Chagas Disease - Parasitology Lecture 1 PDF
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Mansoura University
Dr. Ziad Mahana
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Summary
This lecture covers Chagas disease, a parasitic infection caused by Trypanosoma cruzi. It details the morphology, life cycle, transmission, and clinical manifestations of the disease. Key topics include the acute and chronic phases, and associated complications.
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LECTURE (1) Chagas disease About 8 million people in Mexico, Central and South America have Chagas´ disease cause by Trypanosoma cruzi, causing 12,000 deaths yearly. It can be found anywhere in the globe. However, vector-borne transmission of the disease only occurs in Americas. Migration...
LECTURE (1) Chagas disease About 8 million people in Mexico, Central and South America have Chagas´ disease cause by Trypanosoma cruzi, causing 12,000 deaths yearly. It can be found anywhere in the globe. However, vector-borne transmission of the disease only occurs in Americas. Migration from Latin America to other regions increased spread of Chagas´ disease, with 75 million at risk of infection. If untreated, the disease is life-threatening (silent killer). Found in muscles, nerve cells & reticuloendothelial cells. Oval bodies. 2-4 μm. Having a nucleus and kinetoplast No free flagellum. Indistinguishable from Leishman- Donovan bodies. Multiplication of the parasite in host occurs in this stage. Found in peripheral blood of man & lymph & CSF other mammalian hosts, insect vector and in culture. About 25 μ in length. C or S shape. Deeply stained central nucleus, large kinetoplast, long undulating membrane & free flagellum. Non multiplying form. Found in the insect vector and in culture. Elongated body, about 20 μ in length. It has a kinetoplast near to the nucleus, short undulating membrane & free flagellum. Divides by binary fission in midgut of the vector Man Dogs, cats, domestic and wild animals Reduviid or kissing bug (Silent Killer) Metacyclic trypomastigotes in feces or urine of reduviid bugs These bugs can live in cracks and holes indoors and in outdoor spaces. Most are night biting, defecate while feeding. A tiny kiss causing a mega syndrome. ① Contamination of the bite, skin or mucous membrane abrasion by bug's feces or urine. ② Blood transfusion. ③ Organ transplantation. ④ Accidental exposure in labs. ⑤ Vertical transmission. ⑥ Sexual transmission Parasites uptake by host cell at site of bite & transform into amastigotes that multiply by binary fission. After 5 days, cell ruptures liberating trypomastigotes, invade blood & lymph, and disseminate to tissues. Inside cells, they are transformed into amastigotes that multiply, fill up cells, mainly cardiac muscle fibers. Intracellular multiplication is repeated & cells rupture → damage to affected organs. INCUBATION PERIOD: 1-2 weeks. ’ May last for 1- 4 months. Usually seen in children. CHAGOMA Localized swelling with erythema & localized lymphadenopathy. Inoculation of parasite in conjunctiva causes. ROMANA'S SIGN Unilateral painless oedema of eyelids, with conjunctivitis. Enlargement of lymph nodes (Classical sign of acute Chagas). IN SEVERE Manifestations of meningoencephalitis, acute myocarditis & acute INFECTIONS congestive heart failure. ↑↑ = Fever, generalized lymphadenopathy, hepatosplenomegaly ↑↑ OR ↓↓ ↓↓ = depression of bone marrow & anemia. Death may occur OR DEATH OR RECOVERY Recover (good immune response) OR OR CHRONICITY Pass to a chronic stage. CHAGOMA ROMANA'S SIGN 60% -70% 30% - 40% Dormant form Deadly form Enter the indeterminate form of chronic Years to decades after initial infection. infection. Remain in this subclinical state with no They progress to the determinate form further consequences. of disease. ’ It is found in adults. Multiplication of T. cruzi in tissue cells causes inflammation, irreversible cellular destruction & fibrosis of muscles and nerves that control the tone of hollow organs, manifested by Mega syndrome: Cardiomegaly. HEART DISEASE Cardiac arrhythmias. Congestive heart failure. Due to destruction of intramural plexus. MEGAESOPHAGUS Manifested by dysphagia & aspiration pneumonia. Due to destruction of mesentric plexus. MEGACOLON Manifested by intractable constipation & abdominal distention. As small intestine OTHER MEGAVISCERA Ureters. NERVE DISEASE Peripheral nervous involvement as spastic paralysis. Thyroiditis THYROID DISEASE Thyroid insufficiency CHAGAS´ DISEASE : 7-14 days incubation period. Often in children: chagoma, Romaña sign, flu-like symptoms, ACUTE FORM lymphadenopathy, enlargement of liver and spleen, myocarditis, encephalitis. CHRONIC FORM Asymptomatic (dormant). INTESTINAL DISEASE Megaesophagus, Megacolon. HEART DISEASE 10-30% of cases, sudden death from aneurism. Chronic chagas patients with HIV infection or low immunity are manifested by: ① Meningoencephalitis ② Space-occupying CNS lesions. CONGENITAL INFECTION: It is possible in both phases of the disease. It causes myocardial and neurological damage. ① History of exposure to Reduviid bug bite. ② History of travelling or residence in endemic area. ③ Recent blood transfusion in an endemic area. ④ Chagoma is similar to injury caused by trauma, insect bite, bacterial or fungal infection. ACUTE CHAGAS CHRONIC CHAGAS Should be considered in patients in endemic areas with: Febrile illness Signs of cardiomegaly. Lymphadenopathy. Sever constipation or dysphagia. Detection of T. cruzi in peripheral blood, aspirate or tissue biopsy of lymph node, muscle, liver, spleen and bone marrow by: ① Microscopy: a. Examination of peripheral blood (wet mount, thin and thick blood, or buffy coat smears) stained with Giemsa, show monomorphic trypanosomes (C or S shape). b. H & E stained tissue specimens show amastigotes ① DIRECT ② Culture: Epimastigotes & trypomastigotes are found on NNN medium 1-6 weeks post incubation. ③ Animal inoculation: Intra-peritoneal injection of specimen in experimental animal & blood examined after 10 days for trypomastigotes. ④ Xenodiagnosis: Detect very low parasitaemia, mainly in chronic disease. ① Immunological diagnosis: a. Serological tests: Antigen detection: in urine and sera by ELISA. Antibody detection: IHA, IFA, ELISA, CFT, and rapid immunochromatographic test. b. Cruzin intra-dermal test. ② Molecular technique: For diagnosis of acute, chronic & congenital Chagas. ③ Endoscope: ② INDIRECT Valuable for diagnosis of megaviscera. ④ Barium dye meal and barium dye enema: For visualization of megaoesophagus & megacolon using x-ray. ⑤ X-ray chest and electrocardiography (ECG): For diagnosis & prognosis of cardiomyopathy in chronic Chagas´ disease ① Nifurtimox. ② Benznidazole. Both are used for all ages, and for acute & early chronic cases. ③ Diuretics: for congestive heart failure (acute or chronic disease). ④ Treatment of megacolon: by surgery. ① Control of winged bugs by: Insecticides (Gammaxene, Lindane) Elimination of cracks in wall by cement. ② Control of reservoir hosts. ③ Personal protection by using repellants and bed net. ④ Serological screening of blood & organ donors for T. cruzi. ⑤ Use of riboflavin & UV to reduce level of transfusion infection. ⑥ Detection and treatment of infected cases. ⑦ Early diagnosis & treatment of: Infected women of child-bearing age. Newborns with congenital Chagas Chagas´ disease is a vector-borne disease caused by Trypanosoma cruzi. The classical sign for acute Chagas´ is the Romana's sign. Cases may remain asymptomatic for decade before chronic manifestations. Chronic Chagas´ is characterized by mega viscera, mainly cardiomegaly. Acute stage is diagnosed by microscopy or culture. Chronic disease is diagnosed by at least two different antibody detection tests. Treatment is by nifurtimox or benznidazole A 16-year-old male with no significant past medical history presented to emergency department complaining of fever, headache, and left eye swelling 2 weeks after returning from a 3-week trip to Costa Rica. The patient visited a small village, where he slept on a wooden bed in a one-room cottage that lacked netted windows and doors. These symptoms progressed rapidly over the next few days until the patient’s left eye was swollen shut. He was treated for blepharo- conjunctivitis with no initial response. The patient was then evaluated for periorbital cellulitis. On physical examination, there was periorbital edema and mild erythema of the left eye, and no visible discharge. The right eye was normal. He had one small non-tender, freely mobile right posterior cervical lymph node, and otherwise, he had no significant lymphadenopathy. Systems examinations were normal. Physical examination was otherwise unremarkable. Wet mount of peripheral blood showed flagellated S-shape like- organism, about 25μ in length.