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Triatomine-borne diseases and how they are transmitted

SCOTT TYTHERIDGE: Hello, my name is Scott Tytheridge, and I’m an assistant trial manager at ARCTEC based at the London School of Hygiene & Tropical Medicine. The aim of this step is to understand the pathology, epidemiology, and transmission of Chagas disease, which is transmitted by triatomine bugs. We’ll do this through meeting several objectives, so that by the end of this step, you should be able to recognise the symptoms of Chagas disease and briefly understand the concerns with treating the disease. You should also be able to describe the epidemiology of Chagas and connect it with disease control programmes. Triatomines are the noncompetent vectors of Trypanosoma cruzi, the blood trypanosome responsible for Chagas disease. Chagas has been around for a very long time.
The DNA of the parasite that causes it has been isolated in mummies from present Northern Chile dating back 9,000 years. It is closely related to the saliva-transmitted parasite that causes African sleeping sickness and probably diverged between six and eight million years ago. Modern day Chagas disease was first discovered in triatomine bugs by Carlos Chagas, a Brazilian bacteriologist in 1909. I will later come on to the specific impact of Chagas and its epidemiology, but briefly, there have been worrying reports of its spread into US states, Canada, Australia, Japan, and parts of Europe. There is limited data on autochthonous cases, but numbers in the US are in the low 30s. Competent triatomine species are present in the Southern United States.
A similar epidemiological complication seen in Colombia is the coinfection of HIV and Chagas, which can lead to reactivation of dormant amastigotes in the tissue. You can see here in the picture, the trypomastigote on a thin blood film stained with Giemsa, where nuclear material appears dark purple. The largest sphere is the nucleus of the parasite and sits anterior compared to the smaller sphere, the kinetoplast, which is a mass of mitochondrial DNA. This is what gives its family name, the kinetoplastids. The size of the kinetoplast can help to distinguish species. Trypanosoma cruzi has a much larger kinetoplast compared with its cousin, Trypanosoma brucei, for example.
The whip-like flagellum is actually at the front of the parasite and it kind of drags the parasite forward. Onto the signs, and symptoms, and how to treat the disease. Foremost, Chagas is a chronic disease and most symptoms are associated with long-term infection. Acute symptoms can include an immune reaction at the bite site. If this is located near the eye, then one can get Romaña’s disease, which is where contaminated bug faeces is rubbed into the eye. Other acute symptoms include fever and rarely, inflammation of the heart muscle and/or brain tissue. The chronic symptoms become apparent 30 to 40 years post-infection and often result in death. The main symptom is megasyndrome affecting the oesophagus and the colon or the heart.
I’ll mention this varying pathology again when I discuss the disease epidemiology. Typical blood loss from triatomine feeding can exceed 2 ml per person per night, and so this contributes to states of anaemia over time.
Treatment for Chagas is difficult as the drugs available are not effective during the chronic phase of the infection. And side effects are fairly common with both drugs, tending to be more severe with increasing age of the patient. Nifurtimox was shown to be effective against Trypanosoma brucei, the causative agent of African sleeping sickness, but contains a nitro group which is highly toxic to both the host and the parasite. It is no longer marketed in Brazil nor is it FDA approved as an alternative treatment to benznidazole due to the emergence of resistant T cruzi strains and genotoxic effects. Benznidazole is approved by the FDA and is the drug of choice for now.
As mentioned during the chronic phase, these nitro derivatives are not effective and their long-term administration leads to severe side effects in the patients. When compliance is low in a patient or drug treatment is ignored during the acute phase, the disease progresses to a chronic phase over 20 to 30 years. And after this, the only treatment option is surgery on the affected organs. And now, I’ll talk about the epidemiology. Here is a figure of the estimated Chagas cases globally between 2006 and 2010. The majority of these are found in South America where the triatomine vectors are found, but the disease also occurs in other regions where transmission routes are mostly through organ transplants and congenitally.
Most cases are asymptomatic for life, but around 20% to 30% develop the debilitating symptoms that I mentioned before. The burden of a disease can be estimated using disability-adjusted life years, which can be thought of as years lost of healthy life. It is the combined years of life lost due to premature mortality and the years of life lost due to disability. In a 2013 study, the global annual burden was 806,170 dailies and $627 million in health care costs.
The global consensus is that there are six T cruzi Discrete Typing Units or DTUs. These are transmitted by different triatomine bug species, infect different sylvatic hosts, and are located in different regions of the continent. TcI is primarily transmitted by Rhodnius species, whereas DTUs TcII, V, and VI are thought to be transmitted in the Southern Cone region by Triatoma infestans. TcIV is transmitted by all three of the main genera– Panstrongylus, Triatoma, and Rhodnius. TcIII has been found to be associated with armadillos, whilst the natural host of TcI is the Delphinus opossums in the arboreal palm ecotype. TcI has a primary and secondary transmission form– the primary form being found in lowland tropical, semi-tropical USA, Central, and South America.
The secondary form is referred to as north of Amazon Chagas and is found in Central Brazil and the Eastern Andean foothills. In addition, DTUs lead to different pathologies. Tc1 is responsible for Chagasic cardiomyopathy in the Amazonia and the Andean region. TcII, V, and VI are associated with megasyndromes. TcIII is rarely found in humans or causes no pathology. The likelihood of Chagas infection is increased with poor-quality housing and close contact with arboreal and terrestrial sylvatic habitats for subsistence farming. And this is because of increased exposure to the triatomine bugs as we saw in the previous step. The bugs like to hide behind cracked walls and in roof crevices. And now, looking at the transmission. Here is the transmission cycle.
The infective agent of Chagas is the faeces of the triatomine bug, which contains metacyclic trypomastigotes. This is either scratched into skin abrasions, the puncture site, or mucosal membranes. Note that unlike some STHs, for example, the parasite cannot penetrate unbroken skin. Once this stage has been inoculated into the human host, the trypomastigotes travel to various tissues and penetrate various cells. There, they transform into amastigotes. Amastigotes multiply by binary fission in the cells of infected tissues. Some of these transform back into trypomastigotes, though slightly different from metacyclics, and burst out of the cell, entering the bloodstream and infecting new cells. This infective cycle is what results in cardiomyopathy and megasyndromes.
It is the continued damage and breakdown of tissue through infection and division. Here is a microscopic view of amastigotes in heart muscle tissue. They are filling a muscle cell, and we call this a pseudocyst. They appear purple as they are stained with Giemsa, and this picks up nuclear material. Amastigotes of T cruzi are indistinguishable from another trypanosomatid called Leishmania.
Circulating trypomastigotes that are yet to enter surrounding tissues can be taken up when a triatomine bug takes a blood meal. Inside the midgut of the insect, the trypomastigotes transform into epimastigotes, which are better adapted to survive the bug’s immune system and trypanolytic compounds. Epimastigotes multiply by binary fission in the posterior part of the midgut before moving to the hindgut, where they attach to the rectal cuticle and transform into metacyclic trypomastigotes before being eliminated in the bug’s faeces, thereby completing the cycle.
And now, some further notes. Chagas disease is zoonotic. It cycles in various sylvatic hosts. Some examples are seen here in the pictures. As with many diseases, it only affects humans when they come into contact with triatomine bugs, so control is largely focused around reducing vector contact. Natural infection rates of bugs have been shown to be relatively high in multiple locations across Brazil, including the Pantanal region, Caatinga, Cerrado, and in Southern US states like Texas and Arizona.

In this video, we join Scott Tytheridge as he speaks about the transmission, epidemiology and pathology of Chagas disease, which is transmitted by Triatomine bugs.

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