Trypanosomes Flashcards
two diseases caused by trypanosoma?
chagas disease and african sleeping sickness
once kinetoplastids infect you (trypanosoma/leishmania)….
you are infected for life
kinetoplastids are found
in the blood (different forms w flagella or no flagella)
the kinetoplast structure? function?
contains DNA organized into minicircles and maxicircles similar to mitochondrial DNA function and need for etensive posttranslational editing is unknown in close association with the basal body in the base of the flagellum
trypanosoma cruzi vector? parasite form in vector? parasite form in blood? parasite form in tissue? distribution?
triatomine bugs epimastigote, metacyclic tryp trypomastigote amastigote americas
trypanosoma brucei vector? parasite form in vector? parasite form in blood? parasite form in tissue? distribution?
tsetse fly epimastigote, metacyclic tryp trypomastigote extracellular sub-saharan africa
leishmania vector? parasite form in vector? parasite form in blood? parasite form in tissue? distribution?
sand fly promastigote - (blood) amastigote global except australia
trypanosoma lifecycle
remale reduviids prefer to lay eggs…
in cracks crevices
high in rural/poor housing
transmission of trypanosomes
animal reservoir for trypanosomes/reduviids = rats,, racoons, skunks, dogs
human-human via blood transfusion/organ transplant
sugarcane juice, guava juice, acai juice
in chagas disease, what kills you?
heart disease
how many people in US infected w chagas disease?
300,000 with T cruzi
phases of T cruzi infection
romana sign
eye infection
T cruzi acute phase infection
acute chagas disease
febrile; can cause myocarditis and meningoencephalitis
romanas sign = unilateral painless periorbital edema
indurated lesion at site of parasite entry = chagoma
1-2 weeks incubation
**amastigotes in heart muscle
After a stage of initial parasitemia, trypomastigotes pass to the cardiac muscle and smooth muscle lining the intestinal tract. Here they transform into the amastigote
stage. In the heart, this causes myocarditis in the early stages.
amastigote vs trypomastigotes
Amastigotes are intracellular form with short/no flagella
trypomastigotes travel in blood and have long flagella
t cruzi strains 1 vs 2
type 1 strains are LESS pathogenic than type 2
type 2 occur in southern south america and are human/peridomestic types
type 1 are sylvatic
congenital chagas
1-10% of + mothers will past to baby
–severe respiratory distress, meningoencephalitis, hepatosplenomegaly, or myocarditis
ekg findings from chagas
conduction issues!
-widened QRS
RBBB (right bundle branch block)
chronic chagasic cardiopathy
80% of chronic chagas disease causes heart disease!
conduction issues, arrhythmias, sudden cardiac death, heart failure, thromboembolism, aneurysms
chagas GI disease
mega-esophagus or mega-colon (chagasic colopathy) / distended belly
severe constipation and difficulty swallowing
(disrupted autonomic fx)
reactivated chagas disease
in immunocompromised host
CNS abscess-like lesions (ring enhanced)
meningoencephalitis
acute myocarditis
febrile episodes + transplant rejection
panniculitis
diagnosis of acute chagas
blood smear
peripheral blood will show C shaped trypomastigote with prominent kinetoplast
diagnosis of chronic chagas
T cruzi specific antibody (IgG)
–use 2 different serologic test with 2 different antigens
chagas treatment
benznidazole (1st line) and nifurtimox
*not FDA approved; get from CDC
very effective for acute phase! less for chronic
sleeping sickness - other name?
african trypanosomiasis
african sleeping sickness outlook
300-500K infected in africa–> FATAL infection (death in 2 years)
very toxic drugs with increasing resistance
HAT = human african trypanosomiasis
epidemiology?
subsaharan Africa
T.b. gambiense (west coast)
T.b. rhodesiense (east coast)
east african trypanosmiasis (rhodes) is more common in travelers; BUT west (gambi) is more common in endemic populations
what do tourists do in east africa to get HAT?
safari!!!!
it is a zoonosis
very aggressive biting fly! (tsetse)
vector for HAT
tse tse fly (glossina species)
G.palpalis breeds along rivers, streams, lakes (West Africa)
G.morsitans breeds in wooded savannah (East Africa)
*charateristic cleaver wing
what explains the persistence and resistance of trypanosomiasis
antigenic variation/change!
it changes its dense coat of variant surface glycoproteins (VSG)
-variant clones that express an alternate VSG gene lacks antigenic cross-reactivity and persists!
east and west HAT comparison
presentation and progression of HAT
fatal if untreated
infected tsetse fly bite –> parasites injected and replicate into blood (haemo-lymphatic stage) -> fever, itching, headahces, myalgias, hepatomegaly, anemia
winterbottoms sign = posterior cervical adenopathy
–> meningoencephalitic stage
winterbottoms sign
posterior cervical adenopathy
sign of HAT
rhodesiense (east) vs gambiense (west) prognosis
Rhodes –> death in weeks to months, fulminant illness, shock–> death may occur before CNS invasion occurs
Gambiense –> early stage unrecognized, CNS invasion after 1-2 years –> death due to coma/malnutrition
what do you see in CSF when sleeping sickness is being diagnosed?
lymphocytes!
PSG syndrome of sleeping sickness
(PSG = polysomnography)
An alteration of the normal distribution of sleep and wakefulness, proportional to the severity of symptoms.
An alteration of the structure of sleep episodes, with the abnormal occurrence of REM sleep.
travelers with sleeping sickness do not present with
sleeping issues
usually just an acute febrile illness
lumbar puncture for HAT/sleeping sickness will show…
CSF with elvated wBC, IgM, total protein, ICP
and
MOTT cells = large eosinophilic plasma cells that have failed to secrete their antibodies
MOTT cells in CSF indicate
afircan sleeping sickness
HAT/sleeping sickness treatment
early gambiense?
late gambiense?
early rhodes?
late rhodes?
EG = pentamidine
LG = eflornithine + nifurtimox
ER = suramin (doesnt cross BBB)
LR = melarsoprol (arsenical = very toxic)
