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University of Tripoli

Mohamed Lashal

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toxoplasmosis medical parasitology parasitology disease

Summary

This document provides a detailed overview of toxoplasmosis, a parasitic infection caused by the parasite _Toxoplasma gondii_. It covers various aspects of the disease, including its morphology, the life cycle of the parasite, different infective stages, symptoms, and diagnostic procedures. Also included are various treatment options and preventative measures.

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Toxoplasmosis Prepared by: Mohamed Lashal Lecturer of medical parasitology Faculty of Medicine Tripoli university Phylum apicomplexa (sporozoa) : *General Features : - They obligate intracellula...

Toxoplasmosis Prepared by: Mohamed Lashal Lecturer of medical parasitology Faculty of Medicine Tripoli university Phylum apicomplexa (sporozoa) : *General Features : - They obligate intracellular Parasites. they Have a structure called the apical complex attach to and penetrate host cells Have complex life cycle with alternating sexual and asexual generation. all apicomplexa are known as coccidian parasite. members of this phylum are : Toxoplasma gondii is an intestinal parasite of cat (definitive host) man is an intermediate host in which asexual cycle of the parasite occurs in many organs & tissue( tissue coccidian). Four species of plasmodium & Babesia Spp Cryptosporidium parvum & Isopora belli Are intestinal coccidian of man Toxoplasma gondii Toxoplasmosis Geog. Distribution: worldwide(except Antarctica) Toxoplasma attacks man, animals (cats). Tachyzoite There are 3 major genotype (type I , type II & type III ). These genotype differ in their pathogenicity & prevalence. T. gondii infect large number of the population (perhaps 1/3). It is uncommonly causes clinically significant disease. Individuals such as immunologically impaired patients, fetuses & newborn are at high risk of life threating toxoplasmosis. Sporulated oocyst Pseudo cyst (tachyzoite) Morphology of Toxoplasma gondii A sexual forms 1-Tachyzoite (trophozoite): The actively multiplying, asexual form in human It is is an obligate intracellular parasite pyriform in shape called tachyzoite. Death and rupture of the infected cell freeing the parasite to spread the infection to new cells. Apical Complex at the Pointed end. (Apical complex is made of many structures → Polar rings, Conoid, Micronemes & Rhoptries: facilitate the parasite entry to host cells by their secretion). Multiply by a specialized division within the host cell (Endodyogeny = Internal budding) → wherein 2 daughter trophozoites are formed, each surrounded by a membrane, while still within the parent cell. They are susceptible to drying, freeze-thawing, and gastric digestion 2-Bradyzoite.Tissue Cyst (Encysted Stage)(resting form): A collection of tachyzoite can fill up a host cell develop a parasite membrane and become a cyst in the encysted stage ,the organism is called a bradyzoite. Bradyzoite are slowly Multiplying & -Oval In shape. metabolically Inactive. Cysts are susceptible to desiccation, freezing, and thawing, and heat above 60°C Tissue cyst (bradyzoites) Morphology of Toxoplasma gondii non effective ~ 3-Sexual Form:( Oocyst) : Elongated or Ovoid with blunt ends & Surrounded by 2 layered cyst wall. & Immature Oocyst (Unsporulated): unsegmented Mass Of Protoplasm → 2 Sporoblasts → secrete Cyst Wall to become sporocysts → More Divisions INFECTIVE inside the Sporocystes → 4 Curved nucleated Sporozoites. STAGE Mature ( Sporulated) Oocyst : Contains 2 Sporocysts + Each Sporocysts Contain 4 Sporozoites (Total 8 Sporozoites). The Maturation Process Occurs outside the body (in Feces on Soil ), it takes 1-5 Days. to be infected Oocyst is very resistant to environmental conditions, acids, alkalis & can remain infective in soil for about an year. (Susceptible To Drying). Infective Stage of toxoplasma - > sporulated oocyst Life cycle of Toxoplasma gondii Zoonotic Infection. Definitive Host: Cats and other felines.( Both sexual & Asexual Multiplication). { Complete Cycle). Intermediate Host: Human and other mammals (e.g.: Sheep , Cattles, Pigs , Birds & Mice). (Asexual Multiplication Only). Infective Stage: All Forms of T.gondii are Infective to Human Habitat 1- In cat a- Intestinal: inside epithelial lining of intestine where the parasite multiplies asexually by Schizogony then sexually by Gametogony. b- Extra-intestinal in other body organs where the parasite multiplies asexually. 2- In man and other mammals In RES cells of spleen, liver, lymph nodes, muscles, heart, bone marrow, brain, eye, kidney where the parasite multiplies asexually. I Mode of infection by toxoplasma gondii : 1. Eating raw or undercooked beef, pork or mutton containing toxoplasma cysts. 2. Ingestion of oocysts in material contaminated with infected cat feces. 3. Trans placental (tachyzoite is the infective stage) during active infection. 4. Blood, white cells or platelet transfusion (intra cellular tachyzoite is the infective stage).pack red-cell transfusion are safe. 5. Organ transplantation (Cyst is the infective stage ). 6. Contamination of mucous membrane & skin abrasion (in research workers & butchers) Life cycle of Toxoplasma gondii Development of Toxoplasma in Cat Intestines Sporulated oocyst Sporozoite, bradyzoites & tissue cyst attack epithelial cells Infective stages Unsporulated oocyst Pass in stool of the cat Zygote ♂ merozoites gametocyte Sexual cycle(enteric cycle): Cat is the definitive host Development of Toxoplasma in the human intestine Lamina Blood vessels propria Villi of small intestine contents penetrate the lamina propria, multiply as tachyzoites & enter the circulation Villi of small intestine Lamina Blood vessels propria Pathogenesis and Clinical Picture of toxoplasmosis Toxoplasmosis is considered an opportunistic infection Acquired infection: acquired toxoplasmosis. Congenital infection: congenital toxoplasmosis reoccurence ~ Recrudescence Toxoplasmosis in Immunocompromised patients Symptoms of Acquired toxoplasmosis: brain Toxoplasmosis is considered an opportunistic infection Depends on: eyes Immune status of infected person age of infected person. Skeletal muscles Virulence of infecting strain of Toxoplasma. Tachyzoite pass to the circulation, heart it reaches various tissues & form tissue cysts which persist for human’s life Most cases are asymptomatic. Mild form: lymphadenopathy (cervical & axillary LNs), myalgia, low irregular fever, slight anemia with lymphocytosis, fatigue simulate infectious mononucleosis. Rarely sever form : skin rash (maculopapular) in addition to the above symptoms and some time hepatitis, encephalomyelitis or myocarditis. Very few cases have Retinochorditis which may progress to blindness. Symptoms of congenital toxoplasmosis Depends on : 1- Protective immunity of the mother 2- Age of the fetus at the time of infection Most infections are quite sever. Microcephaly Hydrocephalus encephalomyelitis, intra cerebral calcification hydrocephalus or microcephalus Retinochorditis, macular scar and blindness. Mental retardation and convulsion. Many of those infected in the last trimester are normal at birth but develop Retinochorditis later. Visceral & Muscular Lesions (Hepatosplenomegaly , jaundice , lymphadenopathy polymyositis). Abortion & still birth (rare complication). Reactivation toxoplasmosis (opportunistic infection) Toxoplasmosis known to occur as an opportunistic infection because reactivation of a latent infection is seen in immunosuppressed host ( Post Organ Transplantation, Chemotherapy for Neoplastic Disease, HIV patient and chronic use of steroids ).. Neurological symptoms is the most frequent presentation as - Headache, confusion & altered mental state - Encephalitis. - convulsions, ataxia, & hemiparesis. – Retinochorditis & myocarditis. Encephalitis leading to death. It is due to reactivation of latent cerebral cysts Organ transplant (heart) patients develop acute disseminated toxoplasmosis Diagnosis of toxoplasmosis: -Serological test: - IgM detect recent infection. - IgG which change in titer indicate recent infection. - IgG unchanged titer indicate old infection. - In congenital infection maternal IgG Cross the placenta while IgM do not. So: IgM at birth or up to several months of age indicate congenital infection. -new born IgG persist or increase in titer during the first 6 months also indicate congenital infection. -Sabin Feldman dye test: methylene blue stains T.gondii tachyzoites obtained from mouse peritoneal exudate but the uptake of dye is inhibited by antibody-containing serum. -IFA,CFT. -PCR. Treatment of toxoplasmosis : Combination of Pyrimethamine + trisulfapyrimidines is the treatment of Choice C/I during pregnancy. Spiramycin (during pregnancy). Clindamycin treat encephalitis in AIDS or for sulfur-allergic patient. Control & prevention: Proper personal hygiene Wear gloves during gardening Proper wash of vegetable & fruits. Avoid raw & undercooked meat. Carful handling of cats litter box. Do not feed cats raw or undercooked meat.

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