• 1.

    Bern C, 2015. Chagas’ disease. N Engl J Med 373: 456466.

  • 2.

    Stevens L, Dorn PL, Schmidt JO, Klotz JH, Lucero D, Klotz SA, 2011. Kissing bugs. The vectors of Chagas. Adv Parasitol 75: 169192.

  • 3.

    Moser DR, Kirchoff LV, Donelsen JE, 1989. Dectection of Trypanosoma cruzi by DNA amplification using the polymerase chain reaction. J Clin Microbiol 27: 14771482.

    • Search Google Scholar
    • Export Citation
  • 4.

    Bern C et al. 2007. Evaluation and treatment of Chagas disease in the United States: a systematic review. JAMA 298: 21712181.

  • 5.

    Klotz SA, Schimdt JO, Dorn PL, Ivanyi C, Sullivan KR, Stevens L, 2014. Free-roaming kissing bugs, vectors of Chagas disease, feed on humans in the southwest. Am L Med 127: 421426.

    • Search Google Scholar
    • Export Citation
  • 6.

    Klotz SA, Shirazi M, Boesen K, Beatty NL, Dorn PL, Smith S, Schimdt JO, 2016. Kissing bug (Triatoma spp.) intrusion into homes: troublesome bites and domiciliation. Environ Health Insights 10: 4549.

    • Search Google Scholar
    • Export Citation
  • 7.

    Klotz S, Schmidt J, Dorn P, 2013. Trypanosoma cruzi carriage by Triatoma rubida and Triatoma protracta in a zoological park near Tucson, Arizona. J Kans Entomol Soc 86: 373374.

    • Search Google Scholar
    • Export Citation
  • 8.

    Reisenman CE, Lawerence G, Guerenstein PG, Gregory T, Dotson E, Hildebrand JG, 2010. Infection of kissing bugs with Trypansoma cruzi, Tucson, Arizona, USA. Emerg Infect Dis 16: 400405.

    • Search Google Scholar
    • Export Citation
  • 9.

    Stevens L, Dorn PL, Hobson J, de la Rua NM, Lucero DE, Klotz JH, Schmidt JO, Klotz SA, 2012. Vector blood meals and Chagas disease transmission potential, United States. Emerg Infect Dis 118: 646649.

    • Search Google Scholar
    • Export Citation
  • 10.

    Arce-Fonseca M, Carrillo-Sánchez SC, Molina-Barrios RM, Martínez-Cruz M, Cedillo-Cobián JR, Henao-Díaz YA, Rodríguez-Morales O, 2017. Seropositivity for Trypanosoma cruzi in domestic dogs from Sonora, Mexico. Infect Dis Poverty 6: 120.

    • Search Google Scholar
    • Export Citation
  • 11.

    Tibrayenc M, 2017. Genetics and Evolution of Infectious Diseases, 2nd edition. London, United Kingdom: Elsevier.

  • 12.

    Hernandez S, Flores CA, Viana GM, Sanchez DR, Traina MI, Meymandi SK, 2016. Autochthonous transmission of Trypanosoma cruzi in southern California. Open Forum Infect Dis 3: ofw227.

    • Search Google Scholar
    • Export Citation
  • 13.

    Bern C, Kjos S, Yabsley MJ, Montgomery SP, 2011. Trypanosoma cruzi and Chagas’ disease in the United States. Clin Microbiol Rev 24: 655681.

  • 14.

    Harris N, Woc-Colburn L, Gunter SM, Gorchakov R, Murray KO, Rossmann S, Garcia MN, 2017. Autochthonous Chagas disease in the southern United States: a case report of a suspected residential and military exposures. Zoonoses Public Health 64: 491493.

    • Search Google Scholar
    • Export Citation
  • 15.

    Meyers AC, Meinders M, Hamer SA, 2017. Widespread Trypanosoma cruzi infection in government working dogs along the Texas-Mexican border: discordant serology, parasite genotyping and associated vectors. PLoS Negl Trop Dis 11: eooo5819.

    • Search Google Scholar
    • Export Citation
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Evidence of Likely Autochthonous Transmission of Chagas Disease in Arizona

Norman L. BeattyDivision of Infectious Diseases, Department of Medicine, University of Arizona College of Medicine, Tucson, Arizona;

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Carlos M. Perez-VelezPima County Health Department, Tucson, Arizona;

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Hayley D. YaglomArizona Department of Health Services, Office of Infectious Disease Services, Bureau of Epidemiology and Disease Control, Phoenix, Arizona;

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Sharon CarsonPima County Health Department, Tucson, Arizona;

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Eugene LiuParasitic Diseases Branch, Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia;

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Zain I. KhalpeyDivision of Cardiothoracic Surgery, Department of Surgery, University of Arizona College of Medicine, Tucson, Arizona;

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Stephen A. KlotzDivision of Infectious Diseases, Department of Medicine, University of Arizona College of Medicine, Tucson, Arizona;

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Sean P. ElliottDivision of Pediatric Infectious Diseases, Department of Pediatrics, University of Arizona College of Medicine, Tucson, Arizona

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A healthy 16-year-old girl born and raised in Tucson, AZ, had screening and confirmatory testing revealing Chagas disease; clinical evaluation established that she had the indeterminate form of chronic Chagas disease with evidence of likely autochthonous transmission. Trypanosoma cruzi DNA was detected by conventional polymerase chain reaction in Triatoma rubida captured at her home.

CASE REPORT

A 16-year-old girl was referred to the pediatric infectious diseases outpatient clinic after attempting to donate blood. On routine blood donor screening, her blood was reactive by Trypanosoma cruzi qualitative chemiluminescent immunoassay and enzyme strip immunoassay (ESA) Chagas test. These results were reported to the Arizona Department of Health Services (AZDHSs). Confirmatory diagnostic testing was performed at the Centers for Disease Control and Prevention (CDC) in Atlanta, GA. Trypanosoma cruzi antibody enzyme immunoassay (EIA) was reactive and trypomastigote excreted and secreted antigen immunoassay was positive (Table 1).

Table 1

Patient blood donor screening and confirmatory diagnostic testing for Chagas disease

LaboratoryTrypanosoma cruzi serological testingResults
American Red CrossPRISM® Chemiluminescent immunoassay (Abbott Laboratories, Abbott Park, IL)Reactive
American Red CrossESA Chagas test (Abbott Laboratories, Abbott Park, IL)Reactive
CDCT. cruzi Ab EIAReactive (OD = 0.513)*
CDCT. cruzi Ab IB (trypomastigote excreted-secreted antigen-immunoblot)Positive

Ab = antibody; CDC = Centers for Disease Control and Prevention; EIA = enzyme immunoassay; ESA = enzyme strip immunoassay; OD = optical density.

Reactive: OD > 0.330, nonreactive: OD < 0.270, indeterminate: OD 0.270–0.

Clinical evaluation and course.

The patient was seen within 2 months of her attempt to donate blood. She was in normal health and had no physical complaints. Complete review of systems was unremarkable. She was afebrile with a blood pressure of 142/69 mm of Hg and an unremarkable physical examination of the heart and abdomen. A complete blood count and comprehensive metabolic panel were within normal limits. A 12-lead electrocardiogram demonstrated a normal sinus rhythm at 62 beats per minute with a borderline-prolonged PR interval of 196 ms (normal < 200 ms). A 2-D transthoracic echocardiogram demonstrated a structurally normal heart with normal physiologic parameters for her age group. No dysrhythmias were noted after continuous cardiac rhythm monitoring for 14 days. Magnetic resonance imaging of the heart with flow mapping was unremarkable and without evidence of myocardial fibrosis or ventricular dysfunction. Based on the two separate highly specific diagnostic tests performed at CDC in the absence of signs or symptoms of disease, she was considered to have the indeterminate form of chronic Chagas disease.1 After discussion with the patient, her guardian, and the Parasitic Diseases Branch at CDC, the patient received oral benznidazole at 5.3 mg/kg/day divided into two daily doses for 60 days. A pregnancy test was negative and serial complete blood counts and renal and liver function tests were normal. She tolerated the drug without any adverse reactions.

Assessment of patient’s possible environmental exposure to T. cruzi.

After screening tests were reported positive, AZDHS and local public health officials interviewed the patient and guardian for travel, food-borne, and vector-borne exposures. The patient resided with her parents and siblings in a single-family home located in the foothills of the Santa Catalina Mountains in Tucson, AZ. The home is less than 20 years old. She was born in Tucson and lived there her entire life. Her only travel outside the United States was to Europe (France, Germany, Spain). At the age of 13 years, she stayed 4 days in a modern condominium in Puerto Peñasco located in the northern state of Sonora, Mexico, approximately 120 miles south of Tucson. She did not camp out or participate in any outdoor activities aside from going to the beach. The patient did not recall consuming any raw fruit drinks while outside the United States. She had no history of receiving blood transfusions or an organ transplant. The patient’s mother and siblings were negative for T. cruzi antibody by EIA tests. The family reported using outdoor lighting at night and an active pack rat (Neotoma albigula) infestation on their property with multiple attempts at extermination without success. This rodent is the most common blood meal source for Triatoma rubida in the southwest United States.2 The family had two dogs confined indoors, but no other pets. Nighttime trapping with black lighting on three collection days during June and July 2017 resulted in the collection of three adult T. rubida from around the patient’s home, one specimen per night. The family also provided a collection of insects captured inside the home, one of which was a T. rubida nymph. Trypanosoma cruzi DNA was detected in all three adult T. rubida, but not in the nymph by conventional PCR using T. cruzi–specific primers TCZ1 and TCZ2.3 DNA was extracted from the terminal 1/3 of the abdomen using a separate sterile razorblade, Petri dish, and tweezers. The positive control was DNA-purified from cultured T. cruzi (gift of P. L. Dorn). Negative controls included no DNA and, second, laboratory-grown T. rubida without parasites (gift of J. O. Schmidt). This study was approved by the University of Arizona Institutional Review Board (IRB).

DISCUSSION

We describe evidence of likely autochthonous transmission of Chagas disease in Arizona in a 16-year-old girl. She was found to have positive serologies to T. cruzi on routine screening of her blood donation. Chagas disease is a reportable communicable disease in the state of Arizona which prompted the AZDHS and local public health officials to conduct an investigation into the patient’s travel, food-borne, and vector-borne exposures. Confirmatory immunoglobulin G serologic testing, preferably with two different test formats using different antigen preparations, is needed to confirm a diagnosis of chronic Chagas disease.1 In the United States, the CDC’s Division of Parasitic Diseases and Malaria offers this confirmatory testing at their reference laboratory. Our patient was in a normal state of health with no evidence of cardiac and/or gastrointestinal disease but with positive serologies (Table 1). Therefore, she has an indeterminate stage of chronic Chagas disease. Among persons chronically infected with T. cruzi, 20–30% are estimated to progress to Chagas cardiomyopathy,1 and antitrypanosomal therapy is recommended to reduce the risk of progression to clinical disease, especially in children and adolescents.1,4 Our patient was treated with benznidazole without serious adverse effects. In general, benznidazole is well tolerated in children and young adults. Benznidazole is now approved by the U.S. Food and Drug Administration, but not yet commercially available. Our patient obtained the drug through the expanded access for treatment of Chagas disease program at CDC (CDC IRB Protocol #5765).

The patient’s exposure to triatomines in Tucson was the likely source of her infection. The patient lived in an area of Tucson where triatomines commonly feed on pack rats, which are a wildlife host reservoir for T. cruzi. The patient reported seeing kissing bugs and their hosts (pack rats), around her home. Three adult T. rubida captured in the peridomiciliary area of her home were positive for T. cruzi by PCR. Also, environmental factors such as routinely using outside nighttime lighting and the presence of pets in the home may have increased her chances of contact with triatomines.2 Kissing bug domiciliation or infestation of human dwellings has been described in this region of southern Arizona.5,6 Furthermore, T. rubida in Tucson often harbor T. cruzi: 128 T. rubida captured in a zoological park had a rate of carriage of T. cruzi of 25%.7 An earlier study by Reisenman et al.8 demonstrated a rate of carriage of T. cruzi by T. rubida to be 41% (N = 158 bugs). Interestingly, T. rubida and Triatoma protracta captured in Arizona and California demonstrated that 38% of the bugs had a human blood meal in the abdomen.9 We considered the possibility that infection was acquired during her travel to Puerto Peñasco, Mexico, on a short trip. One study conducted in Sonora, Mexico, showed seropositivity in domestic dogs for exposure to T. cruzi,10 but no human cases to our knowledge have been described in Puerto Peñasco, Mexico. Regardless, it is unlikely that transmission took place at that time because of the short duration of the visit, her stay in a modern resort complex at a beachside condominium, and her denial of ingesting raw fruits or seeing triatomines during that trip.

Triatominae can be found worldwide and are classified into five tribes and 15 genera, including 147 described species most of which are exclusively found in the New World. Trypanosoma cruzi vector-borne transmission only occurs in the Americas because the parasite is harbored by the triatomines that inhabit the New World.11 In our patient, her travel to Europe is not considered an exposure risk because T. cruzi vector-borne transmission is not found in that part of the world. Reports of presumed autochthonous transmission of T. cruzi in the United States are increasing because of blood donation screening. Infected blood donors often present with chronic indeterminate Chagas like our patient.12 Autochthonous T. cruzi infections have been reported in multiple states including California, Louisiana, Texas, Tennessee,13 and, perhaps now, Arizona. One other case of autochthonous Chagas disease may have arisen in Arizona, but the patient was also potentially exposed to T. cruzi on a military base in south Texas,14 an area endemic for canine Chagas disease.15

The risk of autochthonous transmission of T. cruzi infection in the United States is undefined and likely low, but reporting probable autochthonous cases such as this will be important for identifying the risk factors for acquiring Chagas disease in the United States.

Acknowledgments:

We would like to thank the patient and family for helping us with this thorough investigation. We also would like to thank Susan Montgomery from the U.S. Centers for Disease Control and Prevention, Parasitic Diseases Branch, for her professional review and annotation of the manuscript. We want to acknowledge the help of Nicole Bradley-Behrens and Maria Love from the University of Arizona College of Medicine, Department of Immunobiology, for their technical assistance with the detection of T. cruzi.

REFERENCES

  • 1.

    Bern C, 2015. Chagas’ disease. N Engl J Med 373: 456466.

  • 2.

    Stevens L, Dorn PL, Schmidt JO, Klotz JH, Lucero D, Klotz SA, 2011. Kissing bugs. The vectors of Chagas. Adv Parasitol 75: 169192.

  • 3.

    Moser DR, Kirchoff LV, Donelsen JE, 1989. Dectection of Trypanosoma cruzi by DNA amplification using the polymerase chain reaction. J Clin Microbiol 27: 14771482.

    • Search Google Scholar
    • Export Citation
  • 4.

    Bern C et al. 2007. Evaluation and treatment of Chagas disease in the United States: a systematic review. JAMA 298: 21712181.

  • 5.

    Klotz SA, Schimdt JO, Dorn PL, Ivanyi C, Sullivan KR, Stevens L, 2014. Free-roaming kissing bugs, vectors of Chagas disease, feed on humans in the southwest. Am L Med 127: 421426.

    • Search Google Scholar
    • Export Citation
  • 6.

    Klotz SA, Shirazi M, Boesen K, Beatty NL, Dorn PL, Smith S, Schimdt JO, 2016. Kissing bug (Triatoma spp.) intrusion into homes: troublesome bites and domiciliation. Environ Health Insights 10: 4549.

    • Search Google Scholar
    • Export Citation
  • 7.

    Klotz S, Schmidt J, Dorn P, 2013. Trypanosoma cruzi carriage by Triatoma rubida and Triatoma protracta in a zoological park near Tucson, Arizona. J Kans Entomol Soc 86: 373374.

    • Search Google Scholar
    • Export Citation
  • 8.

    Reisenman CE, Lawerence G, Guerenstein PG, Gregory T, Dotson E, Hildebrand JG, 2010. Infection of kissing bugs with Trypansoma cruzi, Tucson, Arizona, USA. Emerg Infect Dis 16: 400405.

    • Search Google Scholar
    • Export Citation
  • 9.

    Stevens L, Dorn PL, Hobson J, de la Rua NM, Lucero DE, Klotz JH, Schmidt JO, Klotz SA, 2012. Vector blood meals and Chagas disease transmission potential, United States. Emerg Infect Dis 118: 646649.

    • Search Google Scholar
    • Export Citation
  • 10.

    Arce-Fonseca M, Carrillo-Sánchez SC, Molina-Barrios RM, Martínez-Cruz M, Cedillo-Cobián JR, Henao-Díaz YA, Rodríguez-Morales O, 2017. Seropositivity for Trypanosoma cruzi in domestic dogs from Sonora, Mexico. Infect Dis Poverty 6: 120.

    • Search Google Scholar
    • Export Citation
  • 11.

    Tibrayenc M, 2017. Genetics and Evolution of Infectious Diseases, 2nd edition. London, United Kingdom: Elsevier.

  • 12.

    Hernandez S, Flores CA, Viana GM, Sanchez DR, Traina MI, Meymandi SK, 2016. Autochthonous transmission of Trypanosoma cruzi in southern California. Open Forum Infect Dis 3: ofw227.

    • Search Google Scholar
    • Export Citation
  • 13.

    Bern C, Kjos S, Yabsley MJ, Montgomery SP, 2011. Trypanosoma cruzi and Chagas’ disease in the United States. Clin Microbiol Rev 24: 655681.

  • 14.

    Harris N, Woc-Colburn L, Gunter SM, Gorchakov R, Murray KO, Rossmann S, Garcia MN, 2017. Autochthonous Chagas disease in the southern United States: a case report of a suspected residential and military exposures. Zoonoses Public Health 64: 491493.

    • Search Google Scholar
    • Export Citation
  • 15.

    Meyers AC, Meinders M, Hamer SA, 2017. Widespread Trypanosoma cruzi infection in government working dogs along the Texas-Mexican border: discordant serology, parasite genotyping and associated vectors. PLoS Negl Trop Dis 11: eooo5819.

    • Search Google Scholar
    • Export Citation

Author Notes

Address correspondence to Stephen A. Klotz, Division of Infectious Diseases, Department of Medicine, University of Arizona College of Medicine, 1501 N. Campbell Ave., Tucson, AZ 85724. E-mail: sklotz@deptofmed.arizona.edu

Authors’ addresses: Norman L. Beatty, University of Arizona, Department of Medicine, Tucson, AZ, E-mail: norman.beatty@bannerhealth.com. Carlos M. Perez-Velez, Division of Infectious Diseases, Pima County Health Department of Tuberculosis Clinic, Tucson, AZ, E-mail: cmperezvelez@gmail.com. Hayley D. Yaglom, Division of Infectious Diseases, Arizona Department of Health Services, Phoenix, AZ, E-mail: hayley.yaglom@azdhs.com. Sharon Carson, Division of Infectious Diseases, Pima County Health Department, Tucson, AZ, E-mail: sharon.carson@pima.gov.com. Eugene Liu, Centers for Disease Control and Prevention Prevention Research Centers, Parasitical Diseases, Atlanta, GA, E-mail: ixq8@cdc.gov. Zain I. Khalpey, Department of Surgery, University of Arizona, Tucson, AZ, E-mail: zkhalpey@surgery.arizona.edu. Stephen A. Klotz, Section of Infectious Diseases, Arizona Health Sciences Center, Tucson, AZ, E-mail: sklotz@u.arizona.edu. Sean P. Elliott, Pediatric Infectious Diseases, University of Arizona Health Sciences Center, Tucson, AZ, E-mail: selliott@peds.arizona.edu.

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