kinetoplastids- trypoanosoma cruxi and leshimania Flashcards
what does trypanosoma cruzi cause
causative agent of chagas diseas with approx 8 million infected and more than 100 million at risk
- leading cause of cardiac diseas in sentral and south america
what did chagas determine
man who discovered the parasite
- parasite life cycle
- that it was a zoonotic disease
infects more than 150 species of mammals including humans
how is trypanosoma cruzi spread
vector born parasite from kissing bugs aka genera triatoma, rhodnius and panstrongylus
aka assassin bugs or triatomine bugs
1) bugs feed on blood
2) parasite transmitted in bug faeces unlike trypansoma gambinease or rhodanaisea which is by saliva
3) faeces holds trypomastigotes which penetrate mucous membranes ect
what are the other less common ways of spreading trypanosoma cruzi
blood transfusion
organ tranplant
contamination of food and drink
transplacental transmission from mother to baby
outline and describe the 3 phases which occur when infected with trypanosoma cruzi
1) acute - can last 4-8 weeks and go away
- romanas sign which is swelling of the eye usually at the bite site or where faeces rubbed into the eye
- fatique, fever, swollen liver and spleen, vomiting
- infants can cause encephalitis
2) intermediate
3) chronic- develops 10-20 yrs after infection
- especially prelevant in immunosuppresant individuals
- enlarged heart
- extensive fibriosis of heart muscles, megacolon (swollen digestive tract)
outline some of the chronic symptoms which occur after infection of trypanosoma cruzi
45% of pateints experience enlarged heart, fibrosis of heart muscle and heart failure
20% experience swollen oesophagus and digestive tract and sever constipation and difficulty swollowing
outline the cyclical spread of trypanosoma cruzi
1) enter via bite wound, mucous membranes or hair follicals
2) trypanomastigotes enter blood stread and are non-dividing entering different cell types e.g. liver, lymph nodes
3) trypomastigotes invade cells and convert to amastigotes which replicate by binary fission in cytoplasm forming pseudocysts
4) amastigotes convert to trypomastigotes when leaving cell and cycle continues or they enter new vector during feeding
5) trypomastigotes transform into epimastigotes in the midgut of vector
outline the different life morphologies of the kinetoplastid in species trypanosoma cruzi
1) epimastigotes multiply by binary fission as they pass into hindgut and attach to epithelium of rectal gland where they differenciate into
2) trypomastigotes which remain in the lumen of rectum awaiting excretion
3) amastigotes occur once parasite enters host cell
why cant epimastigotes invade host cell
they are lysed by host complement and therefore are non infective for the host where as tyrpomatigotes are more mature and can infect the host by avoiding immune system
compare modes of vector transmission between parasites trypasoma brucei and trypanosoma cruzi
brucei= transmitted via mouth parts, transmitted via saliva
- more efficient as being directly deposited into blood
- lower infection rate in vectors as few naturally infected
cruzi= transmitted via hindgut and by contaminated bug faeces
- ineffcient as parasite must find entry route into host
- infection rate higher in vectors
why is there a low transmission efficiency for trypansoma cruzi
inefficent as parasite not direclty depositied into host has to find entry which means that considerable contatc between humans and vectors is needed for infection to occur as repeated feeding over long periods of time allows for tranmission
- only possible as bug infects human habitats and not really found in wild
- prevelant in rural and disadvantaged communities
how can trypansoma cruzi be diagnosed early
1) microscope and giemsa stain
2) detected by PCR
3) chronic disease confrimed by finding parasite antibodies in host blood
what is xenodiagnosis and how can it be used to diagnose trypanosoma cruzi
expose patient to a parasite free vector and see if the parasite then becomes present in the vector
- using another species to diagnose a person
how can chagas disease be treated
1) using benznidazole and nifurtimox, the efficacy decreases the longer the person has been infected
- acute 50-80&
- chronic 20-60%
what is leishmania
a parasite which can either be cutaneous or viceral
88 countires affected mostly in tropics and subtropic but also in south europe
350 million individuals at risk
what vectors transmit the parasite leishmania
sandflies
1) lutzomyia - new world, southeren texas to northern argentina
2) phlebotomus- old world asia, africa, middle east and mediterranean
the flies make little noise and bites dont hurt so hard to tell you have been infected
what factors help determine the form of leshimania disease
1) the species and geographic region
2) immune responce of the host
3) which definitive host is infected
what are the symptoms of cutaneous leishmaniasis
- skin lesion and ulcers produced on parts of the body where sandflies feed
- can be up to 200 lesions
- lesions cause disability and leave patient permanently scared and can cause partial or total destruction of mucosal membranes of nose, mouth and throat cavities
what are some symptoms of viceral leishmaniasis
aka kala azar
irregular bouts of fever, weight loss, swelling of the spleen and liver and anaemia
major coinfection in people with HIV and AIDS
how have cases of leishmaniasis and HIV been thought to be co-infected
HIV destroyed immune responce allowing many faculative and opportunistic parasites to become more apparent
HIV has allowed the study of a range of parasites we didnt know were there at the time
outline the lifecycle of leishmania
1) sandflies become infected by feeding from infected reservoir host of from infected people
2) promastigotes are phagocytized by macrophages from immune responce and transform into amastigotes
3) replication within macrophage to produce pseudocyst full of amastigotes which are released
4) follwing ingestion from vector amastigotes transform to promastigotes in midgut of vector
5) pro,astigotes pass to fly mouthparts
how to diagnose leshmania
examine biopsies- microscopic examination of amastigote in spleen and bone marrow
culture biopsy material to allow proliferation of promastigotes
PCR on blood
animal inoculation to allow development
how can leshmania be controlled
- depends on local transmission
- avoid bites using insecticde treated nets
but this may affect wide range of habitats and non target species - destruction of reservoir hosts
vaccination= side effects
how to treat leishmaniasis
1) cryotherapy
2) infiltration of sodium stiboglyconate
3) heat therapy at 40-42 degrees
4) tropical antibiotics and urea mixtures
