kinetoplastids- trypoanosoma cruxi and leshimania

Question 1

what does trypanosoma cruzi cause

Answer 1

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

Question 2

what did chagas determine

Answer 2

man who discovered the parasite
- parasite life cycle
- that it was a zoonotic disease
infects more than 150 species of mammals including humans

Question 3

how is trypanosoma cruzi spread

Answer 3

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

Question 4

what are the other less common ways of spreading trypanosoma cruzi

Answer 4

blood transfusion
organ tranplant
contamination of food and drink
transplacental transmission from mother to baby

Question 5

outline and describe the 3 phases which occur when infected with trypanosoma cruzi

Answer 5

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)

Question 6

outline some of the chronic symptoms which occur after infection of trypanosoma cruzi

Answer 6

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

Question 7

outline the cyclical spread of trypanosoma cruzi

Answer 7

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

Question 8

outline the different life morphologies of the kinetoplastid in species trypanosoma cruzi

Answer 8

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

Question 9

why cant epimastigotes invade host cell

Answer 9

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

Question 10

compare modes of vector transmission between parasites trypasoma brucei and trypanosoma cruzi

Answer 10

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

Question 11

why is there a low transmission efficiency for trypansoma cruzi

Answer 11

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

Question 12

how can trypansoma cruzi be diagnosed early

Answer 12

1) microscope and giemsa stain
2) detected by PCR
3) chronic disease confrimed by finding parasite antibodies in host blood

Question 13

what is xenodiagnosis and how can it be used to diagnose trypanosoma cruzi

Answer 13

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

Question 14

how can chagas disease be treated

Answer 14

1) using benznidazole and nifurtimox, the efficacy decreases the longer the person has been infected
- acute 50-80&
- chronic 20-60%

Question 15

what is leishmania

Answer 15

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

Question 16

what vectors transmit the parasite leishmania

Answer 16

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

Question 17

what factors help determine the form of leshimania disease

Answer 17

1) the species and geographic region
2) immune responce of the host
3) which definitive host is infected

Question 18

what are the symptoms of cutaneous leishmaniasis

Answer 18

• 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

Question 19

what are some symptoms of viceral leishmaniasis

Answer 19

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

Question 20

how have cases of leishmaniasis and HIV been thought to be co-infected

Answer 20

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

Question 21

outline the lifecycle of leishmania

Answer 21

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

Question 22

how to diagnose leshmania

Answer 22

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

Question 23

how can leshmania be controlled

Answer 23

• 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

Question 24

how to treat leishmaniasis

Answer 24

1) cryotherapy
2) infiltration of sodium stiboglyconate
3) heat therapy at 40-42 degrees
4) tropical antibiotics and urea mixtures