Protozoan Infections Flashcards
acanthamoebic keratitis caused by
acanthamoeba castellani
non arthropod amoeba
epi acanthamoebic keratitis
worldwide air soil water
accidental human infection
life cycle acanthamoeba castellani
in fresh water it multiplies as amoebas forming cysts which can revert back to amoebas in soil
which part of cycle damages humans of acanthamoeba castellani
and what does it damage
both amoebic and cystic forms
- lungs eyes skin uterus following exposure to soil swimming how tubs OR CONTACT LENSES
how does acanthamoeba castellani damage eyes
it has to enter through a DAMAGE in the eye tissue, like chlorinated pool/ eye infection
it loves pseudomonas! which is often found in contact solution
acanthamoebic path
what plays a role in infection
characteristic***
bacterial confection (pseudomonas)
enzymes released by amoebas causes a characteristic stromal infiltrate in the shape of a ring within the eye**
acanthamoebic immunity?
antibody dependent dependent cellular rxn (lymphokines and opsonization of amoeba by antibody)
no partial immunity
s/s acanthamoebic immunity
what do you have to keep in mind
uveitis, optic neuritis corneal keratitis
can lead to granulomatous amoebic encephalitis in immunosuppressed patient!
skin lesions present as ulcers, nodules or accesses
dx acanthamoebic*
amoebas or star like cysts in tissue exudates
tx acanthamoebic
propamidine
trichomoniasis cause by? description
trichomonas vaginallis
non arthropod flagellated protozoan
trichomoniasis reservoir
humans only
its the only definitive host
bad thing about trichomonas
they can survive 1-2 hours on moist surfaces
viable up to 24 hours in urine or semen
life cycle of trichomonas
transmitted by sexual contact OR droplets on contaminated fomites
no cyst stage*
can live in vagina and prostate of humans and are passed directly to uninfected person
path trichomonas
damage is caused by the proliferation of colonies in vagina or Urinary tract
it c causes destruction of epithelial cells causing infiltration inflammation vaginitis
s.s trichomoniasis
vaginitis with frothy green yellow vaginal secretions
foul odor and intense irritation
urethritis and petechiae
male- urethritis, prostatitis or sterility
(1/2 are asymptomatic)
dx trichomoniasis
pyriform flagellated moline trophozoites in vaginal or wet preparations
tx trichomoniasis
metronidazole
tx all sex partners
but 3-4 weeks it self cures
leishmaniasis caused by
leishmania braziliensis
leishmania donovani
leishmania mexicana
leishmania tropica
leishmania tropica location
africa asia europe
leishmania donovani location
africa asia europe and south americal
leishmania braziliensis and mexicana location
central and south america
humans and non humans as reservoirs
how is leishmania transmitted
direct contact with infected tissue
congenitally from mother to child d
leishmania vector
amastigote v trypomastigote
biting female sand fly
amastigote- no flagella
trypomastigote- flagella
life cycle of leishmania?
sandfly ingest macrophages containing amastigote (no flagella) from infected person or animal
amastigote develops into trypomastigote in sandflies which are infected into new host
trypomastogote enters macrophage and turns into amastigote to replicate and multiply in tissues
incubation leishmania
cutaneous- weeks to months
visceral- weeks to years
path leishmania
infiltration of lymphocytes and plasma cells result in hyperkeratosis, necrosis and ulceration of skin and mucoid membrane
which leishmania is visceral
leishmania donovani- they are distributed throughout the reticuloendothelial system by macrophages
immunity leishmania
protective immunity to SPECIES that causes infection!
leishmania tropica ss
papules nodules and scars on skin
leishmania brazilensis and tropicana s s
ulcers on skin and mucous membranes
leishmania donovani s s
fever edema anemia diarrhea weakness conjunctivitis keratitis photophobia
THEIR ORGANS GET HUGEE
dx leishmania
biopsies of organs (tissue and bone biopsy) and skin
- shows intracellular amastigotes
tx leishmania
antimony sodium gluconate
Schistosome dermatitis
by
AKA
by schistosome species (trematode)
aka swimmers itch
leishmania reservoirs*
cattle
dogs
rats
SLOTHS
schistosome dermatitis
caused by
AKA
schistosome species
aka swimmers itch
epi schistosome
host
intermediate host
dead end host
found in fresh or salt water
animals or birds are reservoirs and definitive hosts
intermediate- snail
humans- dead end host
life cycle of schistosome
adult worms live in blood vessels of animals and birds– release eggs via poopy
miracidia hatch and penetrate snails – which develop into cercaria
cercaria penetrate the skin of humans when contact is made
in humans which life cycle of schistosome do we have>?>
Cercaria*
(they Never turn into adult worms)
they just live under the skin but don’t enter the blood vessles
path schistosome
the proteins of cercaria induce inflammatory response in skin– producing serpiginous tunnels where they die
immunity/ sensitivity schistosome
delayed hypersensitivity
no immunity
s/s schistosome
tunnel lesions ==
vesicles papules and hemorrhagic rash that can elead to secondary bacterial infections
lesions go away but sensitivity is present
dx schistosome
observation of symptoms
finding of larva in tissue biopsy
tx schistosome
antihistamines