Table of Contents
Credits
Host: Sara Dong
Guests: Jacob Ricci, Akankcha Alok, Norman Beatty
Writing: Jacob Ricci, Akankcha Alok, Norman Beatty
Edited and Produced by Sara Dong with support from the Infectious Diseases Society of America (IDSA)
Our Guests
Jacob Ricci
Jake is an MD/PhD student currently in his fourth year of the program and second year of his PhD at the University of Florida. His research centers around sex and age differences in myocarditis, with a specific focus on cardiac macrophages in the lab of Dr. Katelyn Bruno. He is originally from Milwaukee, Wisconsin and earned his Bachelors in Neuroscience at the University of Notre Dame before completing a masters in Medical Physics at the University of Florida. Outside of medicine and research, Jake enjoys photography, spending time outdoors, and is a drummer in a band with medical students in his class
Akankcha Alok, MD
Akankcha is an Infectious Diseases and Global Medicine Fellow at the University of Florida. Originally from India, she completed her medical school at Kasturba Medical College, Manipal, India and her residency at the University of Central Florida/HCA Florida North Florida Hospital, Gainesville. Her passions include global health, planetary health, tropical medicine, travel medicine, antibiotic stewardship, and infection prevention. Dr. Alok is especially committed to improving healthcare access in underserved communities and hopes to use her training to make a meaningful impact. Outside of medicine, she enjoys traveling and exploring new cultures.
Norman Beatty, MD
Norman L. Beatty is an Associate Professor of Medicine at the University of Florida College of Medicine, Department of Medicine, Division of Infectious Diseases and Global Medicine. He graduated from the University of Central Florida College of Medicine with a B.S. in Molecular Biology and Microbiology, and a B.S. in Biotechnology. He then went on to study at Ross University School of Medicine and graduated with High Honors with his M.D. degree. He completed his Internal Medicine residency and Fellowship in Infectious Diseases at the University of Arizona College of Medicine – Tucson.
Dr. Beatty has been studying triatomines (kissing bugs) the insect vector responsible for transmitting the parasite that causes Chagas disease in humans and other mammals and Chagas disease since 2015. He is currently researching the prevalence of Chagas disease in Florida as well as throughout the United States. His research has been presented at several conferences, including both the Infectious Diseases Society of America, the American Society of Tropical Medicine and Hygiene annual scientific meetings. Dr. Beatty has a clinic dedicated to Chagas disease which offers advanced testing and management.
Culture
Jacob shared Gainesville’s music scene
Akankcha loves traveling and recently spent the weekend in a camper van in a national forest
Norm is a runner and is prepping for another marathon
Consult Notes
Case Summaries
Case 1: 70 yo man with Chagas cardiomyopathy
Case 2: 40 yo previously healthy woman with positive Chagas screening from blood donation
Key Points
Introduction to Chagas disease!
- An NEJM Review: Bern C. Chagas’ Disease. N Engl J Med. 2015;373(5):456-466. doi:10.1056/NEJMra1410150
- Chagas disease is due to an infection from the kinetoplastid protozoan Trypanosoma cruzi
- There are currently six distinct lineages of T.cruzi classified into discrete typing units (TcI-VI), which vary in their geographic occurrence, host specificity, and pathogenicity
- Chagas disease is transmitted throughout the Americas
- The World Health Organization (WHO) and the Pan American Health Organization (PAHO) highlight 21 countries in the Americas to which Chagas disease is endemic (excluding the US, more on that later)
- The prevalence of T. cruzi is highest in Bolivia, Argentina, Paraguay, Ecuador, El Salvador, and Guatemala: Pérez-Molina JA, Molina I. Chagas disease. Lancet. 2018;391(10115):82-94. doi:10.1016/S0140-6736(17)31612-4
- The epidemiology of Chagas has changed with migration of individuals within and outside of endemic areas as well as due to successful public health programs that reduced transmission in endemic areas. Here is another map/figure that looks at the global distribution of Chagas but highlights historically endemic areas, newly emerging areas, and potential future spread with climate change: Ferreira MDS, Maldonado RA, Farani PSG. Chagas Disease in the 21st Century: Global Spread, Ecological Shifts, and Research Frontiers. Biology (Basel). 2025 Nov 20;14(11):1631. doi: 10.3390/biology14111631. PMID: 41300419; PMCID: PMC12650115.
- Transmitted by several known mechanisms:
- Vector borne
- Contact with triatomine insect (kissing bug) feces which contain the parasite
- Can contaminate the skin or environment and inadvertently be introduced to mucous membranes, breach in skin, or even ingested
- Oral transmission from contaminated food and drink containing the parasite
- Most commonly happens through certain fruit juices such as Açaí berries, guava and palm wine that is unpasteurized
- Some vectors are found in certain ecosystems where the bug or feces can contaminate the juice preparation process
- Congenital transmission
- Approximately 1-10% of chronically infected mothers living with untreated Chagas disease will transmit T.cruzi to the fetus en utero
- Transplantation
- Chronically infected organ donor transmits to recipient
- Blood transfusion
- In certain regions of the world the blood donor servicing agencies are not screening for chronic Chagas disease. In the United States this practice started around 2007.
- Laboratory accidents
- In research and other laboratory settings where parasites are grown in culture.
- Vector borne
More on kissing bugs
- In addition to humans, a number of mammals serve as reservoir hosts for T.cruzi such as armadillos, opossums, raccoons, woodrats, some other rodents, and domestic dogs
- Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus
- You can find more details, characteristics, and pictures of triatomine bugs in the US on the CDC website
- Triatomine bugs often live in domestic and peridomestic environments – they can live indoors and outdoors
- When indoors, they might be found in cracks and holes of housing
- If a kissing bug enters a human home, it spends daylight hours hiding in cracks and crevices (likes to be in contact with surfaces above and below its body)
- The kissing bug emerges at night to take its blood meal and often bites around the exposed face of the victim, thus gaining its moniker. While feeding, the bug defecates and then the patient may scratch at the bite in their sleep / make contact with mucous membranes, etc —> parasite enters the bloodstream
- Since consuming infected insects or their feces can also transmit T.cruzi – another example may be a kissing bug that lives in a thatched roof of home that defecates directly into food on the table below
- When outdoors, they might be found beneath porches, between rocky structures, under cement, in rock/wood/brush piles, in rodent nests or animal burrow, in outdoor dogs houses/kennels, in chicken coops/houses
- In the United States, triatomine bugs rarely infest homes because houses are well-sealed and have plastered walls. However, finding them indoors, especially younger, wingless nymphs, may indicate an infestation. If these bugs are inside, they are often found near where pets sleep, where rodents are present, or around beds and bedrooms, especially under or near mattresses or nightstands.
- When indoors, they might be found in cracks and holes of housing
Images below courtesy of Dr. Norman Beatty:
Top showing some kissing bugs from Florida with adults and nymphal stages
Bottom showing T.cruzi life stages
Clinical manifestations of Chagas disease
- Chagas disease is characterized by two phases: acute and chronic
- Acute T.cruzi infection
- The incubation period after exposure is 1-2 weeks
- The acute phase of infection lasts 8-12 weeks, during which circulating trypomastigotes may be detectable in peripheral blood
- Many patients will be asymptomatic or potentially have mild, nonspecific, self-limited illness that doesn’t lead to clinical attention
- In some patients, acute infection may be associated with a chagoma (inflammation and swelling at the site of inoculation, typically on face or extremities)
- Inoculation via the conjunctivae may lead to very characteristic painless unilateral swelling of the upper and lower eyelid, known as Romaña’s sign (you have likely seen this classic image / test question from Joy D Jester, Rolando E Saenz, Lee T Nesbitt, Jr, and WA Krotoski. The Skin and Infection: A Color Atlas and Text, Sanders CV, Nesbitt LT Jr (Eds), Williams & Wilkins, Baltimore, 1995 )
- Severe acute disease can occur but is rare (<1%), with parasitemia and manifestations such as acute myocarditis, pericardial effusion, and/or meningoencephalitis or disseminated disease
- The acute phase ends when the host immune system gains control of parasite replication, patent parasitemia disappears, and the remaining parasites reside largely in the deep tissues
- Infection is lifelong without treatment
- Chronic T.cruzi infection
- The subsequent chronic phase is initially asymptomatic, and most immunocompetent individuals will remain asymptomatic for life
- Indeterminate chronic Chagas disease: Patients with serologic evidence of T.cruzi infection but no evidence of clinical disease / organ damage
- 20-30% of indeterminate Chagas patients ultimately progress to have clinical disease that is irreversible and potentially fatal
- This phase may persist for decades
- Determinate chronic Chagas disease: Patients with evidence of organ involvement, which can include cardiac, esophageal, colonic, and CNS forms
- Chronic disease may manifest years later
- Chagas cardiomyopathy is a chronic inflammatory disease associated with early conduction system abnormalities
- Inflammation can involve all cardiac chambers leading to progressive dilated cardiomyopathy, frequently with apical aneurysm formation and progressive arrhythmias
- Chagas heart disease stages:
- Stage A: asymptomatic, normal ECG and no structural abnormalities on echocardiography, LVEF ≥55%, complex ventricular arrhythmia usually absent(24-h Holter), cMRI may show myocardial fibrosis
- Stage B1: ECG abnormalities, segmental ventricular dysfunction may be present with structural changes on echocardiography, no symptoms of heart failure, LVEF ≥55%, functional Class (NYHA) I. Complex ventricular arrhythmia may be present(24-h Holter), cMRI usually shows myocardial fibrosis.
- Stage B2: ECG abnormalities, structural changes on echocardiography, no symptoms of heart failure, LVEF 41-54%, functional Class (NYHA) I. Complex ventricular arrhythmia usually present (24-h Holter), cMRI usually shows myocardial fibrosis.
- Stage C: ECG abnormalities, segmental ventricular dysfunction may be present with structural changes on echocardiography, symptoms of heart failure, LVEF <40%, functional Class (NYHA) I,II, III or IV. Complex ventricular arrhythmia present (24-h Holter), cMRI shows myocardial fibrosis.
- Stage D: ECG abnormalities, segmental ventricular dysfunction present with structural changes on echocardiography, symptoms of heart failure, LVEF ≤25%, functional Class (NYHA) IV. Complex ventricular arrhythmia present (24-h Holter), cMRI shows myocardial fibrosis. Refractory to optimized medical treatment.
- Primary GI disease can involve esophagus or colon. More common in pts infected in southern countries of S. America, possibly due to exposure to selected genotypes
- Reactivation due to immunosuppression is also possible. Here is a really nice figure showing the natural history of Chagas disease (but also includes the impact of immunosuppression – hopefully a topic of a future episode): Clark EH, Messenger LA, Whitman JD, Bern C. Chagas disease in immunocompromised patients. Clin Microbiol Rev. 2024 Jun 13;37(2):e0009923. doi: 10.1128/cmr.00099-23. Epub 2024 Mar 28. PMID: 38546225; PMCID: PMC11237761.
Diagnosis of Chagas disease
- A diagnosis of Chagas disease relies on serologic testing (in addition to the clinical presentation and history-taking of course)
- Utilize two different anti-T.cruzi antibody assays looking at different antigen profiles or methodologies (ELISA, IFA, LFA, immunoblot)
- **As discussed in episode, blood donor Chagas screening which is reactive needs additional serologic testing to ensure appropriate diagnosis
- In the acute phase of Chagas infection, the level of parasitemia is high so motile trypomastigotes could be detected by microscopy/smears. PCR is also another available diagnostic tool for acute phase of Chagas disease (and potentially for monitoring for reactivation in transplant recipients, which we didn’t really discuss this episode)
Who should be screened for Chagas disease in the United States?
Any of the following:
- Born in Mexico, Central and South America
- Lived in these Latin America regions for more than 6 months
- Family member known to have Chagas disease
- Lived in housing made of natural materials (adobe, thatch, palm leaves) in Latin America (Mexico, Central or South America)
- Known exposure to triatomine vector (kissing bug) in the Americas (USA, Mexico, Central and South America)
In both cases, a detailed history of potential exposures to Chagas disease was crucial! A few additional notes/details to the list above:
- Often exposures may include living in rural settings within farming communities. Ask about which regions they have lived in and what their childhood was like. Were they outdoors a lot?
- Asking about the structure of housing (such as adobe, thatched roofing, or other materials porous to the environment) helps determining if the housing is amenable to invasive or colonization of triatomine vectors. You may see the term “domiciliation” of bug, which is really an infestations (which is occurring even in places in the US in certain scenarioes)
- Ask the patient or family if they know what a kissing bug is?
- Do they recall ever seeing this insect in their house? Being bitten?
- Have they seen the insect in their home? Did they find the bug at night or in their bed?
- Do they have dogs or cats sleeping in the house?
- Consider showing a picture of the insect that may be the common vector in a particular region
- Dr. Beatty mentioned that patients may use native terms for the insect depending on the region, such as:
- Chinche, common term in Mexico and Central America
- Barbardo/barbeiro in Brazil
- Vinchucha in regions like Bolivia, Argentina, Paraguay
- Chipo in Colombia and Venezuela
- Any family member with Chagas disease? Family members who have died from cardiovascular disease such as sudden cardiac death? Early in life?
Next steps when someone has confirmed serologic diagnosis?
- Complete review of systems and physical examination (assessing for clinical evidence of determinate disease).
- Routine labs: CBC with diff, CMP, CRP, Quantiferon gold or TST, Strongyloides serology (used as baseline if antiparasitic treatment is given)
- 12-lead ECG and transthoracic echocardiogram (all patients)
- Consider holter monitor or cardiac MRI (if available)
- Barium swallow Xray or evaluation for esophageal manometry (if swallow difficulties present)
- Abdominal Xray for colonic distension (if progressive chronic constipation)
- A few notes on cardiac MRI given discussion during the episode
- Akankcha mentioned this systematic review and meta-analysis on diagnosing myocardial fibrosis by cardiac MRI and its outcomes in Chagas Disease: Gómez-Ochoa SA, Rojas LZ, Hernández-Vargas JA, et al. Myocardial Fibrosis by Magnetic Resonance and Outcomes in Chagas Disease: A Systematic Review and Meta-Analysis. JACC Cardiovasc Imaging. 2024;17(5):552-555. doi:10.1016/j.jcmg.2023.11.003
- This article showed how cardiac MRI especially with late gadolinium enhancement can detect myocardial fibrosis even in indeterminate forms of Chagas disease where EKG and echo results are pretty much normal
- Cardiac MRI also gives us the extent and pattern of myocardial fibrosis which can also give us a clue on the prognosis of the disease
- Cardiac MRI can also reveal structural abnormalities such as apical aneurysms, which are consistent with Chagas disease
- Akankcha mentioned this systematic review and meta-analysis on diagnosing myocardial fibrosis by cardiac MRI and its outcomes in Chagas Disease: Gómez-Ochoa SA, Rojas LZ, Hernández-Vargas JA, et al. Myocardial Fibrosis by Magnetic Resonance and Outcomes in Chagas Disease: A Systematic Review and Meta-Analysis. JACC Cardiovasc Imaging. 2024;17(5):552-555. doi:10.1016/j.jcmg.2023.11.003
Who should be considered for antiparasitic treatment?
- All congenital cases, children and women of child-bearing age
- Acute Chagas disease
- Adults with indeterminate chronic Chagas disease ≤ 50 years
- Adults with indeterminate chronic Chagas disease ≥ 50 years (shared decision making after risks/benefits discussion)
- Adults with Chagas heart disease stage B1 (shared decision making after risks/benefits discussion)
WHO/PAHO Guidelines for the diagnosis and treatment of Chagas disease (version from 2019)
SBC Guideline on Chagas Cardiomyopathy: Marin-Neto JA, Rassi A Jr, Oliveira GMM, et al. SBC Guideline on the Diagnosis and Treatment of Patients with Cardiomyopathy of Chagas Disease – 2023. Diretriz da SBC sobre Diagnóstico e Tratamento de Pacientes com Cardiomiopatia da Doença de Chagas – 2023. Arq Bras Cardiol. 2023;120(6):e20230269. Published 2023 Jun 26. doi:10.36660/abc.20230269
Who will likely not benefit from antiparasitic treatment?
- Chronic Chagas heart disease stage B2, C and D
- Esophageal forms with achalasia
- Colonic forms with advanced megacolon
What treatment options are available for Chagas disease? What are potential side effects and recommended monitoring for these antiparasitic medications?
- Two antiparasitic drugs are available for treatment of Chagas disease: benznidazole and nifurtimox
- Programs are available for reduced medication costs.
- Discussion about the risks and benefits should occur with all patients. Side-effects do occur with both medications. They occur more commonly in adults than in children.
Monitoring while on Benznidazole or Nifurtimox:
- Cutaneous reactions (usually develop around 7-10 days; more common with benznidazole)
- Nausea/vomiting, decreased appetite, general fatigue
- Abdominal pain (more common with benznidazole)
- Headache (more common with Nifurtimox)
- CNS side effects (more common Nifurtimox)
- Cytopenias, transaminitis
A publication from Dr. Beatty with an example of a cutaneous adverse drug reaction from benznidazole
Chagas disease in the USA
- As Dr. Beatty mentioned, there has been a push to challenge the label of the US being nonendemic for Chagas
- Beatty NL, Hamer GL, Moreno-Peniche B, Mayes B, Hamer SA. Chagas Disease, an Endemic Disease in the United States. Emerg Infect Dis. 2025;31(9):1691-1697. doi:10.3201/eid3109.241700
- This recent article reviews the available evidence establishing a robust presence of T.cruzi parasites in the US – not only among insect vectors, wildlife, domestic animals – but also among humans without travel histories who are assumed to be locally infected
- Here is a map summarizing the data of here triatomines or kissing bugs occur naturally in the US
Infographics
Goal
Listeners will be able to raise awareness of the diagnosis and treatment of Chagas disease
Learning Objectives
After listening to this episode, listeners will be able to:
- Describe the epidemiology and modes of transmission of Chagas disease, especially the vector triatomine bugs
- Discuss the natural history of Chagas disease including the acute and chronic phases
- Identify which patients should receive antiparasitic treatment for Chagas disease
Disclosures
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Citation
Beatty, N., Alok, A., Ricci, J., Dong, S. “#129: Cruzi’n USA”. Febrile: A Cultured Podcast. https://player.captivate.fm/episode/0b68301d-5d68-4d03-9238-f772b24d3e0d/