Printer Friendly

A case of Chagas cardiomyopathy following infection in South Central Texas.

Human Chagas disease is caused by the protozoan parasite Trypanosoma cruzi, acquired primarily through contact with infected excreta of triatomine insects (known as "kissing bugs"). Although vector-borne transmission predominates, humans can also become infected congenitally, orally through contaminated food or beverages, or hematogenously through blood transfusion or organ transplantation. (1) During the first 4-8 weeks of infection, considered the acute phase, symptoms are usually mild, nonspecific, or unappreciable; potentially fatal myocarditis or meningoencephalitis occur rarely. Approximately 70% to 80% of infected persons enter a chronic indeterminate phase, characterized by lifelong infection without symptoms, electrocardiographic changes, and radiographic evidence of disease. The remaining 20% to 30% develop chronic disease, often presenting years or decades after infection as clinical cardiac and/or digestive disease. (2)

With approximately 5 to 8 million people infected worldwide, (1,3) Chagas is classified by the World Health Organization as one of the most important neglected tropical diseases. (1) There are an estimated 240,000 prevalent cases in the United States among immigrants from endemic areas of Latin America. (4) Fewer than 30 locally-acquired infections have been reported in the United States since 1955, (5) when a resident of Corpus Christi, Texas, became the first documented autochthonous case in the country. (6) In 2013, the Texas Department of State Health Services added Chagas disease to the state's Notifiable Conditions list, which requires the reporting of confirmed and suspected human cases to local or regional health departments. Twelve autochthonous human infections were confirmed in Texas during the first 2 years of mandatory reporting, (7) one of which was associated with left ventricular dysfunction. (8)

Case Report

In October 2016, an 18-year-old US Air Force trainee screened positive for T cruzi infection when he donated blood at Joint Base San Antonio (JBSA), Texas. Blood from all first-time donors at the JBSA-Lackland donation center is screened for T cruzi with an enzyme-linked immunosorbent assay from Ortho-Clinical Diagnostics. Per standard protocol, he was referred to the installation's trainee health clinic, where he was found to have normal vital signs and an unremarkable physical exam. He reported being in excellent health and had not experienced any recent chest pain, shortness of breath, dizziness, or gastrointestinal symptoms.

A chemiluminescence immunoassay and enzyme strip assay (Abbott Laboratories) were ordered and found to be positive for anti-T cruzi IgG antibodies. A whole blood sample was sent to the Reference Diagnostic Laboratory at the Centers for Disease Control and Prevention for further testing. An enzyme immunoassay was reactive and an immunoblot of trypomastigote excreted-secreted antigens was positive, confirming the diagnosis. The patient was notified of these results and referred to the Department of Infectious Disease at San Antonio Military Medical Center (SAMMC) for further evaluation and treatment.

After notifying the patient of his laboratory results, Infectious Disease conducted a 12-lead electrocardiogram (ECG), which demonstrated normal sinus rhythm, first-degree atrioventricular block, and left anterior hemi-block with right bundle branch block. This prompted referral to the Division of Cardiology at SAMMC. Cardiovascular physical exam was benign with normal heart sounds, normal jugular venous pressure, normal apical impulse, and no evidence of congestive heart failure. A battery of noninvasive tests was performed in order to assess for common cardiac manifestations of Chagas disease, including, but not limited to, left ventricular dilatation and dysfunction, wall motion abnormalities, aneurysms, diastolic dysfunction, pathologic bradyarrhythmias and tachyarrhythmias, and ischemic heart disease. (9)

The majority of tests were within normal limits. Chest x-ray showed no evidence of cardiomegaly. Holter monitoring was negative for any pathologic dysrhythmias. Transthoracic echocardiogram demonstrated normal diastolic, valvular, and global systolic function. Exercise testing with Bruce protocol established no exercise-induced arrhythmias, ischemic electrical changes, or anginal symptoms. Cardiopulmonary exercise testing found an appropriate V[O.sub.2]max, early anaerobic threshold, and normal VE/VC[O.sub.2] slope, consistent with a subclinical reduction in exercise capacity with preserved ventilatory efficiency. Cardiac magnetic resonance imaging confirmed the diagnosis of early heart disease, demonstrating left ventricular cavity dilation with preserved global systolic function (ejection fraction of 76%); the imaging was otherwise normal with no wall motion abnormalities, late gadolinium enhancement, abnormal T1 relaxation, or myocardial edema on T2 weighted images.

Given his exposure history, serologic findings, abnormal ECG, and left ventricular cavity dilation, the patient was determined to have chronic Chagasic cardiomyopathy. Per the Brazilian Consensus Classification and American College of Cardiology/American Heart Association classification schemes, he was classified as Stage B1 and Stage B, respectively, (10,11) and at low risk for cardiac death according to 2 validated risk calculators. (11,12) Since cardiomyopathy is a disqualifiable condition for accession into the US military, (13) the patient was processed for medical discharge from training. Infectious Disease advised the patient to complete a 60-day regimen of oral benznidazole, (14) but he declined. He was strongly encouraged to seek follow-up in the civilian health care sector and to notify household contacts that they should be screened for Chagas disease. (15)

Public health personnel interviewed the patient to facilitate case reporting to the Texas Department of State Health Services. The patient was raised on a ranch in south central Texas and had never traveled outside the continental United States. He camped occasionally near his home but never hunted or skinned animals. When shown a display case with triatomine insects of various species and at different stages of development, the patient immediately recognized them, saying they "were all over the place" on the ranch, including within the residence. He did not recall ever receiving a bite. A number of reservoir animals were also present on the property, including cats, dogs, raccoons, and armadillos. The patient was not aware of any relatives having Chagas disease, although he was adopted at a young age and had no knowledge of his biological mother. He had never received a blood transfusion. A week before his blood donation, he had spent 5 days and 4 nights on the JBSA Medina Training Annex for a field training exercise, during which he slept in a permethrin-treated bed net and reported no known insect bites.

Comment

Although neither congenital acquisition nor vectorborne acquisition during military training can be definitively ruled out, this patient was likely infected with T cruzi while growing up on a ranch in south central Texas. Ecologic modeling has predicted that this region of the United States is at increased risk for autochthonous Chagas disease. (16) Situated at the interface of tropical and temperate biomes, south central Texas has a number of environmental and cultural factors that may facilitate human exposure to T cruzi: a diverse array of wildlife reservoirs and indigenous triatomine species; the popularity of high-risk outdoor activities, especially hunting and camping; and the presence of scattered colonias (impoverished, primarily Hispanic communities). As compared to modern urban and suburban houses, poorly constructed ranches, cabins, and colonias are more susceptible to colonization by triatomine insects and wildlife reservoirs, thus increasing the likelihood of human exposure to infected vectors. (17)

The southern United States is inhabited by 11 recognized species of triatomine insects, listed in the Table, most of which are competent T cruzi vectors and likely to be involved in enzootic transmission cycles among indigenous wildlife reservoirs. (18) All species may exist as nest parasites and feed on a variety of vertebrate hosts. Competence for transmitting the parasite to humans is affected by environmental distribution, dispersal capacity, feeding and defecation behaviors, and ability to invade human domiciles, attributes of which vary according to species. (18-20)

In south central Texas, Triatoma gerstaeckeri insects have been found to enter human dwellings and to feed upon humans and domestic animals. (21,22) This medium-to-large triatomine species inhabits much of the Edwards Plateau and South Texas Brush Country between the 96th and 103rd parallels, the southeastern corner of New Mexico, and northeastern Mexico.23 The T cruzi infection rate of this species may exceed 60% in south central Texas,21,22 and adult insects often have detectable human blood in their midgut.24

Although the case patient was likely infected prior to arrival at JBSA, this report highlights the risk for autochthonous Chagas disease in the southern United States and underscores the importance of preventing Chagas and other vector-borne diseases while training in endemic areas. In order to decrease vector habitats, engineering controls should focus on reducing vegetation around military field sites to the maximum extent possible without disrupting the training mission. Administrative controls emphasizing site cleanliness should help minimize the population of woodrats, an important reservoir animal. (25) Finally, the 4 components of optimal personal protective measures should be meticulously used: a properly-worn field uniform (sleeves rolled down, wrist openings secured, undershirt tucked into the pants, and pant legs tucked into the boots); permethrin treatment of the uniform blouse and pants; the application of either DEET*-based (20% to 40% concentration) or picaridint-based (20% concentration) insect repellent to exposed skin; and sleeping in a permethrin-treated bed net. (26) Finally, diligent public health surveillance and health care provider education for Chagas disease are warranted.

References

(1.) Rassi A Jr, Rassi A, Marin-Neto JA. Chagas disease. Lancet. 2010; 375(9723); 1388-1402.

(2.) Bern C. Chagas' disease. N Engl J Med. 2015; 373(5):456-466.

(3.) World Health Organization. Chagas disease in Latin America: an epidemiological update based on 2010 estimates. Wkly Epidemiol Rec. 2015; 90(6):33-43.

(4.) Manne-Goehler J, Umeh CA, Montgomery SP, Wirtz VJ. Estimating the burden of Chagas disease in the United States. PLoS Negl Trop Dis. 2016; 10(11):e0005033.

(5.) Montgomery SP, Parise ME, Dotson EM, Bialek SR. What Do We Know About Chagas Disease in the United States?. Am J Trop Med Hyg. 2016; 95(6):1225-1227.

(6.) Woody NC, Woody HB. American Trypanosomiasis (Chagas' disease): first indigenous case in the United States. JAMA. 1955; 159(7):676-677.

(7.) Texas Department of State Health Services. Chagas disease [internet]. Available at: https://www. dshs.texas.gov/WorkArea/linkit.aspx?LinkIdentifi er=id&ItemID=22929. Accessed January 10, 2017.

(8.) Garcia MN, Murray KO, Hotez PJ, et al. Development of Chagas cardiac manifestations among Texas blood donors. Am J Cardiol. 2015; 115(1):113-117.

(9.) Nunes MA, Dones W, Morillo CA, Encina JE, Ribeiro AL. Chagas disease: an overview of clinical and epidemiological aspects. J Am Coll Cardiol. 2013; 62:767-776.

(10.) Acquatella H. Echocardiography in Chagas heart disease. Circulation. 2007; 115:1124-1131.

(11.) de Souza AC, Salles G, Hasslocher-Moreno AM, et al. Development of a risk score to predict sudden death in patients with Chaga's heart disease. Int J Cardiol. 2015; 187:700-704.

(12.) Rassi A Jr, Rassi A, Little WC, et al. Development and validation of a risk score for predicting death in Chagas' heart disease. N Engl J Med. 2006; 355(8):799-808.

(13.) Department of Defense Instruction 6130.03: Medical Standards for Appointment, Enlistment, or Induction in the Military Services. Washington, DC: US Department of Defense; April 28, 2010. Available at: http://dtic.mil/whs/directives/corres/ pdf/613003p.pdf. Accessed January 10, 2017.

(14.) Bern C, Montgomery SP, Herwaldt BL, et al. Evaluation and treatment of Chagas disease in the United States: a systematic review. JAMA. 2007; 298(18):2171-2181.

(15.) Wagner N, Jackson Y, Chappuis F, Posfay-Barbe KM. Screening and management of children at risk for Chagas disease in nonendemic areas. Pediatr Infect Dis J. 2016; 35(3):335-337.

(16.) Sarkar S, Strutz SE, Frank DM, Rivaldi CL, Sissel B, Sanchez-Cordero V. Chagas' disease risk in Texas. PLoS Negl Trop Dis. 2010; 4(10):e836.

(17.) Garcia MN, Woc-Colburn L, Aguilar D, Hotez PJ, Murray KO. Historical perspectives on the epidemiology of human Chagas disease in Texas and recommendations for enhanced understanding of clinical Chagas disease in the southern United States. PLoS Negl Trop Dis. 2015; 9(11):e0003981.

(18.) Klotz SA, Dorn PL, Mosbacher M, Schmidt JO. Kissing bugs in the United States: risk for vector-borne disease in humans. Environ Health Insights. 2014; 8(suppl 2):49-59.

(19.) Kjos SA, Snowden KF, Olson JK. Biogeography and Trypanosoma cruzi infection prevalence of Chagas disease vectors in Texas, USA. Vector Borne Zoonotic Dis. 2009; 9(1):41-50.

(20.) Martinez-Ibarra JA, Alejandre-Aguilar R, Paredes-Gonzalez E, et al. Biology of three species of North American Triatominae (Hemiptera: Reduviidae: Triatominae) fed on rabbits. Mem Inst Oswaldo Cruz. 2007; 102(8):925-930.

(21.) Curtis-Robles R, Wozniak EJ, Auckland LD, Hamer GL, Hamer SA. Combining public health education and disease ecology research: using citizen science to assess Chagas disease entomological risk in Texas. PLoSNegl Trop Dis. 2015; 9(12):e0004235. doi: 10.1371/journal.pntd.0004235.

(22.) Wozniak EJ, Lawrence G, Gorchakov R, et al. The biology of the Triatomine bugs native to south central Texas and assessment of the risk they pose for autochthonous Chagas disease exposure. J Parasitol. 2015; 101(5):520-528.

(23.) Bern C, Kjos S, Yabsley MJ, Montgomery SP. Trypanosoma cruzi and Chagas disease in the United States. Clin Microbiol Rev. 2011; 24(4):655-681.

(24.) Gorchakov R, Trosclair LP, Wozniak EJ, et al. Trypanosoma cruzi infection prevalence and bloodmeal analysis in Triatomine vectors of Chagas disease from rural peridomestic locations in Texas, 2013-2014. JMedEntomol. 2016; 53(4):911-918.

(25.) Shender L, Niemela M, Conrad P, Goldstein T, Mazet J. Habitat management to reduce human exposure to Trypanosoma cruzi and western conenose bugs (Triatoma protracta). Ecohealth. 2016; 13(3):525-534.

(26.) AFPMB Technical Guide No. 36: Personal Protective Measures Against Insects and Other Arthropods of Military Significance. Silver Spring, MD: Armed Forces Pest Management Board: November 6, 2015. Available at: http://www.acq.osd.mil/eie/ afpmb/docs/techguides/tg36.pdf. Accessed January 10, 2017.

Maj Bryant J. Webber, USAF, MC

Lt Col Edward J. Wozniak, TXSG, MRC

CPT David Chang, MC, USA

Maj Kelvin N. Bush, USAF, MC

Maj Matthew C. Wilson, USAF, MC

LTC James A. Watts, MC, USA

Lt Col Heather C. Yun, USAF, MC

Authors

Maj Webber is the Preventive Medicine Element Chief, 559th Trainee Health Squadron, Wilford Hall Ambulatory Surgical Center, JBSA-Lackland, Texas.

Lt Col Wozniak is Chief Public Health Officer, Texas State Guard Medical Brigade, Camp Mabry, Texas.

CPT Chang is a Fellow in the Department of Infectious Disease, San Antonio Military Medical Center, JBSAFort Sam Houston, Texas.

Maj Bush is a Fellow in the Cardiology Division, San Antonio Military Medical Center, JBSA-Fort Sam Houston, Texas.

Maj Wilson is Medical Director, 559th Trainee Health Squadron, Wilford Hall Ambulatory Surgical Center, JBSA-Fort Sam Houston, Texas.

LTC Watts is Chief of Cardiology, Cardiology Division, San Antonio Military Medical Center, JBSA-Fort Sam Houston, Texas.

Lt Col Yun is Infectious Disease Fellowship Program Director, San Antonio Uniformed Services Health Education Consortium, San Antonio Military Medical Center, JBSA-Fort Sam Houston, Texas.

Caption: Figure 1. Triatoma in the United States (continued).

Caption: Figure 2. Triatoma in the United States (continued).

Caption: Figure 3. Triatoma in the United States (continued).

Caption: Figure 4. Triatoma in the United States (continued).

Caption: Figure 5. Triatoma in the United States (continued).

Caption: Figure 6. Triatoma in the United States (end).
COPYRIGHT 2017 U.S. Army Medical Department Center & School
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2017 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Webber, Bryant J.; Wozniak, Edward J.; Chang, David; Bush, Kelvin N.; Wilson, Matthew C.; Watts, Jam
Publication:U.S. Army Medical Department Journal
Article Type:Report
Geographic Code:1U7TX
Date:Jan 1, 2017
Words:2482
Previous Article:Biosurveillance and morphological variations of larvae and pupae of common malaria vectors, Anopheles (Anopheles) Hyrcanus group species in the...
Next Article:Direct detection of Leishmania from clinical samples.
Topics:

Terms of use | Privacy policy | Copyright © 2021 Farlex, Inc. | Feedback | For webmasters |