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142 Cards in this Set
- Front
- Back
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how do amoeba move?
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by extending cytoplasmic protrusions (pseudopodia)
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what are cytoplasmic protrusions of amoeba called?
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pseudopodia
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what refers to the motile, feeding stage of amoeba?
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trophozoite
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non-motile resting stage of amoeba resistant to environmental effects?
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cyst
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which parasites are irregular and consistently changing shape?
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amoeba
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which amoeba is the only pathogen?
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entamoeba histolytica
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what is the mode of transmission for amebiasis?
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ingestion of cysts via fecal-oral contamination of fruits, vegetables, water
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what are the clinical syndromes for amebiasis?
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intestinal and disseminated
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what are the characteristics of intestinal amebiasis?
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can be asymptomatic or cause amoebic dysentery (diarrhea with cramping and abdominal pain)
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what are the characteristics of disseminated amebiasis?
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hematogenous spread to liver (most common), spleen, lung, brain with 'anchovy-pastelike' abscesses
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which form of entamoeba histolytica is most commonly found in watery stools?
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trophozoites
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what does trophozoites in stool indicate?
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active infection
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which form of entamoeba histolytica is most commonly found in formed stools?
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cysts
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what do cysts in stool indicate?
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quiescent infection
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where does amebiasis have a higher incidence?
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developing countries
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who is at risk of amebiasis in industrialized countries?
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male homosexuals, travelers, recent immigrants
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what is most pathogenic parasitic infection in humans?
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giardiasis
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how is giardiasis transmitted?
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contaminated water and sometimes food
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what organism causes giardiasis?
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giardia (intestinalis) lamblia
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what makes the cyst of giardia particularly dangerous?
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cysts resistant to chlorine
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where does giardia reside in human?
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duodenum/small intestines
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what are clinical symptoms of giardiasis?
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mild to severe diarrhea, cramping, maladsorption
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the presence of red 'kite-shaped' intraluminal organisms indicates infection with what?
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giardia
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what organism causes cryptosporidiosis?
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cryptosporidium parvum
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how is cryptosporidiosis spread?
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fecal contamination of food or water
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what makes cryptosporidium difficult to eradicate from contaminated food or water?
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chlorine is ineffective
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presence of acid-fast oocysts in stool is diagnostic of what condition?
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cryptosporidiosis
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what are the clinical symptoms of cryptosporidiosis?
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abdominal pain, watery diarrhea (severe in immunocompromised) leading to dehydration, wt loss, fever, nausea, vomiting
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where does cryptosporidium typically infect?
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small intestine, but possible digestive tract, lungs, conjunctiva
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which organism attaches to brush border and promotes engulfment?
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cryptosporidium
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what promotes oocyst of cryptosporidium to release sporozoites?
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acid
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what is the segmented, flattened tapelike body of the tapeworm called?
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storbila
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specialize attachment organ of tapeworm?
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scolex
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crown of scolex, which may have hooks, of tapeworm?
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rosteilum
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each segment of the tapeworm is hermaphoroditic and referred to as?
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proglottid
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the fish tapeworm?
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diphyllobothrium latum
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which tapeworm competes with the host for vit B12?
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diphyllobothrium latum
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where is diphyllobothrium latum found in the human?
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small intestine
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what does cestode refer to?
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tapeworm
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pork tapeworm?
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taniea solium
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beef tapeworm?
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taniea saginata
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what is cysticercosis?
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when larvae migrates into brain, eye, or muscle and encysts
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how can tell taniae eggs apart?
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can't, look very similar
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what is the difference in proglottids of t. soleum and t. saginata?
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the number of uterine branches; solium has <12, saginata has >12
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what organism causes hyatid disease?
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echinococcus granulosus/multilocularis
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what are the definitive and intermediate hosts of echinococcus granulosus?
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definitive = dog; intermediate = sheep
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what are the definitive and intermediate hosts of echinococcus multilocularis?
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definitive = fox; intermediate = rodent
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what are clinical manifestations of hydatid disease?
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jaundice (cysts in the liver), cough, hemoptysis, seizures/increased cranial pressure from brain cysts
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what is a danger of cysts from hydatid disease?
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rupture with following anaphylaxis
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what is the disease process of echinococcus?
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penetrate intestines --> travel to different organs --> form hydatid cysts
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what is the most common location of hydatid cysts?
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liver
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where is hydatid sand found?
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at the center of hydatid cysts
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what is hydatid sand made of?
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degrading hooklets
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chinese or oriental liver fluke?
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clonorchis sinensis
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where is clonorchis sinensis found?
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endemic in asia (korea, china, taiwan, vietnam); rare in US
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how is clonorchis sinensis acquired and what phase is the parasite in?
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eating undercooked or pickled freshwater fish containing metacercariae phase of the parasite
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what is the intermediate host of clonorchis sinensis?
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snail
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what is the general life cycle of clonorchis sinensis?
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eggs release miracidia --> develop in snail (sporocysts, rediae, cercariae) --> cercariae released from snail --> penetrate fish and encyst as metacercariae --> human ingests --> metacercariae excyst in duodenum
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what is the pathogenesis of clonorchis sinensis?
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inflammation and intermittent obstruction of biliary ducts
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what is characteristic of acute phase of clonorchis sinensis infection?
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eosinophilia, abdominal pain, nausea, diarrhea
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what is characteristic of chronic infection with clonorchis sinensis?
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cholangitis, cholelithiasis, pancreatitis, cholangiocarcinoma
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how diagnose clonorchis sinensis?
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observation of characteristic eggs (small, operculated) containing miracidium
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what phase of shistosoma is infectious from the environment?
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cercariae
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how acquire schistosomiasis?
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cercariae penetrate skin
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what is the life cycle of schistosoma outside the body?
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eggs released from infected individuals --> release miracidia --> penetrate snail and undergo further development --> sporocysts mature to cercariae --> cercariae released into water and are free living
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what is the life cycle of schistosoma upon encountering a human host?
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penetration and lose tail to become schistosomulae --> migrate to portal blood where mature into adults --> paired adult worms migrate to mesenteric venules to lay eggs --> eggs circulate to liver and are shed in stools
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where does schistosoma masonii migrate to?
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large intestinal mesenteric veins
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where does schistosoma japonicum migrate to?
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small intestinal mesenteric veins
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where does schistosoma haematobium migrate to?
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veins of urinary bladder
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what are clinical features of schistosomiasis?
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swimmer's itch; weeks later - fever, cough, abdominal pain, diarrhea, hepatosplenomegaly, eosinophilia
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what rare condition is associated with schistosoma japonicum?
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cerebral granulomatous disease caused by eggs in the brain
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what rare condition is associated with schistosoma masonii?
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granulomatous lesions around ectopic eggs in the spinal cord
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what rare condition is associated with schistosoma haemotobium?
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transverse myelitis with flaccid paraplegia
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what clinical conditions are associated with schistosoma haemotobium infection?
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pelvic pain, hematouria, urinary obstruction, urinary bladder squamous cell carcinoma
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continuing infections with schistosoma can cause?
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granulomatous reactions and fibrosis in affected organs
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how diagnose schistomiasis?
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microscopy of stool (s. mansonii/japonicum) or urine (s. haematobium); rectal (all) or bladder (s. haematobium) biopsy
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how differentiate schistosomas?
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+/- spine and its location
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which trematode has a lateral spine?
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schistosoma mansonii
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which trematode has a terminal spine?
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schistosoma haematobium
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which tematode has an absent spine?
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schistosoma japonicum
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oriental lung fluke?
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paragonimus westermanii
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where is paragonimus westermanii located?
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far east
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how is paragonimus westermanii acquired?
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ingestion of inadequately cooked or pickled crustaceans containing metacercariae
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what is life cycle of paragonimus westermanii in human body?
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excyst in duodenum --> migrate to lung where lay eggs --> aspirate to excrete in feces (possible to find in sputum but unlikely)
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clinical features of acute phase of paragonimus westermanii infection?
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diarrhea, abdominal pain, fever, cough, urticaria, heptosplenomegaly, pulmonary abnormalities and eosinophilia
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clinical features of chronic phase of paragonimus westermanii infection?
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pulmonary manifestations, cough, expectoration of discolored sputum, hemoptysis, chest radiographic abnormalities
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when are eggs of paragonimus westermanii demonstrated in stool?
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2-3 months post infection; will not be detected in early disease
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what does plasmodium cause?
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malaria
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what are characteristic clinical features of malaria?
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splenomegaly, periodic shaking chills as rbcs rupture, followed by spiking fevers, sweats, anorexia, and joint pain; leukopenia and normocytic anemia may also be present
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which species of malaria are most common?
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p. falciparum and p. vivax
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what is the infectious stage of plasmodium?
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sporozoite
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which stage of plasmodium infects rbcs?
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merozoite
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what is the extraerythrocytic cycle of plasmodium?
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sporozoites divide asexually in the liver into schizonts (filled with merozoites) --> merozoites infect rbcs
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what is the erythrocytic cycle of plasmodium?
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infect --> merozoites transform to trophozoites (feeding stage with ringlike shape followed by amoeboid shape) --> back to merozoites --> infect other rbcs or become gametes
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which plasmodium species is most severe and what are its clinical manifestations?
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p. falciparum; cerebral malaria, acute renal failure, severe anemia, ARDS
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how is diagnosis of malaria made?
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microscopy of blood smears
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what type of rbcs does p. falciparum infect?
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nondiscriminatory
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what morphology is expected to be observed in p. falciparum infection?
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head phone/double ring shapes in rbcs
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what type of rbcs does p. malariae infect and how long can recurrences be expected?
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older, smaller rbcs; mild recurring up to 40 years
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what type of rbcs does p. vivax infect and how long can recurrences be expected?
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large rbc; common relapse for next 5 years
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what blood group in AA is protective for p. vivax?
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Duffy
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what type of rbcs does p. ovale infect and how long can recurrences be expected?
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young rbcs, relapses up to 5 years
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which parasite is endemic to massachusetts?
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babesia
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how is babesia transmitted?
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from cattle and deer by deer ticks
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what are clinical manifestations of babesiasis?
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fever, sweats, headache, arthralgia, myalgia; severe will see jaundice, hemoglobinemia, hemolytic anemia
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what is babesiasis often misdiagnosed as and what is used to distinguish the infections?
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malaria; identical ring forms however babesia lacks pigment and occasionally forms four ring complexes (Maltese cross)
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which organism produces a high level of parasitemia and can vary in symptoms from asymptomatic to severe?
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babesia
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which organism is especially problematic in asplenic patients?
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babesia
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what organism is the model for filiariasis?
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wuchereria bancrofti
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what does infection with wuchereria bancrofti cause?
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lymphatic dysfunction leading to lymphedema and elephantiasis, typically of lower extremities; febrile lymphangitis and lymphadenitis episodes
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how is the diagnosis of wuchereria bancrofti infection made?
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identification of microfilariae in blood samples or, preferably, lymph node biopsies
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what is the infective form of wuchereria bancrofti?
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microfilariae
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what is important in treatment of those with filiariasis?
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antibacterial cream on wounds to prevent secondary bacterial infection as skin gets thin
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what is the amastigote form of leishmania?
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round or oval, about 2-5 um, intracellular, prominent nucleus and dark staining and bar-shaped structure
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what is the kinetoplast form of leishmania?
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includes very short flagellum
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what is the promastigote forme of leishmania?
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in insect vector, elongate with flagellum projecting from anterior end
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what cell does leishmania inhabit?
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macrophage
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what is characteristic of cutaneous leishmaniasis?
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multiplication of amastigotes may last months to life; usually confined to skin with raised papules, ulcers on exposed parts of body
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what are clinical characteristics of visceral leishmaniasis?
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persistent fevers with splenomegaly and pancytopenia
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how diagnose cutaneous leishmaniasis?
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aspiration of lesion edge
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what is the most common form of leishmaniasis?
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cutaneous
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what is preferred treatment for leishmaniasis?
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amphotericin B
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which cell type harbors amistagotes of leishmania?
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macrophages
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what is the vector for trypanosoma brucei?
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tsetse fly
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what is the vector for trypanosoma cruzi?
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cone nosed, nonflying Reduviid bug
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how are the trypanosomes able to evade the immune system?
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by shifting surface antigens during infection
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what linkage is cleaved in order to change glycoprotein coat?
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ethanolamine linkage is quickly cleaved by an enzyme
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what disease does t. brucei cause?
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African sleeping sickness
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what disease does t. cruzi cause?
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chagas disease originally in south america spreading to central america and US
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is t. brucei extracellular or intracellular?
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extracellular
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is t. cruzi extracellular or intracellular?
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intracellular
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how does the clinical progression of the trypanosomiasis related to the clinical signs of the disease?
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after 5-7 days the parasites switch to a new VSG conformation with peaks of infection every 7-14 days
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what is the overall cycle for t. brucei from vector to host and back?
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tsetse fly ingests trypomastigotes during feeding --> asexual reproduction in tsetse fly gut --> migrate to fly salivary glands --> transform to metacyclic trypomastigotes --> infected into host during feeding --> transform into trypomastigotes --> asexual reproduction in circulation --> tsetse fly feeds to ingest trypomastigotes
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what form of t. brucei is ingested by the tsetse fly?
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trypomastigote
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what form of t. brucei is the host infected with?
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metacyclic trypomastigote
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what are the clinical symptoms of t. brucei infection?
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early: high fever, weakness, constant headaches, pain in joints, rash, transitory edema; late: endocrine and cardiovascular disorder, abortion, kidney disorders; eventually: CNS invasion leading to lethargy, comatose state, eventually death
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what are the clinical symptoms of t. cruzi infection?
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acute: less than 5% suffer from anemia, loss of strength, nervous disorders, muscle and bone pain, heart enlargement and failure, then death after 3-4 wks of infection; chronic: megaorgan, cardiac symptoms, 27% mortality
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what is the overall cycle of t. cruzi?
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bug feeds on infected individual to ingest trypomastigote stage --> matures to promastigote in bug gut --> migrates to anus and transforms to metacyclic trypomastigote --> bug bites and defecates on host --> host inoculates wound, eyes, etc with parasite --> parasite becomes systematic and matures into amostigote phase --> penetrates smooth and cardiac muscle --> forms pseudocyst and undergoes binary fission --> multiplies until bursts and penetrates more tissue with some transforming into trypomastigotes entering bloodstream
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what form of t. cruzi is ingested by the bug?
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trypomastigote
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what form of t. cruzi infects the host?
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metacyclic trypomastigote
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what form of t. cruzi penetrates muscle?
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amastigote
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what is one of the few infectious causes of cardiovascular disease?
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t. cruzi
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