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Chagas disease – Symptoms and causes


Chagas (CHAH-gus) disease is an inflammatory, infectious disease caused by the parasite Trypanosoma cruzi. This parasite is found in the feces of the triatomine (reduviid) bug. This bug is also known as the “kissing bug.” Chagas disease is common in South America, Central America and Mexico, the primary home of the triatomine bug. Rare cases of Chagas disease have also been found in the southern United States.

Also called American trypanosomiasis, Chagas disease can infect anyone. Left untreated, Chagas disease later can cause serious heart and digestive problems.

During the acute phase of infection, treatment of Chagas disease focuses on killing the parasite. In people who have chronic Chagas disease, it’s no longer possible to kill the parasite. Treatment in this later phase is about managing signs and symptoms. You can also take steps to prevent infection.


Chagas disease can cause a sudden, brief illness (acute), or it may be a long-lasting (chronic) condition. Symptoms range from mild to severe, although many people don’t experience symptoms until the chronic stage.

Acute phase

The acute phase of Chagas disease, which lasts for weeks or months, is often symptom-free. When signs and symptoms do occur, they are usually mild and may include:

  • Swelling at the infection site
  • Fever
  • Fatigue
  • Rash
  • Body aches
  • Eyelid swelling
  • Headache
  • Loss of appetite
  • Nausea, diarrhea or vomiting
  • Swollen glands
  • Enlargement of your liver or spleen

Signs and symptoms that develop during the acute phase usually go away on their own. In some cases, if the infection isn’t treated, Chagas disease will advance to the chronic phase.

Chronic phase

Signs and symptoms of the chronic phase of Chagas disease may occur 10 to 20 years after initial infection, or they may never occur. In severe cases, Chagas disease signs and symptoms may include:

  • Irregular heartbeat
  • Heart failure
  • Sudden cardiac arrest
  • Difficulty swallowing due to enlarged esophagus
  • Stomach pain or constipation due to enlarged colon

When to see a doctor

See your doctor if you live in or have traveled to an area where Chagas disease is widespread and you have signs and symptoms of the condition. Symptoms may include swelling at the infection site, fever, fatigue, body aches, rash and nausea.


The cause of Chagas disease is the parasite Trypanosoma cruzi, which is spread from an insect known as the triatomine bug, or “kissing bug.” These insects can become infected by this parasite when they swallow blood from an animal that is infected with the parasite.

Triatomine bugs live primarily in mud, thatch or adobe huts in Mexico, South America and Central America. They hide in crevices in the walls or roof during the day and come out at night — often feeding on sleeping humans.

Infected bugs defecate after feeding, leaving behind parasites on the skin. The parasites can then enter your body through your eyes, mouth, a cut or scratch, or the wound from the bug’s bite.

Scratching or rubbing the bite site helps the parasites enter your body. Once in your body, the parasites multiply and spread.

You may also become infected by:

  • Eating uncooked food contaminated with feces from bugs infected with the parasite
  • Being born to a person who is infected with the parasite
  • Getting a blood transfusion or an organ transplant from someone who was infected with the parasite
  • Being accidentally exposed to the parasite while working in a lab
  • Spending time in a forest that contains infected wild animals, such as raccoons and opossums

Risk factors

The following factors may increase your risk of getting Chagas disease:

  • Living in poor rural areas of Central America, South America and Mexico
  • Living in a residence that contains triatomine bugs
  • Receiving a blood transfusion or organ transplant from a person who carries the infection

It’s rare for travelers to the at-risk areas in South America, Central America and Mexico to catch Chagas disease because travelers tend to stay in well-constructed buildings, such as hotels. Triatomine bugs are usually found in structures built with mud or adobe or thatch.


If Chagas disease progresses to the long-lasting (chronic) phase, serious heart or digestive complications may occur. These may include:

  • Heart failure. Heart failure occurs when your heart becomes so weak or stiff that it can’t pump enough blood to meet your body’s needs.
  • Enlargement of the esophagus (megaesophagus). This rare condition is caused by the abnormal widening (dilation) of your esophagus. This can result in difficulty with swallowing and digestion.
  • Enlargement of the colon (megacolon). Megacolon occurs when your colon becomes abnormally dilated, causing stomach pain, swelling and severe constipation.


If you live in a high-risk area for Chagas disease, these steps can help you prevent infection:

  • Avoid sleeping in a mud, thatch or adobe house. These types of residences are more likely to harbor triatomine bugs.
  • Use insecticide-soaked netting over your bed when sleeping in thatch, mud or adobe houses.
  • Use insecticides to remove insects from your residence.
  • Use insect repellent on exposed skin.

Nov. 12, 2020

Found a Bug? | Kissing Bugs and Chagas Disease in the U.S.

Community science is when non-scientists and scientists work together to collect data to answer scientific questions. Our community science project loves help from community scientists like you! You can participate by sending us kissing bugs from Texas and throughout the United States. We are trying to learn more about where different kinds of kissing bugs live. We are also working to learn more about how many kissing bugs are infected in different places. And we want to learn more about which animals kissing bugs feed on. We have lots of questions, and any kissing bugs you send us help us get closer to answering the questions. If you think you have found kissing bug in or around your home, kennel, yard, or other area, please reach out to us!

It’s best to NOT squish a bug, but sometimes it happens! After the bug is squished, do not touch the bug with your bare hands. The T. cruzi parasite may be in the feces of kissing bugs, and their bodies may have the parasite on them. Use an item like a small plastic bag to pick up the bug and throw it away where other people and animals cannot get it. If you squished the bug and there is a mess, consider using a bleach solution to clean the surfaces where the bug was found. Read the label on the bleach container before using. If you want to send us the squished bug for research, read below about how to send us a bug.

SUBMITTING A BUG FOR TESTING — How to prepare a bug to send to us for research

Do not touch a kissing bug with your bare hands! The T. cruzi parasite may be in the feces of kissing bugs, and their bodies may have the parasite on them. Use a glove or small plastic bag to collect the bug so you do not touch the bug directly. Keep the bug in a closed plastic bag, a vial, or other small container. To kill the bug, you can put it in the freezer for a few hours or you can set the container outside in the sun until the bug dies. Contact us with any questions!

When you find a kissing bug, write down the date, time of day you found it, where it was caught (indoors or outdoors), and any possible bites on people or animals. If you are in Texas, you can submit kissing bugs that bit a person to the Texas Department of State Health Services. Our lab at Texas A&M University is a research lab, and we mostly test kissing bugs that are NOT associated with bites.

KISSING BUGS — How to identify

Kissing bugs have some parts that make them easier to recognize. They have a ‘cone-shaped’ head, thin antennae, and thin legs. All of the kinds of kissing bugs found in the United States are mainly black or very dark brown, with red, orange or yellow ‘stripes’ around the edge of their bodies. Since they try to bite and feed without being noticed, their bites are generally not painful. Kissing bugs are mostly active at dusk or night. Some of the most common kinds of kissing bugs in Texas are shown here:

NON-KISSING BUGS — Send us a picture!

There are many bugs that look like kissing bugs. Many of these non-kissing bugs feed on plants or insects. They can have strong mouthparts that cause a painful bite if they are bothered or feel threatened. No insects other than kissing bugs are known to carry the parasite that causes Chagas disease. We’ve assembled pictures of some of the most common non-kissing bugs here. Please take a look and see if your bug resembles these bugs; if so, it might not be a kissing bug. If you have any questions, please feel free to send a picture and a message. The bug can be put in a freezer for a few hours to kill it. This will also preserve the DNA for our testing.

Feel free to download and print our pamphlets on kissing bugs and canine chagas disease.

Funded under cooperative agreement number UG4LM012345 with the University of North Texas Health Science Center – Gibson D. Lewis Library, and awarded by the DHHS, NIH, National Library of Medicine. Funded in part by Texas Ecological Laboratory program.

All rights reserved. All images are copyrighted by their respective copyright owners.

American trypanosomiasis. Chagas disease | DermNet NZ

Author: Marie Hartley, Staff Writer, 2009. DermNet NZ Update March 2021. Copy edited by Gus Mitchell

What is American trypanosomiasis?

American trypanosomiasis, commonly known as Chagas disease, is a systemic infection caused by the zoonotic protozoan parasite Trypanosoma cruzi.

Who gets American trypanosomiasis?

American trypanosomiasis is endemic in the southern half of the United States, and 21 countries in South and Central America. It has spread to at least 19 non-endemic countries including through Europe and the Asia-Pacific due to migration and international travel. An estimated 8–10 million people worldwide have Chagas disease, including approximately 500,000 in the US and 100,000 in Europe. In Latin America alone there are 28,000 new cases each year. The WHO estimated more than 16 million people migrated from endemic areas to non-endemic countries between the years 2000 and 2009. Active transmission has then occurred in several non-endemic countries. The majority of cases in non-endemic countries are adult Latin-Americans, most of whom are unaware of their diagnosis. Serological studies in Europe have shown an overall prevalence of 4% in immigrant Latin Americans, and 18% in Bolivians. In 2006, New Zealand had 6315 permanent residents born in endemic countries, with an estimated prevalence of Chagas disease of 98 cases. In 2011, Australia had a predicted 1928 cases in 116,430 migrants.

Distribution of Chagas disease

Red indicates endemic areas where transmission is through vectors; yellow indicates endemic areas where transmission is occasionally through vectors; non-endemic areas are in blue where transmission is vertical or via blood transfusions or organ transplants. Acknowledgement Liu and Zhou Infectious Diseases of Poverty (2015) 4:60.

What causes American trypanosomiasis?

T. cruzi is a zoonotic intracellular parasite that has been identified in pre-Columbian mummies but was only described on April 14, 1909 by Carlos Ribeiro Justiniano Chagas. The parasite spread to humans from mammalian hosts such as armadillos, rodents, and raccoons in the wild following the clearance of forests and jungles for timber and farming. Humans are an accidental host, and infections were initially noted in poor rural workers whose homes were invaded by the triatomine bugs seeking night-time blood meals, but most cases are now identified in urban areas. Domesticated animals have subsequently become infected. In Australia, the animal form of Chagas disease must be notified to the Department of Agriculture.

Triatomine bugs, also known as reduviid or kissing bugs, collect T. cruzi during an infected blood meal and excrete the protozoa in their faeces.

Routes of transmission of American trypanosomiasis to humans include:

  • Vector spread: Following a blood meal, the triatomine bug deposits trypomastigotes in its faeces which can enter broken skin or through adjacent intact mucous membranes such as the conjunctiva
  • Ingestion: Accidental intake of food/drink contaminated with infected triatomine bugs or their urine or faeces
  • Transplacental vertical spread of T. cruzi from an infected mother to her baby – risk of infection 5–10%.
  • Blood/platelet transfusion or organ/tissue transplantation from an infected donor – risk of infection 20–40%.

In endemic countries, spread is predominantly by triatomine bugs whereas in non-endemic countries transfusions/transplants and vertical spread are the major routes.

Trypanosoma cruzi

What are the clinical features of American trypanosomiasis? 

Acute American trypanosomiasis

  • Incubation period 1–2 weeks
  • Asymptomatic parasitaemia
  • Symptomatic – non-specific febrile illness, nausea/vomiting/diarrhoea, headache, myalgia, lymphadenitis, hepatosplenomegaly
  • Vector inoculation site — chagoma at skin portal of entry, Romaña sign if entry through periorbital mucosa.

Parasitaemia resolves after 4–8 weeks and clinical features resolve in 90% of cases.

Chronic American trypanosomiasis

  • Indeterminate asymptomatic Chagas disease — 60–70% — rest of life
  • Cardiac/gastrointestinal chronic Chagas disease — 30-40%, develops 10–30 years after initial infection
    • Chronic chagasic cardiomyopathy — 1/3, diffuse myocarditis, dilated cardiomyopathy, heart failure
    • Gastrointestinal form of Chagas disease – denervation of gastrointestinal (GIT) nervous system causing dysphagia, GIT hypomotility, dilatation of colon, and constipation
    • Cardiodigestive Chagas disease.

The severity of chronic Chagas disease is assessed using the Kuschnir classification system ranging from Class 0 having reactive serology, normal ECG, and heart size, through to Class 3 with cardiac enlargement and apical aneurysm.

Cutaneous features of Chagas disease

  • Chagoma — red indurated swelling at skin inoculation site
  • Romaña sign — purplish swelling of the lids of one eye, conjunctivitis
  • Schizotrypanides — diffuse measles-like eruption.

Clinical features in special groups

Congenital American trypanosomiasis in newborns

  • Prematurity, low birth weight
  • Hepatosplenomegaly, jaundice
  • Tachycardia
  • Uncommon – chagoma, rash, oedema, lymphadenopathy, myocarditis, sepsis

Reactivation Chagas disease in immunocompromised patients

  • HIV infection, organ transplant recipients, drug-induced immunosuppression
  • Chagas disease is an AIDS-defining illness
  • Neurological and cardiac involvement are the commonest manifestations
  • May present with fever and erythematous nodules and plaques
  • Panniculitis and erythema nodosum-like skin lesions have been reported
  • Sequential monitoring for parasitaemia if positive serology prior to commencing immunosuppression
  • Treat if parasitaemia detected.

What are the complications of American trypanosomiasis?

  • Reactivation of Chagas disease — immunomodulators, HIV
  • Cardiac disease — dilated cardiomyopathy, heart failure
  • Gastrointestinal disease — megaoesophagus, megacolon, constipation
  • Neurological disease — encephalitis, pseudotumoural mass.

How is American trypanosomiasis diagnosed?

Screening of blood/tissue/organ donors, transplant recipients, and before other planned immunomodulatory treatments

  • Blood smear and serological testing — routine in endemic countries and some non-endemic areas with significant numbers of Latin-American immigrants

Acute, congenital, and reactivated American trypanosomiasis

  • Circulating parasites in peripheral blood seen on thick blood smear
  • Xenodiagnoses — uninfected triatomine insects are fed on the patient’s blood, and their gut contents examined for parasites 4 weeks later
  • Blood culture
  • Detection of T. cruzi DNA by polymerase chain reaction (PCR)
  • Skin biopsy — intracellular amastigotes are seen in chagomas and skin lesions of acute and reactivated Chagas disease, but not in schizotrypanides.

Chronic American trypanosomiasis

  • Serology — at least two of the following tests should be positive: indirect immunofluorescence, haemagglutination, ELISA
  • ECG, chest X-ray
  • Other investigations as clinically indicated.

In Australia and New Zealand there are very few laboratories performing serological testing for Chagas disease and confirmatory tests have to be performed overseas. Blood services screen patients based on a questionnaire, excluding potential donors who have a history of Chagas disease, were born in an endemic area, or who received fresh blood components in an endemic area. The former should never become a blood or organ donor, and the latter two groups require negative serology before becoming donors.

What is the treatment for American trypanosomiasis?

Prevention in endemic areas

  • Education
  • Vector surveillance and control
  • Insecticide-treated bed and window netting, building codes
  • Insect repellent and protective clothing
  • Vaccines are under development.

Resistance to pyrethroid insecticides was first detected in triatomine bugs in the 1970s associated with vector control failures, and has become more widespread.

Prevention in non-endemic areas

  • Screening of blood and organ donors
  • Diagnosis and treatment of identified cases
  • Education of health professionals

Acute phase

Chronic phase

  • Role of anti-trypanosomal medications controversial
  • Supportive
  • Symptomatic

What is the outcome for American trypanosomiasis?

Adequate treatment in the parasitaemic phase is effective in nearly all cases. Chronic Chagas disease, and rarely acute Chagas disease, can be fatal resulting in 50,000 deaths annually worldwide, including 12,000 deaths in Latin America per year.



  • Bern C, Messenger LA, Whitman JD, Maguire JH. Chagas disease in the United States: a public health approach. Clin Microbiol Rev. 2019;33(1):e00023-19. doi:10.1128/CMR.00023-19. Journal
  • Coura JR, Viñas PA, Junqueira AC. Ecoepidemiology, short history and control of Chagas disease in the endemic countries and the new challenge for non-endemic countries. Mem Inst Oswaldo Cruz. 2014;109(7):856–62. doi:10.1590/0074-0276140236. Journal
  • Hemmige V, Tanowitz H, Sethi A. Trypanosoma cruzi infection: a review with emphasis on cutaneous manifestations. Int J Dermatol. 2012;51(5):501–8. doi:10.1111/j.1365-4632.2011.05380.x. PubMed Central
  • Jackson Y, Pinto A, Pett S. Chagas disease in Australia and New Zealand: risks and needs for public health interventions. Trop Med Int Health. 2014;19(2):212–218. doi:10.1111/tmi.12235. Journal
  • Lattes R, Lasala MB. Chagas disease in the immunosuppressed patient. Clin Microbiol Infect. 2014;20(4):300–9. doi:10.1111/1469-0691.12585. Journal
  • Lidani KCF, Andrade FA, Bavia L, et al. Chagas disease: from discovery to a worldwide health problem. Front Public Health. 2019;7:166. doi:10.3389/fpubh.2019.00166. Journal
  • Liu Q, Zhou XN. Preventing the transmission of American trypanosomiasis and its spread into non-endemic countries. Infect Dis Poverty. 2015;4:60. doi:10.1186/s40249-015-0092-7. Journal
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  • Vallejo M, Reyes PP, Martinez Garcia M, Gonzalez Garay AG. Trypanocidal drugs for late-stage, symptomatic Chagas disease (Trypanosoma cruzi infection). Cochrane Database Syst Rev. 2020;12:CD004102. doi:10.1002/14651858.CD004102.pub3. Journal

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Chagas disease – PAHO/WHO | Pan American Health Organization

Chagas disease is associated with multiple social and environmental factors that expose millions of people to infection.  Among the main risk factors for Chagas disease are living in poorly constructed housing – particularly in rural and suburban areas – having limited resources, residing in areas of poverty that are socially or economically unstable or have high rates of migration, and belonging to groups linked to seasonal farm work and crop harvests. This disease contributes and perpetuates the cycle of poverty, reduces learning capacity, productivity, and the ability to generate income.

In the early 1990’s, the countries affected by Chagas disease, especially those where the disease was endemic, were organized to combat this public health threat. Along with the Pan American Health Organization/ World Health Organization, country representatives generated a successful scheme for horizontal technical cooperation between countries, called the Sub-regional Initiatives for Prevention and Control of Chagas Disease. These initiatives have been developed in the Southern Cone (1992), Central America (1997), Andean countries (1998), Amazonian Countries (2003), and Mexico (2004). These countries have contributed in creating substantial improvements in the situation through the interruption of vector transmission in all or part of the territory of the affected countries, the elimination of exotic species of vectors, the introduction of universal screening of blood donors, the detection of congenital cases, the reduction of prevalence in children, reduction in morbidity, expansion of access to diagnosis and treatment, and improvement of the quality of diagnosis, clinical care, and treatment of infected and ill persons.

The initiatives in the Americas have helped achieve significant reductions in the number of acute cases of disease and the presence of domiciliary triatomine vectors in endemic areas. The estimated number of people infected with T. cruzi worldwide dropped from 30 million in 1990 to 6 to 8 million in 2010. In those 20 years, the annual incidence decreased from 700,000 to 28,000 new cases of infection and the burden of Chagas disease decreased from 2.8 million in  1990-2006 to disability-adjusted life years lost to less than half a million years.

While substantial progress has been made, not all countries have managed to achieve the goals that have been proposed. New challenges have emerged such as the spread of disease due to the migration of people living in endemic countries to non-endemic countries, the need to ensure the sustainability of programs, confronting the emergence or re-emergence of cases of Chagas disease, recovering from natural disasters, expanding coverage of diagnosis and treatment, and achieving universal access to treatment.

Geographical distribution of Chagas disease in the Americas according to the status of transmission by the main vector in each area. Year: 2011.

Chagas disease | UF Health, University of Florida Health

Speak with a Chagas disease expert

Call for an appointment with one of our infectious diseases expert, Dr. Norman Beatty, if you think you may have Chagas disease.

What is Chagas Disease?

Chagas disease is a tropical disease caused by the parasite Trypanosoma Cruzi. The transmission occurs through direct interaction with insect vectors, known as the “kissing bugs,” which are only found in the Americas. A person can become infected by different routes. Fecal material of the bug carrying the parasite enters the body via skin bite or oral ingestion. Another route is congenital infection (passed down from mother to child). Other less common forms of transmission include blood transfusion and organ transplantation.

Who is at Risk?

  • Individual born or having lived in Mexico, Central or South America, excluding the Caribbean Islands
  • Individual whose mother was born in Mexico, Central America or South America
  • Individual who lived in the regions mentioned above for longer than 6 months
  • If there was a known exposure to the kissing bug (refer to images)
  • Those who screen positive for Chagas disease after blood donation

What are the Phases of Chagas disease?

Acute Phase – Signs and Symptoms

  • A majority of people will not present symptoms
  • Symptoms that may develop are non-specific, such as fever, enlarged lymph nodes, fatigue
  • Chagoma: skin inflammation at the site where the parasite entered
  • Romaña’s sign: swelling around the eye of person who contracted the parasite through mucous membranes
  • A serious acute infection may occur if the person has a weakened immune system

Indeterminate Phase – Signs and Symptoms

  • No clinical evidence of Chagas disease-related illness
  • Positive screening and confirmatory testing for parasite exposure
  • Majority of people remain asymptomatic (parasite may be detected in blood)
  • Parasite can reactivate if the person develops a condition that weakens immune system causing serious disease
  • Person should be monitored with a clinical provider for the potential development of the chronic phase

Chronic Phase – Signs and Symptoms

  • Heart disease (most common organ affected):
    • Abnormality in electrical activity
    • Sudden cardiac arrest
    • Dilated cardiomyopathy and congestive heart failure
  • Gastrointestinal tract disease (abnormal enlargement of esophagus and/or colon):
    • Trouble swallowing liquids and solids
    • Chronic constipation and abdominal pain
    • Colon enlargement can distend the abdomen
  • Thromboembolic disease: higher rates of pulmonary embolism and stroke

How to Get Tested?

Chagas testing may be arranged by a primary care provider or by an infectious disease specialist. Exams and tests consist of the following:

Physical Examination

  • Signs of heart failure: elevated jugular venous distension, edema in lower extremities
  • Irregular, slow and/or rapid heartbeat
  • Lymph nodes enlargement
  • Delayed bowel sounds
  • Distended abdomen
  • Enlarged spleen and/or liver


  • Chest X-Ray
  • Echocardiogram
  • Electrocardiogram
  • Cardiac magnetic resonance imaging
  • Blood tests to investigate for antibodies present in the blood

How Does Treatment Work?

  • The acute phase of the disease should be treated in children and most adults. Infants born with the infection should also be treated.
  • Adults in the indeterminant or chronic phases should discuss with a medical provider whether treatment will be necessary.
  • Antiparasitic drugs used for treatment are benznidazole and nifurtimox. These drugs may cause side effects and patients should be monitored
  • Cardiac devices, such as pacemakers and defibrillators are sometimes placed when certain abnormal heart rhythm is detected.
  • Advanced cardiac care is needed if the heart becomes too weak, which includes ventricular-assist devices, and even heart transplantation.

Outlook (Prognosis)

  • About one third of infected people likely develop chronic or symptomatic Chagas disease.
  • It can take more than 20 years from the time of the original infection to develop chronic illness, typically heart or gastrointestinal dysfunction.
  • Abnormal heart rhythms may cause cardiac arrest and sudden death.
  • Those who develop heart failure without management or heart transplant, usually die within several years.

Possible Complications

Chagas disease can cause these complications:

  • Enlarged heart
  • Heart failure
  • Arrhythmias or abnormal electricity of the heart
  • Sudden cardiac arrest
  • Enlarged colon
  • Enlarged esophagus with difficulty swallowing
  • Ischemic stroke
  • Reactivation due to immunocompromising condition or medication

Frontiers | Precision Health for Chagas Disease: Integrating Parasite and Host Factors to Predict Outcome of Infection and Response to Therapy

Trypanosoma cruzi and Chagas Disease

Chagas disease, American trypanosomiasis, is caused by infection with the protozoan parasite Trypanosoma cruzi which displays a complex life cycle involving human and animal hosts as reservoirs of disease and triatomine insects of the Reduviidae family as vectors. Although the route of infection was originally felt to be restricted to contamination of the wound or mucous membrane with T. cruzi-contaminated excreta of hematophagous insects, other forms of transmission are also important, including oral infection through consumption of food and drink contaminated with the parasite, blood transfusion, organ transplantation, and congenital infection (Moncayo, 2003; Coura, 2014; Dolhun and Antes, 2016; Alarcón de Noya et al., 2017). Although 6–7 million infected individuals live in the Americas (WHO, 2020), migration of T. cruzi-infected people throughout the world, many of whom are unaware of being infected, has contributed to the globalization of the disease (Steverding, 2014). Of the 238,000 infected people which are believed to reside in the United States, mostly immigrants from South America (Meymandi et al., 2017), 30,000 are found in Los Angeles, where Dr. Sheba Meymandi oversees a large Chagas clinic and a Center of Excellence for Chagas Disease (Meymandi, 2020). A few dozen cases of vector-borne transmission have been documented in the United States, although infection is widespread in wild animals throughout the southern half of the country (Montgomery et al., 2016; Kruse et al., 2019). The lack of an effective vaccine against T. cruzi, and the moderate effectiveness and toxicity of first-line drugs aggravate the situation (Schaub et al., 2011; Nunes et al., 2013; Rodríguez-Morales et al., 2015). Considering these aspects of epidemiology, continued surveillance of insects and wild animals, continued screening of the blood supply, and perhaps implementing screening of women of childbearing age will help to reduce transmission of T. cruzi through various routes.

In the human host, T. cruzi trypomastigotes, the infective forms of the parasite, can enter a wide variety of host cells. Trypomastigotes then differentiate into amastigotes which replicate in the cytoplasm and differentiate back to trypomastigotes again, which lyse the host cell membrane and exit the cell to continue the infectious cycle in the human. Cardiac and smooth muscle tissues are preferential cellular targets of T. cruzi. The adverse sequelae of infection described below depend on the tissues and organs involved, which is a highly variable and unpredictable factor. Chagas disease is highly complex. While traditionally considered as having acute, indeterminate (chronic–asymptomatic) and chronic (symptomatic) phases, this illness is highly heterogeneous and best considered to be a unique illness for each patient (Bonney et al., 2019). Most infected individuals live normal lives and eventually die of causes other than Chagas disease, completely unaware of their lifelong infection, whereas around 30% of infected people develops clinical manifestations. The acute phase of T. cruzi infection, lasting 4–8 weeks, often has no associated symptoms, despite the fact that the parasite is replicating and spreading throughout the body (Bastos et al., 2010; De Bona et al., 2018). In the case of vector transmission, it is possible to see Romaña’s sign around 5% of the time, when parasites deposited by the triatomine on the face enter the conjunctiva, leading to periorbital inflammation and edema. Chagoma, an inflammatory skin lesion at the site of the insect bite, is also occasionally observed (Bastos et al., 2010). In most cases, however, acute infection is not recognized due to the non-specificity of signs and symptoms (fever, anorexia, and/or flu-like symptoms like body ache). In very rare cases acute infection leads to sudden death, due to parasitization of the cardiac conduction system and a fatal dysrhythmia. In most people, parasite-specific adaptive immunity develops, keeping overall tissue parasitosis and blood parasitemia at very low levels for life. In contrast, approximately one-third of infected individuals develop cardiomyopathy or, to a lesser degree, mega disease of the esophagus or colon, occurring many years after infection. Disease pathogenesis is extremely complex with multiple known and proposed mechanisms of tissue-specific damage. Current data highlight the persistence of parasites in cardiac tissue as a key factor to disease progression, whether by anti-parasite immunity, autoimmunity or other mechanisms, suggesting that reduction of parasitosis through trypanocidal treatment is key to combatting the illness (Hyland et al., 2007; Viotti et al., 2009; Bastos et al., 2010; Bocchi et al., 2017; Bonney et al., 2019). We have recently reviewed pathogenesis (Bonney et al., 2019) and will not discuss this further in this review.

Treatment of

Trypanosoma cruzi Infection

Current Treatment for Chagas Disease

Trypanosoma cruzi infection is treated with Benznidazole (BNZ) or Nifurtimox (NFX), nitroimidazole compounds that have been used for decades. The approach currently practiced by most is to treat all acutely infected individuals, newborns with congenital infection, and anyone under 50 years of age. Further, all immunocompromised individuals such as those with HIV/AIDS or other immunosuppressive disorders or treatments, should be treated to prevent reactivation of chronic infection, normally maintained at very low levels by effective adaptive immunity (Pinazo et al., 2013). BNZ is administered to adults a dose of 5–8 mg/kg/day for 60 days. Children’s doses are somewhat higher because they are more tolerant to the drugs and show quicker resolution of the common hepatic and renal toxicity upon drug cessation. Adults over 50 years of age with chronic T. cruzi infection should be considered individually, balancing the potential benefits and risks based. BNZ treatment is contraindicated for pregnant women and people with significant hepatic and renal illness (WHO, 2020). NFX is recommended as a second line drug, only in the cases of BNZ failure and in the absence of neurological and psychiatric disorders. NFX is administered at 8–10 mg/kg/day for 90 days in adults, and at 15–20 mg/kg/day for 90 days in children (Bern et al., 2007).

Although there are cases in which BNZ has been found to be more effective than NFX, both in the laboratory and in patients, the reasons for these differences are not known (Olivera et al., 2017; Crespillo-Andújar et al., 2018). Limitations of BNZ monotherapy includes the lower probability of parasitological cure in cases of chronic infection in contrast to the high probability of parasitological cure in the acute phase when treatment is maintained for the entire 60 day treatment period (Meymandi et al., 2018). It is also possible that BNZ-resistant T. cruzi clones emerge after partial treatment (Hughes and Andersson, 2017). Finally, the relatively short half-life of the drug (about 12 h), the low penetration of some tissues (Perin et al., 2017) and the occasional serious side effects are additional limitations. These adverse side effects are well-known, and include allergic dermatitis, peripheral neuropathy, anorexia, weight loss, and insomnia (Castro and Diaz de Toranzo, 1988). When they do develop, these side effects occur early in treatment and often become intolerable, causing patients to abort treatment; this can occur in up to 40% of individuals (Castro and Diaz de Toranzo, 1988; Castro et al., 2006; Viotti et al., 2009).

There have been a number of attempts to improve BNZ and NFX therapy, both to increase efficacy and to reduce toxicity, by decreasing the daily dose, giving the drug intermittently, or preemptively treating potential side effects (Bastos et al., 2010; Álvarez et al., 2016; Morillo et al., 2017; Rassi et al., 2017; Cardoso et al., 2018). During the last decade, two important randomized clinical trials were conducted to evaluate the capacity of BNZ to modulate the evolution of Chagas heart disease in adult patients with established cardiomyopathy—the BENEFIT study (Morillo et al., 2015) and the TRAENA trial (Riarte, 2012). Both used a dose of 5 mg/kg/day of BNZ or placebo for 60 days and patient follow up over 5–10 years. Both found that BNZ was able to significantly reduce parasitemia and parasite-specific serum antibodies. However, these trials also showed that BNZ did not significantly reduce progression of clinical cardiac disease through 5 years of follow-up. Additional studies confirmed the low efficacy of BNZ to prevent progression of cardiomyopathy in patients with documented heart disease (Rassi and Rassi, 2010; Rassi et al., 2017). What these trials did not address is the potential benefit of therapy to indeterminate patients. Can drug treatment prevent the development of cardiomyopathy in chronically infected people with no cardiac disease? A retrospective study addressed this directly and showed that treatment with BNZ prevents the development of ECG alterations and decreases parasite-specific antibody titers in indeterminate patients (Fragata-Filho et al., 2016). Taken together, and considering additional studies (Villar et al., 2014; Pérez-Molina et al., 2015), these data suggest that trypanocidal therapy benefits acutely infected individual and chronically infected people who have not yet developed clinical heart disease.

Approaches to Improve Treatment of Chagas Disease

Research on new treatments involves two main strategies: a search for new candidate drugs that are more effective and less toxic to replace BNZ, and a search for adjunctive agents that can either increase the efficacy of BNZ/NFX or reduce their doses to prevent adverse effects. Typically, compounds tested for efficacy as monotherapy are also tested in combination with BNZ/NFX.

The main approaches to preclinical drug discovery for T. cruzi drugs involve seven main groups of inhibitors: (1) inhibitors of ergosterol biosynthesis (e.g., posaconazole and other antifungal azoles), (2) trypanothione metabolism (amiodarone and dronedarona), (3) pyrophosphate metabolism (biphosphonates), (4) cruzipain inhibitors (K777 and derivates), (5) calcium metabolism (amiodarona, dronedarona), (6) protein and purine synthesis inhibitors, and (7) compounds that impair the redox metabolism (nitroaromatic compounds like BNZ, NFX and fexinidazole). Unfortunately, only a few clinical trials for treatment are ongoing or were performed recently for these candidates (Apt, 2010; Sales Junior et al., 2017).

Inhibitors of ergosterol biosynthesis affect the production of the parasite cell membrane and show trypanocidal effects, similar to what they do in fungi. For T. cruzi, a number of antifungals drugs have been found to have good in vitro and in vivo efficacy (Bustamante et al., 2014; Molina et al., 2014; Torrico et al., 2018), both as single agents and in combination with BNZ. Posaconazole, for example, demonstrated trypanocidal activity particularly in combination with BNZ (Bustamante et al., 2014). However, in clinical trials, no advantage was observed with the combined therapy vs. BNZ monotherapy (Morillo et al., 2017). In addition, posaconazole showed no curative effects in patients on its own (Molina et al., 2014). Ravuconazole and E-1224, a ravuconazole prodrug with better drug absorption and bioavailability, are antifungal azoles with potent in vitro activity against T. cruzi. However, E-1224 failed to show sustained efficacy 1 year after treatment in comparison with BNZ and presented some safety issues at high doses (Torrico et al., 2018).

Besides antifungals azoles, the most advanced candidates in clinical trials are amiodarone and fexinidazole, which have ongoing or completed Phase II clinical studies, respectively. One advantage of amiodarone is its potential dual role in patients with cardiomyopathy since it is an antiarrhythmic drug as well as a potent and selective anti-T. cruzi agent (Benaim and Paniz Mondolfi, 2012). Dronedarone, a derivate of amiodarone developed to reduce thyroid toxicity, showed a better profile at a lower dose, and will hopefully be tested in a clinical trial soon (Benaim et al., 2012).

The Drugs for Neglected Diseases initiative (DNDi) has actively chosen to investigate nitroaromatic compounds. Their investigations have proved fruitful, resulting in a trypanosomatid portfolio that contains several agents. The DNDi portfolio published in December 2019 lists fexinidazole as in a Phase IIa clinical trial, whereas new BNZ regimens are in Phase IIb/III. Fexinidazole can induce high levels of parasitological cure in mice infected with BNZ-susceptible, partially resistant and resistant T. cruzi strains in acute and chronic experimental Chagas models (Bahia et al., 2012). These and other data have encouraged DNDi to include fexinidazole in clinical studies. In addition, the BENDITA (Benznidazole New Doses Improved Treatment & Associations) trial showed that a BNZ 2-week treatment course for adult patients with chronic Chagas disease displayed similar efficacy and significantly fewer side effects than the standard treatment duration of 8 weeks, when compared to placebo (DNDi, 2019). DNDi will now continue to work with national programs, partners, and health ministries of endemic countries to confirm these results and encourage the necessary steps to register the new regimen.

Other interesting strategies in preclinical studies are nanoparticle therapy and natural compounds. Considering that a major disadvantage of BNZ is its high toxicity, recent work has employed nanotechnology to attempt deliver this drug in an effective but safe way. The development of nanoparticles for drug delivery is an area of great promise. The earliest particles investigated were liposomal formulations of BNZ, which were developed to target the drug to the liver (Morilla et al., 2004). Since that time a variety of particles have been tested, including polymethacrylate interpolyelectrolyte complexes (García et al., 2018) and the amphipathic poloxamer P188 (Scalise et al., 2016). While these formulations were tested in different in vitro and in vivo systems, they show great promise in delivering BNZ and other trypanocidal agents to parasites and parasitized cells at lower effective BNZ doses with lower associated toxicity.

Natural compounds constitute a newer but nonetheless active area of Chagas drug discovery. Many plants extract display trypanocidal properties, with some demonstrating activity more potent than BNZ or NFX. Like other drugs, natural trypanocides can be useful either as independent agents, or through enhancing the activities of BNZ or NFX by enhancing their uptake by host cells, killing of intracellular amastigotes, or reducing toxicity. Drug repurposing is also being applied to T. cruzi as it is to many infectious and non-infectious diseases (Bellera et al., 2015). Some effective drugs can come from unlikely places, like agents used in cancer chemotherapy (Epting et al., 2017), antivirals, antibiotics, and cardiac medicines (Bellera et al., 2015).

Despite much research by hundreds of researchers over several decades, we still do not have an agent or regimen that is superior to BNZ/NFX for the treatment of T. cruzi infection. Several candidates showed good trypanocidal activity in vitro, but fail preclinical or clinical trials. There are many factors determining the outcome of infection and susceptibility of the parasite to treatment beyond what can be measured through typical studies. In the rest of this Mini Review we discuss other aspects of the host-pathogen interaction that impact the outcome of infection and treatment, which should be considered in whether, when and how to treat infection.

Outcome of

T. cruzi Infection and Efficacy of Treatment Depend on Many Factors

It is difficult to extrapolate the results of in vitro tests to in vivo animal studies and even harder to extend those results to humans. Besides being human, people are highly heterogeneous genetically, and physiologically and respond to most challenges and interventions, including infections and drug treatments, with great variation; this can lead to treatment failures (Francisco et al., 2015). Although success of any treatment can be measured by the reduction of parasitemia and even of parasite-specific serum antibodies, success is ultimately measured by reduction in the development of long-term sequelae such as cardiomyopathy and megacolon. As mentioned above, treatment with intermittent low doses of BNZ in patients with established chagasic cardiomyopathy significantly reduced parasitemia, but not progression of cardiomyopathy (Morillo et al., 2015). Also T. cruzi displays a high degree of genetic and pathogenetic heterogeneity and are commonly present as mixtures of distinct parasite clones in a single infected triatomine or infected host (Pronovost et al., 2018). However, it is theoretically possible to predict the outcome of infection—subclinical for life, cardiomyopathy, mega disease—if we knew more about the genetic and physiologic basis of parasite virulence (broadly defined) and host susceptibility (also broadly defined). We are a long way from this understanding today. Variability in host physiologic factors such as nutrition, immune status, existence of coinfections, etc., further complicate the issue. The balance among host genetics, host physiology and parasite genetics determine outcome of infection and response to treatment. A number of these are discussed below. The reader should keep in mind that these factors are ultimately based in large part on the genetics of host and parasite, which makes a systems approach to Chagas disease management possible in the future.


In the absence of other information, epidemiologic data can be of modest help in predicting the outcome of T. cruzi infection. Information about patient origin, possible form of transmission (insect, congenital, oral), presence of other conditions such as immunosuppressive states such as cancer, HIV coinfection, or treatment with immunosuppressive drugs, may inform patient management. Clearly, infected individuals who are immunocompromised need treatment. Other aspects of the infection, such as the location where infection takes place, and by extension the characteristics of the human and parasite populations, can be useful. An estimated two-thirds of infected Brazilians are infected with the TcII strain of T. cruzi (Brenière et al., 2016; Zingales, 2018), one of seven discrete typing units (DTU) TcI-TcVI, plus TcBat (Zingales et al., 2009; Lima et al., 2015). Some of these DTUs can be identified serologically (Bhattacharyya et al., 2019). TcII strains, represented by the common laboratory strain Y, generally exhibit high virulence and may produce mega disease as well as cardiac disease in chronic infection (De Oliveira et al., 2008; Oliveira et al., 2017). In contrast, people from Argentina and Bolivia frequently are infected with TcV strains and frequently develop cardiomyopathy (Zuñiga et al., 1997; Messenger et al., 2015; Quebrada Palacio et al., 2018; Zingales, 2018). Other DTUs such as TcI (e.g., Colombian) or TcVI (e.g., Tulahuen) have a tendency not to cause clinical disease and are often used in chronic indeterminate mouse models of infection (Chandra et al., 2002; Santana et al., 2014). Unfortunately, the DTU system alone is not sufficient to predict disease outcome or response to therapy since there is no single outcome associated with any given DTU. No physician would withhold drug treatment in an acutely infected individual simply based on the fact that they may be infected with one particular T. cruzi strain or another.

Parasite Virulence

Virulence is a complex term in its own right. It is important to carefully define at each use. Virulence could be the capacity of T. cruzi to invade host cells, replicate, and emerge after host cell lysis. This leads to high parasitemia in experimental animals. It could refer to tissue tropism, with some tissue infections being more harmful to the host than others. Virulence might refer to the ability of the parasite to kill its host. At some level, considering the parasite alone, virulence is based on genetic elements. Virulence may be conferred by specific parasite surface proteins or secreted proteins that signal host cells, facilitating parasite entry and replication. Molecules from trans-sialidase and cruzipain families are well-established virulence factors of T. cruzi and validated targets for drug discovery. Cruzipain also participates in the modulation of the host cell immunity, highlighting the key role of the host response in the establishment and outcome of T. cruzi infection (Guiñazú et al., 2004; San Francisco et al., 2017). High virulence is usually defined as the ability to cause high parasitemia and/or tissue parasitosis and/or death of experimental animals (Sales-Campos et al., 2015). This is based in part on the ability to invade and/or replicate in host cells more rapidly than do low virulence isolates. Low virulence strains are more likely to cause low-level chronic infection that may never cause clinical disease (Cardillo et al., 2015). As mentioned above, the commonly used high-virulence Y strain of T. cruzi causes death in young C57BL/6 mice between 14 and 21 days post-infection in conjunction with maximal parasitemia (Casassa et al., 2019). By contrast, the K98 strain causes chronic infection. It should be emphasized that virulence is equally influenced by the host (Ferreira et al., 2018), as discussed in more detail below.

Tissue Tropism

Another characteristic of T. cruzi is differential tissue tropism. Some isolates of this parasite have a propensity to infect certain tissues over others. This may be due to specific affinity for certain host cell surface molecules, preferential ability to replicate in some cells better than others, or specific attraction to an organ-specific vascular bed. If a person becomes infected with a myotropic strain, it is more likely that cardiac pathology or skeletal myositis will develop. On the contrary, a pantropic strain may affect many organs and promote development of megaesophagus or megacolon. Tropism can be ascertained by in vitro testing using different cell lines. A strain with cellular myotropism will prefer H9C2 cardiac myoblasts or human skeletal myoblasts (Jorge et al., 1986; Mirkin et al., 1997; Aridgides et al., 2013), while a pantropic strain will not have a preference, for example affecting kidney cells and embryonic fibroblasts equally (Piras et al., 1982; Jorge et al., 1986; Medina et al., 2018). Information about the tropism of parasite clone or clones could potentially be important in guiding treatment decisions, including a decision not to treat. The challenge of course is to determine potential tropism or other characteristics of a clone without having isolated and cultured parasites for laboratory study. There may be ways to do this in the future using a combination of advanced imaging and molecular approaches (see below). In the meantime, it is really not possible to predict the tissue tropism of a strain based on the region of origin or DTU.

Drug Resistance

The differential resistance of T. cruzi to BNZ among isolates has been documented (Bustamante et al., 2014; Abegg et al., 2017; Vieira et al., 2018). This intrinsic resistance in some strains could explain why some patients receiving the same BNZ treatment show parasitological cure while others do not. Similar to virulence, the capacity of parasites to resist or be susceptible to a drug is genetically determined by the presence of specific factors. The T. cruzi Colombian and V-10 strains are highly resistant to BNZ, while the Y and Dm28c strains are partially resistant and the CL strain is highly sensitive (Filardi and Brener, 1984; Bahia et al., 2012; Reigada et al., 2019). Somewhat paradoxically, intracellular replication of some strains is enhanced by the presence of BNZ and the associated production of reactive oxygen species (Paiva et al., 2018). Several have proposed that different T. cruzi DTU have different resistance to BNZ and NFX (Cencig et al., 2012; Teston et al., 2013). Some DTU are more resistant to BNZ than others, although even within a single DTU there can be variability in BNZ sensitivity (Quebrada Palacio et al., 2018). Interestingly, parasite strains of different DTUs do show common BNZ susceptibility and resistance patterns (Revollo et al., 2019). Clearly there can be much greater refinement in genetic characterization of T. cruzi than the DTU system but it is a measure that has shown great utility in many studies. However, data from genotyping could be used to predict the susceptibility of an isolate to drug treatment. As mentioned above and discussed below, the challenge is to be able to genotype or phenotype parasites without isolating them, since in many chronically-infected patients circulating parasites are rare or absent. As a relatively crude measure of T. cruzi sensitivity to BNZ, quantitative PCR to detect parasite DNA in blood before and after BNZ treatment is the best we have at the moment (Britto et al., 1999; Maffey et al., 2012; Barros et al., 2017; Rodrigues-dos-Santos et al., 2018). It is also possible that parasite dormancy may play a role in drug resistance (Sánchez-Valdéz et al., 2018).

Host Factors in Parasite Susceptibility and Resistance

As in many diseases, the outcome of T. cruzi infection is determined not only by the pathogen, but also by the host. We tend to focus on immunity but there are other intrinsic (innate) factors that may also contribute to susceptibility and resistance. These known and unknown attributes are bundled in the vague term “genetic factors.” Beyond the genetic factors there is also host nutritional status, possible presence of coinfections, and other environmental factors that may influence outcome. This concept is best exemplified by the finding that most T. cruzi-infected individuals have no clinical signs or symptoms of infection—ever. Regarding host genetic background, T lymphocytes in chronic patients with no clinical disease have a high frequency of CD4+ and CD8+ T cells expressing HLA-DR and CD45RO (Dutra et al., 1994), with little to no costimulatory CD28 (Dutra et al., 1996; Menezes et al., 2004; Albareda et al., 2006). This profile positively correlates with the expression of the regulatory cytokine IL-10 (Menezes et al., 2004) and also with the presence of CTLA-4, a costimulatory molecule which leads to T cell modulation (Souza et al., 2007). Since CD8+ T cell destruction of parasitized cells can lead to tissue inflammation and clinical disease, it is possible that immunoregulatory mechanisms in these patients prevent pathology and facilitate lifelong indeterminate, subclinical disease. The balance between proinflammatory and anti-inflammatory immune responses is central to the outcome of infection. Although a pro-inflammatory adaptive immune response is necessary to control T. cruzi, immunoregulation is necessary later on to prevent tissue destruction and possible subsequent autoimmune damage (Bonney and Engman, 2015). In this way, IL-10 plays an essential modulating role in controlling disease development. The ability to express IL-10 at sufficiently high levels may be genetically determined and may influence disease outcome. Studies in experimental models of T. cruzi infection demonstrate the influence of host immune response in the outcome of infection. BALB/c mice, which develop a Th3-skewed response upon T. cruzi infection, are hypersensitive to infection and do not survive the acute phase. In contrast, C57BL/6 mice, which develop Th2 immunity through the IL-12/IFN-γ/iNOS axis, control the parasite and show low parasitemia and mortality during the acute phase (Michailowsky et al., 2001).

Toward Precision Health Management of Chagas Disease

As described above, T. cruzi infection and Chagas disease are highly complex. At the present time, no single factor or combination of factors can predict disease outcome or response to therapy in an infected individual. The assignment of T. cruzi strains to DTUs and the assessment of a person’s HLA haplotype and other immunogenetics are starting points. In chronic infection it is often not possible to isolate parasites for analysis and, even if successful, the parasite isolated may not represent all parasite clones present in the patient, which might have different pathogenic potential. Detection of parasites in chronically infected individuals is most frequently accomplished by PCR (Schijman et al., 2011) and this method has also been used to monitor the effect of therapy on parasite persistence (Morillo et al., 2015; Sulleiro et al., 2019). Unfortunately, the sensitivity of PCR is problematic—only 60% in the large BENEFIT Trial of several thousand patients (Morillo et al., 2015). Although there are many possible reasons for this, a likely reason is suboptimal sampling. Perhaps a proteomic approach would be better and recent work detecting T. cruzi antigens in circulating immune complexes from infected individuals is promising (Ohyama et al., 2016). A major breakthrough in patient management would be the ability to assess the distribution of parasites in the body, much as is done today with nuclear medicine scans for cancer. We can do this in mice employing bioluminescent imaging of engineered luminescent parasites (Hyland et al., 2008) but obviously this is not possible in patients. Interestingly the infection in mice is highly dynamic with migration of parasite foci around the body over time (Lewis et al., 2014). Development of approaches to image parasites in an infected person to determine location(s) and burden would enhance the care of Chagas patients if these are found to be linked to organ-specific dysfunction. Another would be the detection of parasite-free T. cruzi DNA in blood or body fluids, much as is done today for circulating tumor cell DNA. In this way it is theoretically possible to genotype all parasite clones in an infected individual, perhaps quantitatively, by next generation sequencing (NGS), in the absence of circulating parasites. This is an active area of investigation in a number of laboratories (Domagalska and Dujardin, 2020).

A more refined genetic analysis of T. cruzi than the DTU system will no doubt emerge through large scale NGS whole exome or genome analysis of parasites and integration of this information with detailed clinical information and patient outcomes, including response to treatment. In this way, the complex interplay between parasite and host genetics that ultimately determines the outcome of infection might emerge. This may not happen tomorrow, but it is a major goal of the medical field as applied to many diseases, both infectious and otherwise. Unfortunately genome wide association studies have not been successful in identifying gene polymorphisms associated with disease progression (Deng et al., 2013). Regarding drug treatment, a comprehensive, systems approach to parasite and host will essentially allow a pharmacogenomic approach to treatment, much as is done today for personalized treatment decisions for cancer, arrythmias and pain management (Wang et al., 2011).

How will this happen? Until now, associations between biological data and biological behaviors were deduced from simultaneous consideration of small numbers of data features from a laboratory experiment or clinical trial. This limitation has hindered our understanding of polygenic diseases like diabetes and coronary heart disease. The advent of machine learning now allows the simultaneous analysis of hundreds or even thousands of features across a very large number of biological samples employing supercomputing to identify relationships among the features (Rajkomar et al., 2019). For some applications, the machine needs to be “trained,” for example by “learning” the associations of histologic images with cancer types. If all goes well with the training, the computer can then type the cancer with high accuracy (Esteva et al., 2017; Gertych et al., 2019). Extending the histology example further, there is information in a complex image like tissue histology that reflects underlying genetic modifications, such as DNA methylation, and machine learning can identify those subtleties in a way that the human eye never could (Zheng et al., 2020). This approach can also be applied to molecular data de novo for gene discovery (Wood et al., 2018). Ultimately, the promise of precision health will be realized by the application machine learning to a wider variety of data features and, for Chagas disease, this means clinical data, basic patient information, including demographics, baseline genome sequence, behavioral and physiological data and, of course, genomic information of the parasite clone(s) infecting the person. We believe that it is only a matter of time when this will be science and not just science fiction.

As an intermediate step between the present and future, we propose a highly simplistic theoretical approach to categorizing T. cruzi infection and treatment. Refinement of this model over time by adding levels of sophistication might eventually yield a useful tool for patient management. For example, considering five attributes derived from host or parasite it is possible to generate a pictorial representation of the infection (Figure 1). This is based loosely on the modeling of Santi-Rocca (Santi-Rocca et al., 2017). Each attribute—parasite genetics, host genetics, T helper phenotype, epidemiology, and response to BNZ can be “scored” from 1 to 5, with 1 corresponding to the lowest level of a particular attribute and 5 the highest. When applied to two different infections, Patient 1 having a low-level, chronic infection with no clinical disease and Patient 2 having significant cardiomyopathy, a pictorial representation of the infection can be generated. The attributes are listed below each patient in clockwise order from the top. Clearly this is so simplistic that it is not useful today. These attributes are not really “scorable” in this way and do not correlate in the manner shown in these examples. However, simplistic, this approach does give a preliminary glimpse into a future analytic scheme that shows how specific features of host and parasite might contribute the ultimate outcome of infection and responsiveness to treatment.

Figure 1. Preliminary simplified model for assessing a Trypanosoma cruzi-infected individual. See text for description and discussion.

In terms of refinement, the field really does need to move beyond studies of laboratory strains to analyze strains present in patients and insects in a systematic and non-biased way through NGS. It is possible that the DTU structure will have value over time since if nothing else DTU by definition reflects the genetic relatedness of strains. We foresee a day when genotyping of the strain(s) present in each patient will become part of the standard workup of T. cruzi infection and that NGS genotyping of circulating parasite DNA will solve this problem. The premise underlying this entire discussion is that, ultimately, disease outcome and response to therapy can be predicted based on the genotypes of parasite and host, both as independent factors and in combination. The latter notion is based on the well-known fact that an individual parasite strain shows differential virulence depending on the host, and that an individual host has different disease outcome depending on the parasite strain. This complexity is challenging but no more so than in many other polygenetic diseases affecting millions.


Since its discovery more than 100 years ago (Chagas, 1909), Chagas disease has proven to be a major clinical and public health challenge due to the extreme heterogeneity in the outcome of infection, the wide range of mammalian hosts and reservoirs, the large geographic range of its triatomine insect vectors, worldwide migration of infected individuals, and paucity of drugs. While we have discussed the potential future for disease diagnosis, prognosis and patient management, the ultimate solution is the development of an effective and curative treatment having low toxicity. Better yet, a safe and effective vaccine that provides sterilizing immunity or even immunity sufficient to minimize the parasite burden to prevent clinical disease. Science and medicine are developing rapidly and we are hopeful that someday T. cruzi and Chagas disease will be considered manageable infections, much like the viral and bacterial infections that were previously deadly and now are managed through vaccination and effective drug treatments.

Author Contributions

All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.


This work was funded in part by NIH grants R01-HL075822 and GM93359. SM was supported by a Wood-Whelan Fellowship from the International Union of Biochemistry and Molecular Biology.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


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  • Nine creatures drinking other people’s blood

    • Zaria Gorvett
    • BBC Future

    Photo author, NPL

    Photo caption,

    This bird does not look like Dracula. But she loves other people’s blood no less than

    Thanks to pop culture, the vampire is usually represented as either the gloomy Transylvanian Count Dracula, or the immortal teenager from The Twilight Saga gleaming in the sun. But on our planet there are also real, not fictitious bloodsuckers, the correspondent was convinced

    BBC Earth.

    Sharp-billed earthen finch (Geospiza difficilis septentrionalis)

    Photo author, NPL

    Photo caption,

    Sharp-billed earthen finch (Geospiza difficilis) drinks the blood of a blue-faced booby (Sula dactylatra)


    novel. Around Wolf Island, the Pacific Ocean stretches for a thousand kilometers in all directions.

    This is the farthest frontier of the Galapagos, a hot wasteland covered with sharp lava rocks and tangled scrub.And vampires rule here.

    Tiny and outwardly unremarkable, sharp-billed ground finch is a close relative of the seed-eating ground finch. But do not let its nondescript appearance deceive you.

    His diet also includes grains and vegetation, but at the same time he has also adapted to the island life in a special way.

    Sharp-billed earthen finches sit on a larger bird – for example, a blue-footed booby – and with a sharp beak pierce the skin in the area of ​​the tail feathers, extracting blood.They often attack defenseless chicks sitting in nests.

    Surprisingly, the victims of the vampires have little to no resistance. One possible explanation for this behavior is that finches first bit off parasites from bird feathers – and then evolved into bloodsuckers. Or maybe large birds are just too lazy to drive them away.

    Thanks to its vampirism, Sharp-billed Ground Finches survive even in the driest months and are the most abundant bird species on the island.

    Sometimes several finches even line up for a victim, patiently waiting for their chance to feast on blood.

    Predators (Reduviidae family)

    Photo Credit, NPL

    Forests and jungles around the world are teeming with cold-blooded killers. The name of the predators speaks for itself, and they have all the necessary deadly tools – stealth, insidious strategy and lethal weapons.

    Approximately 7000 species of these bugs have a very different diet – some hunt bees, others drink the blood of vampire bats.But they are all equipped with a deadly proboscis.

    Most predators usually kill their prey before they eat it. Predators, on the other hand, inject digestive secretions into their prey through the proboscis instead.

    After its insides turn into a nutritious soup, the proboscis begins to act as a straw through which the predator sucks in the contents of the victim, without thinking about whether she is still alive or not.

    Most predators feed on insects and use various tricks in the hunt.For example, the species Stenolemus bituberus hunts for spiders sitting in their webs – an enterprising predator twitches the strings, imitating the movements of entangled prey, and ambushes a spider that has come to check what is the matter.

    The termite-hunting Salyavata variegata is even more cunning. To begin with, the predator finds the first prey: after waiting for the worker termite at the entrance to the termite mound, it pierces it with its proboscis and sucks it out, and then pushes the remains into the nest.

    After some time, new prey appears, pulling out the corpse of a comrade: instinct makes termites remove dead relatives from their homes.

    Another predator species, Acanthaspis petax, feeds on ants. They use the shells of the eaten victims in a particularly cynical way, sticking them on themselves for additional protection.

    Scientists have met predators with up to 20 dead ants.

    Predators do not disdain people either. Kissing bugs have been drinking human blood for thousands of years. They owe their name to the habit of sticking to the face of a sleeping person, which at one time irritated the most famous biologist in history.

    Charles Darwin encounters kissing bugs while cruising the Beagle around the world. “It’s disgusting to feel like soft wingless insects about an inch long crawling all over your body,” he wrote about the experience.

    Kissing bugs are the main vector for Chagas disease, a parasite that lives in the bugs’ digestive system and infects the wound when bitten.

    This chronic disease is gradually undermining heart health, and some experts believe that Darwin died from it in the end.

    Flying vampire frog (Rhacophorus vampyrus)

    Photo by Jodi Rowley

    The foggy jungle of South Vietnam is one of the wettest places on our planet. They are constantly submerged in clouds, which soak tree crowns with water.

    This environment is ideal for amphibians, but you probably don’t expect to see vampires here.

    This is what biologist Jody Rowley, who came on a business trip in 2010, also thought. But very soon a group of scientists under her leadership discovered a flying frog, hitherto unknown to science.

    Back at the Australian Museum in Sydney, where she works, Rowley tried to get a good look at the tiny eyes of the captured tadpoles by placing one specimen under a microscope.

    “To my great amazement, I saw protruding black fangs! And I assumed they would have the usual mouthparts of a tadpole – such, you know, an unremarkable beak-shaped thing,” Rowley told BBC Earth. But why does a tadpole need fangs?

    Photo author, Jodi Rowley

    Photo caption,

    Tadpole Rhacophorus vampyrus

    Adult vampire frogs spend their entire life in the crown of trees, planning from branch to branch with the help of large membranes between the fingers.

    To prevent eggs from becoming prey for predators, female frogs lay them not in streams or puddles on the ground, but near water-filled depressions in tree trunks, whipping eggs into sticky foam with their hind legs.

    When tadpoles are born, the foam liquefies, and they fall down into a hollow with water. They have nothing to eat there, so after a while the female returns and lays new eggs.

    “They don’t suck blood – they use their fangs to grab eggs into their big mouths, swallowing them whole,” explains Rowley.

    Kenyan jumping spider (Evarcha culicivora)

    Photo author, Robert Jackson


    The jumping spider Evarcha culicivora eats the Anopheles gambiae mosquito

    The Kenyan jumping spider is even partly a pity. This spider, which lives in the Lake Victoria region in eastern Africa, simply adores human blood.

    But fate is unfair to him: he does not have specialized mouth devices that allow him to pierce the skin.

    Therefore, spiders have to get blood through intermediaries, namely, to feed on sucked mosquitoes.This is the only species of living creatures known to science that chooses prey depending on what it ate.

    At the same time, jumping spiders are very picky in their eating habits.

    If given the opportunity, they prefer to feed exclusively on female Anopheles gambiae mosquitoes, the main vector of malaria in Africa. But hunting just one species in an insect-infested region is challenging.

    Spiders recognize malaria mosquitoes by the 45-degree angle of the abdomen in a sitting position, and are able to distinguish a blood-filled mosquito from a hungry mosquito by smell.

    Ximena Nelson of the University of Canterbury in New Zealand tried to understand how they distinguish between females who drink blood and males who do not.

    To figure this out, Nelson set up a bizarre experiment, in preparation for which she built monster mosquitoes resembling the creation of Dr. Frankenstein.

    She took the heads, breasts and abdomens of females and males of two mosquito species and glued them together in different combinations. Then she fixed these stuffed animals in the poses characteristic of them in life and showed them to the spiders.

    It turned out that spiders first of all notice the characteristic fluffy antennae: they always chose a stuffed animal with a female head.

    Lingual wood lice (Cymothoa exigua)

    In January 2015, the Internet shuddered in disgust after a woman from Nottingham, English opened a can of tuna and found two beady eyes staring at her.

    The culprit of the network phenomenon with the tag #tunagate turned out to be the tongue wood louse. The way of life of this creature is so strange that you can’t imagine such a thing on purpose.

    This parasite starts life as a male and looks for a suitable fish, and when it finds it, it penetrates into it through the gills, crawls into its mouth and begins to transform.

    He hooks his feet on the base of the fish’s tongue and begins to drink its blood, rapidly increasing in size and at the same time turning into a female. In woodlice, the eyes are smaller and the legs are lengthened.

    Sooner or later, the dried tongue of the fish falls off, and woodlice comes to replace it. From this moment on, the fish uses the parasite as a prosthetic tongue.

    The female woodlouse mates with males living in the gills and gives birth to offspring, which spreads to the sides in search of a new host.

    Crested scoop (Calyptra thalictri)

    Night moths look harmless, but not all of them feed on flower nectar. Calyptra butterflies are found throughout Europe and typically use their pointed proboscis to drink from the flowers and pierce the fruit rind.

    But some have evolved into less harmless habits.So, male crested scoops, originally from Siberia, drink the blood of mammals, including humans, with the help of their proboscis.

    And males of some species of Asian scoops stick to larger animals: cows, rhinos and even elephants.

    Ordinary Vandellia cirrhosa

    Piranhas, you say? What about the small, translucent kandiru fish found in the Amazon? That’s where the tourist’s nightmare is!

    This miniature catfish can crawl into even the narrowest bodily openings and anchor itself inside with backward-pointing spines on the gills.

    Some species of this fish do not exceed a centimeter in length, but there are also those that grow up to 40 centimeters.

    Candiru became widely known in the 1990s, after reports that one of these fish allegedly climbed into the urethra of an unlucky man through the stream of his urine and settled there. But, fortunately, there is hardly any truth in this myth.

    In fact, kandiru are usually taken into the gills of other catfish, although cases are known when they were found in open wounds.

    Vampire bacteria

    Photo author, Daniel Kadouri

    Photo caption,

    Micavibrio aeruginosavorus (yellow) attacks the bacterium Pseudomonas aeruginosa (pink)

    Micavibrio aeruginosavorus is the smallest known predator. This bacterium, shaped like a tadpole, feeds on other microorganisms, sinking “teeth” into their outer membranes and sucking juices.

    It was discovered more than 30 years ago, but it is difficult to study, because in laboratory conditions its genetic information is clogged with the genes of the bacteria that it feeds on.

    “Even if you give it all the nutrients it needs to survive, it won’t grow,” says Martin Wu, professor of biology at the University of Virginia.

    But this is a useful vampire.

    His favorite food is a pathogen called Pseudomonas aeruginosa, which causes a life-threatening lung infection in patients with cystic fibrosis.

    Pseudomonas aeruginosa is very difficult to destroy, since the colonies of these bacteria are able to form a protective film that protects them from antibiotics.

    However, Micavibrio aeruginosavorus is able to overcome this barrier and kill harmful microorganisms that are protected from conventional drugs.

    “This is possibly the first live antibiotic we know of,” says Wu.

    Dodder (genus Cuscuta)

    Photo author, NPL

    This weed is quite a match for the predatory plant monsters from the fantasy horror novel “Day of the Triffids”.

    Dodder sniffs out the victim, puts it in a doze and eats it alive.Once, dodder grew only in Europe, but now it has spread over most of the continents of our planet.

    Dodder stems, like other plants, can absorb solar energy – but they don’t.

    Usually, plants tend to leave the shaded corner and get out into the sun, but dodder, using similar light and shadow recognition mechanisms, moves in the opposite direction in search of prey.

    “However, she seems to be able to smell the plants,” says Jim Westwood, professor of phytopathology at the Wygryn Polytechnic Institute in the USA.“Perhaps this helps her to choose a target.”

    Having attached to the host plant through special suction cups, the parasite receives almost all the necessary nutrients from it. the target intercepts the messages encoded in RNA.

    But the matter is not limited to this: the parasite also sends its own signals.The host appears to be directly manipulated, “Westwood says.

    Fight Neglected Diseases – Bayer Pharmaceuticals Russia

    Tropical Disease refers to infectious diseases that develop in the hot, humid conditions of the tropics. Almost synonymous with Neglected Diseases ”Refers to infectious diseases that primarily affect the most vulnerable segments of the population in the poorest countries, where methods of prevention and treatment of these diseases are not available.This is especially true for residents of remote rural areas.

    Chagas disease

    Chagas disease is an infectious disease caused by unicellular parasites and transmitted to humans by blood-sucking bugs. In the context of globalization, Chagas disease is increasingly evolving from an endemic disease in Latin America to a global threat to health systems in North America and Europe.

    How dangerous is Chagas disease?

    Chagas disease can be lifelong if left untreated, causing severe organ damage and life-threatening.

    Who is at risk?

    People living in rural areas of endemic countries are at the highest risk of infection. The main route of transmission of infection is vector-borne. Transfusions of blood products, organ transplants or transmission from an infected mother to a newborn are also serious risks of infection.

    How many people have Chagas disease?

    An estimated 6 to 8 million people worldwide are infected with Trypanosoma cruzi, the parasite that causes Chagas disease.Due to the absence of pathognomonic symptoms, most of them do not know about the infection in the body until serious signs of organ damage appear, which manifests itself many years later.

    Where does Chagas disease occur?

    Chagas disease is most common in some areas of 21 countries in Latin America. Due to massive urbanization and migration to other regions of the world, Chagas disease is increasingly being detected in cities in Latin America and countries that were not previously considered the territory of its distribution – the United States of America, Canada, Europe and some countries of the Western Pacific Ocean.

    How do people get Chagas disease?

    Chagas disease is not transmitted from person to person, but mainly through a transmission route. The insect vectors are called triatomite bugs. After being bitten and consuming blood, they defecate on human skin. A person can become infected if Trypanosoma cruzi parasites enter the body through mucous membranes or skin defects from the bugs’ feces. A person can accidentally rub stool into a bite wound, or bring it into scratches on the skin, eyes, or mouth.

    Other routes of infection:

    • vertical – from an infected pregnant woman to a child;
    • for blood transfusions;
    • for organ transplantation;
    • when eating raw food contaminated with the faeces of infected bed bugs;
    • in case of incidents in the laboratory.

    Bayer Contribution

    Bayer has developed one of two existing effective treatments for Chagas disease for the treatment of Chagas disease.Its active ingredient – nifurtimox – is included in the WHO list of vital medicines. Since 2000, Bayer has supported WHO in meeting the growing demand for this drug. The company has conducted a major clinical trial to obtain data on the safety and efficacy of the drug in children aged 0- <18 years and is currently developing a new dosage form suitable for use in children.

    African sleeping sickness

    African sleeping sickness is insidious and deadly, and social rejection only adds to the suffering of patients.This disease, also known as human African trypanosomiasis, threatens millions of people in many sub-Saharan countries.

    How dangerous is human African trypanosomiasis?

    African trypanosomiasis can be fatal if not treated promptly. In addition, if treatment is not carried out early, there is a high risk of patient disability.

    Who is at risk?

    People living in rural areas and dependent on agriculture, fishing, livestock or hunting are at the highest risk of infection.Even in the regions where the disease is spread, most flies do not tolerate parasites – the risk of infection increases with the number of tsetse fly bites of a person. Tourists are not at high risk of contracting African trypanosomiasis if they do not spend a lot of time in rural areas of tropical Africa – for example, in nature reserves where the disease is common. City travelers are not at risk of infection.

    How many people have this disease?

    Thanks to large-scale WHO interventions, the number of reported cases in 2009 fell below 10,000 for the first time in 50 years, and in 2017 did not reach 2,000.However, due to hostilities in some areas, many cases remain undiagnosed to this day.

    Where is African trypanosomiasis found?

    Sleeping sickness occurs in 36 countries in sub-Saharan Africa, which are home to tsetse flies, which are carriers of the disease. The most common type of disease, Trypanosoma brucei gambiense infection, occurs in 24 countries in West and Central Africa. This form accounts for 98 percent of reported cases of sleeping sickness and is a chronic infection.More than 95 percent of cases are reported in the Democratic Republic of the Congo, Angola, Sudan, the Central African Republic, the Republic of the Congo, Chad and Northern Uganda.

    Where is African trypanosomiasis found?

    Sleeping sickness occurs in 36 countries in sub-Saharan Africa, which are home to tsetse flies, which are carriers of the disease. The most common type of disease, Trypanosoma brucei gambiense infection, occurs in 24 countries in West and Central Africa.This form accounts for 98 percent of reported cases of sleeping sickness and is a chronic infection. More than 95 percent of cases are reported in the Democratic Republic of the Congo, Angola, Sudan, the Central African Republic, the Republic of the Congo, Chad and Northern Uganda.

    How do people get this disease?

    A person becomes infected with African trypanosomiasis through the bite of an infected tsetse fly. Sometimes a pregnant woman can pass the infection on to her baby.In theory, the infection can be transmitted through blood transfusion, but such cases are rarely documented.

    Bayer Contribution

    Bayer offers two substances for the fight against human African trypanosomiasis. Both are included in the WHO List of Essential Medicines. Since 2000, Bayer has provided these drugs to WHO at no cost. Since 2013, the company has been financially contributing to the establishment of WHO mobile emergency medical teams in the Republic of the Congo, the country with the highest burden of African sleeping sickness.

    River blindness

    Onchocerciasis is an infection caused by a parasitic worm transmitted by the bite of an infected midge, which occurs primarily in agricultural areas of sub-Saharan Africa. The disease is called river blindness because the transmitting fly reproduces in fast flowing streams, and the infection itself can cause blindness.

    How dangerous is onchocerciasis?

    Among the infectious causes of blindness in the world, onchocerciasis is second only to trachoma and can also cause debilitating and disfiguring skin lesions.

    Who is at risk?

    People living near rivers with Simulium midges, mainly in sub-Saharan Africa, are at greatest risk of contracting onchocerciasis. Many bites usually occur before infection. People who are less than three months in areas where the parasite lives are at a low risk of contracting O. volvulus.

    How many people have onchocerciasis?

    The WHO expert committee on onchocerciasis estimates that at least 25 million people are infected with it, and a total of 123 million people live in areas where the disease is spread.About 300,000 people were blinded by the parasite’s bites, and another 800,000 suffered from visual impairment.

    Where is onchocerciasis found?

    Onchocerciasis occurs mainly in tropical regions. More than 99% of infected people live in 31 countries in sub-Saharan Africa: Angola, Benin, Burkina Faso, Burundi, Cameroon, Central African Republic, Chad, Republic of the Congo, Côte d’Ivoire, Democratic Republic of the Congo, Equatorial Guinea, Ethiopia, Gabon, Ghana, Guinea, Guinea-Bissau, Kenya, Liberia, Malawi, Mali, Mozambique, Niger, Nigeria, Rwanda, Senegal, Sierra Leone, South Sudan, Sudan, Togo, Uganda, United Republic of Tanzania.The disease also occurs in Yemen, Brazil, and Venezuela.

    How do people get onchocerciasis?

    Onchocerciasis is transmitted to humans through repeated bites of infected midges from the genus Simulium.

    Bayer Contribution

    In 2014, Bayer signed an agreement with Drugs for Neglected Diseases (DNDi) to jointly develop a new treatment for river blindness. DNDi is a patient-centered, non-profit drug research and development organization dedicated to developing new treatments for neglected diseases.The existing drugs for river blindness are effective only against microfilariae of parasites, that is, larvae and young worms. However, adults live to the end of their natural life and produce more and more new generations of offspring. Thus, drugs must be prescribed as part of a mass-use program for up to 15 years. The compound Bayer is working on is a macrofilaricide that also kills adult nematodes. It will help to significantly shorten the duration of treatment, thus allowing tremendous progress in the long-term fight against river blindness.

    Science: Science and Technology: Lenta.ru

    Scientists at the University of California have discovered a new substance that can help in the treatment of COVID-19. K777, which is considered a potential drug against Chagas disease, has surprisingly been shown to be an effective inhibitor of cathepsin L, an enzyme that contributes to the infecting of human cells with the virus. The discovery is reported in an article published in the journal ACS Chemical Biology.

    It is known that SARS-CoV-2 cannot attach to and infect human cells unless a human enzyme called cathepsin L breaks down the S-protein (spike protein) of the virus.At the same time, cathepsin is very similar in structure to cruzain, which is produced in the parasite Trypanosoma cruzi , the causative agent of Chagas disease (American trypanosomiasis). It is a chronic, tropical disease that contributes to the development of heart failure and other irreversible damage to internal organs.

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    Scientists have been looking for protection from coronavirus all year.Will they be able to defeat him?

    00:01 – April 4, 2020

    Researchers have shown that low concentrations of K777 inhibit cathepsin L, which can reduce SARS-CoV-2’s ability to infect cells without harming them. Different cell lines were used in the experiments, but not all of the inhibitor had an effective effect. Experts attribute this to the fact that not all cell lines produce the same amount of cathepsin L or the same amount of ACE2. ACE2 is a cellular receptor that the viral spike protein uses to bind to the cell membrane after it has been cleaved by cathepsin L.

    The cell lines tested were obtained from African green monkey kidney epithelium, human cervical epithelium and two types of human lung epithelium. They are cancer cells, so their molecular characteristics may differ from healthy human lung or cervical cells.

    At the same time, an experimental therapeutic agent based on K777 has been shown to prevent lung damage from coronavirus infection in animals and is well tolerated by people who participated in clinical trials.

    Fast news delivery – in the “Feed of the Day” in Telegram

    sickness and disease – Translation into Russian – examples English

    These examples may contain rude words based on your search.

    These examples may contain colloquial words based on your search.

    Dwindling stocks of food and medicines are adding to the vulnerability of the civilians to sickness and disease .

    Dwindling supplies of food and medicine further increase the vulnerability of civilians to diseases .

    Poverty weakens the body, making it susceptible to sickness and disease .

    The health program focused on supporting the consolidation of government-sponsored primary health care services, and on educating communities to create healthful habits and to prevent sickness and disease .

    The health program focuses on helping to consolidate government-funded primary health care services and educating communities to create healthy environments and prevent diseases and diseases .

    The widespread use of contract or agency labor at mines can undermine the very notion of sustainable development by condemning current workers and future generations in many countries to poverty, sickness and disease .

    The widespread practice of hiring temporary workers to work in mines under contracts or through recruitment agencies can undermine the very idea of ​​sustainable development, as such practices doom current and future generations of workers in many countries to poverty, hunger and disease.

    There is sickness and disease that is everywhere.

    Azerrad also noted that “irtually every song contains some image of sickness and disease “.

    This lack of availability of and accessibility to food has had significant negative impact on the nutrition and health status of people as it can cause immune systems to weaken, making people vulnerable to sickness and disease .

    This food shortage is causing serious nutritional and health problems, resulting in a weakened immune system and an increased vulnerability of the body to diseases and diseases .

    Suggest an example

    Other results

    The optional scheme adds family benefits and benefits for sickness and occupational diseases .

    The optional scheme concerns family benefits for diseases and for occupational diseases .

    Vector control can reduce the transmission of dengue, sleeping sickness and Chagas disease .

    Vector control can reduce transmission of dengue, sleeping disease and Chagas disease .

    I want to learn how to cure cataracts, side sickness and all other diseases .

    The Special Rapporteur received testimony from reliable sources indicating that detainees are very often forced to sleep on cold cement, and that many of them suffer from sickness and serious diseases .

    The Special Rapporteur has received testimony from reliable sources that very often prisoners are forced to sleep on cold concrete floors and that many of them suffer from serious diseases .

    In addition, several parasitic conditions continue to cause considerable morbidity and disability: schistosomiasis, lymphatic filariasis, trachoma, trypanosomiasis, or sleeping sickness , and Chagas disease .

    In addition, several parasitic diseases continue to cause a large number of diseases and disabilities: schistosomiasis, lymphatic filariasis, trachoma, trypanosomiasis, or sleeping disease , and Chagas disease .

    The ILO recognizes both the right to a safe and healthy working environment and the protection of the worker against sickness , disease and injury arising out of his employment to be fundamental human rights.

    Last year, hundreds of volunteer biology and chemistry researchers around the world worked together to sequence the genome of the parasite responsible for some of the developing world’s worst diseases : African sleeping sickness , leishmaniasis and Chagas disease .

    Last year, hundreds of volunteers – biologists and chemists – from all over the world worked together to sequence the genomes of parasitic organisms that cause the most common infections in Third World countries – sleeping disease , leishmaniasis and Chagas disease .

    He is immune to aging, conventional disease , sickness and most forms of injury.

    Provided further that a veteran is disabled owing to sickness , disease or injuries sustained in the line of duty he shall be given a monthly disability pension.

    If the veteran, due to illness , ill health or injuries, is not able to remain in the service, he is assigned a monthly disability pension.

    Heads of household with a low income are entitled to free medical aid on account of bodily or mental impairment, sickness or disease which does not require treatment in hospital.

    Low-income heads of households are entitled to free medical care for physical or mental disabilities, disease or disorder , which do not require hospital treatment.

    He sees you, your ideas, as a sickness , as a disease .

    Disease and sickness wreak havoc on the lives of children, men and women.

    Diseases destroy the lives of children, men and women.

    It has also been suggested that the Red Death is not a disease or sickness at all but a weakness (like “original sin”) that is shared by all of humankind inherently.

    It has also been hypothesized that the Red Death is not disease at all; it must be understood as a weakness inherent in all people (like “original sin”).

    90,000 Kissing bed bugs: 12 people are infected with Chagas disease in Texas and between 7 and 8 million worldwide.

    American media reports that people living or traveling in Texas may contract Chagas disease./epochtimes.ru/

    Chagas disease (American trypanosomiasis) is spread by the parasite Trypanosoma cruzi (T. cruzi) (triatomaceous bug). It is called the “kissing bug” because it bites people on the thin skin around the eyes and mouth, often while they sleep, WebMD reports.

    “It is not the bite of a parasite that causes the infection, but the faeces. If a bug bites an animal or person, it becomes a carrier of T. cruzi. The bug leaves droppings that enter the human body through the eyes, nose, mouth or bite wound, ”says the WebMD article.

    People can also get sick by eating meat from an infected animal, blood transfusion or organ transplant from an infected person.

    Triatoma infestans is a major vector of Chagas disease. Photo: CDC / World Health Organization, public domain

    Latent danger

    US Department of Health officials told NBC that 12 people are infected. The media company warns of the danger of the spread of Chagas disease.

    But the statement from the federal government does not say that people are getting infected here. This disease is rare outside the tropics.

    However, Candice Stark, who did not leave the United States, contracted the disease after donating blood in 2013. Her doctor knew little about Chagas disease. Stark found the bug in a closet at her parents’ home in Lagrange, and Texas A&M researchers confirmed it was a kissing bug.

    Since then, researchers have obtained these bugs from various parts of the state.

    “During peak season, we receive bags of bedbugs every day, each containing one to 10 bedbugs or more,” said Sarah Hamer, a researcher at Texas A&M.

    Shocking discovery

    Ed Wozniak from the Texas Department of Public Health went in search of bed bugs himself and found 500 of them. “I’m shocked. I didn’t expect to find so much, ”Wozniak said.

    Bed bugs breed because agricultural areas are turning into suburbs.

    The bugs tested by researchers at Baylor Medical Schools in Houston are infectious and contain human blood, which means they’ve already bitten people.

    Little done

    NBC said the Department of Public Health does not take the issue seriously and barely mentions Chagas disease publicly.

    The Centers for Disease Control and Prevention (CDC) is investigating: “There needs to be a thorough study to find out what the risks of contracting Chagas disease are in Texas,” Dr. Susan Montgomery told NBC.

    Symptoms and treatment

    The disease has two phases. The former presents with mild symptoms: rash, pain, vomiting, diarrhea, loss of appetite, swollen eyelids, and flu-like symptoms. These symptoms disappear after a few weeks or months, but the parasite remains in the body.

    Boy from Panama suffering from Chagas disease. Acute infection presents with swelling in the area of ​​the right eye. Photo: CDC / Dr. Mae Melvin, public domain

    The second phase can be fatal for weak individuals if the parasite causes heart failure or esophageal hypertrophy.

    Treatment with enznidazole and nifurtimox, preferably immediately after infection. The drugs are only available through the CDC.

    According to the WHO, between 7 and 8 million people are infected worldwide, mainly in Latin America, where Chagas disease is endemic. In Colombia, the cost of treating the disease in 2008 was US $ 267 million.

    The disease is named after the Brazilian physician Carlus Ribeiro Justiniano Chagas, who discovered it in 1909.

    English version

    Tropical diseases keep Americans in poverty

    Homeless in San Francisco. Photo by Flickr user Evan Blaser

    America’s poverty statistics are sobering. The Census Bureau’s annual income statement shows that one in five American children lives in poverty, and that compared to 2007, Americans are earning less, and the average annual income of black families is about $ 23,000 lower than that of whites. families.Last year, a report from the National Poverty Center showed that the number of households living on less than $ 2 a day per person increased from 636,000 in 1996 to 1.650 thousand in 2011.

    Part of the reason for this plight is the spread of so-called neglected tropical diseases in the United States, particularly in the south and along the Gulf Coast, and especially among black and Hispanic communities. Up to 1 million people are infected with the parasites that cause Chagas disease, a chronic infection that leads to heart disease or intestinal damage in 40 percent of cases.

    There are a number of diseases like Chagas disease that can be traced back to how impoverished Americans are being rejected by the rest of society. One of those who understands this problem is Dr. Peter Hotez, who collaborates with the Sabin Vaccine Institute and Texas Children’s Hospital in Houston. He has been working with neglected tropical diseases his entire life, so I met with him to discuss this topic.

    VICE: I understand that the tropical diseases you are working with are classified as neglected.Do you feel like your work is forgotten too?
    Dr. Peter Hotez : There is a group of these diseases. Our original list, published in 2005, had 13 or 14 “neglected tropical diseases,” and now the World Health Organization has expanded that list to 17, which is the correct list. I like to call them the most important diseases that you have never heard of. They are actually very common among the poor. The problem is that only poor people get sick, so no real attention is paid to these diseases.One of the reasons for such an active fight against HIV / AIDS was the strongest propaganda that began in the United States, North America and Europe, but this does not happen with regard to other diseases, because only extremely poor people are sick with them.

    One of my studies showed that neglected tropical diseases affect the poor in rich countries, including the United States. This is not only a sub-Saharan African affliction.

    Dr. Peter Hotez

    What previously unseen diseases are now emerging in America?
    Well, it’s not like they weren’t there before; just no one was looking, which in itself is interesting.One of these is called Chagas disease; It is a parasitic heart infection transmitted by the bite of a kissing bug, a disease common in Texas.

    Do you think these diseases are being ignored because they affect the poor?
    That’s right. If these diseases hit the middle class or wealthy people in North America or England or elsewhere in Europe, no one would tolerate it. But they are not visible because only the poorest suffer.

    How do you work on these diseases in such a situation?
    I think you want to ask “how do you get people to do this kind of work?”

    Yes, where do you get people to take care of them, and how do you get people to work on the disease in a situation where the disease has not become something that requires you to intervene as a kind of savior?
    Well, one of the things I say is that such diseases do not only occur in conditions of poverty; we now have strong evidence that these diseases themselves cause poverty.Diseases such as schistosomiasis, a parasitic disease caused by blood flukes (trematodes), and toxocariasis, which is common among Americans living in poverty, actually reduce intelligence. They reduce the IQ of children, and there is research showing that chronic infections during childhood [can] reduce future wages by 40 percent. Other infections make people too sick to work.

    This is the hidden reason why a billion people at the bottom are unable to lift themselves out of poverty: because they are too sick.In most cases, we can implement some kind of intervention that is so cheap that we could lift these people out of poverty quite easily. In fact, we call these vaccines that we develop in our research laboratories “vaccines against poverty” because they have the potential to affect not only better health but also economic development.

    Is there support for the development of these vaccines? I suppose you tell politicians and big companies that many people who find themselves in poverty suffer from this very disease that causes their poverty, and you hear a lot of questions, but in the end nothing happens.Since some people are working on research on these diseases, do you receive support or do you feel like you are banging your head against a brick wall?
    I would say that this and that happens. We have good times and bad times and we have done a fairly good job of attracting donor support from the EU; they are supporting the development of our hookworm vaccine. The Carlos Slim Health Institute provides vaccine support for Chagas disease and leishmaniasis.There was support from the (Bill) Gates Foundation, the American government and the National Institutes of Health, and also from the largest Michelson Foundation for Medical Research. This allowed us to develop vaccines that went through the early stages of clinical trials. The subsequent stages of clinical trials, which are a condition for obtaining a license, will be a difficult task – we do not know who will be able to provide funding for this purpose. Thus, we have not yet completed the development of all the elements, but we have made tremendous progress in preparing these vaccines for the clinical trial phase.

    Life Cycle of Schistosomiasis (Click to Enlarge)

    You say that many of the decisions regarding these diseases are indeed very simple; Is this the case when, along with other diseases, you have vaccinations, there are pills, but the question is their distribution, education and how they will get to those in need?
    Yes, this issue is sometimes referred to as a global access issue and how can you provide global access? We think we have a good strategy in terms of effective drugs for deworming and treating schistosomiasis.And it seems that they get to those who need them. In fact, the US Agency for International Development has just celebrated giving treatment to the first billion people, so people seem to get these drugs and they are pretty simple to use. We participated in the development of packaging for these drugs in 2005 and 2006. We hoped that it would be quite simple and easy, given that the drugs are provided free of charge and can be taken without a doctor.

    How is the distribution of these drugs in the United States compared to the rest of the world?
    The irony is that we have to literally convince people of how widespread these neglected tropical diseases are in the United States.Many are reluctant to admit that there are poor people in this country, but we have 1,650,000 American families living on less than $ 2 a day. We are working with Congress to ensure that some legislation is passed. Congressman Chris Smith of New Jersey recently filed with Congress the Neglected Tropical Disease Eradication Bill, which addresses not only neglected tropical diseases such as female genital schistosomiasis in Africa, but also those diseases here in the United States.

    So the presence of neglected tropical diseases in the US is proving something that America really doesn’t want to talk about – the existence of widespread poverty across the country?
    This is true, and it is again relevant now in connection with the immigration debate, you know, 50,000 Central American children are currently in detention at the border with Mexico. One of the reasons for the deportation of these children is that they can be carriers of all these diseases, although in fact, these diseases are already here, and they have been here for a very long time.

    I have always been amazed at the number of American citizens who are heading to “save Africa” and do not realize that they themselves have huge poverty problems on their own.
    I think that an impressive part of them live in extreme poverty. You know, we have nearly 20 million Americans living at half the level of poverty in the United States, and thus we are approaching the level of poverty in many middle-income countries, mainly in the American South and along the Gulf Coast.This is complete poverty. We call them “tropical diseases,” but sometimes that’s a little bit wrong. These are diseases of extreme poverty. That is, the climate is a component, but the main determining factor is poverty.

    Have you seen an increase in the number of poor people during your work as a doctor?
    It was necessary, in the sense that before, no one counted, and only now we started counting. So we came to Texas three years ago to create this National School of Tropical Medicine, modeled on those in London and Liverpool.The difference is that we are working in a country with an epidemic of the disease: the southern US and Houston, so I support the decision to work not only for people in Africa, but for neglected diseases among poor people here at home. Pharmaceutical companies are doing a good deed by donating drugs, but convincing their shareholders to invest in research and development of new projects is quite another matter, the results of which they will eventually simply have to give away. In this regard, we feel that we must work in the non-profit sector.

    Follow Oscar on Twitter.

    Chagas disease in Chaco – nature


    • Developing world
    • Parasitic infection
    • Healthcare

    Studying disease transmission in poor rural areas is part scientific research and part diplomacy.

    You wouldn’t know this if you went to his little farm, but Ramon Raul Alegre is the owner of a unique mud hut.It looks like all the other buildings from the raw warehouse are dotted with dusty muddy paths in Pampa del Indio, a municipality in Argentina’s northern province of Chaco, except that it is more dilapidated than most. This is because the walls of Alegre’s hut have been torn apart, every few months, by scientists at the University of Buenos Aires (UBA) in Argentina, who are looking for the blood-sucking insects Triatoma infestans. It is the main vector of the Trypanosoma cruzi region, which is the parasite that causes Chagas disease.

    Live T. infestans collected from a chicken coop near the unique Alegre mud hut. Image: Anna Peterik

    The reason for this partial eradication is that the first insects appeared in Alegre’s hut and somehow developed resistance to pyrethroids, a class of insecticides that has dominated Chagas disease vector control programs since the mid-1980s. Curiously, beetles developed this resistance in the absence of repeated exposure to pyrethroids.No one is sure how this happened. It is possible that these insects were recently transported from a site in the western part of Gran Chaco – a vast flat plain that spans parts of Argentina, Bolivia and Paraguay – or that resistance was spontaneous among the local population.

    The initial sign appeared when Alegre was bitten at sunset in a nearby field shortly after the hut was first sprayed. This sparked an experiment. Four times, at 2-month intervals, Juan Manuel Gurewitz, a UBA graduate student, re-sprayed the hut with pyrethroids and collected the dead beetles.Between each application, Gurewitz placed a tent with a mosquito net all over the structure to keep insects out or re-infest the hut, and to prevent the Alegre goats from devouring fallen insects.

    “We have tried every approach to maximize the effectiveness of pyrethroid,” says Uriel Kitron, professor of environmental science at Emory University in Atlanta, Georgia, USA, who oversees the study site. “All the time, the beetles were able to reproduce and reconstruct their numbers.”Today’s test shows that a fifth spraying in 2 years, this time with malathion – a much more toxic insecticide that cannot be bought without a prescription in Argentina – has finally nailed. The Alegre problem. Pyrethroid resistance has been confirmed in blind laboratory tests on bedbugs.

    Chagas Life Man

    Both Gurewitz and Kitron work with Ricardo Gürtler. At the age of 55, Gürtler has been studying the basics of transmission and control of Chagas disease since he was a graduate student.In about the first half of his career, Gürtler watched with optimism as the large-budget, militaristic Southern Cone Initiative interrupted vector transmission of Chagas disease in three of Argentina’s five neighboring countries. This happened in several provinces of Argentina. However, after 2001, when the country suffered the largest sovereign default in economic history, Argentina’s control programs have been deteriorated by inconsistent funding and vague or absent governance.The number of Argentines with acute symptoms of Chagas disease has since increased in eight of the 22 provinces.

    Alegre’s unique mud hut, partially dismantled for science. Image: Anna Peterik

    Most of Gürtler’s research comes from the province of Santiago del Estero in Argentina, where he and his colleagues followed the study sites from 1984 to 2006 (Ref. 1). They have collected a huge database. Over the years, they monitored the density of bugs, counted how many insects were infested at different stages of development, checked dogs, cats, and residents, and organized communities to plaster the walls of some houses to close the crevices in which these insects like to hide.They used this information for a mathematical transmission model T. Cruzi 2 . Policy recommendations fell out of their models.

    “For example, Ricardo showed that if you have fewer than two dogs in your family, you are unlikely to get infected,” says Rick Tarleton, a professor at the University of Georgia who has researched Chagas disease since the 1980s. “This information was helpful in planning dog vaccination programs.” A group at the Autonomous University of Yucatan in Merida, Mexico began testing a therapeutic DNA vaccine against T.cruzi in mongrel dogs. In 2008, they published the results of a pilot clinical trial that showed some success. Over the past decade, researchers have increasingly used dogs as guardians of T. cruzi transmission, and new research has shown that their immune response against salivary bug antigens can be used as a surveillance tool.

    “The dog problem is a classic example of the heterogeneity we constantly find with Chagas,” Kitron says as an old ragged dog limps by.”This guy is more likely to be the source of the infection than the other dogs here.” Similarly, 20–30% of buildings in each community appear to act as pockets of infested insects that quickly infest other buildings after a spraying campaign. 3 “But that means control can be the goal,” adds Gürtler.

    The Santiago del Estero project showed the main dynamics of Chagas disease in Gran Chaco. Now that this work has been completed, Gürtler has focused on understanding how they differ from each other.To this end, he created three new training centers in Gran Chaco: one in Bolivia, one in Paraguay and one in Argentina. The plots have different vegetation, climate and ethnic groups. Gürtler hopes that an added bonus of the new system will be to encourage closer collaboration between scientists and disease vector control officials in the three countries.

    Tobas and triatoms

    Pampa del Indio is Gürtler’s new location in Argentina. The population is £ 15,000.One third of the inhabitants live in the city of the same name; The rest live in huts scattered along several trails that traverse the municipality and along the edges of dense forest. It is one of the poorest municipalities in Argentina and probably has the highest percentage of people of indigenous origin of any of the municipalities in the country. The indigenous people in Pampa del Indio are of the Toba ethnic group. Tobas lived a largely nomadic life, hunting and fishing, until deforestation and agriculture arrived in the area in the early decades of the twentieth century.The government of Juan Perón, who was three times famous ruler of Argentina, gave some titles of the land of Toba – 60 years ago. This pushed them towards a more agricultural existence.

    Alegre is Toba. His other hut – where he lives – shows why Toba’s homes are much more likely to be infected with T. infestans than Creole homes in Pampa del Indio. Tobas often prefers to sleep on the floor. They tend to straw the roofs of their homes, providing T. infestans with a better habitat than just mud walls.In general, Tobas is poorer than non-indigenous residents, so it is not easy for them to afford insecticides and it is more difficult for them to travel to a small city hospital where they can learn about Chagas disease and receive treatment. The population of Toba is also in constant flux: Toba is attracted to Pampa del Indio because it is there that their community gains political power, and that is why the city serves as a springboard for those who migrate to the main cities of Argentina looking for work or large social benefits.,

    For these reasons, monitoring of T. cruzi transmission in indigenous populations is often difficult. “Sometimes Toba asks,“ Why do you want my blood? “Explains Gürtler, who pioneered the testing of household dogs and presented the results to owners to reassure them that the blood test was in their best interest. “You can’t take samples from people and leave. You have to build trust – it takes time – and the local medical staff can’t do it because they don’t have enough staff. “

    Gürtler (left) and Alegre (right). Image: Anna Peterik

    Tobas also treats their homes differently. For example, last year, Gürtler and his team found more than 500 vectors in a single house, just 15 minutes after spraying, suggesting that a total of 5,000 beetles may have been infested in the hut. Instead of treating the house, the family decided to burn it down to the ground. “They often do the same if a relative dies in the house – burn it down and build another house nearby,” explains Gürtler.Understanding these idiosyncrasies is part of what he calls the “human element,” which Gürtler believes is ignored by most Chagas disease control programs – a sentiment echoed by field researchers in other countries (Box 1).

    Politically, it is regrettable that the majority of known foci of pyrethroid-resistant Triatoma infestans are located in the western part of Gran Chaco Island in Bolivia. Bolivian immigrants are often and mistakenly blamed for many of Argentina’s woes.The discrimination is such that one Argentine news recently reported that “two people and a Bolivian” were killed in a car accident. Ricardo Gürtler faced this in his own research.

    In 2007, he and entomologist Delmi Canale of the national Chagas disease program in Argentina traveled to the Patagonian province of Chubut to find out if T. infestans existed so far south. They went at the invitation of local officials who were concerned about the number of Bolivian migrants in their province who tested positive for T.cruzi. Gürtler and Canale were unable to locate T. infestans. “But a few months after I went there, an adult error appeared at a medical center in downtown Komodoro Rivadavia. He was found by a janitor who said that the Bolivians had been in the center a few days earlier, ”recalls Gürtler.

    Gradually the insect was sent from an official to an official in Chubut. He was eventually mailed to Gürtler, dead, but laid a few eggs in a plastic container.Gürtler and Romina Piccinali, who were one of his postdoctoral researchers, used their database of common T. infestans haplotypes to compare the sequence of the Patagonian beetle mitochondrial oxidase I gene with typical DNA sequences from around Gran Chaco. “It was 100% Argentine beetle, probably from the western provinces of San Juan, Mendoza or Rio Negro,” Gürtler says with a wry smile. Shortly thereafter, he returned to Comodoro Rivadavia and found that most of the Chagas migrants in the city were in fact from these three Argentine provinces and lived in a middle-class area.

    From Chagas to Kafka

    The purpose of this trip is to show Kitron a new study site. As part of the tour, Gürtler visits a local hospital. Seems to be clean with a dedicated but under-trained staff. Director Arturo Navajas is open about his concerns. He does not have good statistics on the prevalence of Chagas disease at the local level. Its best data relates to pregnant women who visit the hospital, of which 10% tested positive.The true figure is almost certainly higher. In addition, the hospital only has two boxes of medicine – enough for 15 people – who arrived a year after they were ordered.

    Inefficiency at every level surrounds scientists trying to study Chagas disease. In 2002, at the height of the economic crisis in Argentina, Gürtler and Kitron received a grant from the US National Institutes of Health, of which more than US $ 500,000 went to work in Argentina.Meanwhile, to reduce the rate at which cash was leaving the country, the Argentine government passed legislation limiting the amount of money that can be withdrawn from bank accounts to a few hundred dollars a week. This meant that Gürtler had to buy reagents and ancillary equipment when traveling to the United States. “Even today, we have to justify every dollar that goes into the laboratory’s bank account as if we were laundering money. It’s really not anyone’s fault. ”He shrugs.“Everything works here. This is a kind of Kafka story. It is difficult for people from abroad to understand. Funding is difficult everywhere […], but here the question of how you get the money takes about a third of the researchers’ time. ”

    Like many countries in Latin America, Argentina has a decentralized public health system. In provinces and municipalities, vector control is carried out in a bizarre, individual way. For example, in Pampa del Indio, no official is responsible for ensuring that houses are sprayed with insecticides; however, services may occasionally change.The morning after Gürtler shows Kitron the hospital, he returns to speak with Navajas. He called Hector Frelius, who is a friend of his in Buenos Aires and is tasked with coordinating the fight against Chagas disease at the national level. Frelij agreed to ship more drugs directly to Pampa del Indio. In response, Navajas says he will help Gürtler organize cross-community blood tests to assess the local prevalence of the disease.

    Data dark side

    Good data is scarce, and the more scientists dig, the more they seem to disprove the assumptions on which the Southern Cone Initiative was based. In the beginning, elimination of T. infestans was considered feasible because the vector was thought to be highly susceptible to pyrethroids and lack the genetic variability necessary to develop resistance. Several groups, including Gürtler, have denied these assumptions. It was also believed that bugs fly badly and cannot be reinfected from afar.However, Gürtler’s data from Santiago del Estero show that they can cover distances of 500–2000 m 4 .

    It was also assumed that once all T. infestans in a settlement have been eliminated, re-infestation from nearby forests will be impossible. With the exception of the melanic version or “dark morph” of T. infestans, which lives in the Andean valleys of Bolivia, T. infestans were thought to be unable to survive and reproduce in the wild. Again, this is not true. In the summer of 2006 and 2007, several members of the Gürtler group identified dark morphs in a forest 40 km from Fuerte Esperanza in northeastern Argentina, near Pampa del Indio 5 and 1000 km from the Andean valleys of Bolivia.They did this based on a study of the local population of the parrots Amazona aestiva and Aratinga acuticaudata. These birds tend to nest in deciduous trees with trunks made by hollow fungus. When Gürtler’s group placed cans of live mice in trees (as bait), they found dark T. infestans morphs glued to sticky paper placed around the mouths of the cans. Trapped bed bugs appear to be genetically much closer to hut-dwelling insects in Pampa del Indio than to dark morphs in Silvata in Bolivia, suggesting that some of the recontamination in eastern Gran Chaco Island comes from not home populations.

    “It’s just that no one has looked for them before,” suggests Gürtler. Likewise, no one thought to study urban vectors until recently – or systematically check, after spraying campaigns, whether bugs were really dying. These revelations point to why the original Southern Cone Initiative did not work across the board, and offer some hope that programs can be devised to revitalize it.

    Returning to the unique muddy hut of Alegre, Gurewitz found T.infestans in a nearby chicken coop. It is not known whether they came from a resilient population in a hut or flew into the chicken coop from another house 500 meters away. Gürtler, Gurewitz and Kitron travel to Alegre’s house to try to find him. His wife appears. “More mistakes?” she asks, disappointed. “Don’t worry, we’ll get rid of them. We will be back, ”promises Gurewitz.


    1. Search for Anna Peterik in:

      • Nature Research Journals •
      • PubMed •
      • Google Scientist


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