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85 Cards in this Set
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Primary/definitive host
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In a heteroxenous life cycle, this is the host in which sexual reproduction occurs, and where the adult form resides.
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Secondary Host
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Essential for the life cycle of a heteroxenous parasite.
Viz. snail in schistosomiasis |
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Reservoir host
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Wild animal host in which a heteroxenous parasite's life cycle is completed. Usually commensal.
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Vector
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Biological vectors most commonly an arthropod, mechanical vectors can be anything (flies that transfer amoebiasis)
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Nematodes (roundworms)
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Helminths that are unsegmented, dioecious.
Tm: ingestion of eggs/encysted larvae, penetration of larvae, arthropod vector. Ascaris lumbricoides, Trichuris trichiura (whipworm), hookworms, stronglyoides, pinworm |
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Cestodes (tapeworms)
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Segmented monoecious worms.
Tm: encysted larvae Taenia spp., fish tapeworm |
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Trematodes (flatworms)
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Unsegmented, usu. monoecious.
Tm: larvae through intact skin. |
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Malaria
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Agents: Plasmodium spp.
Vector: anopheles mosquito Sxs: paroxysmal fever, chills (rigor) during rupture of merozoites. Recur for weeks. Cerebral malaria Path: fever, anaemia, tissue hypoxia, immune complexes Dx: parasites in blood smear, thick smear for screening, thin smear for specificity. |
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Plasmodium falciparum
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Disease: malaria
Most virulent spp, invades all RBCs. Forces RBC expression of sequestrins, results in knobby irregularities that bind to ICAM on endothelial cells; haemostasis. Fever cycle: 48 hrs. Severe manifestations: many, including cerebral malaria, renal failure, DIC, acidosis, black water fever, severe anaemia. Dx: high parasitaemia, multiple ring forms in single RBC, crescent gametocytes. |
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Plasmodium vivax
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Disease: malaria
Invades only immature RBCs Oddities: sporozoites may remain dormant in liver for years (like P. ovale). |
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Plasmodium ovale
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Disease: malaria
Invades only immature RBCs. Like P. vivax, can remain dormant in liver. Fever cycle: 48 hrs |
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Plasmodium malariae
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Invades only senescent RBCs.
Fever cycle: 72 hrs Associated w. glomerulonephritis. |
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Splenic Manifestations of Malaria
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Gross: enlarged/congested
Histo: Macs laden w. hemozoin aka malarial pigment. (pigment from breakdown of Hb). Can become fibrotic in chronic disease. |
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Hepatic Manifestations of Malaria
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Gross: mild enlargement in acute disease.
Histo: Kupffer cell hyperplasia w. hemozoin accumulation. Chronic: fibrosis, dark pigmentation. |
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Cerebral Manifestations of Malaria
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Ring haemorrhages around BVs, focal ischaemic necrosis, Duruk's granuloma (focal microglial proliferation).
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Black Water Fever
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Manifestation of malaria
Path: due to haemolysis in kidneys resulting in renal failure. |
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Cerebral Malaria
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Severe manifestation of P. falciparum malaria.
Sxs: coma, prevalent in children. |
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Sporozoites
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Malarial form that develops within an oocyte. After oocyte ruptures, it migrates to mosquito salivary glands. Upon injection inot human, it invades hepatocytes and becomes a schizont, or lies dormant as a hypnozoite (P. vivax, ovale)
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Schizont
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Sporozoites develop into tissue schizonts within hepatocytes over 1-2wk period, until hepatocytes rupture, releasing thousands of what are now merozoites.
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Merozoites
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Formerly schizonts, these are released upon hepatocyte rupture. Binds to and invades RBCs, then ring form → trophozopite → schizont → burst into merozoite.
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Malarial Gametocytes
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Develops from few merozoites. Macrogametocyte = female, micro- = male. Ingested by mosquito during blood meal, becomes gametes in mosquito gut.
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Ookinete
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Malarial gametes fuse into a zygote, which then transforms into the motile ookinete that migrates through the gut wall, transforming into an oocyst.
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Oocyst
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From ookinete, sporozoites develop inside, then oocyst bursts, releasing the sporozoites.
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Chagas Disease
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Agent: Trypanosoma cruzi
Range: central/south America Manifestations: acute and chronic forms Path: Multiplying amastigotes destroy cells, causes autoimmune response cross-reacting w. myocardial cells, neurones, lymphocytes, extracellular proteins. |
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Trypanosoma cruzi
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Vector: triatomid insects (kissing, assassin, cone bug)
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Acute Chagas Disease
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Manifestations: localised inflammation at site of entry (chagoma), myocarditis, lymphadenopathy, hepatosplenomegaly. Reactive hyperplasia of lymphoid tissue. RES, macs, blood involved.
Sx: fever, malaise, anorexia, oedema (face, lower extremities), Romaña's sign. Dx: Detect motile trypomastigotes in blood or buffy coat. Xenodiagnosis very sensitive but stupid. |
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Chronic Chagas Disease
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5-15 yrs after acute
Manif: Heart (biventricular dilation, mural thrombi, atrophy), GI (oesophageal/colonic dilation "megadisease", atrophy of myenteric plexus), encephalitis, hepatosplenomegaly, lymphadenopathy, bone marrow hypoplasia. Sxs: arrythmias, CHF, emboli, dysphagia, chest pain, aspiration, constipation, abdominal pains. Dx: serology for T. cruzi Abs. (Actual organism rare) |
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Romaña's Sign
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Sx of acute Chagas Disease. Painless oedema of periorbital soft tissues.
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trypomastigote
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Motile, flagellated form of Trypanosoma spp. (Chagas, sleeping sickness) that is ingested by triatomid insects from mammal. Enters insect gut and becomes promastigotes and multiply.
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metacyclic trypomastigote
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Infective form of trypanosoma spp. Multiplying promastigotes change into this in insect gut, then discharged via faeces during blood meal. You scratch it in.
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amastigote
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Non-flagellated form of Tryapnosoma spp and Leishmania spp. Metacyclic trypomastigotes enter macs and change into amastigotes, which then divide by binary fission. Macs carry these back to lymph node and lyse, releasing amastigotes. These transform back into trypomastigotes, enter blood, and reach most tissues. Changes back into amastigotes within tissues.
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Leishmaniasis
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Agent: Leishmania spp.
Path: visceral leishmaniases grow at 37C, cutaneous at 34C. Intact CMI limits infection and/or forms granulomas. Sx: self-healing skin ulcers, fever, malaise, wt. loss, severe visceral disease (pancytopaenia, haemorrhage). Dx: Bone marrow aspiration, peripheral blood smear, clture, serology (false neg >40% if HIV+) |
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Leishmania spp.
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Visceral Leishmaniasis: L. donovani, infantum, chagasi.
Cutaneous: L. major, tropica, aethiopica. Mucocutaneous: L. braziliensis, amazonensis, mexicana. Vector: sandfly; Phlebotomus (Old World), Lutzomyia (New World). Virulence: Proton ATPase that moderates phagosome pH (allowing intraphagosome multiplication); lipophosphoglycans against enzymes, free radicals. |
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Visceral Leishmaniasis (kala azar)
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Most serious form of Leishmaniasis.
Sx: severe hepato/splenomegaly (filled with amastigotes), pancytopaenia, bone marrow disease, glomerulonephritis, amyloidosis. |
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Cutaenous Leishmaniasis (bouton d'orient, Baghdad ulcer, tropical/Oriental sore, Delhi boil)
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Most common form of Leishmaniasis.
Sx: single ulcer, usu. heals spontaneously in 6 months w. scarring. Histo: granumlomatous inflammation w. few parasites. |
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Mucocutaneous Leishmaniasis (espunida)
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Sx: skin ulcers that enlarge, esp. of nose/mouth. Lesions heal spontaneously w. lots of scarring, but may reactivate.
Histo: mixed chronic inflammatory infiltrate, or overtly granulomatous. Variable # of parasites in macs. |
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Disseminated Cutaneous Leishmaniasis
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Rare form of leishmaniasis, usually due to anergy.
Sx: cf. lepromatous leprosy, w. diffuse chronijc skin lesions, keloids, verrucae. Histo: numerous dermal amastigotes. |
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African trypanosomiasis
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Agents: Chronic form: Trypanosoma brucei gambiense (cent., w. Africa) Acute form: T. brucei rhodesiense (S., E. Africa)
Vector: Tsetse fly Path: Trypomastigotes cause lymphocytes to relase INF-γ and IL-2, activating macs and damaging BBB. Trypanomastigotes then proliferate in CNS, leading to focal demyelination, haemorrhage. Dx: trypomastigotes in blood or tissues, serology, PCR. |
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Acute Sleeping Sickness
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Agent: T. brucei rhodesiense
Sxs: (few weeks after inoculation) high persistent fever, headache, vomitting, rigors, bone pain, anaemia, marked neurologic impairment (meningoencephalitis), progress to coma. Almost always fatal w/o Tx. |
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Chronic Sleeping Sickness
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Agent: T. brucei gambiense
Sx: month/years after inoculation. Low grade, irregular fevers, headaches, backaches, skin rashes, cachexia, anaemia, progressive CNS impairment. Usually fatal w/o Tx. |
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Skin manifestations of Sleeping Sickness
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Firm, tender, painful chancre (hyperaemic nodule). Oedema, chronic inflammation, vasculitis.
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Cerebral Manifestations of Sleeping Sickness
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Meningoencephalitis, oedema, focal demyelination, necrosis, haemorrhage, microgliosis (cf. Duruck's granuloma in malaria), reactive astrocytosis.
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Lymphatic Manifestations of Sleeping Sickness
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Reactive hyperplasia, lymphocytic depletion in late disease.
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Miscellanous Manifestations of Sleeping Sicknessq
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Cardiac: chronic endocarditis, myocarditis, pericarditis.
Marrow: hypoplasia. |
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Toxoplasmosis
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Agent: toxoplasma gondii
Range: WW, but more in warm, humid climates. Vector: loveable cats Path: T. gondii binds soluble laminin, then uses that to bind to laminin RR to sneak into cell. Dx: serology (reliable only in immunocompetent hosts), detect parasite in tissues (usu. in immunocompromised) |
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Acute Toxoplasmosis
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Tachyzoites multiply in host cells, leading to rupture until CMI activates macs. Usually minimal injury before CMI activated.
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Latent Toxoplasmosis
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After acute infxn, T. gondii forms dormant tissue cysts, can persist for decades, activating in times of immunodeficiency.
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Congenital Toxoplasmosis
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T. gondii readily crosses placenta. Foetus lacks CMI to fight off infxn.
Path: necrotising meningocencephalitis (variable neurologic impairment), chorioetinitis (born blind), necrotising hepatitis, myocarditis, pneumonia, adrenitis. Spontaneous abortion possible. |
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Necrotising Meningoencephalitis
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Sequelae of congenital toxoplasmosis.
Gross: sign. loss of brain tissue; hydrocephalus, cerebral calcifications. Histo: glial nodules w. many tachyzoites in periventricular, periaqueductal regions. |
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Chronic Toxoplasmosis
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Some acute infxns goes into chronic phase. T. gondii transforms into bradyzoite, multiplies slowlyu within intracellular cysts.
Path: slow tissue destruction. |
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Immunocompetent Toxoplasmosis
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Path: most commonly lymphadenopathy/-itis. Hepatitis, myocarditis, encephalitis, pneumonia possible.
Sx: 90% asymptomatic. Mono-like. |
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Immunodeficient Toxoplasmosis
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Most cases from reactivated disease.
Path: Brain most commonly affected. Multifocal necrotising encephalitis, chorioretinitis. Sx: focal CNS abnormalities (seizures, hemiparesis, CN palsies, visual disturbances), general CNS (heachache, confusion, stupor, behavioural abnormalities, coma) High mortality rate. |
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Amebiasis (Amoebic Dysentery)
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Agent: Entamoeba histolytica
Range: cent., S.A., Africa, India. Tm: food, water, sex, flies/roaches (mechanical vectors.) Sxs: Carriers (pass cysts in stool), dysentery (lasts 2-6wks, fulminant necrotising colitis seen in the weak), non-dystenteric colitis (milder diarrhoea). Dx: observe organism in stool (≥3 samples), biopsy (colonoscope), serology (reverts to neg 6-12 months after active disease) |
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Entamoeba histolytica
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Disease: amebiasis
Virulence: chitin wall (protection) surface lecithin (binds to colonic epithelial cells) proteinase (breaks down ECM) Channel forming protein (lyses host cells) |
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Intestinal Amebiasis
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Signs: Flask shaped ulcers in colon.
Path: trophozoites burrow in lamina propia, mucosa becomes focally necrotic. Rarely, ameboma (granuloma) may form. Muscularis mucosa forms barrier to deeper invasion, preforation of bowel is rare. |
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Extraintestinal Amebiasis
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Site: usu. liver
Sxs: amoebic liver abscess (~40%), may become 2°ly infected with bacteria. Other sites: lungs, brain, skin, GU. |
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Giardiasis
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Agent: giaria lamblia
Range: Rockies, Cent. America, India. Tm: drinking from mountain streams. Beavers, geese are reservoirs Path: Trophozoites attach to surface of enterocytes. May cause villous atrophy, resulting in malabsorption. Sx: Watery diarrhoea (1-3wks after infxn), fat steatorrhoea, iron-microcytic anaemia, lactose intolerance. Dx: Cysts/trophozoites in stool, duodenal fluid; Giardia Ag. |
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Giardia lamblia
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Disease: Giardiasis
Virulence: Lectin: binds to surface of enterocytes Sucker-like discs: firm attachment Surface Ag variation: protects Giardia from secretory IgA. |
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Cryptosoridiosis
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Agent: Cryptosporidium parvum
Range: 3rd world Tm: contaminated water Pts: AIDS, children Sx: self-limiting diarrhoea or cholera-like chronic diarrhoea (immunocompromised). Path: Disrupts microvilli; infxn usu. limited to S.I., but in AIDS can metastisise through G.I., and villi can atrophy. Dx: Acid-fast stain to see oocysts in stool; Ag in stool more sensitive. |
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Crytosporidium parvum
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Disease: Crytosporidiosis
Notes: intracellular; appear as ~2μm bluish dots on enterocytes in LM. Virulence: Surface Lectin: adhesion to enterocytes. |
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Microsporidiosis
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Agent: Microscporidia or Encephalitozoon (most common)
Path: chiefly opportunistic in AIDS. No morphologic change to intestinal mucosa. Virulence: Polar tubes allow invasion. Sx: Chronic diarrhoea, wasting. Variety of extraintestinal inflammatory disorders possible. Dx: EM is gold standard. Detect spores w. modified trichrome. |
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Ascariasis (roundworm)
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Most common helminthic infxn.
Agent: Ascaris lumbricoides Path: Larvae may cause pneumonitis, eosinophilia, enter biliary tract and obstruct ducts (cholangitis, liver abscesses, acute pancreatitis). Sx: most asymptomatic, signs of obstruction, malnutrition if severe. Transient resp. manifestations during lung migration. Dx: ova in stool. Bolus of worms/larvae sts vomitted up. |
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Ascaris lumbrioides
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Disease: ascariasis
Range: world-wide, esp. warm moist, poor sanitation. Virulence: attaches to S.I., feeds on intestinal contents. Outer cuticle may cause mechanical irritation. |
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Trichuriasis (whipworm)
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Agent: Trichuris trichiura
Range: world-wide, esp. warm moist, poor sanitation. Children ↑'d risk Tm: Food, etc. Eat ova. Path: worm lives in caecum, small erosions/focal inflam., peripheral eosinophilia. Rectal prolapse if severe. Worms drink lots of blood. Sxs: Usu. none. Cramps, bloody diarrhoea, mild anaemia, wt. loss/growth retardation if severe. Dx: ova in stool. |
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Hookworm Infection
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Agent: Ancylostoma duodenale (Old World); Necator americanus (New World).
Range: world-wide, esp. warm moist, poor sanitation. Tm: filariforms in soil penetrate intact skin! Path: worms feed on blood. Pneumonitis, eosinophilia. Sx: pruritis at site of entry, cough from lung migration, severe iron-def. anaemia possible. Dx: ova in stool. |
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Strongyloidiasis
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Agent: strongyloides stercoralis
Range: world-wide, esp. warm moist, poor sanitation. Path:Larvae cause pneumonitis, eosinophilia. Sx: pruritis, cough (lung migration), disseminated hyperinfxn assoc. w. gram- sepsis. (immunocompromised). Dx: Larvae in stool, resp. secretions (in hyperinfxn) |
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Enterobiasis (pinworm)
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Agent: Enterobius vermicularis
Range: temperate zones; usu. infect kids. Path: usu. no damage; worms small and non-invasive. Sx: perianal/perineal pruritis. Dx: Scotch-tape test to detect ova. |
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Taeniasis
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Agent: Taenia spp.
Range: pork/boeuf-eating areas (T. saginata is boeuf tapeworm) Path: infxn of S.I. by adult form of Taenia spp. Suckers and hooklets (T. Solium only) allow attachment. Sx: usu. none. Dx: ova or proglottids in stool. |
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Cysticercosis
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Agent: Taenia solium
Range: Pork-eating areas of the world (pork tapeworm) Path: infxn of tissues by larvae of T. solium. Human is dead-end host. T. solium has hooklets. Injury due to expanding cysticerci in brain, sk mm, skin, heart. Scarring/calcification of cysts. Sx: Brain cysts can cause CNS sxs. Retinal: blindess. Cardiac: arrhythmias. Sx: imagining studies, serology for cysticercus Abs. |
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Fish Tapeworm
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Agent: Diphyllobothrium latum
Tm: sashimi Range: AK, MN, MI, Canada, Scandanavia, Japan. Path: worms attach and feed in intestinal mucosa, competing for B-12, rarely causing megaloblastic anaemia. Very low damage. Dx: ova or gravid proglottis in stool. |
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Schistosomiasis
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Agent: S. mansoni, japonicum, haematobium.
Range: Mostly sub-Sahara. Tm: skin penetration in water. Snail is int. host. Path: Transient inflammation at site of entry, pruritis (Swimmer's itch)Schistosomules fool immune system, cause no inflammation by sharing host proteins. Ova are highly immunogenic however; cause granulomatous response, results in progressive fibrosis/organ dysfuxn. Dx: Ova in stool, urine, or tissue. Serology, imaging, eosinophilia. |
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Schistosoma mansoni
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Range: Africa, S.A, Haiti, PR.
Disesae: Liver and GI tract schistosomiasis. Notes: female worms migrate to mesenteric venules to deposit eggs (like S. japonicum), affecting regions drained by inf. mesenteric vein (distal colon, rectum). Dx: ovum is oval w. lat. spine. |
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Schistosoma japonicum
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Range: E. Asia
Disease: liver, GI schistosomiasis. Notes: migrates to mesenteric venules to deposit eggs (like S. mansoni), usu. affects regions drained by sup. mesenteric vein. (SI, ascending colon). Dx: ovum is round w. lat. nub. |
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Schistosoma haematobium
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Range: Africa, Middle East
Disease: bladder schistosomiasis. Notes: deposits ova in peliv venous plexus. Dx: ovum is oval w. terminal spine. |
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Intestinal Schistosomiasis
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Agent: S. mansoni, S. japonicum.
Path: polyps, abscesses, ulcers, fibrosis, fistulae Sx: bloody diarrhoea, abdominal pain, cramping. Obstruction from fibrotic strictures. |
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Hepatic Schistosomiasis
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Agent: S. mansoni, S. japonicum.
Path: Ova cause periportal granulomatous inflammation, progressive periportal fibrosis. Severe cases cause portal HTN. Sx: Ascites (due to portal HTN), GI haemorrhage from varices. |
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Urinary Schistosomiasis
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Agent: S. haematobium
Path: Ova cause granulomatous inflammation; polyps, ulceration, fibrosis, calcification, fistulae, hydroureter, hydronephrosis. Sxs: Haematuria, dysuria, polyuria, renal insufficiency (due to ureter constriction) Notes: associated w. ↑'d risk of squamous cell carcinoma of bladder. |
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Katayama Fever (Snail Fever)
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Caused by migration of schistosomas.
Sxs: urticaria w. eosinophilia, fever, abdominal pain, tender hepatosplenomegaly. |
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Filariasis
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Agent: Wucheria bancrofti, Brugia malayi.
Range: equatorial. Tm: mosquitoes Path: provokes inflammation in lymphatics → fibrosis, obsruction. Sx: usu. none where endemic. Recurrent fever, malaise, lymphadenopathy, small subset develop elephantiasis after 20-30 yrs. Tropical pulmonary eosinophilia possible. Dx: microfilariae in peripheral blood. |
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Tropical Pulmonary Eosinophilia
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Asthma-like clinical manifestation of Filariasis, due to filarial Ags provoking hypersensitivity rxn.
Sx: cough, wheezing, pulm. infiltrates, low grade fever, peripheral eosinophilia. |
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Trichinosis
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Agent: Trichinella spiralis
Range: E./Cent. Europe, Americas. Path: GI infxn, encysts in sk mm. Sx: usu. none, self-limited. Abdominal pain, diarrhoea, sk mm invasion = severe pain, tenderness, fever, weakness, malaise. Dx: Peripheral eosinophilia, serology, cysts or calcified nodules in mm (late stage). |
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Trichinella spiralis
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Disease: Trichinosis
Tm: eating raw, undercooked meat (usu. porc) w. encysted larvae. Path: Larvae penetrate bowels, migrate, only viable in sk mm. Transforms myocyte into cyst. Larva dies (dead end), cyst calcifies years later. |
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Visceral Larva Migrans
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Helminthic larva migrating in incidental host.
Pts.: usu. children Agents: Toxocara canis, cati (dog/cat roundworm) Path: ova hatch in GI, larva penetrates and invades BV, but dies in tissues. Dead worm provokes granulomatous response. Sx: inflam., focal haemorrhage, necrosis, fibrotic scarring. Visual loss (ocular larva migrans), pneumonitis, myocarditis, hepatomegaly. Usu. self-limited. Dx: eosinophilia, serology, clinical. |
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Echinococcosis (Hydatid disease)
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Agent: Echinococcous granulosus, multilocularis, vogeli.
Pts.: Herders. Range: pastorial area w. sheep. Path: Humans dead end, slowly expanding cysts cause mechanical compression or allergic rxn. Liver, lungs most common. Sx: Compression of bile ducts (jaundice), cyst rupture (peritoneal pain, pneumothorax/empyaema, anaphylaxis). Dx: Serology, radiology (cysts), needle aspiration possible. |
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Echinocoocus spp.
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Echinococcus granulosus: hydatid cystic disease.
E. multilocularis: alveolar hydatid disease. E. vogeli: polycystic hydatid disease. |