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Fatal acute Chagas disease by Trypanosoma cruzi DTU TcI, Ecuador

Abstract

Background

Chagas disease is caused by the haemoflagellate protozoan Trypanosoma cruzi. Currently, T. cruzi recognizes seven discrete typing units (DTUs): TcI to TcVI and Tcbat. The genetic diversity of T. cruzi is suspected to influence the clinical outcome. Acute clinical manifestations, which include myocarditis and meningoencephalitis, are sometimes fatal; occur most frequently in children and in immunocompromised individuals. Acute disease is often overlooked, leading to a poor prognosis.

Case presentation

A 38-year-old man from a subtropical area of the Andes mountains of Ecuador was hospitalized after 3 weeks of evolution with high fever, chills, an enlarged liver, spleen, and lymph nodes, as well as facial edema. ECG changes were also observed. T. cruzi was identified in blood smears, culture and amplification of DNA by PCR. Tests for anti-T. cruzi IgG and IgM and HIV were negative. Molecular typing by restriction fragment length polymorphism (PCR-RFLP) determined the parasite to DTU TcI. In the absence of a timely anti-T. cruzi medication, the patient died.

Conclusions

This is a case of severe pathogenicity and the virulence of a DTU TcI strain in an adult patient. The severe acute Chagas disease was probably overlooked due to limited awareness and its low incidence. Our findings suggest that T. cruzi DTU TcI strains circulating in Ecuador are capable of causing fatal acute disease. Early diagnosis and prompt treatment is of paramount importance to avoid fatalities in acute infections.

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Background

Data from the World Health Organization indicate that 6–7 million individuals are infected by Trypanosoma cruzi, from the south of the United States to the north of Argentina and Chile, with approximately 60–70 million people at risk of infection; Chagas disease is considered a neglected tropical disease [1].

Infected individuals may present with clinical manifestations of different levels of severity. The genetic diversity of T. cruzi is suspected to influence the clinical outcome although no definitive associations have been unequivocally identified [2, 3]. Seven genetic lineages or discrete typing units (DTUs) are currently recognized, named TcI through TcVI and Tcbat [3]. All lineages are present throughout the Americas, although TcI predominates in northern region of South America, and occurs in both domestic and sylvatic cycles of the parasite [2]. In addition, TcI infections are frequently reported in the northern section of the Amazon, where patients can display severe acute clinical manifestations, including cardiomyopathy and death [2]. TcI has also been isolated from chronic chagasic cardiomyopathy and reactivation disease [4]. TcII, TcV, and TcVI are associated with chronic cases presenting megaesophagus and megacolon in the southern cone countries [5, 6].

The acute phase of Chagas disease is usually asymptomatic; however, when symptoms do occur, they may include high fever, malaise, enlargement of the liver, spleen, and lymph nodes; as well as subcutaneous edema (localized or generalized) [7]. ECG changes are also common [2]. Death can occur in the acute phase (< 5–10% of symptomatic cases) due to severe myocarditis, meningoencephalitis, or both [7,8,9] and in some cases due to acute kidney failure (AKF) [10]. In addition, fatal cases with disseminated and diffuse foci have been observed [5]. Severe acute Chagas disease and related deaths occur most frequently in children, the elderly and immunocompromised individuals or in those who are receiving immunosuppressive drugs or organ transplants [4, 6, 7].

Chagas disease is endemic in Ecuador, country located in the northwest region of South America. TcI is clearly the predominant DTU, and has been the only DTU isolated from triatomines, rodents and opossums in the central Pacific coast and in southern Ecuador [4, 11]. However, a couple of reports exist in the literature suggesting the presence of genetic lineages other than TcI in Ecuador [12, 13]. T. cruzi infection is considered a public health problem in Ecuador, because it is endemic in the Amazon, the Pacific coast and in some subtropical areas of Andes mountains [7, 14]. The Pan-American Health Organization (PAHO) and the Ecuadorian Ministry of Public Health (MPH) estimate the general prevalence of T. cruzi infection to be 1.38% of the general Ecuadorian population with annual mortality of 7.7 per 1000 seropositive, meaning that there are 1300 deaths annually due to Chagas [http://chagas.zoonosis.gub.uy/Documentos/Ecuador/ Control_dela_Enfermedad_de_Chagas_en_Ecuador_OPS_Chagas.pdf. CP 17-1106292]. However, information is scarce regarding the genetic diversity of human isolates. Herein, we report a case of Chagas disease in a 38-year-old man who died in the acute phase due to myocarditis and renal failure. The patient was infected in the western foothills of the Andes close to the central Pacific coastal region, and the parasite isolated from his blood was determined to belong to T. cruzi DTU TcI.

Case presentation

A farmer of 38-year-old man was admitted to a hospital with fever (39 °C), chills, malaise, anorexia, generalized pallor, hepatosplenomegaly, lymphadenopathy, weight loss, facial edema, and an ulcerous skin lesion in his left leg. The patient was born and always lived in a locality of La Maná-Cotopaxi province; a subtropical area located in the western foothills of the Andes, close to the central Pacific coastal region, some 130 km from the capital Quito. The patient reported neither receiving blood transfusions nor travelling within or outside Ecuador.

Since December 2014, he had a 22-day history of high fever, chills and malaise being treated with antibiotics and antipyretics in a public health center. Five days prior to hospital admission, he was diagnosed with T. cruzi infection via microscopic observation in peripheral blood. Due to unavailability of anti-T. cruzi drugs, he was transferred to a hospital. The patient reported of having an insect bite in his left leg approximately 10 days prior to the development of the fever. The bite became a pruritic indurated papule, which subsequently ulcerated and did not heal even with the use of an antibiotic cream. The patient was hospitalized with a diagnosis of acute Chagas disease, in order to receive treatment with benznidazole, the drug recommended by the Ecuadorian MPH [14].

At the beginning of hospitalization, microscopic examination of thick and thin smears of peripheral blood confirmed the presence of T. cruzi, and was negative for malaria parasites. T. cruzi was cultured in LIT medium. The parasites were spotted on FTA Classic Card (Whatman, Newton Center, MA). Blood tests showed a white blood cell count of 6.8 × 109/L, with 44.8% neutrophils, 45.9% lymphocytes, 7.3% monocytes, 1.2% eosinophils and 0.8% basophils. The erythrocyte sedimentation rate was 40 mm/hour, with a hemoglobin of 8.4 g/dL, a hematocrit of 25.4%, and a platelet count of 152,000/μL. VDRL, HBsAg, HBcAg, HCV, ELISA and Western blot for HIV, and the test for febrile agglutinations (Brucella spp., typhoid and paratyphoid fevers), were all negative. Serum glucose, urea and creatinine were 77, 173 and 7.7 mg/dL, respectively. Serological tests for anti-T. cruzi IgG and IgM (Chagatest ELISA recombinant, Version 3.0. Wiener-Argentina) were negative. Blood, urine and skin ulcer cultures for bacteria were negative. Paracetamol (1 g) was administered every 8 h as an anti-febrile agent.

The EKG showed left anterior fascicular hemi block, QRS 0.10mms, marked deviation of the axis to the left (positive QRS in I and negative in AVF), small R waves and large S waves in III and AVF. The chest X-ray demonstrated an increased heart area. An abdominal CT scan showed bilateral pleural effusion, liver and spleen enlargement, and liquid in the pelvic cavity.

During the 11-day hospitalization period, the patient’s temperature fluctuated from normal to 38 °C. Hydration and electrolytes were normal. Creatinine levels initially rose to 10.4 and later to 13.1 mg/dL, requiring hemodialysis. The patient received six blood transfusions in total, elevating the hemoglobin to 11.8 g/dL. The patient died of respiratory distress due to acute failure of heart and kidneys. He never did receive benznidazole because of hospital shortage. Parents did not consent to an autopsy.

T. cruzi DNA was extracted from the FTA card. Genotyping was performed by PCR-RFLP, following the methodology developed by Lewis et al. (2009) [15]. Briefly, fragments of the D7 divergent domain of the 24Sα rRNA locus (LSU rDNA), glucose-6-phosphate isomerase (GPI) and heat shock protein 60 (HSP60) genes were amplified with specific primers; the size of amplicons and restriction fragments after digestion with restriction enzymes (Eco RV for HSP60 and Hha I for GPI) were compared to those of reference T. cruzi strains (Fig. 1). Additionally, a multiplex PCR assay targeting the mini-exon gene [16] was also performed (Fig. 2). In both cases, the T. cruzi isolate from the patient matched the pattern of DTU TcI. Written consent to publish the case was provided by the patient’s wife.

Fig. 1
figure1

T. cruzi genotyping by PCR-RFLP. As indicated by the brackets on the right side, specific fragments from the LSUr DNA, HSP60 and GPI genes were amplified by PCR. GPI and HSP60 amplification products were digested with HhaI and EcoRV restriction enzimes, respectively. L: DNA molecular weight ladder, with the corresponding molecular weights in base-pairs indicated on the left of the gels. TcI-TcVI: DTU controls. N: Negative (no template) control. P: DNA isolated from the patient’s blood. Tr: T. rangeli DNA. Lanes containing restriction products are labeled with an asterisk (*). Only restriction products are shown for controls

Fig. 2
figure2

T. cruzi genotyping by mini-exon multiplex PCR. Parasite genotyping was performed using the multiplex PCR assay targeting the mini-exon gene, which differentiates TcI from the other T. cruzi DTUs. L: DNA molecular weight ladder, with the corresponding molecular weights in base-pairs indicated on the left of the gel. P: DNA isolated from parasites cultured from the patient’s blood. TcI. DTU TcI control DNA (Cutia Cl1 strain), yielding a 200 bp band. TcII-V-VI. Control DNA from DTU TcII DNA (Tu18Cl93 strain), yielding a 250 bp band, corresponding to DTUs TcII, V or VI. TcIII-IV. DTU TcIV (CAN III Cl1 strain), yielding a 150 bp band, corresponding to DTUs III or IV. NC. Negative (no template) control. Tr. T. rangeli control DNA, yielding a 100 bp band

Discussion and conclusions

This is the first time in Ecuador to genotype T. cruzi TcI (DTU) from a human source, although the patient did not survive in the acute phase of the Chagas disease. To date, TcI is the predominant DTU in Ecuador, as evidenced in studies but involving reservoirs and vectors from different geographic regions [4, 11]. It is in concordance with previous reports from the northern region of South America that showed DTU TcI being predominant in the neighboring countries of Colombia and Venezuela [17, 18]. It has been hypothesized that TcI can escape the host’s acute immune response, remain in the peripheral blood mononuclear cells and then parasitize organs faster [5, 19]. The present case suggests that the TcI strain circulating in the country are capable of causing fatal acute disease. Hence, further research is needed to identifying the genetic lineages of T. cruzi DTU in different clinical presentations and the severity of the Chagas disease.

Acute Chagas cases resulting in death have been documented, mostly from oral contamination and found most frequently in the Amazon region [20]. Most of these cases were due to TcI, with rare cases due to TcIII and TcIV [21,22,23], TcI in Venezuela and French Guiana [24, 25] and TcII in southern Brazil [26]. However, in this case, the infection apparently occurred via the vectorial route, as suggested by the presence of a chagoma, i.e. the pruritic papular lesion that evolved into an ulcer in the left leg, starting 10 days before the appearance of fever and malaise. The presence of T. cruzi vectors has been reported in Cotopaxi province, specifically Triatoma carrioni and T. dispar [27].

Symptoms frequently reported in acute fatal cases of Chagas disease are hepatomegaly (100%), myocarditis (75%), pericardial effusion (50%), cardiomegaly (25%) or acute kidney failure (AKF) [10, 17, 20]. In the present case, the patient was clearly in the acute phase, because of the duration of the symptoms and the absence of anti-T. cruzi IgM and IgG antibodies. The absence of antibodies would be explained because 1) In order to develop detectable antibodies, it generally takes at least 3 to 4 weeks [28]. 2) In acute cases reported in Venezuela, specific IgM antibodies were demonstrated only in 87.3% of cases, and the transmission was oral, that is considered more severe, because of the rapid entry of parasites into the blood stream [24]. Hence, prompt development of antibodies can occur when compared to a natural infection caused by a triatomine bite, as probably occurred in our case. 3) Another explanation could be because of the different antigens used in the ELISA techniques performed, in-house with the delipidised antigen specific for T. cruzi epimastigotes [24] would detect prompt antibodies rather than we used the commercially ELISA method Chagatest ELISA recombinant, Version 3.0. Wiener-Rosario, Argentina, based on six recombinant proteins. Severe symptomatology is known to occur in immunocompromised patients [7]. However, our patient had no history of taking immunosuppressive drugs and was HIV-negative. The symptoms present in our patient including edema, EKG alterations, cardiomegaly, bilateral pleural effusion and the elevation of creatinine and blood urea nitrogen, strongly suggested acute myocarditis and AKF. The latter condition is usually marked by a rise in serum creatinine concentration or by azotemia.

High mortality in acute cases of Chagas disease has been linked to lack of prompt diagnosis and treatment. Both may have contributed to worsening of the patient’s condition and his subsequent death. We strongly advise health-care providers, lab technicians, physicians, as well as decision-makers in the central health entities to increase awareness about Chagas disease, and to improve the availability and distribution of anti-T. cruzi medication in the country. This case exemplifies the challenges faced by the local healthcare system in this regard, and constitutes an urgent call for action in order to ensure early diagnosis and prompt treatment is available to all chagasic patients in Ecuador.

Availability of data and materials

All relevant data and materials are included in the manuscript.

Abbreviations

AKF:

Acute kidney failure

DTUs:

Discrete typing units

EKG:

Electrocardiogram

ELISA:

Enzyme-linked immunosorbent assay

HBcAg:

Anti-core hepatitis

HBsAg:

Hepatitis B surface antigen

HCV:

Hepatitis C Virus

HIV:

Human Immunodeficiency Virus

MPH:

Ministry of Public Health

PAHO:

Pan American Health Organization

PCR-RFLP:

Polymerase Chain Reaction-Restriction fragment length polymorphism

VDRL:

Venereal Disease Research Laboratory test

WHO:

World Health Organization

References

  1. 1.

    World Health Organization. Chagas disease (American trypanosomiasis). Geneva: World Health Organization Washington; 2018. Accessed 19 June 2018: http://www.who.int/news-room/fact-sheets/detail/ chagas-disease (american-trypanosomiasis)

    Google Scholar 

  2. 2.

    Messenger LA, Miles MA, Bern C. Between a bug and a hard place: Trypanosoma cruzi genetic diversity and the clinical outcomes of Chagas disease. Expert Rev Anti Infect Ther. 2015;13(8):995–1029. https://doi.org/10.1586/14787210.2015.1056158.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  3. 3.

    Zingales B. Trypanosoma cruzi genetic diversity: something new for something known about Chagas disease manifestations, serodiagnosis and drug sensitivity. Acta Trop. 2018;184:38–52.

    CAS  Article  Google Scholar 

  4. 4.

    Costales JA, Jara-Palacios MA, Llewellyn M, Messenger LA, Ocaña-Mayorga S, Villacís AG. Trypanosoma cruzi population dynamics in the Central Ecuadorian Coast. Acta Trop. 2015;151:88–93.

    Article  Google Scholar 

  5. 5.

    Diaz-Bello Z, Thomas MC, Lopez MC, Zavala-Jaspe R, Noya O, Alarcón de Noya B. Trypanosoma cruzi genotyping supports a common source of infection in a school-related oral outbreak of acute Chagas disease in Venezuela. Epidemiol Infect. 2014;142(1):156–62.

    CAS  Article  Google Scholar 

  6. 6.

    Nicholls RS, Cucunubá ZM, Knudson A, Flórez AC, Montilla M, Puerta CJ, Pavía PX. Enfermedad de Chagas aguda en Colombia, una entidad poco sospechada. Informe de 10 casos presentados en el período 2002 a 2005. Biomédica. 2007;27(Supl.1):8–17.

    Article  Google Scholar 

  7. 7.

    World Health Organization. Control of Chagas Diseases. Geneva: WHO Technical Report Series. Second report of the WHO Expert Committee; 2002. p. 1–106.

    Google Scholar 

  8. 8.

    Hollowed J, McCullough M, Sanchez D, Traina M, Hernandez S, Murillo E. Rapidly progressing Chagas cardiomyopathy. Am J Trop Med Hyg. 2016;94:894–6.

    Article  Google Scholar 

  9. 9.

    Carme B, Aune I, Nguyen G, Aznar C, Beaudet B. Four Cases of Acute Chagasic Myocarditis in French Guiana. Am J Trop Med Hyg. 2001;64:162–3.

    CAS  Article  Google Scholar 

  10. 10.

    Pinto AYN, Valente SAS, Valente VC. Emerging Acute Chagas Disease in Amazonian Brazil: Case Reports with Serious Cardiac Involvement. Brazilian J Infect Dis. 2004;8(6):454–60.

    Google Scholar 

  11. 11.

    Ocana-Mayorga S, Llewellyn MS, Costales JA, Miles MA, Grijalva MJ. Sex, subdivision, and domestic dispersal of Trypanosoma cruzi lineage I in southern Ecuador. PLoS Negl Trop Dis. 2010;4(12):e915 [PubMed: 21179502].

    Article  Google Scholar 

  12. 12.

    Garzón EA, Barnabé C, Córdova X, Bowen C, Paredes W, Gómez E, Ouaissi A, Tibayrenc M, Guevara AG. Trypanosoma cruzi isoenzyme variability in Ecuador: first observation of zymodeme III genotypes in chronic chagasic patients. Trans R Soc Trop Med Hyg. 2002;96(4):378–82.

    Article  Google Scholar 

  13. 13.

    Bhattacharyya T, Mills EA, Jansen AM, Miles MA. Prospects for Trypanosoma cruzi lineage-specific serological surveillance of wild mammals. Acta Trop. 2015;15:182–6.

    Article  Google Scholar 

  14. 14.

    Abad-Franch F, Aguilar M. Control de la Enfermedad de Chagas en el Ecuador. Quito, Diciembre 2002 - Febrero: OPS/OMS – Ministerio de Salud Pública del Ecuador; 2003.

    Google Scholar 

  15. 15.

    Lewis MD, Ma J, Yeo M, Carrasco HJ, Llewellyn MS, Miles MA. Genotyping of Trypanosoma cruzi: systematic selection of assays allowing rapid and accurate discrimination of all known lineages. Am J Trop Med Hyg. 2009;81(6):1041–9.

    CAS  Article  Google Scholar 

  16. 16.

    Fernandes O, Santos SS, Cupolillo E, Mendonça B, Derre R, Junqueira AC, Santos LC, Sturm NR, Naiff RD, Barret TV, Campbell DA, Coura JR. A mini-exon multiplex polymerase chain reaction to distinguish the major groups of Trypanosoma cruzi and T. rangeli in the Brazilian Amazon. Trans R Soc Trop Med Hyg. 2001;95(1):97–9.

    CAS  Article  Google Scholar 

  17. 17.

    Añez N, Crisante G, da Silva FM, Rojas A, Carrasco H, Umezawa ES, Stolf AM, Ramirez JL, Teixeira MM. Predominance of lineage I among Trypanosoma cruzi isolates from Venezuelan patients with different clinical profiles of acute Chagas'’ disease. Trop Med Int Health. 2004;9(12):1319–26.

    Article  Google Scholar 

  18. 18.

    Mejia-Jaramillo AM, Pena VH, Triana-Chavez O. Trypanosoma cruzi: Biological characterization of lineages I and II supports the predominance of lineage I in Colombia. Exp Parasitol. 2009;121(1):83–91 [PubMed: 18950627].

    CAS  Article  Google Scholar 

  19. 19.

    Cassini AL, de Abreu Vieira PM, Mendes Roatt B, Oliveira Aguiar-Soares RD. The TcI and TcII Trypanosoma cruzi experimental infections induce distinct immune responses and cardiac fibrosis in dogs. Mem Inst Oswaldo Cruz. 2014;109(8):1005–13.

    Article  Google Scholar 

  20. 20.

    Cavalcante dos Santos VR, de Meis J, Savino W, JA AA, dos santos Vieira JR, Coura JR, Verissimo Junqueira AC. Acute Chagas disease in the state of Pará, Amazon Region: is it increasing? Mem Inst Oswaldo Cruz. 2018;113(5):e170298.

    Google Scholar 

  21. 21.

    Coura JR. Transmission of chagasic infection by oral route in the natural history of Chagas disease. Rev Soc Bras Med Trop. 2006;39:113–7.

    PubMed  Google Scholar 

  22. 22.

    Marcili A, Lima L, Valente VC, Valente SA, Batista JS, Junqueira AC, Souza AI, da Rosa JA, Campaner M, Lewis MD, Llewellyn MS, Miles MA, Teixeira MM. Comparative phylogeography of Trypanosoma cruzi TCIIc: new hosts, association with terrestrial ecotopes ans spatial clustering. Infect Genet Evol. 2009;9(6):1265–74.

    Article  Google Scholar 

  23. 23.

    Valente SA, da Costa VV, das Neves Pinto AY, de Jesus Barbosa César M, dos Santos MP, Miranda CO, Cuervo P, Fernandes O. Analysis of an acute Chagas disease outbreak in the Brazilian Amazon: human cases, triatomines, reservoir mammals and parasites. Trans R Soc Trop Med. 2009;103:291–7.

    Article  Google Scholar 

  24. 24.

    Alarcón de Noya BA, Díaz-Bello Z, Colmenares C, Ruiz-Guevara R, Mauriello L, Muñoz-Calderón A, Noya O. Update on oral Chagas disease outbreaks in Venezuela: epidemiological, clinical and diagnostic approaches. Mem Inst Oswaldo Cruz. 2015;110(3):377–86.

    Article  Google Scholar 

  25. 25.

    Coura JR. Chagas disease: control, elimination and eradication. Is it possible? Mem Inst Oswaldo Cruz. 2013;108(8):962–7.

    Article  Google Scholar 

  26. 26.

    Steindel M, Pacheco LK, Scholl D, Soares M, de Moraes MH, Eger I, Kosmann C, Sincero TC, Stoco PH, Murta SM, de Carvalho-Pinto CJ, Grisard EC. Characterization of Trypanosoma cruzi isolated from humans, vectors and animal reservoirs following an outbreak of acute human Chagas disease in Santa Catarina state, Brazil. Diagn Microbiol Infect Dis. 2008;60:25–32.

    CAS  Article  Google Scholar 

  27. 27.

    Abad-Franch F, Paucar A, Carpio C, Cuba CA, Aguilar HM, Miles MA. Biogeography of Triatominae (Hemiptera: Reduviidae) in Ecuador: implications for the design of control strategies. Mem Inst Oswaldo Cruz. 2001;96(5):611–20.

    CAS  Article  Google Scholar 

  28. 28.

    Janeway CA, Travers P, Walport M, Shlomchik MJ. In: Janeway CA, Travers P, Walport M, Shlomchik MJ, editors. Adaptative immunity to infection. 5th ed. New York: Churchill Livingstone; 2001. p. 381–423. Immunobiology.

    Google Scholar 

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Acknowledgements

The authors would like to thank Camila Cilveti and Jalil Maiguashca Sánchez for technical assistance, and Ronald Guderian for reviewing this manuscript.

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MC: Overall coordination, writing, editing and revision of manuscript. WC, GS: Diagnosis and management of patient, writing and editing of manuscript. YV, JA, AG: Parasitological and molecular diagnosis, writing and editing of manuscript. All authors read and approved the final manuscript.

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Correspondence to Manuel Calvopina.

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The Hospital Director and the patient’s wife signed a consent to obtain the data from the clinical record, after patient death.

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The authors declare that they have no competing interests.

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Calvopina, M., Segovia, G., Cevallos, W. et al. Fatal acute Chagas disease by Trypanosoma cruzi DTU TcI, Ecuador. BMC Infect Dis 20, 143 (2020). https://doi.org/10.1186/s12879-020-4851-0

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Keywords

  • Trypanosoma cruzi
  • TcI
  • DTU
  • Fatal acute Chagas disease
  • Ecuador