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ID Case Conference January 16, 2008

ID Case Conference January 16, 2008. Carlos M. Perez, MD, FACP Associate Professor of Medicine Pontificia Universidad Catolica de Chile. The Case.

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ID Case Conference January 16, 2008

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  1. ID Case ConferenceJanuary 16, 2008 Carlos M. Perez, MD, FACP Associate Professor of Medicine Pontificia Universidad Catolica de Chile

  2. The Case HPI: ♂, 52 yo, h/o chronic renal insufficiency s/p bilateral nephrectomy and living donor transplantation (1978)  rejection cadaveric donor transplantation (1987)chronic rejection. Type 2 Diabetes mellitus, Hepatitis C, Right atria mass Myxoma? diagnosed one year before current admission.

  3. The Case HPI: Transferred from another hospital where he was admitted for altered mental status. Hypoglycemia was found. Also developed MRSA bacteremia treated with Vancomycin. Leucocyturia on UA, received po Ciprofloxacin. No urine cultures available. Transesophageal echocardiogram showed R atria mass.

  4. PMH: Type 2 Diabetes mellitus insulin dependent. Hepatitis C, no treatment. R atria mass PSH: Bilateral nephrectomy, kidney transplantation X 2 Medications: Insulin NPH. Prednisone 10 mg qd. Cyclosporine. NKDA SH: Married. No Etoh use. No tobacco use. No pets exposure. No recent travels. ROS: Altered mental status. No fever. No GI symptoms.

  5. Physical exam P: Normal Pulse and BP. Afebrile. Normal saturation on room air. Pale. Hydrated. No lymphadenopathy. No skin rash HEENT wnl, Lungs clear, Heart RRR, no murmurs, abdomen soft, no tender. Kidney on RLQ, non tender. Neurological examination: Mental status: Awake. Mutism. Bilateral upper an lower extremities moderate weakness. Generalized rigidity. Normal reflexes. Sensation difficult to asses. No meningeal signs.

  6. Laboratory Hematocrit 2. Hb 7. WBC 5,800 (3 % bands, 15 % lymphocytes), Platelets 126,000. Sed rate 114. CRP 2.7 (NV < 0.9). Glucose 154. Creatinine 3.32. BUN 48. Albumin 2,8. ALT 35 AST 27 GGT 36 AP 45. TB 0.86. INR 1,1. UA: WBC 2. RBC 12. Bacteria (-) Urine culture (-)

  7. MRI

  8. MRI

  9. Laboratory CSF: Clear. Glucose 123. Protein 56. WBC 3. RBC (-). GS (-). Aerobic culture (-). AFB stain (-) Adenosin deaminase 13,97 (NV < 8)

  10. Discussion

  11. Laboratory Ig G Toxoplasma gondii: 1,667. RPR (-). CMV antigenemia (-). Blood cultures(-) CSF repeated: Glucose 77, Protein 56, WBC 40 (100 % mono), and the Lab Technician call us that night because he saw…

  12. Laboratory Trypomastigote of Trypanosoma cruzi

  13. Laboratory Ig G Trypanosoma cruzi: (+) 1/1,280 PCR T. cruzi serum and CSF (+) PCR T. gondii CSF (-)

  14. Clinical course Nifurtimox started 8 mg/kg/day (120 mg every 6 hr.,NG tube) Generalized tonic-clonic seizures. Antiepileptic drugs started (Fenitoin, Valproic acid, Levetiracetam, Topiramate). Head CT: Lesions became hemorrhagic Toxoplasma therapy initiated

  15. Clinical course

  16. Chagas´disease American trypanosomiasis, or Chagas' disease, is caused by the protozoan flagellates parasite, Trypanosoma cruzi. Although T. cruzi is a zoonotic parasite, humans can become infected with resulting acute or chronic disease. Chagas' disease is found only in Central and South America, Mexico and the southern United States. The World Health Organization has estimated that 16 to 18 million people are infected with T. cruzi, with an estimated annual infection rate of 300,000 and an annual mortality rate of >50,000 patients. The infection is endemic in Argentina, Brazil, Bolivia, Chile, Colombia, Costa Rica, Ecuador, El Salvador, Guatemala, Honduras, Mexico, Nicaragua, Uruguay, Paraguay, Peru, and Venezuela.

  17. Chagas´disease Individuals of all ages can be infected, although acute Chagas' tends to be diagnosed most frequently in children. The mean age of acquisition of infection is estimated to be approximately four years in endemic areas. Seventy to 90 percent of infected individuals are asymptomatic carriers of T. cruzi and never develop any symptoms. However, when chronic disease occurs, the manifestations are usually delayed and typically do not arise until 40 to 50 years of age.

  18. Chagas´disease • T. cruzi is transmitted by various species of bloodsucking triatomine insects, or kissing bugs. • There are more than 100 different triatomine species. Most infection are transmitted by one of seven species, the most common of which is Triatoma infestans. These insects measure 5 to 45 mm in length, depending upon the species. Once a bug is infected, it remains so for life and can transmit infection for several years.

  19. Chagas´disease Life cycle: Involves three distinct morphologic stages. The triatomine bug becomes infected when it ingests blood from an infected mammal that has circulating trypomastigotes. The parasite enters the midgut of the insect and transforms into an epimastigote form. It undergoes multiplication, migrates to the hindgut, and becomes an infective form known as the metacyclic trypomastigote.

  20. Chagas´disease Life cycle: When the vector takes a blood meal, it defecates around the bite site. The resulting irritation causes the host to scratch the site and contaminate the wound with parasites discharged in the feces. Humans are characteristically bitten on the face at night while sleeping, and inoculation of parasites can occur via breaks in the skin or directly into mucous membranes or into conjunctivae.

  21. Chagas´disease Life cycle: Once in the host, the infective metacyclic forms multiply and spread systemically. They then enter cells and transform into amastigotes, which are the dividing form found in host tissues. They can be found in any organ or tissue but have a predilection for striated muscle, glial, and nerve cells. They can differentiate into trypomastigotes to spread hematogenously to distant sites. When an infected host is bitten by another bug, the Triatome bug becomes infected, thereby completing the life cycle.

  22. Chagas´disease Pathogenesis: Unclear. There is extensive debate over whether the complications that arise are due directly to parasite invasion or to secondary autoimmune mechanisms. Organs involved in disease show chronic inflammatory changes and diffuse fibrosis. The conduction system and the muscle are affected in the heart. In the GI tract, loss of neurons of myenteric plexus, inflammation and fibrosis of the gut wall develop.

  23. Chagas Disease • Clinical manifestions : • Acute infection: Chagoma (indurated area of erythema and swelling + local lymphadenopathy). Unusual meningoencefalitis, myocarditis. • Chronic infection: CHF, Rhythm disturbances, thromboembolism. Megaesophagus, Megacolon. • Immunocompromissed host: HIV infections. Transplant.

  24. Chagas´disease Clinical manifestions : Immunocompromissed host: T cruzi can reactivate in chronic carriers under immunosupression. Myocarditis, meningoencephalitis cases have been reported. In HIV (+) several cases. In kidney transplant only one case of meningoencephalitis successfuly treated with benznidazole See Abstract(Jardim, E.J Trop Med Hyg. 1994;97:367-70)

  25. Chagas´disease Diagnosis: Ig G. PCR. Xenodiagnosis Treatment: Nifurtimox (Lampit). Benznidazole.

  26. Search PubMed Chagas Disease Case Reports Review Drug Therapy Differential Diagnosis Note: In order to see PubMed results, use ViewSlide Show, or hit F5.

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