It is a tropical parasitic disease that can betransmitted via many insect vectors, with the Triatominae bug or assassin bug, which is a blood- sucking insect, being one of the best known and proliferant. The most common species to spread trypanosomiasis include vectors in the genera Triatoma, Rhodinius, and Panstrongylus.
Regardless of the individual vector, they are infected with the protozoan Trypanosoma curzi. It is the parasite which causes Chagas' Disease, with the vector being the mode of transmission. Furthermore transmission is also possible through blood transfusion, organ transplantation and contaminated food and from mother to unborn child. (CDC, a, n.d.)
1.1 Its importance
The estimated infection figures of Chagas' Disease are between 8 to 11 million individuals in Central America, Mexico and South America. Most individuals are unaware of their infection and if not treated the infection can remain lifelong or become life threatening. (CDC, a, n.d.)
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2. Life cycle
Chagas' disease is caused by the protozoan parasite Trypanosoma cruzi. As previously described, the transmission is primarily through blood sucking insects to humans via triatomine bugs. (CDC, a, n.d.)
Below is a diagram representing the typical life cycle of Chagas' disease or Human America Trypanosomiasis. (CDC, a, n.d.)
Fig 2. The lifecycle of Chagas' disease (picture from CDC website). http://www.dpd.cdc.gov/dpdx/HTML/TrypanosomiasisAmerican.htm
The life cycle begins with the insect vector, an infected triatomine.
1. It ingests a blood meal from the host, human or animal and through doing so trypomastigotes are released in the form of faeces near to where the bite occurred. Then via direct contact with the wound or through the intact musosal membranes the trypomastigotes enter the host. This is demed the infective stage.
2. Trypomastigotes invade the cells near to the inoculation site inside the host where the trypomastigotes differentiate into intracellular amastigotes.
3. Then the amastigotes undergo binary fission multiplication in the infected tissue cells.
4. Then these amastigotes differentiate in the cell into trypomastigotes and then are expelled into the bloodstream. At this stage diagnosis can be achieved.
' At this stage multiple tissue infections and transformations into intracellular amastigotes can occur to infect new regions of the body. The trypomastigotes present in the bloodstream do not replicate, instead only replicate when another cell is invaded or ingestion from another vector occurs. This as a consequence of how the vector becomes infected with the parasite through consuming the blood of the animal or human.
5. The life cycle then moves on to the triatomine bug stage where trypomastigotes are ingested into the vectors midgut where they transform into epimastigotes.
6. These epimastiogtes in the midgut multiply and differentiate.
7. This further progresses through differentiation from epimastiogotes to infective metacyclic trypomastigotes located in the hidgut.
3. Disease location
The disease is not present in the UK and the main continent where risk of infection is present includes Central and South America and Mexico. Infection outside of these continents usually occurs when isolated individuals travel back from countries that harbour chagas' disease and they are found to be already infected on arrival. (eMedicine, n.d.)
The estimated infection figures of Chagas' disease are between 8 to 11 million individuals in Central America, Mexico and South America. Most individuals are unaware of their infection and if they are not treated the infection can remain lifelong or become life threatening. (CDC, a, n.d.)
In the initial stages of the disease some die from excessive levels of parasitosis, where some live past the initial infestation and the disease progresses on to a chronic stage. However patients can be asymptomatic, suffering no visible illness and go on to die from other causes.
Treatments for individuals infected with T.cruzi focus on eliminating the parasite load and to deal with the symptoms and physical implications of the disease, most notoriously the lesions in which accompany the disease and for the most part are irreversible.
The most well known specific treatments for the disease include the use of benznidazole and nifurtimox. These drugs how ever have limited function in eradicating the total parasitic load and so to cure the individual.
Furthermore utilisation of these drugs in the treatment of Chagas' disease remains controversial in chronic cases due to limited research currently available on its effectiveness.
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4.1 Acute phase
' Patients are commonly prescribed either benznidazole or nifurtimox. This is usually as a result of patients becoming immune compromised through either suffering chronic infection or congenital infection.
' Cure rates are highest in young babies and a parasitologic cure can be expected in younger and newly infected individuals, although some physical remains of the disease may remain such as the accompanying lesions.
' Research has suggested that completed eradication of the parasitic load of people suffering acute Chagas' disease is 70% although the data has not been verified. If the data collected from Argentina is examined it shows that if treatment is administered before the patients first birthday that 90% of cases can be cured.
' Treatments of corticosteroids and interferon- y can also be administered to suffering from acute Chagasic myocarditis or meningoencephalitis but the success rates have yet to be established.
' At the indeterminate ' phase benznidazole or nifurtimox is recommended for treatment in children with chronic infection and data supports this with high cure rates parasitologically being observed.
' However, parasitological cure for a long term infection in adults where the individual was most likely infected at infancy, with the use of these drugs is less than 10%.
' Transient suppression is achieved by using this treatment to restrict infection and lower the risk of parasite isolation through xenodiagnosis or hemoculture, the overall effect remains unknown.
' Comprehensive research in this area regarding the long ' term outcome for these patients has not occurred and is a possible future area of research with a trial currently being undertaken with the use of benznidazole in Colombia and Brazil.
' Information is also not available for infected individual which are either pregnant or are immunosuppressed (through either preparing for transplantion or individuals suffering from HIV.
' For the chronic symptomatic stage of the disease, consensus is that antiparasitic medication should be withheld from patients already suffering cardiac and/or gastrointestinal disease as risk out weights the benefit.
The protozoan T.cruzi is transmitted by Triatomines. A misconception is that all reduviids transmit T.cruzi where only a select few in the family Reduviidae can as most are phytophagus or insectivorous.
T.cruzi is able to be transmitted to humans from all triatomine species but only a fraction is able to reside and these consequently become important vectors.
The parasite is transmitted by select triatomine species but many more aid the spread of sylvatic cycles. This is due to the five nymphal (instar) stages of triatomines which can all act as harbourers for T.cruzi and can later transmit the parasite on to a host.
The main vector species in the transmission of T.cruzi to humans include Triatoma infestans, Rhodnis prolixus, and Trimatoma dimidiate. In the Sub ' Amazonian endemic regions the main vector has historically been T.infestans. (eMedicine, n.d.)
Control programmes have been established in the 1990s to eliminated dominciliary of T.infestans with success in Brazil, Urugauy and Chile and as a direct result are confirmed by the Pan American Health Organisation as transmission free.
Furthermore control programmes in Argentina and Bolivia have made significant progress. In Central America and the nations surrounding the Andeas R.Prolixus is the common vector and T.dimidata is similar in distributional range but extends also to Mexico
Other vectors are restricted to more specific areas and are so less involved in transmitting T.cruzi Protozoan to the human population.
Sylvatic species have the ability to invade houses and in so doing increases the risk of transmission.
New infections of T.cruzi occur in low standard housing which allows the sylvatic cycle to be present. The housing is infested with triatomines which are infected with T.cruzi remain in the house.
These triatomines infected with parasites consume a blood meal from there hosts (animal or human) after which faeces containing the parasite are deposited near to the bite site. (eMedicine, n.d.)
5.1 Reservoir hosts
There are two different category reservoirs of T.cruzi these include domestic and sylvatic reservoirs. This shows the disease as a zoonosis with transmission between animals to humans, such animals include dogs, cats, rats, mice and guinea-pigs.
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The suggested correlation between the domestic and sylvatic cycle is through humans becoming infected with sylvatic parasites from the Opossum, species Didelphis virginiana. The parasitic load is retained throughout its life time.
Sylyvatic hosts that harbour the t.cruzi parasite are mammals amounting to approximately 150 species such as lagomorpha, chiroptera and primates. (Molyneux, 1983)
It is therefore suggested that a reservoir isolate, when introduced to laboratory mice creates infection with the corresponding morphology including amastigotes in tissues, cultures and the ability to infect triatomine insects. It is believed that this could aid in parasitic identification and and provide increasingly important epidemiological data.
Significant sylvatic reservoirs include the anteater tamandua, armadillo dasypus, opossum didelphis and several different species of bat and primate.
The parasite t.curzi has been documented in feral animals within the United States of America. These feral animals include such animals as the opossum didelphis, armadillo dasypus, skunk mephitis, ringtailed cat bassaricus with particular reference to the wood rat neotoma.
Transmission pathway cycles can be defined into three categories:-
' Soley sylvatic or enzootic cycle ' consisting of sylvatic bugs
' Sylvatic and somestic transmission ' consisting of cycling or overlapping between the two, transmitted by either sylvatic or domicillary insect vectors.
The above transmission classification is simplified due to possible impact on ecological conditions due to human activities creating disturbance of the vectors and reservoir resulting in variation in behaviour and distribution.
Sylvatic reservoir hosts maintain habitats which commonly correspond with a specific species of triatomine bug which can be located in close proximity, most commonly in burrows and nests.
Triatomine bugs are opportunistic feeders but the preference remains with human and dog hosts. Guinea pigs have also contributed to the spread of the disease in the Andean countries, especially so as the animal is usually raised in the kitchens of traditional dwellings. Predators of the traitomine bugs include rats, mice, cats and chickens, lowering the population.
Carlos chaga discovered that humans have evolved to be the principal host with the second being cats.
Dogs are also vital reservoir hosts particularly at night due to their close proximity to humans. This is also seen in guinea pigs, in Bolivia they were found to have substantial levels of infection which created a high risk as they where commonly bred indoors. (Bastien, 1998)
6. Control Strategies
Chagas' disease that is untreated does not automatically mean that the disease will result in fatality and it is also possible for patients to have the disease and suffer with no or mild symptoms as a result of chronic Chagas Disease.
Treatment has been seen as a first control mechanism and with patients with acute Chagas' Disease, treatment does provide benefit but with lampit treatment taking up to 120 days being time consuming and medication less effective in the chronic stage other strategies needed to be adopted.
Chemotherapeutic control has been investigated but due to the vast infection rates this would be impractical to implement on a large scale.
As a result of these short comings the emphasis has been moved on to vector control.
The use of alternative insecticides instead of chlorinated hydrocarbons is under evaluation such as organophorus compounds, carbarnates and synthetic pyrethroids. Furthermore compounds such as malathroin have been used in Argentina and insecticidal spraying is conducted with knapsack spraying equipment inside individual houses.
This however as a result of spraying has resulted in some areas eradicating the undesired species but for then another species to invade and replace it.
An insecticide to deal with this issue needs to be able to cover the crevices in walls, produce a prolonged effect on surfaces with the capability of eradicating eggs and preventing resistance to the insecticide.
Tests with third generation pesticides are occurring and these include the use of pheromones, attractants and insect growth regulators.
The utilisation of this combined with natural pathogens and updates house construction with an integration of pest control could be a viable.
Experimentation on the fifth instar nymph stages has been undertaken using juvenile hormone analogues in the attempt to produce a control but for the most part the effectiveness's seems limited due to the short period. This would prevent the adult hormone characteristics from developing.
Research has suggested that the use of mermithid meatode neoaplectana could be used in humid climates as a control for triatomines as it penertrates the instars of all bugs.
With a further possibility that could involve the predators or the parasitoids but there part in controlling the population is un known.
Another possible area of expansion includes the use of the parasitic hymenoptera which has a wide distribution. The possibility of this can be seen with t.rangeli, able to control populations in the wild, it posses flagellum and blastocrithida triatomae. It is already known to affect rhodnius prolixus.
Although the methods examined have the possibility of success the most potentially effective universal approach would be to update the poor housing. The correlation between the lowering of infection rates and the upgrading of the quality of housing is already established.
Two ' thirds of children who are seroreactive living in traditional housing comprised of local materials and mudstick. Research concluded that two thirds of children have over a 90% infestation of p.megistus.
Housing materials that could help prevent the transmission of these parasites and the disease include concrete, tiles or corrugated iron.
Construction of houses in brick and concrete would produce a significant reduction in transmission but one major setback is the cost, with most people previously effected not being able to afford to re construct their homes.
One control strategy that can both be combined or used on its own is by the removal of litter and waste and the eradication of areas in which the insect can conceal itself. (Molyneux, 1983)