of RSV. |
Transmission by direct contact. Spread occurs cell-cell down RT. Self-limited.
Causes bronchiolitis or pneumonia. Tx primarily supportive: O2 and hydration. Bronchodilators sometimes useful. Steroids not effective. Prevention: anti-RSV monoclonal antibody (Palivizumab) in high-risk infants. |
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What is AIDS?
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Result of depletion and dysfunction of T helper (CD4) lymphocytes and other immune cells by HIV.
CD4+T-lymph <200 cells/uL or CD4+ T-lymph %/total lymph <14 or documentation of AIDS-defining condition. |
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What is the most common human retrovirus?
What retrovirus is common in West Africa? What other retroviruses infect lymphocytes? |
HIV-1.
HIV-2. Not as virulent, not as prevalent, less infectious. HTLV-I: Japan, Carribean, S Africa. HTLV-II. |
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What envelope glycoprotein is important for HIV to attach to cells for infection?
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gp120 + gp41 = gp160 (target for vaccines).
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What is Toxoplasma gondii?
How is it acquired? What animal hosts sexual stage? How does it manifest? When does risk start for HIV? Tx? |
Obligate intracellular protozoan parasite.
Acquired by ingestion of undercooked meat. Cat hosts sexual stage. Usually asymptomatic at first, but can be mononucleosis-like. Can cause toxoplasma encephalitis. Congenital infection. CD4 < 100. Tx is Pyrimethamine & Sulfadiazine. Prevent w/ daily Trimethoprim-sulfamethoxazole. |
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What is acute HIV?
How do you test for it? |
Acute mononucelosis-type illness (fever, swollen glands, mouth/genital sores, pharyngitis). Occurs 1-3wks after high risk exposure. Think of acute HIV for dd of mono.
HIV antibody test usually (-), may take 1-3mos to turn (+). Can diagnose acute HIV by testing for HIV RNA. |
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Sx of hepatitis (regardless of cause).
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Nausea, vomiting.
Abdominal pain (URQ). Loss of appetite, fever, fatigue. Diarrhea, light stools, dark urine. Jaundice, icterus. |
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What types of hepatitis often cause acute infection?
What types of hepatitis often cause chronic infection? |
A,E cause acute hepatitis.
B,C,D cause chronic hepatitis. |
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How common is Hepatitis C (HCV)?
Is it acute or chronic? How is it transmitted? Is there a vaccine? |
Most common chronic bb infection in US.
May be acute, but usually chronic - can lead to cirrhosis and liver cancer. Transmitted via blood (IVDU). No vaccine. |
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What is the structure of HCV (Hepatitis C)?
How many genotypes are there? What genotypes respond best to therapy? |
Linear, positive ssRNA, enveloped, icosahedral capsid.
6 genotypes (1 most common). Genotypes 2 and 3 respond best to therapy. |
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Perinatal transmission of HCV (Hepatitis C).
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5% transmission rate.
No need to avoid pregnancy or breastfeeding. No association w/ delivery method. Prophylaxis not available. Test infants born to HCV-infected women at birth. |
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What is the incubation period of HCV?
What is HCV's mechanism of injury? |
Average 6-7wks.
HCV not directly cytopathic - host immune system response causes fibrosis. Antibody response not protective --> reinfection can occur. |
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Tx for chronic HCV.
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Combination therapy with PegIFN + Ribavirin (6-12mos).
Goal is sustained virologic response (SVR): undetectable HCV RNA in patient's blood 6mos after stopping tx. |
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Adverse effects of HCV tx: PegIFN and Ribavirin.
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Adverse effects of PegIFN dose-dependent and resolve after tx stops. Fatigue, flulike, anemia, neutropenia, thrombocytopenia, depression, suicidality, anorexia, thryroid toxicity, ophalmologic toxicity.
Adverse effects of Ribavirin: dose-dependent reversible hemolytic anemia, teratogenicity. |
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Structure of Hepatitis B virus (HBV).
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Enveloped, circular, dsDNA genome that replicates through RNA intermediate.
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HBV replication.
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HBV enters hepatocytes via HBsAg interacting w/ receptors.
After uncoating, HBV DNA to nucleus. Partially dsDNA --> fully dsDNA, covalently closed circular DNA (cccDNA). cccDNA is template for transcription of viral RNA. cccDNA most resistant to antiviral therapy and host immunological responses - stuck in DNA permanently - not curable! HBV replication through RNA intermediate from cccDNA. |
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Transmission of Hepatitis B (HBV).
Is there a vaccination? |
Blood and body fluids.
Pregnant woman who is infected to newborn. Sexually transmitted - 100x more infectious than HIV. Vaccination for all infants, children not previously vaccinated, at risk adults. |
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What is a HBV infection usually like?
|
More often acute infection is symptomatic vs. HCV. Hepatitis sx. Acute HBV infection in adults usually complete recovery w/ production of HBsAb for protection. Most newborns and immunodeficient adults develop chronic infection due to failure to eliminate virus. Chronic HBV may have no sx.
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What is the incubation period of HBV?
|
Incubation ~60-90d.
Often asymptomatic until late stage. |
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What is the mechanism of liver injury in HBV?
What mediates HBV viral clearance? |
HBV not cytopathic, immune response causes liver damage - fibrosis + inflammation.
Clearance mediated by the humoral immune response (anti-HBs) 1-6mos later - protective immunity from reinfection. |
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What i the goal of HBV tx?
What is tx for HBV? |
Reduce likelihood of long-term sequelae of HBV infection (cirrhosis, hepatocelular carcinoma).
Tx: immunotherapy, inhibitors of viral DNAp, nucleoside analogues (Lamivudine, Entecavir, Telbivudine), nucleotide analogues (Adefovir, Tenofovir), Emtricitabine. No indication for Combination therapy IFN + oral antivirals. |
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Lamivudine or Emtricitabine in HBV tx.
|
Lower cost, safety, activity against HBV and HIV.
High rate of drug resistance, mutations in HBV polymerase gene. |
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Tenofovir in HBV tx.
|
Preferred.
Potent inhibitor of HBV DNAp. Effective in suppressing HBV w/ and w/out 3TC resistance, and in patients w/ Telbivudine or Entecavir resistance. Antiviral activity against HBV and HIV. |
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Adefovir in HBV tx.
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Activity against wtHBV, LAM-resistant HBV.
Low resistance rate. Renal tubular injury, not very potent. |
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Entecavir in HBV tx.
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Preferred.
Potent, effective against WT, 3TC resistant, ADV-resistant HBV. Low rate of drug resistance. Less nephrotoxic than adefovir and tenofovir. Can lead to HIV resistance. |
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Telbivudine in HBV tx.
|
Slightly more potent than lamivudine and adefovir.
Selects for same resistant mutants as lamivudine, but more expensive and no activity against HIV. |
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What type of disease does HAV (Hepatitis A virus) cause?
Tx? Transmission? Vaccine? |
Acute liver disease, lasting days-wks.
Does not lead to chronic infection. Tx is supportive, no antivirals. Transmitted via ingestion of fecal matter, close person-person contact, contaminated food. HAV vaccine for children starting at age 1 and travelers to certain countries. |
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What is the structure of HAV?
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Non-enveloped, ssRNA+.
Single serotype. |
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What happens after HAV infection?
|
Protective antibodies develop and confer lifelong immunity.
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What is the structure of a retrovirus?
What differs between viruses to classify them B-,C-,D-type? What is contained in virion? |
Enveloped, icosahedral, with capsid containing 2 copies of (+)strand RNA.
Only virus that is diploid. Morphology of capsid core differs. Virion contains RT, integrase, 2 tRNAs (primer for replication). |
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What are the 3 major genes retroviruses carry?
|
gag: internal proteins
pol: enzymes env: envelope glycoproteins |
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What are the 3 subfamilies of retroviruses?
|
Oncovirinae (HTLV-1, -2, -5)
Lentivirinae (HIV-1, -2) Spumavirinae (Human foamy virus) |
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What malignancy is HTLV-1 associated with?
How is HTLV-1 transmitted? What does the virus infect? How is infection characterized? Sx of HTLV-1 infection. |
Adult T-cell Leukemia (ATLL).
Transmitted via body fluids: breast milk, semen, blood. Infects CD4 helper T cells. Infection characterized by malignant clone of morphologically altered T cells ("flower cells"). Sx: lymphadenopathy, hepatosplenomegaly, hypercalcaemia. Immunocompromised. HAM/TSP. |
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How are arboviruses transmitted?
Where does the virus replicate? Where is the virus maintained? What kind of viruses are they? Diseases caused? |
Transmitted by bloodsucking arthropods.
Replicates in arthropod vector. Maintained in vertebrate host. RNA viruses (Togaviridae, flaviviridae, bunyaviridae). Encephalitis, febrile disease, hemorrhagic fevers. |
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What causes dengue fever?
What are the host? Vectors? Sx of dengue fever? Why does dengue hemorrhagic fever (DHF) occur? |
Dengue virus (flavivirus family).
Monkey and man are hosts. Mosquitoes are vectors. Sx are fever, headache, rash, bone pain ("breakbone fever"), myalgias, arthralgia. DHF occurs because subsequent infection w/ different serotype. Macrophages become activated and release inflammatory cytokines. Increased vascular permeability major problem. |
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What are Rodent-borne viral pathogens?
|
Arenaviridae
Hantavirus (bunyaviridae) |
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How are Hantaviruses spread?
Where does virus remain? What diseases is it associated with? Best known in US? |
Infected rodents spread virus via saliva, urine, droppings. Can be aerosolized and inhaled.
Virus remains in lung where it causes hemorrhagic tissue destruction and lethal pulmonary disease. Associated with hemorrhagic fever with renal syndrome (HFRS) and severe pulmonary syndrome (HPS). Sin Nombre virus. |
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What viruses are part of Filoviridae?
What is the reservoir? How is it transmitted? Sx? |
Ebola and Marburg viruses.
Reservoir unknown. Transmitted from infected monkeys and other animals, or exposure to body fluids of infected person. Sx are hemorrhagic fever with widespread bleeding into skin, mucous membranes, visceral organs, GI tract. High mortality. |
