hemo Flashcards
T cruzi Disease
Chagas
Tcruzi group
Stercoraria
T crusi mulitply host manner
discountinous
Tcrzui most heavily infrcted cells
Myocytes and reticuloendothelial system
T cruzi vectors
Reduviid Tratoma, Panstrongylus, Rhodnius
T cruzi stages of deevlopment
Amastigote, Promasitote, epimastigote, trypomastigote
Tcruzi stage in bloodstream
Trypomastigote
T crusi stage in tissue cells
Amastigot
T cruzi stage in vevtor midgut
aastigote, epimastogote, promastigote
Tcruzi stage in hindgut
metacyclic trypomastigotes
what parasite and stage oosterior pointed, 2/3 undulations, threadlike flagellum, C U S shaped
Trypomastigotes
T cruzi trypomastigote charactersitic of species
kinetoplast
Tcruzi location where thye multiplu
Macrophages
Tcruzi method of multipliation
hbinary fission as amastigotes
Tcruzi transmission
bite broken skin mucous mebrane
Tcruzi disease stages
acute and chronic
T cruzi acute phase
inflammation of myocardium, fever malaise, lymphadenopathy, Chagomas, Romanas sign
Chagomas
furuncle lile lesion, central edema lympahdenopathy
Romanas sign
Conjunctivities, bipalpebral edema
T cruzi chronic stage
friboic resctions injure myocsrdium, cardiac conduction system p, enteric nervous system
T cruzi chronic stage most affected organ
aheart
T cruzi chronic stage symptoms
cardiomegaly, arrhytmnia, paliptations, GIT form=achalasia due to emegaesphagus, cosntipation due to megacolon 1/3rd affected
T cruzi disease diagnosis
compelte patient hsitory
T cruzi disease definitive diagnosis
visualize parssites in blood smears using giemsa stain, only in 1st 2 months
T cruzi diagnosiis in chronic stage
elisa, hemaglutination , pcr
t cruzi disease cardiac diagnosis
ECG atrial fibrillation, low QRS voltage, cardiomayipathy
T cruzi. disease GIT diagnosis
barium esophagogram, barium enema
Tcruzi treatment and sideeffects
nifurtimox ( weight loss anorexia behavioral changes) and benznidazole (rashes, bone marrow suppression, neuropathy)
nifurtimox moa
oxidative radicals, dna synthesis
T cruzi disease epidemiology
chagas disease, 10 mil worldwide, latin americas, inwho list pf. eglected diseases
Tbrucei gambiense and rhodesiense disease
HAT african sleeping sickness
T brucei family
Salivaria
T brucei vector
Tsetse fly Glossina
T brucei gambiense localise, affects, epidemiology
western pand central subsahara, humnas, reservoir dogs pigs sheep, 95%
T brucei rhodesiense localize, affects, epi
east sfrica, cattle and wild animlas, humans aciddntal, more rapid and fatal 5%
T brucei stages
epimastigot and trypmastigote
T brucei location in body
Bloom lymph and spleen CSF
what parasite and stage selnder, stumpy, flattened and fusiform, large central karyosome, undulatingmembrane, flagellum
trypomastigote
HAT initial lesion
chancre, then eschar, more common in gambiense
HAT 2 stages
hemolymphatic stage and meningocephalic stage
HAT hemolymphatic
fever headache, muscle pain malaise, anemia myocsrditis
lymph nodes enlarged nontender rubbery
Winterbottoms sign HAT gambeiense
HAT hemilymphatic reason
damage in tissue due to toxins or immune reactions
HAT meningoecephalitic
CNS symotms, headache, sleep,apathy, behavour, convuslions speech defects, paralysis
deep delayed hyperesethsia
kerandals sign HAT meningocephalitic
Continously changing surface proteins
antigenic variation T brucei
T brucei diagnosis
trypanosomes in chancre, lymph, CSF, blood
T brucei pathognomic for meningoencepahlitic stage
increased IgM levels
T brucei diagnsotic test
Card agglutination test
T brucei treatment and efects
Suramin sodium for both (fever, rash, renal insufficiency, muscle pain), pentamidine for gambiense (tachycardia hypoglecemia hypotension), melarsoprol for CNS (fatal arsenic ecncephalopathy)
Melasroprol second line drug
Nitrofurazone and eflornithine
Melarsoprol reaction
Jarsih Herxheimer reaction febrile epsiode
T brucei epidemiology
300,00.in subsaharan africacatt
e and game animals like antelopes are reservoir animlas
Leishmania 2 types
New world (amazonensis, barziliensi, mexiacana, guynensis, chaagsi) old world (tropica, aethipica, major)
Leishmania vector
Phlebotomus Lutzomyia sandfly
Leishmania primary reservoirz
Dogs and rodents
zleihsmania in mammalian host
amastigote
Leishmania in vector
promastigote
what stage and parasite ovoid bodies, live in monocytes, leukocytes, large nucelus,axoneme srise from kinetoplast
Amastigote Lesihamnia
what stage and parasite ssingle free flagellum from kinetoplast, invade reticuloendothelial cells
promastigotes zleishmania
leishmania diseases
CL, DCL, MCL VL
Lieshmania immune system response
Leishamnia specific Th1 type CD4+ Tcells, macrophages, cytokines
zlishamnia most common form
CL
erythematous papul or nodule / orientsl button
CL lesihkaniasisis
Chiclero ulcer in ears
L. mexicana
Leptomatous keishmania, localized, non ulcersting papule
DCL
In 2-5% L braziliense, mucous mmebranes
MCL
Nasal stiffiness, discharge, esoitaxis, destruction od nasal septum
Espundia, MCL
Kala azar, by L donovani complex,
VL
VL cause
spread in spleen liver bone marrow
Twice daily fever spikes, chills
acute VL
hepatosplenomegaly efever weakness loss of appetite
Subacute chronic VL
MCL Th1 response
Strong
VL th1 response
low absent
Hypopigmented macules, amlar erythema, nodules, ulcerations
post kala azar dermal leishmaniasis
leishamnia diagnosis
amastigotes in lesions, tissue biopsy
Lieshmania skij test positive in , negative in
CL MCL, DCL VL
Leishamnia treatment
sodium stibogouconate, meglumine (abdmonial pain, nausea, arthralgia, arrythmia), drug of choice is amphotericin B, Miltefosine in VL patients
Lieshamnia disease of poverty
squalid, poor housing malnutrition, weak immune system, lack of resources
coinfection leishmania
HIV/VL
Leishamnia prevention
repelents DEET and permethrin, no chemoprohpylaxis