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- 1. PARASITOLOGY
- 2. Introduction • Parasites occur in two distinct forms: Protozoa---Unicellular Metazoa---Multicellular .Protozoa divided into 4 groups .Metazoa into 2 groups
- 3. Protozoa-Introduction • Are unicellular & widely distributed in nature • Basic structure: Protoplasm differentiated into cytoplasm & nucleus A limiting membrane or plasma membrane which is pliable– some cases Outer coat is more rigid– Majority of protozoa • Locomotion, an important characteristic- three organelles: Flagella, cillia, pseudopodia
- 4. Amoeba-Common Terms • Trophozoite: Motile form • Cyst: Non motile.cystwall/membrane.Infective stage in most • Pre-cyst: Rounded form of Trophozoite preceeding cystic stage • Excystation: Process of emergence of trophozoite from the cyst • Encystation: Process of formation of cyst from trophozoite
- 5. Amoeba- classification 1-Pathogenic intestinal amoeba: Entamoeba histolytica Endolimax nana 2-Non pathogenic intestinal amoeba: Entamoeba hartmanni Entamoeba coli Iodamoeba butschlii 3-Free living amoeba: Naeggleria spp Acanthamoeba spp
- 7. Enatamoeba histolytica (Amoebic Dysentery & Liver abscess) • Two stages in life cycle: .Trophozoite– Motile .Cyst– ----------Non motile .Trophozoite is found in intestinal & extra intestinal lesions & in diarrheal stools. .Cyst mainly found in non diarrheal stool Not highly resistant and readily killed by boiling, also removed by filtration but, not by chlorination
- 9. •Cyst- four nuclei- diagnostic V/S other amoeba Excystation in GIT– Amoeba with four nuclei-divides–).
- 10. These enter large intestine & may: 1-invade host tissues 2- live in lumen of colon without infection 3- Encyst •Only Cysts can survive in external environment for any length of time •Antibodies-not protective but diagnostic
- 11. Pathogenesis & Life cycle • Infection ---------ingestion of cysts Transmission--fecal oral route contaminated food & water •Cysts differentiate into Trophozoites in ileum. •Trophozoites invade colonic epithelium, secrete proteolytic enzymes that cause necrosis. •Invasion results in bleeding & RBCs ingested by trophozoites.
- 13. Pathogenesis & Life cycle • More deeper invasion till reach submucosa. .Destroy tissues near and far & necrosis occurs. .Formation of small abscesses ultimately result in ulcers. • The Ulcers: may be Shallow erroding only Mucosa or Deeper entering Submucosa. • In S/mucosa: Trophozoites multiply rapidly & spread laterally. Flask shaped ulcer (broad based)
- 14. Pathogenesis & Life cycle •Invasion of submucosa– invasion of portal circulation •Most frequent systemic disease site is Liver & Abscesses form. (Lungs & brain)
- 15. Clinical features •Acute Dysentery + Lower abdominal discomfort + Flatulence + Tenesmus .may last for few days or weeks and resolves spontaneously or transforms into chronic disease, •Chronic Diarrhea on & off +Wt. loss +Fatigue •90% are Asymptomatic carriers
- 16. •Intestinal Complications: .Amoeboma : A granulomatous lesion resembling adenocarcinoma colon can occur in some- Sites: Cecum,Rectosigmoid .Perforation .Hemorrhage .Appendicitis
- 17. Clinical features Amoebic liver abscess- .Right upper quadrant abdominal pain .Wt. loss, fever, hepatomegally, .Enlarged tender abdomen. .Leukocytosis & raised ESR .Anchovy sauce- Brownish yellow pus Pus is a mixture of *sloughed liver tissue & blood*.
- 18. Laboratory diagnosis • Intestinal Amoebiasis: .Fecal Examination: for trophozoites & cysts Trophozoites are present in Diarrheal stool Cysts are present in Formed solid stool .Charcot-Leyden crystals .E.histolytica antigen in stool-specific .PCR detects nucleic acids of organism • Serologic test for invasive disease
- 20. Laboratory diagnosis •Extraintestinal Amoebiasis: Cysts or Trophozoites may not be present in faeces - so valuable are, •Serological tests: (+ve in >90% cases) .4 most commonly used: 1.Gel diffusion 2.Indirect hemagglutination 3.Latex agglutination 4. Flourescent antibody test also ELISA
- 21. Lab diagnosis Extraintestinal Amoebiasis •Aspiration of Liver abscess: Bacteriologically sterile .Contains: . Degenerated liver cells . Few RBCs . Occasional leukocytes . Trophozoites may be present
- 22. Giardia • Giardia lamblia is main type- Giardiasis • Two stages in life cycle Trophozoite Pear shaped Resembles Badminton racket two nuclei, flagella (four pairs) suction disk for attachment to intestine Movement: Falling leaf movement (Rolls on itself) Cyst, oval, , four nuclei .thick walled .gives two trophozoites during excystation in
- 23. Pathogenesis • Infection by ingestion of cysts in fecally contaminated food and water • Excystation occurs in duodenum, trophozoite attaches to gut. does not invade mucosa & does not enter blood stream .causes inflammation of duodenal mucosa leading to malabsorption of protein & fat
- 25. Clinical features •Watery, non bloody diarrhea,foul smelling + nausea, anorexia, flatullence, abdominal cramps- No Fever
- 26. Laboratory diagnosis •Examination of Diarrheal stools: Trophozoites or cysts/both—less reliable •Deudenal aspirates-- more reliable •String test •ELISA- Detects Giardia antigen
- 27. Urogenital Protozoa • Trichomonas hominis --- Large intestine • Trichomonas tenax ----- Mouth • Trichomonas vaginalis ---- is main • Life cycle has only one stage (Trophozoite) no cyst stage • A pear shaped organism with a central nucleus & 4 anterior flagella • 5th flagellum turns back & attached to body by undulating membrane
- 28. Pathogenesis •This is only parasite that is transmitted by sexual contact. (Man acting as carrier) Then it resides in vagina & prostate •Women: Vaginitis: watery, foul smelling greenish vaginal discharge with itching & burning •Men: Mostly asymptomatic 10% have urethritis with burning
- 29. Lab diagnosis •Samples: .Vaginal or prostatic secretions or semen .Wet mount film under microscope shows pear shaped trophozoite having typical Jerky motion
- 30. Blood & Tissue Protozoa •Plasmodium •Toxoplasma •Trypanosoma •Leishmania
- 31. Toxoplasma
- 32. Toxoplasma • Toxoplasma gondii . • A very common parasite of human & animals • Causes Toxoplasmosis • Atleast 1/3rd world population contracts Toxoplasma TORCH
- 33. Toxoplasma •Animals involved ---- Range is Wide •Definitive host is domestic cat & felines Humans & other mammals are intermediate hosts. •Host immune system limits spread Organism persists as cysts within tissues
- 34. Life cycle •In Cat (Definitive host): Begins with ingestion of raw meat (eg.mice) •Bradyzoites released from cysts in small intestine, penetrate & infect mucosal cells •1stly: Asexual cycle occurs ---- formation of merozoites----- enter fresh host cells & initiate different cycles
- 36. Life cycle • Some of Merozoites Transform into sexual stages- (initiate gametogony) .Macrogamate---Fertilized by a motile Microgamate----Zygote --- Oocyst formed • Disintegration of host cell epith. reulting in Oocysts passed in cat feces. • Man is infected when ingests soil contaminated with oocysts. • Human infection occurs with ingestion of cysts in undercooked meat (Lamb or pork) from animals that grazed in soil contaminated with cat feces •
- 37. Life cycle Human (Intermediate host): Infection: 1-by accidental contact with Oocysts in cat feces, ingestion of oocysts in food, water, or 2- eating improperly cooked meat (Pork, Mutton ,Beef, Poultry) containig cysts & peudocysts Cysts rupture in small intestine-New forms ingested by macrophages,form Tachyzoites (Rapidly multiplying) .Only Asexual development in man & no oocysts formed. .Merozoites enter lymphatics & blood---- Cysts & Pseudocysts in various organs (Brain muscle etc--Bradyzoites –slowly multiplying)
- 38. Pathogenesis • Route of transmission :By Ingestion of Cysts in undercooked meat or contact with cat feces. Transplacental from mother to fetus Blood transfusion • Spread: Mainly to Brain , lungs, liver & eyes Form pseudocysts,Cysts (Endozoites) • Congenital infection: Can occur only when mother is infected during pregnancy but not if infected before pregnancy because no trophozoites to pass through placenta
- 39. Clinical features • Most are asymptomatic • Congenital Toxoplasmosis: (More severe in congenital form) Active parsitemia can cause severe often fatal cerebral damage Abortion or Stillbirth or, Neonatal disease (in those who recover) (mental defects,Encephalitis, hydrocephalus, intracranial calcifications) + fever, jaundice,.
- 41. Clinical features- (Congenital ) • Less severe lesions as Chorioretinitis (Pigment ringed scar), Congenital Toxoplasmosis, leading cause of blindness in children Hepatosplenomegally generally missed at birth may be observed latter in life. • Mental retardation in some- months or years latter.
- 42. Clinical features- •Acquired Toxoplasmosis: less severe form • May show involvement of Eyes & Lymphatics Eyes : Uveitis, Choroiditis, Choroidoretinitis Lymphatic system : Lymphadenopathy with/ without fever • Rarely-- Myocarditis - Myositis
- 43. Clinical features Toxo. in immunodefficient host (AIDS): (Mostly Result of reactivation of latent infection) .Mild to severe, with encephalitis, fever, headache, mental deterioration and seizures, ending in fatal acute fulminating disease. • Necrotizing Encephalitis, Myocarditis, Pneumonitis (Autopsy findings)
- 44. Lab diagnosis Giemsa staining & microscopy: Crescent shaped trophozoites cabe seen esp in CSF • Isolation or detection of parasite not always possible/successful •Serological tests to detect antibodies .Flourescent antibody test : (a Sensitive test) For acute & congenital infections (IgM) Flourescein labelled anti IgM is used for congenital toxoplasmosis also because IgG may be from mother
- 45. .Dye test of Sabin & Feldman: (Highly sensitive and specific) .Depends on the cytoplasmic lysis of endozoites when they are exposed to the antibody in the presence of a heat sensitive non specific substance found in the serum of certain individuals known as Accessory factor .Modified parasites appear unstained or clear when treated with methylene blue
- 46. .Indirect Haemagglutination test: .A very sensitive test but . D/A is that it takes longer to become positive compared with Dye test & FAT. . Once positive it remains so for years • CBC may show lymphocytosis