This presentation slide includes the disease "Chagas disease" transmitted by protozoan parasite "Trypanosoma cruzi" and vector "Reduviid bug".
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Added: Aug 29, 2018
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REDUVIID BUG AND ASSOCIATED DISEASE Team members: Akhtar Alam Omkar Moore Kapil S. Neupane Milan Oli Shiva Raj Sahani MBBS 1 st YEAR DEVDAHA MEDICAL COLLEGE KATHMANDU UNIVERSITY
CLASSIFICATION Kingdom : Animalia Phylum :Arthropoda Class : Insecta Order : Hemiptera Family : Reduviidae
MORPHOLOGY 4-40 mm in length depending upon species Have elongated head with distinct narrow neck Have long limbs Have prominent mouthparts called proboscis(rostrum) May be brown, black or red
FEEDING May be blood sucking or predators Feeds on cockroach, millipedes, ants, human blood etc Inject lethal saliva in prey Saliva digest tissues and liquifies the inside of prey. DISEASES TRANSMITTED: American trypanosomiasis (Chagas diseases) caused by Trypanosoma cruzi.
Life cycle of T. cruzi T. c ruzi passes its life cycle in 2 hosts: Definitive host- man. Intermediate host- reduviid bug. Extrinsic incubation period: 8-10 days Intrinsic incubation period:1 week Infective form- Metacyclic trypomastigote form found in feces of Reduviid bug. Reduviid bug are large, night biting bugs, which typically defecate while feeding. Feces contain metacyclic Trypomastigote.
Development In Human T ransmitted to human host by contamination of ulcerated skin lesion by feces of Reduviid bug containing metacyclic trypomastigote form of T. cruzi. Development in human- Trypomastigote form invade the reticuloendothelial system and spread to other tissues. Passing through promastigote & epimastigote forms, they again become trypomastigotes which get released into the blood stream- infective stage for Reduviid bug.
Development in Reduviid bug Bug acquire infection by feeding on an infected human host. The trypomastigote are transformed into epimastigote in the midgut in the from where they migrate to hindgut and multiply. After multiplication, develops into non dividing metacyclic trypomastigotes which is excreted in feces- infective stage for human.
CHAGAS DISEASE Infection caused by Trypanosoma cruzi , transmitted by Reduviig bug . Result in acute inflammatory changes in skin (chagomas), eye & many other body tissues, especially those of the heart and intestinal tract. First described by Carlos Chagos in 1909 in Brazil. Not contagious.
EPIDEMIOLOGY About 8-11 million people are infected worldwide(2016). Highly prevalent countries: (WHO 2010) Endemic in Mexico, Argentina, South America and Central America Sporadic in Amazon. Mostly prevalent in rural areas.
ROUTES OF TRANSMISSION Bite of Reduviig bug. Consumption of food contaminated with faeces from infected bugs. Blood transfusion from infected donors. Passage from mother to new born during pregnancy and child birth. Organ transplant from infected donors. Laboratory accidents.
TRANSMISSION Bug live in mud, thatch or huts. They hide in walls or roof during day and come out during night. Bite human during sleeping hours. During feeding, they defecate & leave T. cruzi parasites on skin. Parasites enters into body through eyes, mouth, cut or scratch or the wound from the bug bite site. Once entered inside body the parasite multiply and spread.
PHASES OF DISEASE Acute phase Intermediate phase Chronic phase
SIGNS AND SYMPTOMS 1. Acute phase Histologic changes- presence of parasite within leucocytes cells of subcutaneous tissue and development of interstitial edema, lymphocytic infiltration and hyperplasia of lymph nodes. Ramona sign- Unilateral painless edema of palpebrae and periocular tissues.
SIGNS AND SYMPTOMS Acute phase (Continue…) Chagoma-Swelling and redness at the site of infection Rashes & Fever Head and body aches Fatigue Nausea & Vomiting Hepatomegaly & splenomegaly
SIGNS AND SYMPTOMS 2. Intermediate phase Subpatent parasitemia Easily detectable antibodies to T. cruzi Asymptomatic.
SIGNS AND SYMPTOMS 3. Chronic phase Heart Thinning of ventricular walls Biventricular failure Mural thrombi Arrhythmias Conduction system abnormalities Lymphatic infiltration, diffuse interstitial fibrosis & atrophy of myocardial cells.
SIGNS AND SYMPTOMS b. GIT Dilation of esophagus and colons Abdominal pain and constipation. Focal inflammation lesions with lymphocytic infiltration. Reduced number of neurons in myoenteric plexus.
PREVENTION AND CONTROL Primordial prevention Mass education We should aware the people about kissing bug because it seems friendly but it can transmit the parasite named Trypanosoma cruzi.
PREVENTION AND CONTROL Primary prevention Synthetic pesticide sprays. Personnel protection using mosquito net. Remove wood, brush, rock and piles near the house. Modification of house structure.
PREVENTION AND CONTROL Secondary prevention Screening of blood is done; Transfusion control Mother-Child transmission control Treatment of Chagas disease[Acute phase] Benznidazole Nifurtimox
PREVENTION AND CONTROL Tertiary prevention If disease progress to chronic phase: it is no longer curable so require management of symptoms. Cardiomyopathy; Pacemaker placement, Heart transplant. Megaesophagous; Esophagocardiomyectomy. Megacolon; Duhamel-Haddad operation.
SOURCES Preventive And Social Medicine-K. Park Paniker’s textbook of parasitology Essentials of Medical Pharmacology-K. D. Tripathi