Common Terms in Parasitology 22-02-2017 (1).pptx

Common Terms in Parasitology 22-02-2017 (1).pptxCommon Terms in Parasitology 22-02-2017 (1).pptxCommon Terms in Parasitology 22-02-2017 (1).pptxCommon Terms in Parasitology 22-02-2017 (1).pptx

1. PARASITOLOGY DR.ABID HUSSAIN CHANG

2. Parasitology Classification

3. Parasite Host Reservoir host Intermediate host Definitive host Paratenic host Ectoparasite Endoparasite

4. 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

5. Protozoa-Classification

6. 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 Metacyst : Trophozoite which emerges from cyst

7. 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

8. Intestinal and Urogenital Protozoa

9. 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

10. Cyst- four nuclei- diagnostic Excystation in GIT– Amoeba with four nuclei- divides-- 8Trophozoites – single nucleus, fine, even chromatin lining & central karyosome (nucleolus).

11. 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

12. 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 of tissues results in bleeding & RBCs ingested by trophozoites

13. Pathogenesis & Life cycle 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) Invasion of submucosa – invasion of portal circulation Most frequent systemic disease site is Liver & Abscesses form .

14. 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

15. Clinical features Intestinal Complications: . Amoeboma can occur in some- Cecum,Rectosigmoid A granulomatous lesion resembling adenocarcinoma colon .Hemorrhage .Appendicitis .Perforation

16. 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.

17. 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

18. 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

19. Lab diagnosis Extraintestinal Amoebiasis Aspiration of Liver abscess: Bacteriologically sterile . Contains: . Degenerated liver cells . Few RBCs . Occasional leukocytes . Trophozoites may be present

20. Giardia Giardia lamblia is main type- Giardiasis Two stages in life cycle Trophozoite Resembles Badminton racket Pear shaped , two nuclei, flagella (four pairs) suction disk for attachment to intestine Movement: Falling leaf movement (Rolls on itself) Cyst, oval .thick walled, four nuclei .gives four trophozoites during excystation in intestinal tract

21. 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 malbsorption of protein & fat

22. Clinical features Watery, non bloody diarrhea,foul smelling + nausea, anorexia, flatullence , abdominal cramps- No Fever

23. Laboratory diagnosis Examination of Diarrheal stools: Trophozoites or cysts/both—less reliable Deudenal aspirates-- more reliable String test ELISA- Detects Giardia antigen

24. Cryptosporidium C.pavum causes Cryptosporidiosis(Diarrhea) ++++ Diarrhea in immunocompromised (AIDS) pt Life Cycle : Oocysts release Sporizoites --- Trophozoites --- Schizonts ---- Merozoites --- Microgametes & Macrogametes , unite----Zygote---- Oocyst

25. Pathogenesis Org acquired by Fecal-oral transmission of oocyst -Excysts in S.I- Trophozoites , attach to Gut wall-No invasion Clinical features : Diarrhea (Watery Non bloody) Esp in AIDS pt & +++ fluid loss Lab Diagnosis: Stained by modified Kinyoun acid-fast stain shows Oocysts

26. 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

27. Pathogenesis This is only parasite that is transmitted by sexual contact . Then it resides in vagina & prostate Women: Vaginitis with watery, foul smelling greenish vaginal discharge with itching & burning Men: Mostly asymptomatic 10% have urethritis with burning micturition

28. Lab diagnosis Samples: . Vaginal or prostatic secretions or semen . Wet mount film under microscope shows pear shaped trophozoite having typical Jerky motion

29. Blood & Tissue Protozoa Plasmodium Toxoplasma Trypanosoma Leishmania

30. Plasmodium Malarial parasite Four types of Plasmodia Cause Malaria: 1- P.vivax (common) 2-P.ovale 3-P.malariae 4- P.falciparum (common)

31. Vector is female Anopheles mosquito Life cycle = two phases 1-Sexual cycle occurs in mosquitoes 2-Asexual cycle occurs in humans Other routes of transmission: Transplacental , Blood transfusion

32. Life cycle Life cycle in humans : Begins with the introduction of sporozoites into the blood from saliva of biting mosquito. Sporozoites enter liver cells & change into Merozoites Merozoites are released from liver & infect RBCs- organism changes into ring shaped trophozoite , then changes into schizont filled with many merozoites .

33. Life cycle The periodic release of merozoites causes the typical recurrent symptoms of chills, fever & sweats in malaria Merozoites in human RBCs develop into male & female gametocytes

34. Life cycle in Mosquito These RBCs containing gametocytes are ingested by female anopheles mosquito during bite. Gemetocytes produce male & female gametes fertilization occurs , Zygote is formed-

35. Life cycle in Mosquito Ookinete (motile) penetrates & burrows into gut wall of mosquito & changes into circular body Oocyst whithin which many merozoites produce which migrate to salivary glands & transmitted to humans when mosquito bites for its blood meal.

36. Pathogenesis Pathologic findings are mainly due to destruction of RBCs due to Release of merozoites & lysis in spleen----- S plenomegally

37. Pathogenesis P.falciparum Malaria is more severe than other plasmodia. More number of RBCs are damaged & occlusion of capillaries with aggregates of parasitized RBCs This can lead to severe life threatening hemorrhage & necrosis esp : in brain (Cerebral malaria)

38. Pathogenesis Excessive hemolysis & kidney damage resulting in hemoglobinuria . Urine of pt becomes dark in colour (Black water Fever) ---ARF P.malariae fever 72 hours( Quartan malaria as it recurs every 4 th day) & for 48 hours for other plamodia ( tertiam malria as it recurs every third day) Tertian by P.falciparum is called malignant tertian malaria and that by others is Benign tertian.

39. Clinical features Abrupt onset of fever & chills + headache+ myalgias + Arthralgias about 2 wks after mosquito bite +++Anemia, Spleenomegally & hepatomegally P.falciparum causes life threatening lesions Cerebral malaria with extensive brain damage & Black water fever with kidney damage

40. Lab Diagnosis Examination of blood (Thick & thin Giemsa stained smears) . Trophozoites (within RBCs) Ring shaped . Gametocytes Banana or crescent shaped ( P.falciparum ) spherical in others

41. Toxoplasma

42. Toxoplasma Toxoplasma gondii . A common parasite of human & animals causes Toxoplasmosis Atleast 1/3 rd world population contracts Toxoplasma TORCH

43. Toxoplasma Animals involved ---- Range is W ide Definitive host is domestic cat & felines Humans & other mammals are intermediate hosts. Human infection occurs with ingestion of cysts in undercooked meat (Lamb or pork) from animals that grazed in soil contaminated with cat feces

44. Life cycle In Cat & Man: In Cat : Infective stages: Sporozoites,Cystozoites & Endozoites Ingestion---- Penetrate epith cells of cat intestine Round up & grow within host cells 1stly: Asexual cycle occurs ---- formation of merozoites ----- enter fresh host cells & initiate different cycles

45. 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 feces This is ingested accidentally by man

46. Life cycle Development in human: Infection: 1 -by ingestion of Oocysts from cat or – 2 - eating improperly cooked meat (Pork, Mutton ,Beef, Poultry) containig cysts & peudocysts Cysts – Rupture in small intestine-New forms ingested by macrophages-- Tachyzoites .Only Asexual development in man & no oocysts formed. . Merozoites enter lymphatics & blood---- Cysts & Pseudocysts in various organs-( Bradyzoites –slowly multiplying)

47. Pathogenesis Route : By ingestion of Cysts in undercooked meat or cat feces . Transplacental from mother to fetus Spread: Mainly to Brain , lungs, liver & eyes Form pseudocysts ( Endozoites ) Congenital infection: Can occur only when mother is infected during pregnancy

48. Clinical features Most are asymptomatic Congenital : ( More s evere in congenital form) Abortion or stillbirth or neonatal disease (Encephalitis, hydrocephalus intracranial calcifications) + fever, jaundice,. Most newborns are asymptomatic .

49. Clinical features- ( Congenital ) Less severe lesions as chorioretinitis (Pigment ringed scar),& hepatosplenomegally generally missed at birth may be observed latter in life. Mental retardation in some- months or years latter.

50. 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

51. Clinical features Toxo . in immunodefficient host: (Result of reactivation of latent infection) .Mild to severe, ending in fatal acute fulminating disease. Necrotizing Encephalitis, Myocarditis , Pneumonitis (Autopsy findings)

52. Lab diagnosis Giemsa staining & microscopy : Crescent shaped trophozoites 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 u sed

53. Lab diagnosis Dye test of Sabin & Feldman : 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

54. Indirect Haemagglutination test: .A very sensitive test but . D/E is that it takes longer to become positive compared with Dye test & FAT. . Once positive it remains so for years

55. Extra Toxo Sporogony : During sporogony two sporoblasts form a single cell– these develop a cyst wall & become sporocyst . Each Sporocyst ---- 4 sporozoites Extra intestinal Development can take place simultaneously with intestinal phase Stages are, Cysts & pseudocysts

56. Trypanosoma Three major pathogens 1- Trypanosoma cruzi - Chaga`s disease 2- Trypanosoma gambiens 3- Trypanosoma rhodesiense .Both cause Sleeping sickness

57. Trypanosoma cruzi Causes chaga`s disease Life Cycle : Rueduvid bug is the vector which transmits organism when bites humans or other reservoir hosts (Dogs, cats, rats) .At the time of bite, the bug releases organisms Trypomastigotes in feces which are rubbed into bite site & enter blood of person and penetrate cardiac muscle & change into Amastigote , Epimastigote & Trypomastigote forms. Inside bug- -- Trypomastigotes ××× & change to Epimastigotes before becoming Trypomastigotes Affects many cells as, Myocardial, glial & reticuloendothelial cells

58. Disease occurs mostly in rural areas because the bug resides in rural huts & feeds at night. It bites preferentially arround mouth or eyes hence named also as kissing bug . The parasite produces focal lymohangitis & oedema at bite site.There is facial edema & a nodule ( chagoma ) Cardiac muscle is severely affected,may result in congestive heart failure Neuronal cells are also affected which can result in cardiac arrythmias & loss of tone in colon ( megacolon )

59. Clinical features Primary lesion ( Chagoma ) is usually found on face near eyelids producing swelling of eye & temporal region ( Romana`s sign) + Fever + Lymphadenopathy + Hepatosplenomegally Cardiomyopathy – In Mild, extrasystole+slight tachycardia In severe cases: partial or complete heart block leading to cardiac failure (Cause of death) Some cases:Dilatation of esophagus ( mega esophagus) & megacolon (Dilatation of colon)

60. Laboratory diagnosis Isolation of T.cruzi from blood : a) Can be found by direct examination (stained & wet films) but requires concentration methods as centrifugation so rarely done Bone marrow examination Muscle biopsy ( amastigotes ) B ) culture , on NNN medium is very useful Xenodiagnosis : Atleast 6 clean uninfected laboratory bred reduvid bugs are allowed to feed on suspected pt. & hindgut of bug examined after 2 weeks for epimastigotes

61. Serological methods: are + in majority cases .Indirect haemagglutination . Flourescent antibody test (FAT)

62. Trypanosoma gambiens & Trypanosoma rhodesiense cause Sleeping sickness (African Trypanosomiasis ) Vector: Tsetse fly which bites & injects organism to human skin, where they enter into bloodstream undergo different developmental stages .Spread to lymph nodes & brain

63. Life cycle In tsetse fly : Bite---Ingests Trypomastigotes from reservoir host. .××× in gut and migrate to salivary glands & change to epimastigotes . .××× then form metcyclic trypomastigotes & transmitted by tsetse bite. In man : From injection site in skin enter bloodstream ( Blood form trypomastigotes ) Epimastigotes in tissue---Rare v/s T.cruzi & Leishmania

64. Pathogenesis & Clinical features Spreads from skin to L.N & Brain Sleeping sickness progresses to coma-- due to demyelinating encephalitis.

65. Pathogenesis & Clinical features Skin ulcer occurs at bite site ( Trypanpsomal chancre) Intermittent weekly fever & lymphadenopathy (Organism in enters blood) Winterbottom sign (Enlargement of posterior cevical L.N) Encephalitis characterized by headache, insomnia & mood changes . followed by muscle tremors , slurred speech . .This progresses to somnolence & coma .Untreated case can lead to death

66. Laboratory diagnosis Demonstration of parasite : Blood or aspirate of chancre or L.N CSF (Trypanosomes) Serologic : ELISA CFT FAT

67. Leishmania 4 major pathogens: L.donovani (visceral leishmaniasis ) L.Tropica - L.mexicana L.braziliences ---subcutaneous leishmaniasis -Both cause cause cutaneous leishmaniasis

68. Leishmania donovani Causes kala azar (visceral leishmaniasis ) Life cycle involves sand fly as vector which sucks blood from an infected host( dogs,foxes rodents) and ingests macrophages containing amastigote stage of organism. Dissolution of macrophages releases amastigotes --- change to promastigotes & multiply. Finally migrates to pharynx of sand fly where they can be transmitted during next bite.

69. In humans after bite, Promastigotes are engulfed by & survive within macrophages—change into Amastigotes . Infected macrophages die, progeny organism released which infects other macrophages & reticuloendothelial cells. They are tmted to sand fly during bite.

70. Pathogenesis Organs of reticuloendothelial system (Liver, spleen & bone marrow) are severely affected Reduced bone marrow activity results in Anemia, Leukopenia & thrombocytopenia This results in secondary infection & bleeding tendency S pleenomegally is striking

71. Clinical features Visceral Leishmaniasis - -Kala- Azar : Intermittent fever, weakness, weight loss Massive splenomegally , Hyperpigmentation ( kala azar – Black sickness). .Disease runs for months to years. weakness, infection & GIT bleeding occur. .Death if not treated

72. Muco cutaneous leishmaniasis : Starts as pustular swelling in mouth or on nostrils .May become ulcerative after many months & extends into nasopharyngeal mucous membrane. . 2ndary infection very common-with destruction of nasal cartillage & facial bone

73. Cutaneous leishmaniasis : Starts as . Painless papule on exposed parts (Face etc) . Ulcerates after few months (Circular/oval ulcer with indurated margin)

74. Laboratory Diagnosis Visceral L: Detecting amastigotes in bone marrow spleen, L.N biopsy .Serologic: FAT Indirect immunoflourescence . Formol gel test- A drop of commercial formaldehyde+1 ml pt srum --- a coagulum .Leucopenia, Anemia

75. Lab. Diagnosis Cutaneous & Mucocutaneous Parasite is isolated from margins of ulcers Culture: Lockes solution Montengro test : Consists of intradermal injection 0.1 ml of antigen prepared from cultures of promastigotes --- * Erythema & Induration—48 hours*