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85 Cards in this Set

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Primary/definitive host
In a heteroxenous life cycle, this is the host in which sexual reproduction occurs, and where the adult form resides.
Secondary Host
Essential for the life cycle of a heteroxenous parasite.
Viz. snail in schistosomiasis
Reservoir host
Wild animal host in which a heteroxenous parasite's life cycle is completed. Usually commensal.
Vector
Biological vectors most commonly an arthropod, mechanical vectors can be anything (flies that transfer amoebiasis)
Nematodes (roundworms)
Helminths that are unsegmented, dioecious.
Tm: ingestion of eggs/encysted larvae, penetration of larvae, arthropod vector.
Ascaris lumbricoides, Trichuris trichiura (whipworm), hookworms, stronglyoides, pinworm
Cestodes (tapeworms)
Segmented monoecious worms.
Tm: encysted larvae
Taenia spp., fish tapeworm
Trematodes (flatworms)
Unsegmented, usu. monoecious.
Tm: larvae through intact skin.
Malaria
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.
Plasmodium falciparum
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.
Plasmodium vivax
Disease: malaria
Invades only immature RBCs
Oddities: sporozoites may remain dormant in liver for years (like P. ovale).
Plasmodium ovale
Disease: malaria
Invades only immature RBCs. Like P. vivax, can remain dormant in liver.
Fever cycle: 48 hrs
Plasmodium malariae
Invades only senescent RBCs.
Fever cycle: 72 hrs
Associated w. glomerulonephritis.
Splenic Manifestations of Malaria
Gross: enlarged/congested
Histo: Macs laden w. hemozoin aka malarial pigment. (pigment from breakdown of Hb). Can become fibrotic in chronic disease.
Hepatic Manifestations of Malaria
Gross: mild enlargement in acute disease.
Histo: Kupffer cell hyperplasia w. hemozoin accumulation.
Chronic: fibrosis, dark pigmentation.
Cerebral Manifestations of Malaria
Ring haemorrhages around BVs, focal ischaemic necrosis, Duruk's granuloma (focal microglial proliferation).
Black Water Fever
Manifestation of malaria
Path: due to haemolysis in kidneys resulting in renal failure.
Cerebral Malaria
Severe manifestation of P. falciparum malaria.
Sxs: coma, prevalent in children.
Sporozoites
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)
Schizont
Sporozoites develop into tissue schizonts within hepatocytes over 1-2wk period, until hepatocytes rupture, releasing thousands of what are now merozoites.
Merozoites
Formerly schizonts, these are released upon hepatocyte rupture. Binds to and invades RBCs, then ring form → trophozopite → schizont → burst into merozoite.
Malarial Gametocytes
Develops from few merozoites. Macrogametocyte = female, micro- = male. Ingested by mosquito during blood meal, becomes gametes in mosquito gut.
Ookinete
Malarial gametes fuse into a zygote, which then transforms into the motile ookinete that migrates through the gut wall, transforming into an oocyst.
Oocyst
From ookinete, sporozoites develop inside, then oocyst bursts, releasing the sporozoites.
Chagas Disease
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.
Trypanosoma cruzi
Vector: triatomid insects (kissing, assassin, cone bug)
Acute Chagas Disease
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.
Chronic Chagas Disease
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)
Romaña's Sign
Sx of acute Chagas Disease. Painless oedema of periorbital soft tissues.
trypomastigote
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.
metacyclic trypomastigote
Infective form of trypanosoma spp. Multiplying promastigotes change into this in insect gut, then discharged via faeces during blood meal. You scratch it in.
amastigote
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.
Leishmaniasis
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+)
Leishmania spp.
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.
Visceral Leishmaniasis (kala azar)
Most serious form of Leishmaniasis.
Sx: severe hepato/splenomegaly (filled with amastigotes), pancytopaenia, bone marrow disease, glomerulonephritis, amyloidosis.
Cutaenous Leishmaniasis (bouton d'orient, Baghdad ulcer, tropical/Oriental sore, Delhi boil)
Most common form of Leishmaniasis.
Sx: single ulcer, usu. heals spontaneously in 6 months w. scarring.
Histo: granumlomatous inflammation w. few parasites.
Mucocutaneous Leishmaniasis (espunida)
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.
Disseminated Cutaneous Leishmaniasis
Rare form of leishmaniasis, usually due to anergy.
Sx: cf. lepromatous leprosy, w. diffuse chronijc skin lesions, keloids, verrucae.
Histo: numerous dermal amastigotes.
African trypanosomiasis
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.
Acute Sleeping Sickness
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.
Chronic Sleeping Sickness
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.
Skin manifestations of Sleeping Sickness
Firm, tender, painful chancre (hyperaemic nodule). Oedema, chronic inflammation, vasculitis.
Cerebral Manifestations of Sleeping Sickness
Meningoencephalitis, oedema, focal demyelination, necrosis, haemorrhage, microgliosis (cf. Duruck's granuloma in malaria), reactive astrocytosis.
Lymphatic Manifestations of Sleeping Sickness
Reactive hyperplasia, lymphocytic depletion in late disease.
Miscellanous Manifestations of Sleeping Sicknessq
Cardiac: chronic endocarditis, myocarditis, pericarditis.
Marrow: hypoplasia.
Toxoplasmosis
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)
Acute Toxoplasmosis
Tachyzoites multiply in host cells, leading to rupture until CMI activates macs. Usually minimal injury before CMI activated.
Latent Toxoplasmosis
After acute infxn, T. gondii forms dormant tissue cysts, can persist for decades, activating in times of immunodeficiency.
Congenital Toxoplasmosis
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.
Necrotising Meningoencephalitis
Sequelae of congenital toxoplasmosis.
Gross: sign. loss of brain tissue; hydrocephalus, cerebral calcifications.
Histo: glial nodules w. many tachyzoites in periventricular, periaqueductal regions.
Chronic Toxoplasmosis
Some acute infxns goes into chronic phase. T. gondii transforms into bradyzoite, multiplies slowlyu within intracellular cysts.
Path: slow tissue destruction.
Immunocompetent Toxoplasmosis
Path: most commonly lymphadenopathy/-itis. Hepatitis, myocarditis, encephalitis, pneumonia possible.
Sx: 90% asymptomatic. Mono-like.
Immunodeficient Toxoplasmosis
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.
Amebiasis (Amoebic Dysentery)
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)
Entamoeba histolytica
Disease: amebiasis
Virulence:
chitin wall (protection) surface lecithin (binds to colonic epithelial cells)
proteinase (breaks down ECM)
Channel forming protein (lyses host cells)
Intestinal Amebiasis
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.
Extraintestinal Amebiasis
Site: usu. liver
Sxs: amoebic liver abscess (~40%), may become 2°ly infected with bacteria.
Other sites: lungs, brain, skin, GU.
Giardiasis
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.
Giardia lamblia
Disease: Giardiasis
Virulence:
Lectin: binds to surface of enterocytes
Sucker-like discs: firm attachment
Surface Ag variation: protects Giardia from secretory IgA.
Cryptosoridiosis
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.
Crytosporidium parvum
Disease: Crytosporidiosis
Notes: intracellular; appear as ~2μm bluish dots on enterocytes in LM.
Virulence:
Surface Lectin: adhesion to enterocytes.
Microsporidiosis
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.
Ascariasis (roundworm)
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.
Ascaris lumbrioides
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.
Trichuriasis (whipworm)
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.
Hookworm Infection
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.
Strongyloidiasis
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)
Enterobiasis (pinworm)
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.
Taeniasis
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.
Cysticercosis
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.
Fish Tapeworm
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.
Schistosomiasis
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.
Schistosoma mansoni
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.
Schistosoma japonicum
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.
Schistosoma haematobium
Range: Africa, Middle East
Disease: bladder schistosomiasis.
Notes: deposits ova in peliv venous plexus.
Dx: ovum is oval w. terminal spine.
Intestinal Schistosomiasis
Agent: S. mansoni, S. japonicum.
Path: polyps, abscesses, ulcers, fibrosis, fistulae
Sx: bloody diarrhoea, abdominal pain, cramping. Obstruction from fibrotic strictures.
Hepatic Schistosomiasis
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.
Urinary Schistosomiasis
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.
Katayama Fever (Snail Fever)
Caused by migration of schistosomas.
Sxs: urticaria w. eosinophilia, fever, abdominal pain, tender hepatosplenomegaly.
Filariasis
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.
Tropical Pulmonary Eosinophilia
Asthma-like clinical manifestation of Filariasis, due to filarial Ags provoking hypersensitivity rxn.
Sx: cough, wheezing, pulm. infiltrates, low grade fever, peripheral eosinophilia.
Trichinosis
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).
Trichinella spiralis
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.
Visceral Larva Migrans
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.
Echinococcosis (Hydatid disease)
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.
Echinocoocus spp.
Echinococcus granulosus: hydatid cystic disease.
E. multilocularis: alveolar hydatid disease.
E. vogeli: polycystic hydatid disease.