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18 Cards in this Set

  • Front
  • Back
Entamoeba histolytica (Ameba)
-causes intestinal & extraintestinal infection
-epidemiology: developing countries b/c of hygiene, male homosexuals, travelers, recent immigrants, institutionalized pts.
-trophozoite: active form, lives in intestinal lumen, feeds on RBCs
-cyst: infective form, passed in feces
-lifecycle: direct, ingest mature cysts  trophozoites  multiply  trophozoites & cysts  passed in feces
-clinical manif: asymptomatic: stays in lumen, invasive intestinal: dysentery, colitis, appendicitis, toxic megacolon, polyps, invasive extraintestinal: liver abscess, pulmonary abscess, skin & genital lesions
-diagnosis: I.D. cysts & trophozoites in stool
-treatment: asymptomatic (iodoquinol, interferes w/oxidative phos), symptomatic (metronidazole, disrupts DNA helical structure, inhibits glucose metabolism)
Balantidium coli (Ciliate)
-large & ciliated, pigs are reservoir
-lifecycle: ingest food w/cysts  trophozoite  multiplies  cysts in feces
-clinical manif: most asymptomatic, diarrhea, abdominal pain, weight loss
-diagnosis: trophozoites in stool
-treatment: tetracycline
Giardia lamblia (Flagellate)
-no cyst form, 4 anterior flagella, 1 posterior
-epidemiology: human, most common pathogenic parasite in industrialized countries, multiple sexual partners, people w/other venereal diseases
-lifecycle: lives in female lower genital tract & male urethra & prostate, replicates via binary fission, can’t survive outside host, transmitted via sexual intercourse
-clinical manif: females: vaginitis, copious fowl-smelling yellow discharge, cervical lesions, ab pain, males: asymptomatic, urethritis, epididymitis, prostatitis
-diagnosis: I.D. actively motile orgs in vaginal/prostatic & urethral secretions
-treatment: metronidazole, prophylaxis
Cryptosporidium parvum (Sporozoa)
-epidemiology: in water, worldwide, 80% of the pop has had cryptosporidiosis
-transmission: water contaminated w/oocyst
-clinical manif: watery diarrhea, weight loss, dehydration, ab pain, fever, nausea,vomiting worse in immunocompromised (CD4>200)
-diagnosis: acid-fast staining, antibody, PCR
-treatment: fluid & electrolyte replacement
Trypanosoma brucei
-causes sleeping sickness (Central Africa)
-morphology: single flagellum, undulating membrane, 2 forms: (1) epimastigote in insect host, (2) trypomastigote in humans
-lifecycle: Tsetse fly bites  injects saliva & trypomastigotes in blood  multiply via binary fision  Tsetse fly bites & ingests trypomastigotes  multiply  turn into epimastigotes  multiply in salivary gland  turn into trypomastigotes
-clinical manif: stage 1 (chancre), stage 2 (hemolymphatic: fever, lymphadenopathy, pruritus), stage 3 (meningoencephalitic: headaches, somnolence, abnormal behavior, loss of consciousness, coma)
-diagnosis: I.D. trypanosomes in chancre fluid, lymph node aspirate, blood, bone marrow, or CSF, history of travel & fly-bite, symptoms
-treatment: Suramin or Pentamidine (acute), Melarsoperol (CNS)
Trypanosoma cruzi
-causes Chagas’ disease (Latin America)
-morph: epimastigote (insects), amastigote (human tissue), trypomastigote (human blood)
-epidemiology: w/inc pop mvmt, possibility of transmission via blood transfusion inc in U.S.
-lifecycle: Triatomine bug bites near eye  defecates  rub eye  push trypomastigotes into body  turn into amasitgotes  multiply via binary fission  turn into trypomastigotes  enter bloodstream  Triatomine bug bites  ingests trypomastigotes  epimastigotes  multiply  trypomastigotes  passed in feces
-clinical manif: edematous skin plaque at lesion site = chagoma, acute stage: lymph nodes & heart, chronic stage: hollow organs, cardiomegaly, megaesophagus, megacolon
-diagnosis: history of travel, cardiac problems, chagoma, I.D. org in lesion, lymph, or blood
-treatment: Nifurtimox (acute), Benznidizol (chronic), high toxicity, incomplete cure
-causes leshmaniasis
-morph: promastigote (sand fly, flagellum, infective stage), amastigote (mammals)
-lifecycle: Sand Fly takes blood meal  inject promastigote  phagocytized by macrophages  turn into amastigotes inside macrophage  multiply  Sand Fly takes blood meal  ingests macrophages infected w/amastigotes  turn into promastigotes  multiply
-clinical manif: visceral: liver, spleen, lymph nodes, chills, fever, darkening skin, cutaneous: papular lesion, heals spontaneously, scars, mucocutaneous: lesion doesn’t heal, necrosis of mucoid tissue, very disfiguring to face
-diagnosis: lesions, symptoms, ID org in lesion
-treatment: Pentosam (antimony gluconate)
Toxoplasma gondii
-causes toxoplasmosis
-lifecycle: ingest fecal oocyts (cats) or tissue cysts (undercooked meat)  tachyzoites  localize in neural & muscle tissue
-clinical manif: asymptomatic, flu-like illness, lymphadenopathy, CNS (immunodeficient pts) congenital if mom infected during pregnancy (passes through placenta)  ocular infection
-diagnosis: isolate tachyzoites from blood or lymph, PCR, serologic testing
-treatment: not needed for healthy non-pregnant person, otherwise Pyrimethamine
-causes malaria
-morph: trophozoite, schizont, gametocyte
-lifecycle: 3 stages: (1) Exo-erythrocytic (liver), (2) Erythrocytic (blood),
(3) Sporogonic (sexual, insect, but insect isn’t the definitive host, the human is)
-clinical manif: fever & chills (3 stages: cold  hot  sweating), headache, myalgia, weakness, vomiting, diarrhea, splenomegaly, anemia, pulmonary/renal dysfunction, CNS
-diagnosis: travel history, symptoms, blood
-treatment: Quinine
Ascaris lumbricoides (roundworm)
-intestinal nematode
-lives in upper part of small intestine
-epidemiology: most prevalent in Asia (China, India), rural SE U.S. (Kentucky, Tennessee), children 4-14 yrs, largest nematode (in human)
-lifecycle: direct, eggs ingested by host and hatch in small int  juveniles penetrate tissues of int & enter blood  migrate to lungs then alveoli  coughed up  swallowed  finish development in small int  females prod eggs  passed through host feces  juveniles in eggs mature to infective stage
-diagnosis: microscopic I.D. of eggs in stool
-clinical manif: stunted growth (children), no acute symptoms (adults), ab pain, intestinal obstruction, pulmonary symptoms
-treatment: Albendazole or mebendazole, note: Vitamin A supplements improved growth but de-worming did not
Enterobius vermicularis (pinworm)
-intestinal nematode
-lives in cecum & adjacent areas of large & small intestine, female comes out through anus at night and deposits eggs perianally
-epidemiology: crowded conditions, children 5-10 yrs, most prevalant helminth infection in U.S., more common in temperate climates
-lifecycle: direct, ingest eggs w/infective juveniles  hatched in small int  worms migrate to large int  reach sexual maturity  females crawl out of anus & deposit eggs on perianal skin  eggs hatch  can crawl back into body through anus or eggs become infective and passed via hands, bed clothes, etc
-diagnosis: nocturnal observation perianally, scotch tape test, very characteristic eggs (ovoid & flattened on one side*, thin walled)
-clinical manif: asymptomatic, perianal pruritus esp at night  secondary infections if you scratch too much & push in through skin
-treatment: Albendazole, treat family & school
Strongyloides stercoralis
(card 1 of 2)
-intestinal nematode
-causes Strongyloidiasis, no male worm
-clinical manif: asymptomatic chronic disease of GI tract, can be undetected for decades, if put those pts on steroids for asthma or COPD the org goes into hyperinfection mode and larvae disseminate to extra-intestinal organs (high mortality rates ~87%)
-epidemiology: almost all deaths in U.S. due to parasites are due to this parasite, most prevalent in SE Asia, sub-Saharan Africa, & Latin America, pockets of endemicity in Western countries, in SE U.S.
-lifecycle: free living or in host, (1) female in intestinal mucosa  eggs hatch in intestine  juveniles passed in feces  molt  infective juveniles (filariform larvae) & free-living juveniles (rhabditiform larvae)
(2) infective juveniles  penetrate skin of host  enter blood  migrate to lungs  coughed-up & swallowed
(3) free-living juveniles  if don’t find a host  become adult males & females  sexually reprod eggs  juveniles hatch
Wuchereria bancrofti
-blood/tissue nematode
-epidemiology: tropical areas
-lifecycle: indirect, mosquito vector, mosquito bites  larvae enter bite wound  adults live in lymphatic sys  larvae migrate into blood  mosquito bites infected human  ingests larvae
-diagnosis: I.D. microfilariae at night b/c of nocturnal periodicity of infective form, but antibodies present all day not just at night
-clinical manif: asymptomatic, acute lymphadenitis & filarial fevers, elephantiasis
-treatment: (1) interrupt transmission w/Albendazole, (2) alleviate & prevent disability w/lymphoedema management
Schistosoma (Blood fluke)
-trematodes, flat, nonsegmented, obligate parasites
-causes Schistosomiasis, ranks 2nd behind malaria in public-health importance
-epidemiology: developing countries, children under 14
-characteristics: dioecious, found in blood in pairs, female lives in gynaecophoric canal in male, gets nutrients from male via tegument
-lifecycle: not direct, snail vector, eggs passed in feces/urine  hatch in water  miracidia stage enters snail  sporocyts  circariae larvae w/bifurcated tail  penetrates skin of host  schistosomulae  enter blood  migrate to portal blood in liver  mature  adults move to venules of bowel/rectum  lay eggs  passed in feces
-diagnosis: I.D. eggs in stool/urine, antibodies
-clinical manif: worms not pathogenic, eggs are pathogenic, skin penetration of cercariae  allergic dermatitis at entry site, adult  enlargement of spleen & liver, Katayama fever from immune response to egg antigen
-treatment: Praziquantel
-vaccine: surface mem turnover hypothesis: con’t renews surface to evade immune sys
Fasciolopsiasis buski (Intestinal fluke)
-trematodes, flat, nonsegmented, obligate parasites
-causes inflammation, ulceration, mucous secretion at site of attachment (duodenal & jejunal mucosa)
-epidemiology: China, Thailand, India
-lifecycle: eggs passed in feces  hatch  free-swimming miracidium  enters snail  asexual reprod  cercariae leave snail & prod metacercariae on vegetation  eat veggies  mature adult in small intestine
-diagnosis: I.D. eggs
-prevention: cook/wash veggies thoroughly
-treatment: Praziquantel
Clonorchis sinensis (Liver fluke)
-trematodes, flat, nonsegmented, obligate parasites
-live in bile duct & liver up to 30 yrs!
-epidemiology: China, Japan, Korea, Vietnam, up to ¼ Chinese immigrants to US
-diagnosis: I.D. egg in stool
-lifecycle: eggs passed in feces into water  miracidium hatches from eggs  infects snail  cercariae leave snail  penetrate skin of fish  becomes metacercariae  eat raw or undercooked fish  get into small intestine  goes to bile duct to mature
-clinical manif: inflammation & intermittent obstruction of biliary ducts, GI symptoms
-treatment: Praziquantel
Paragonimus westermani (Lung fluke)
-trematodes, flat, nonsegmented, obligate parasites
-reddish brown color, thick-bodied worms, animal reservoirs (fox, tiger, pig, dog, cat)
-epidemiology: E.Asia, Americas, Africa
-lifecycle: indirect, 2 intermediate hosts, eggs leave via feces or sputum  enters snail  sporocysts  rediae  cercariae  invade crustaceans  become metacercariae  humans ingest undercooked crustaceans  excyst in duodenum  lay eggs in lungs
-diagnosis: I.D. eggs in stool/sputum 2-3 months after infection, biopsy
-clinical manif: acute (diarrhea, ab pain, fever, cough, hepato-spleenomegaly, urticaria (hives), eosinophila), chronic (pulmonary, cough, discolored sputum, hemoptysis (cough-up blood))
-treatment: Praziquantel
Strongyloides stercoralis (card 2 of 2)
-diagnosis: stool, difficult to find, eosinophilic, plate in beef broth  see motile tracks in agar
-clinical manif: unremarkable, nonspecific, GI (abdominal bloating), skin lesion (larva currens), pulmonary symptoms, in hyperinfection: alveolar hemorrhage, bacterial infections b/c leakage of gut flora, septicemia, pneumonia, meningitis, 87% mortality
-treatment: Ivermectin, Thiabendazole, have to kill 100% of the worms b/c even 1 female can keep producing eggs (unlike other worms)