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Lectures 12-13 American Trypanosomes
Terms in this set (68)
what is the causative agent of American trypanosome? and name the disease it causes?
- T. cruzi
How many people are infected with Chagas disease?
- 8-10 million people infected in Latin America (21 countries in southern America are endemic)
- 500,000 new cases with 10,000 deaths per year
what are disability adjusted life years (DALYs)?
a measure of overall disease burden; the number of years lost due to disability, disease or early death.
what is the history behind Trypanosoma cruzi?
- a historically important disease - looking back at 9,000 year old mummies we found that 41% of them were positive for T.cruzi DNA
- humans are a very recent host
-the emergence in humans is as a result of changing vector-host-parasite ecology; resulting in anthropogenic changes.
- due to people invading wild habitats- allowed for the introduction of the vector-human contact
who was the first person to discover T.cruzi and describe the disease and lifecycle?
Carlos Chagas- he helped to characterise the disease
How is T.cruzi transmitted?
via the Triatomine bugs ~ also known as kissing bugs
where is the Triatomine bug found?
- found in Central and South America- a geographic range between Argentina and the USA.
what are some of the characteristics of the Triatomine bugs?
- large insects
- order is Hemiptera and family is Reduviidae
- many different species
- they don't have a pupal stage- will emerge from the egg and go through various molts until the mature to an adult
- only the adults are sexually mature and have wings
- can take 4-24 months for the new borne to reach maturity depending on species
- can survive long periods of starvation-provides longevity
- at every stage of development these bugs feed on blood- lots of opportunity to take up and transmit disease
what is the Trypanosome folklore?
People believe that Charles Darwin was bitten and died from Chagas disease; a report written by Charles Darwin refers to him being bitten by these bugs when in Argentina. After this, he had symptoms that reflected extreme Chagas disease.
describe the transmission cycle of Chagas disease
1. Triatomine bug takes a blood meal and defecates at the same time.
2. As it defecates there is a lot of the infective, highly motile trypomastigotes that are in the feces
3. we as the host spread the infected feces to open wounds/eyes/mouth- allows entry to body
4. inside host, the trypomastigotes invade cells (intracellular division inside host cells)- they multiply inside host cells which either go and infect other host cells or are taken up in another blood meal by another vector.
where do the stages of T.cruzi replication take place inside the vector (Triatomine bug)?
within the vector we see various stages of multiplication in the migut until they move to the hindgut where they transform into this metacyclic trypomastigote ready to transmit.
what are the different routes of Chagas disease treatment?
- vector borne transmission makes up 80%
- transfusion of infected blood is 4-20%
- ingestion of infected sources
- congenital; mother to foetus
what are the two types of Chagas disease transmission cycles?
- one that involves the vector
- one that involves human-human transmission
describe Chagas disease epidemiology across the world
- Latin America- endemic in 21 countries
- sustained transmission is taking place due to urbanization
- non-endemic regions like the USA where 300,000 infected people are found. mostly immigrants from areas of Latin America.
- transmission in the USA is not vector borne but via blood transfusion or congenital transmission
- 68,000-123,000 infected immigrants in Europe. Spain sees the highest frequency of infection due to having 80% of its immigrant being from Bolivia.
- transmission is linked to migration, no vector
-there is also an association between HIV infection and the emergence of Chagas disease- with HIV you can enter the acute stage of Chagas infection.
what are the risk factors of Chagas disease in Latin America
1. the use of domestic animals has allowed T.cruzi to spread which previously existed in wild animals
2. for decades a strictly rural disease- but due to urbanization and socioeconomic changes, deforestation and rural exodus has transformed the epidemiological profile of the disease
3. blood transfusion
4. poverty and house construction - favourable triatomine bug habitats in poorly constructed houses, also individuals might be suffering with malnutrition.
5. congenital transmission
Where are triatomine bugs typically found?
- they live in the walls or roof cracks of poorly constructed homes in rural/suburban areas
- they become active at night, and bite exposed areas of the skin, defecating close to the bite
what is the chronic phase of Chagas disease? (TWO TYPES)
- lifelong disease
- two phases either a lifelong asymptomatic chronic disease or a latency of 10-20 years where reactivation occurs and symptoms are present.
- 20-30% of people who initially have the indeterminate form progress to clinical conditions over decades; e.g cardiac disease and plethora of complications leading to sudden death.
what are the clinical conditions that can progress with Chronic Chagas disease?
Gastrointestinal disease (less common) of the oesophagus/colon, with advancement to megaoesophagus/megacolon. Predominant in southern cone countries; rare in northern south America, central America and Mexico.
Cardiomyopathy occurs in 20-30% of infected individuals, an enlarged heart, develop digestive damage (megaviscera), peripheral nervous involvement. This is due to the parasites invasion of certain tissue- as their pseudocysts rupture there is direct damage to that tissue! cell and tissue damage from parasite enzymes as well
what is the stigma associated with Chagas disease?
It makes it difficult for people with chronic Chagas to get jobs and make money.
This stigma leads people to avoid proper diagnosis and treatment; even though it is important to be treated in the early acute phase (a key component of early intervention).
Chagas disease co-infection with HIV causes what?
can cause re-activation of the early acute phases- very hard to detect due to a very poor human response.
Chagas disease is complicated by HIV co-infection
How is the acute stage of Chagas disease infection determined?
by the high volumes of parasites present in the blood early on in infection
when is the best time to diagnose Chagas disease?
- during the acute stage of infection (a few days after transmission)
- lots of parasite in the blood can be visualised by microscope
- a smear of blood is viewed down a microscope or buffy coat to see the parasite
when does the acute stage of Chagas disease end?
the acute phase ends when there is an immunological balance between the host and parasite
when do we enter the chronic phase of Chagas disease?
we enter the chronic phase where there is immune involvement; few parasites in the blood
if the T.cruzi parasites are not in the blood, where are they?
- cardiac cells
- skeletal muscles and macrophages
- this is to evade the immune system
why is it difficult to detect T. cruzi during the chronic stage?
- the parasite is inside the cells at this point
- can only diagnose by looking at clinical signs, symptoms or serological tests to detect anti T.cruzi antibodies
How is chagas disease treated?
only 2 effective drugs against acute and early chronic phases
what are the 2 drugs that treat Chagas disease? what are the drawbacks?
Nifurtimox and Benznidazole.
both cause serious side effects (40% of cases), these side effects are common with age.
therefore we can only treat young people and those who have early diagnosis.
How does the T.cruzi drugs affect acute infection?
- treatment reduces symptom severity
- shortens clinical duration of infection (helps to drop parasitaemia)
who does the WHO recommend treatment for Chagas disease for?
- acute, congenital and re-activated T. cruzi infection.
- children with chronic infections (more likely for treatment to be successful, lower risk of side effects)
why are there no drugs for the chronic phase of T.cruzi?
does not affect the quality of life.
clinical trials in progress but hindered by no accepted reference assay to detect chronic T.cruzi infection- we cannot determine if the drugs are effective!
when can't T.cruzi drugs be administered?
what are the challenges of T.cruzi treatment?
1. serious side effects
2. accessibility to drugs is problematic - less than 1% of patients have access to Benzimidazole.
3. treatment can only be recommended in areas with vector control or non-endemic regions.
4. disease is poorly understood by health professional in non endemic areas-making detection difficult
5. desperately need new drugs against trypanosomes/improved detection.
there is No vaccine for Chagas, therefore what can we we do to control the disease?
we can focus on prevention! by interrupting transmission by controlling intradomicillar vectors in Latin America, screening blood transfusions worldwide, screening organ transplantation, screening for congenital infection.
what are some effective ways to control the Triatomine bug vector?
1. indoor residual spraying
2. housing program- new modern houses.
3. blood banks
How does vector control affect vector transmission?
vector controls causes a fall in vector transmission
describe the insecticide and control options of Chagas disease
Insecticide impregnated materials- ITNs, IRS.
House improvement (environmental management)- plastering of walls (earth, cow dung, lime or cement mixes).
social interventions (education and community participation)- school teachers, community leaders, focus groups, meetings and house visits, sustainability is a key parameter in community participation.
how does political commitment affect vector control
even when we have success, political interest could be lost, resulting in less sustained control; this is the "punishment of success"
describe the current vector control progression of Chagas disease
1. historic control program in Venezuela led to a continent wide alliance in the fight against Chagas
2. this was known as the SOUTHERN CONTE INITATIVE (1991)
3. involved domestic vector elimination, serological screening blood tests and house improvement
4. very successful! reached targets
what was the first country to achieve an interruption of vector transmission with Chagas?
under the southern cone initiative there were huge reductions in disease incidence in all countries except?
What countries are a part of the SOUTHERN CONE INITIATIVE?
ARGENTINA, BOLIVIA, BRAZIL, CHILE, PARAGUAY, URUGUAY
Why was the southern cone initiative successful?
the main vector (Triatoma infestans) is a highly domesticated vector- therefore it is a good target for control. - likes to live in people's houses so the insecticide works well on them (easy to control)- does not have wild populations, so cannot be easily repopulated
what are some of the issues with the Southern cone initiative? why was it not completely successful?
1. there is more than one species vector, an oversimplification
2. over 100 species of triatomine and 20 species are responsible for chagas
3. ecology of vectors and the environment they occupy varies and provides different niche of control
4. sublte differences in their transmission cycles- both a predomestic cycle and the involvement of a wild/sylvatic cycle.
5. opossum is involved in the wild cycle of chagas disease.
6. Rhodnius prolixus is mostly peridomestic, and in some sylvatic populations (prefers huts with palm thatch roofs and peridomestic palms)- therefore makes control more complicated
what are the most important Chagas disease vectors- specify the binomial names
- triatoma infestans
- triatoma dimidtata
- rhodnius prolixus
what Triatomine species can be found in both wild/sylvatic and predomestic populations?
Triatoma dimidiata and Rhodnius prolixus
How many central countries of South America have managed to eliminate R.prolixus?
infection rates of chagas have dropped from 30 million to what?
6-8 million in the last few years
the southern cone initiative is the most successful, 2 other initiatives to reduce Chagas?
1. central America initiative
2. Andean initiative
what is the anual cost of Chagas disease control?
mortality of chagas disease has reduced from 45,000 to?
What is the Gran Chaco? How does it link to Chagas?
a massive region that includes Argentina, Bolivia and Paraguay!
home to many indigenous communities
there is a high transmission of Chagas in this region!
region is dominated by forest, sparsely populated and very poor!
what is the infection rate of the Gran chaco?
50% infection rate with T. cruzi by T. infestans
Blood of Bolivian origin has a much higher percentage prevalence of T.cruzi infection compared to donors of other Southern American countries, why?
due to the high prevalence of T.cruzi in communities in the Gran Chaco region.
looking at the graph, what are the trends present in the graph?
1. a link between chagas disease prevalence and age in the gran chaco region.
2. there are no age groups where chagas disease is 0- due to congenital transmission
3. a sharp increase in prevalence between the ages of 10-17; this indicates transmission within the population
4. at a certain age, there is 100% prevalence in that age group (between ages 70-90)
what are the risk factors for transmission of Chagas at the ages of 2-15 in the Gran chaco region?
- the head of household having education beyond primary school.
- construction of house- evidence of wall cracks and white wash.
you are 2.35 more likely to be infected with chagas if what? AND How are these odds reduced?
if you have cracks in your walls.
these odds are reduced if plaster is applied to these cracks (whitewash) as a protective effect.
why is the rates of transmission so high in the Gran chaco?
data shows that in peridomestic sites (gardens/yards) and domestic sites when an intervention is put into place (e.g insecticide spraying) - initially the there is reduction in transmission and n.o of bugs, BUT overtime those numbers recover and infestation returns. this is particular in peridomestic sites
why does reinfestation occur in sites that have previously been sprayed with insecticides in the Gran Chaco region?
2. in order for the insecticides to be sprayed on the walls of the house; the occupants belongings must be removed from the house (clothes, beds, etc.)- however, this could mean bringing hidden triatomines outside and protecting them, or those doing the spraying might be lazy and not do their job well- therefore the procedure needs to be improved!
1. another possibility could be re-infestation from other sources/sites; e.g chicken coup, goat corral, pig corral- these are potential blood sources that could support the vector. this peridomestic infestation could be the cause!
How do sylvatic populations in the Gran chaco contribute to re-infestation of T.infestans?
1. as our pests become more domesticated they become less genetically diverse- due to the founder effect.
2. T. infestans and R.prolixus often have low genetic diversity, whereas other species like T. dimidata are more widespread amongst domestic, peridomestic and sylvatic populations- therefore showing high levels of diversity.
3. we do see T. infestans in some sylvatic populations- associated with a greater genetic diversity.
4. domestication also allows enlargement of the vector's geographical distribution, which will also increase its genetic diversity- there is a region in the Gran Chaco that has sylvatic populations
5. genetic diversity allows the insects to have a greater genetic repertoire.
6. insecticide resistance is possible amongst populations
wild and domestic populations of T. infestans have an unusually high genetic diversity, specifically in the Bolivian Andes. what does this suggest about the Bolivian Andes?
this could be the point of origin of dispersal of this species, but there are some difference in the Andean and non-Andean T. infestans populations, associated with wild guinea-pigs and sylvatic cycles
How do Peridomestic populations act as a "bridge" for sylvatic and domestic genetic interchange?
peridomestic and domestic populations are very closely related to each other- lots of gene flow between these two populations, they must be mating together frequently/lots of inbreeding.
very distinct from the sylvatic populations of Triatoma spp. - but there is still some type of link; therefore some gene flow that is less frequent.
allowing that gene flow is giving high diversity; allowing them to adapt to the environment and our protective measures, potentially giving rise to resistance.
How can we prevent gene flow between sylvatic, peridomestic and domestic populations?
improving indoor residual spraying methods and maintaining them to prevent re-infestation to avoid this rise in resitance
How does the climate of the Gran chaco region affect insecticide compounds?
the climate is hot and arid- contributes to the rapid degradation of the insecticide compound. this is a prefect environment in which resistance can rise
Name the different types of insecticide
DDT (not effective against Triatomids).
Dieldrin, benzene hexachloride and propoxur.
Cypermethrin, cyfluthrin, deltamethrin, permethrin, lambdacyhalothrin and denpropathrin
name the different methods of insecticide formulations
wettable powders (WPs) and suspension concentrates (SCs) formulations for porous wall surfaces.
emulsifiable concentrates penetrate and are lost.
Insecticidal paint (but difficult to apply)
what are the issues specifically to the Gran chaco region that makes Chagas disease control difficult?
1. inadequate insecticide spraying and formulation
2. extreme climates degrade active insecticide molecules
3. rapid household re-infestation due to wild T.infestans
4. lack of systemic surveillance and tools to monitor re-infestation.
- variable insecticide resistance facilitated by high genetic variability of T. infestans
- lack of expertise
- poor house structure and lack of political investment
In summary, what are the major difficulties the control of Chagas disease?
1. dissemination ~ disease has spread to endemic and non-endemic areas due to population mobility
2. knowledge and experience of the disease is limited
3. diagnosis and treatment is difficult and inadequate ~ many don't have access
4. chagas disease is chronic so increases the n.o of co-infections and co-morbidities
5. political interest declines after transmission has been controlled
6. persistence - transmission in some areas might involve wild vectors, rather than domestic.
This set is often in folders with...
Lectures 1-3 Bacterial Pathogens
Lectures 4-6 Mycobacteria
Lecture 7-9 African Trypanosomes
Lecture 10-11 Protozoan parasites
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