際際滷

際際滷Share a Scribd company logo
TOXOPLASMOSIS
 HISTORY
 MORPHOLOGY
 LIFECYCLE
 TRANSMISSION
 PATHOPHYSIOLOGY
 CLINICAL MANIFESTATIONS
 DIAGNOSIS
 TREATMENT
 PREVENTION
SIR HENRY NICOLLE
 TOXOPLASMOSIS GONDII DISCOVERED AND
NAMED BY CHARLES JULES HENRY NICOLLE
(1866-1936) AND MONCEAUX IN 1908.
 AN INTRACELLULAR PARASITE WAS ISOLATED
FROM THE LIVER AND SPLEEN OF A WILD
AFRICAN RODENT CTENODACTYLUS GONDII.
 A YEAR LATER THEY CALLED IT TOXOPLASMA
GONDII BECAUSE OF ITS ARCHED SHAPE (TOXON:
ARCH) AND BECAUSE OF THE COMMON NAME IN
WHICH IT WAS FOUND, THE GONDII.
TOXOPLASMOSIS
CLASSIFICATION
KINGDOM
PHYLUM
CLASS
FAMILY
GENDER
SPECIES
PROTISTA
APICOMPLEXA
SPOROZOA
SARCYSTIDAE
TOXOPLASMA
GONDII
1908
1923
Janku
Chorioretinitis
1939
Wolff and Col
Congenital meningoencephalitis
1948
Sabin and Feldman
Reaction
Serological
1949
Frenkel
Hypersensitivity test
1970
renkel &
hutchison
True Form of
Transmission
MORPHOLOGY
 ASEXUAL FORMS TACHYZOITE
BRADYZOITE (TISSUE CYST)
 SEXUAL FORM OOCYST
TACHYZOITES
 ACTIVELY M U LT I P LY I N G F O R M
CRESCENT SHAPE SEEN IN ACUTE
INFECTION
 INFECT ALL THE NUCLEATED
M A M M A L I A N CELLS
 INSIDE THE HOST CELL, THE
TACHYZOITES ARE S U R RO U N DE D BY
A VACUOLE - ASEXUAL
M U LT I P L I C AT I O N OCCURS -
ROSETTES
BRADYZOITES
 RESTING STAGE OF THE PARASITE
 SEEN IN C H RO N I C INFECTIONS
MOST C O M M O N SITE IS MUSCLES
A N D BRAIN
 INSIDE THE CYST - SLOWLY
M U LT I P LY I N G TROPHOZOITES
ARE CALLED AS BRADYZOITES
OOCYST
SEXUAL F O R M OF THE PARASITE F O U N D
O N LY IN CATS A N D FELINES
LIFE CYCLE
TRANSMISSION
 INGESTION OF SPO RU LA TED O O C YSTS FRO M C O N TA M IN A TED
SOIL, F O O D OR WATER
 INGESTION OF TISSUE CYST C O N TA I N I N G BRADYZOITES F RO M
U N D E RC O O K E D MEAT
 BY BL O O D TRA N SFU SIO N , N EED LE STIC K IN JU RIES, O RG A N
TRANSPL ANTATION
 TRANSPLACENTRAL TRANSMISSION
LABORATORY ACCIDENTS (
TACHYZOITES IN BLOOD)
The Tachyzoites
arereproduced
Dissemination
Following route
lymphatic/ hematogenous
Penetrates
the intestinal wall
PATHOPHYSIOLOGY
PATHOGENESIS
 FORMATION OF TACHYZOITES MULTIPLY AND DISSEMINATION
 LYMPHATIC TISSUE-FOLLICULAR HYPERPLASIA
 SKELETAL MUSCLE
 MYOCARDIUM-FOCAL NECROSIS (MUSCLE CYSTS)
 RETINA ,CHOROID-GRANULOMATOUS LESION
 LUNGS-INTERSTITIAL PNEUMONIA
 CNS  NECROSIS AND MICROGLIAL NODULES
 OTHER ORGANS-PANCREATITIS,GLOMERULONEPHRITIS
 IN IMMUNOCOMPETENT INDIVIDUALS,IMMUNE MECHANISMS LIKE
MACROPHAGES,CD8+ CELLS,NK CELLS,INTERFERON GAMMA,IL-2,12
 KILL OR INHIBIT THE REPLICATION
 IMMUNOGLOBULINS A,M,G DEVELOP
 TISSUE CYSTS BECOME ACTIVE WITHIN 7 DAYS AND REACTIVATION OCCURS
ACUTE OR CHRONIC
 THE RAPIDLY MULTIPLYING CRESCENTRIC CELL (TACHYZOITES ) INITIATE THE
ACUTE STAGE OF DISEASE
IN FUTHER DEVELOPMENT THEY PENETRATE NEW CELLS ESPECIALLY EYE
AND BRAIN.
FURTHER DEVELOPMENT SLOWS DOWN IN THESE ORGANS CALLED AS
BRADYZOITES TO FORM A QUIESCENT TISSUE CYSTS
 THE EVENT LEAD TO CHRONIC STAGE OF DISEASE
CLINICAL MANIFESTATIONS
 FEATURES IN I M M U N O C O M P E T E N T INDIVIDUAL
 FEATURES IN IMMUNODEFICIENT INDIVIDUAL
 CO N G E N I TA L TOXOPLASMOSIS
 OCULAR TOXOPLASMOSIS
IMMUNOCOMPETENT
 ACUTE STAGE-ASYMPTOMATIC
 SYMPTOMATIC
 HEADACHE,FATIGUE
 MALAISE
 FEVER
 CERVICAL LYMPHADENOPATHY
 SUBOCCIPITAL,SUPRACLAVICULAR,INGUIN
AL,MEDIASTINAL(DISCRETE,MULTIPLE,VARI
ABLE IN CONSISTENCY)
IMMUNOCOMPROMISED
 ACUTE INFECTION OR REACTIVATION OF BRADYZOITES
 DEADLIEST-TOXOPLASMIC ENCEPHALITIS
 EITHER FOCAL DYSFUNCTION TO NON FOCAL MENINGOENCEPHALITIS
 DUE TO VASCULITIS,EDEMA AND HEMORRHAGE
 ALTERED MENTATION(75%),SEIZURES(33%), FOCAL NEUROLOGICAL
SIGNS(60%), HEADACHE(56%), FEVER(50%)
 BRAINSTEM-CRANIAL NERVE PALSY,DYSMETRIA,ATAXIA
 BASAL GANGLIA-HYDROCEPHALUS,CHOREIFORM MOVEMENTS,
CHOREOATHETOSIS
 DD-CRYPTOCOCCAL MENINGITIS,HSE,TM,CNS LYMPHOMA
 LUNG-ARDS,HEMOPTYSIS,DIC
OCULAR TOXOPLASMOSIS
 BLURRED VISION,SCOTOMA,PHOTOPHOBIA
 MACULAR INVOLVEMENT-LOSS OF CENTRAL VISION,
NYSTAGMUS SECONDARY TO POOR FIXATION
 EOM- CONVERGENCE-STRABISMUS
 FLARE UPS OF CHORIORETINITIS-DESTROY RETINAL
TISSUEGLAUCOMA
 CONGENITAL LESIONS-MASSIVE CHORIORETINAL
DEGENERATION WITH EXTENSIVE FIBROSIS
 IN PATIENTS WITH AIDS,DIFFUSE RETINAL NECROSIS-
FREE TACHYZOITES+CYSTS CONTAINING
BRADYZOITES
CONGENITAL TOXOPLASMOSIS
 OCCURS DURING FIRST TIME IN PREGNANCY
 INFECTION OF PLACENTA-HEMATOGENOUS INFECTION OF FETUS
 AS GESTATION INCREASES-RATE OF TRANSMISSION INCREASES BUT SEVERITY DECREASES
 INFECTED CHILDREN INITIALLY ASYMPTOMATIC,PERSISTENCE OF T.GONDII-
REACTIVATION-MOST FREQUENTLY CHORIORETINITIS
 CHORIORETINITIS,STRABISMUS,BLINDNESS,EPILEPSY,ANEMIA,JAUNDICE,RASH
 MICROCEPHALY,INTRACRANIAL CALCIFICATION,HYDROCEPHALUS,PNEUMONITIS
TRIMESTER FIRST SECOND THIRD
Trasmission rate 10-25% 30-54% 60-65%
DIAGNOSIS
 DIRECT MICROSCOPY
 DETECTION OF TACHYZOITES IN B LO O D A N D TISSUE CYST IN TISSUE
BIOPSY
 STAINING METHODS:
o GIEMSA
o PAS
o SILVER STAINS
o IMMUNOPEROXIDASE STAIN
SEROLOGY
 DETECTION OF TOXOPL ASMA ANTIGEN BY ELISA
 DETECTION OF TOXOPL ASMA ANTIBODY BY
o SABIN F E L D M A N DYE TEST
o INDIRECT FLUORESCENT ANTIBODY TEST
o IGM ELISA
o IGG ELISA
o IGG AVIDITY TEST
 PARALLEL IGG TESTING -4 FOLD RISE IN PAIRED SERA OF 3 WEEKS APART-
ACUTE INFECTION
 IGG LOW AVIDITY-ACUTE INFECTION(<3 MONTHS)
 HIGH -CHRONIC INFECTION(>3 MONTHS)
 PRESENCE OF IGA,M,E ACUTE INFECTION
 OTHER METHODS-DOUBLE SANDWICH IGM ELISA &
IGM IMMUNOSORBENT ASSAY
MOLECULAR METHODS
POLYMERASE CHAIN REACTION
AMPLIFICATION OF B1 GENE DETECTION OF T.GONDII DNA
SAMPLES
o AMNIOTIC FLUID
o PERIPHERAL BLOOD
o CSF
o URINE
o AQUEOUS & VITREOUS FLUID
TREATMENT
 GOAL-TO ARREST THE REPLICATION OF PARASITE AND PREVENT FURTHER
DAMAGE TO ORGANS INVOLVED
 IMMUNOCOMPETENT
 IMMUNOCOMPROMISED
 CONGENITAL
IMMUNOCOMPETENT
 NOT REQUIRE SPECIFIC THERAPY
 IF OCULAR+ ,TREATED FOR 1 MONTH 
PYRIMETHAMINE+SULFADIAZINE/CLINDAMYCIN OR PREDNISONE
IMMUNOCOMPROMISED
 AIDS PATIENTS SEROPOSITIVE FOR T.GONDII CD4+T LYMPHOCYTE
COUNT<100/MCGL(SCREENING AIDS PATIENTS)
 IF CD4+T LYMPHOCYTE COUNT>200,NO NEED OF PROPHYLAXIS
 TRIMETHOPRIM-SULFAMETHOXAZOLE
 NOT TOLERATE-DAPSONE+PYRIMETHAMINE
 ATOVAQUONE +/_ PYRIMETHAMINE
 PROPHYLACTIC MONOTHERAPY-
DAPSONE,PYRIMETHAMINE,AZITHROMYCIN,CLARITHROMYCIN,AEROSOLIZE
D PENTAMIDINE
 PATIENT+HIV- CD4+T LYMPHOCYTE COUNT>200 FOR ATLEAST 6 MONTHS
AFTER ART+ASYMPTOMATIC---DISCONTINUE THE PROPHYLAXIS
CONGENITAL INFECTION
 NEONATES-ORAL PYRIMETHAMINE(1MG/KG)
 SULFADIAZINE (100 MG/KG)
 FOLINIC ACID FOR 1 YEAR
 PREDNISOLONE(1MG/KG PER DAY)-MAY BE USED
 PREGNANT-SPIRAMYCIN(IN ACUTE CASE EARLY IN PREGNANCY)
 PYRI/SULFA/FOLINIC ACID AFTER 18 WEEKS OF PREGNANCY
PREVENTION IS BETTER THAN CURE
 AVOIDANCE OF HUMAN CONTACT WITH CAT FECES IS HIGHLY IMPORTANT
 CHANGING OF CAT LITTER AND SAFE DISPOSAL CAN PREVENT
TRANSMISSION
MEAT SHOULD BE COOKED TO INTERNAL TEMPERATURE OF 74-75DEGREE
CELCIUS
 WASH YOUR HANDS AFTER HANDLING RAW MEAT
 PROTECT CHILDREN'S PLAY AREAS FROM CAT AND DOG DROPPINGS
WASH YOUR HANDS VERY WELL AFTER BEIN G IN CONTACT WITH SOIL
POSSIBLY CONTAMINATED BY ANIMAL FECES
 SCREENING OF IMMUNOCOMPROMISED FOR ANTIBODY TO T.GONDII
 PREGNANT WOMEN SHOULD AVOID CONTACT WITH KITTENS
REFERENCES
 PRINCIPLES AND PRACTICES OF INFECTIOUS DISEASES,8TH EDITION-
MANDELL,DOUGLAS

More Related Content

toxoplasma.pptx

  • 2. HISTORY MORPHOLOGY LIFECYCLE TRANSMISSION PATHOPHYSIOLOGY CLINICAL MANIFESTATIONS DIAGNOSIS TREATMENT PREVENTION
  • 3. SIR HENRY NICOLLE TOXOPLASMOSIS GONDII DISCOVERED AND NAMED BY CHARLES JULES HENRY NICOLLE (1866-1936) AND MONCEAUX IN 1908. AN INTRACELLULAR PARASITE WAS ISOLATED FROM THE LIVER AND SPLEEN OF A WILD AFRICAN RODENT CTENODACTYLUS GONDII. A YEAR LATER THEY CALLED IT TOXOPLASMA GONDII BECAUSE OF ITS ARCHED SHAPE (TOXON: ARCH) AND BECAUSE OF THE COMMON NAME IN WHICH IT WAS FOUND, THE GONDII.
  • 5. 1908 1923 Janku Chorioretinitis 1939 Wolff and Col Congenital meningoencephalitis 1948 Sabin and Feldman Reaction Serological 1949 Frenkel Hypersensitivity test 1970 renkel & hutchison True Form of Transmission
  • 6. MORPHOLOGY ASEXUAL FORMS TACHYZOITE BRADYZOITE (TISSUE CYST) SEXUAL FORM OOCYST
  • 7. TACHYZOITES ACTIVELY M U LT I P LY I N G F O R M CRESCENT SHAPE SEEN IN ACUTE INFECTION INFECT ALL THE NUCLEATED M A M M A L I A N CELLS INSIDE THE HOST CELL, THE TACHYZOITES ARE S U R RO U N DE D BY A VACUOLE - ASEXUAL M U LT I P L I C AT I O N OCCURS - ROSETTES
  • 8. BRADYZOITES RESTING STAGE OF THE PARASITE SEEN IN C H RO N I C INFECTIONS MOST C O M M O N SITE IS MUSCLES A N D BRAIN INSIDE THE CYST - SLOWLY M U LT I P LY I N G TROPHOZOITES ARE CALLED AS BRADYZOITES
  • 9. OOCYST SEXUAL F O R M OF THE PARASITE F O U N D O N LY IN CATS A N D FELINES
  • 11. TRANSMISSION INGESTION OF SPO RU LA TED O O C YSTS FRO M C O N TA M IN A TED SOIL, F O O D OR WATER INGESTION OF TISSUE CYST C O N TA I N I N G BRADYZOITES F RO M U N D E RC O O K E D MEAT BY BL O O D TRA N SFU SIO N , N EED LE STIC K IN JU RIES, O RG A N TRANSPL ANTATION TRANSPLACENTRAL TRANSMISSION LABORATORY ACCIDENTS ( TACHYZOITES IN BLOOD)
  • 12. The Tachyzoites arereproduced Dissemination Following route lymphatic/ hematogenous Penetrates the intestinal wall PATHOPHYSIOLOGY
  • 13. PATHOGENESIS FORMATION OF TACHYZOITES MULTIPLY AND DISSEMINATION LYMPHATIC TISSUE-FOLLICULAR HYPERPLASIA SKELETAL MUSCLE MYOCARDIUM-FOCAL NECROSIS (MUSCLE CYSTS) RETINA ,CHOROID-GRANULOMATOUS LESION LUNGS-INTERSTITIAL PNEUMONIA CNS NECROSIS AND MICROGLIAL NODULES OTHER ORGANS-PANCREATITIS,GLOMERULONEPHRITIS
  • 14. IN IMMUNOCOMPETENT INDIVIDUALS,IMMUNE MECHANISMS LIKE MACROPHAGES,CD8+ CELLS,NK CELLS,INTERFERON GAMMA,IL-2,12 KILL OR INHIBIT THE REPLICATION IMMUNOGLOBULINS A,M,G DEVELOP TISSUE CYSTS BECOME ACTIVE WITHIN 7 DAYS AND REACTIVATION OCCURS
  • 15. ACUTE OR CHRONIC THE RAPIDLY MULTIPLYING CRESCENTRIC CELL (TACHYZOITES ) INITIATE THE ACUTE STAGE OF DISEASE IN FUTHER DEVELOPMENT THEY PENETRATE NEW CELLS ESPECIALLY EYE AND BRAIN. FURTHER DEVELOPMENT SLOWS DOWN IN THESE ORGANS CALLED AS BRADYZOITES TO FORM A QUIESCENT TISSUE CYSTS THE EVENT LEAD TO CHRONIC STAGE OF DISEASE
  • 16. CLINICAL MANIFESTATIONS FEATURES IN I M M U N O C O M P E T E N T INDIVIDUAL FEATURES IN IMMUNODEFICIENT INDIVIDUAL CO N G E N I TA L TOXOPLASMOSIS OCULAR TOXOPLASMOSIS
  • 17. IMMUNOCOMPETENT ACUTE STAGE-ASYMPTOMATIC SYMPTOMATIC HEADACHE,FATIGUE MALAISE FEVER CERVICAL LYMPHADENOPATHY SUBOCCIPITAL,SUPRACLAVICULAR,INGUIN AL,MEDIASTINAL(DISCRETE,MULTIPLE,VARI ABLE IN CONSISTENCY)
  • 18. IMMUNOCOMPROMISED ACUTE INFECTION OR REACTIVATION OF BRADYZOITES DEADLIEST-TOXOPLASMIC ENCEPHALITIS EITHER FOCAL DYSFUNCTION TO NON FOCAL MENINGOENCEPHALITIS DUE TO VASCULITIS,EDEMA AND HEMORRHAGE ALTERED MENTATION(75%),SEIZURES(33%), FOCAL NEUROLOGICAL SIGNS(60%), HEADACHE(56%), FEVER(50%) BRAINSTEM-CRANIAL NERVE PALSY,DYSMETRIA,ATAXIA BASAL GANGLIA-HYDROCEPHALUS,CHOREIFORM MOVEMENTS, CHOREOATHETOSIS DD-CRYPTOCOCCAL MENINGITIS,HSE,TM,CNS LYMPHOMA LUNG-ARDS,HEMOPTYSIS,DIC
  • 19. OCULAR TOXOPLASMOSIS BLURRED VISION,SCOTOMA,PHOTOPHOBIA MACULAR INVOLVEMENT-LOSS OF CENTRAL VISION, NYSTAGMUS SECONDARY TO POOR FIXATION EOM- CONVERGENCE-STRABISMUS FLARE UPS OF CHORIORETINITIS-DESTROY RETINAL TISSUEGLAUCOMA CONGENITAL LESIONS-MASSIVE CHORIORETINAL DEGENERATION WITH EXTENSIVE FIBROSIS IN PATIENTS WITH AIDS,DIFFUSE RETINAL NECROSIS- FREE TACHYZOITES+CYSTS CONTAINING BRADYZOITES
  • 21. OCCURS DURING FIRST TIME IN PREGNANCY INFECTION OF PLACENTA-HEMATOGENOUS INFECTION OF FETUS AS GESTATION INCREASES-RATE OF TRANSMISSION INCREASES BUT SEVERITY DECREASES INFECTED CHILDREN INITIALLY ASYMPTOMATIC,PERSISTENCE OF T.GONDII- REACTIVATION-MOST FREQUENTLY CHORIORETINITIS CHORIORETINITIS,STRABISMUS,BLINDNESS,EPILEPSY,ANEMIA,JAUNDICE,RASH MICROCEPHALY,INTRACRANIAL CALCIFICATION,HYDROCEPHALUS,PNEUMONITIS TRIMESTER FIRST SECOND THIRD Trasmission rate 10-25% 30-54% 60-65%
  • 22. DIAGNOSIS DIRECT MICROSCOPY DETECTION OF TACHYZOITES IN B LO O D A N D TISSUE CYST IN TISSUE BIOPSY STAINING METHODS: o GIEMSA o PAS o SILVER STAINS o IMMUNOPEROXIDASE STAIN
  • 23. SEROLOGY DETECTION OF TOXOPL ASMA ANTIGEN BY ELISA DETECTION OF TOXOPL ASMA ANTIBODY BY o SABIN F E L D M A N DYE TEST o INDIRECT FLUORESCENT ANTIBODY TEST o IGM ELISA o IGG ELISA o IGG AVIDITY TEST
  • 24. PARALLEL IGG TESTING -4 FOLD RISE IN PAIRED SERA OF 3 WEEKS APART- ACUTE INFECTION IGG LOW AVIDITY-ACUTE INFECTION(<3 MONTHS) HIGH -CHRONIC INFECTION(>3 MONTHS) PRESENCE OF IGA,M,E ACUTE INFECTION OTHER METHODS-DOUBLE SANDWICH IGM ELISA & IGM IMMUNOSORBENT ASSAY
  • 25. MOLECULAR METHODS POLYMERASE CHAIN REACTION AMPLIFICATION OF B1 GENE DETECTION OF T.GONDII DNA SAMPLES o AMNIOTIC FLUID o PERIPHERAL BLOOD o CSF o URINE o AQUEOUS & VITREOUS FLUID
  • 26. TREATMENT GOAL-TO ARREST THE REPLICATION OF PARASITE AND PREVENT FURTHER DAMAGE TO ORGANS INVOLVED IMMUNOCOMPETENT IMMUNOCOMPROMISED CONGENITAL
  • 27. IMMUNOCOMPETENT NOT REQUIRE SPECIFIC THERAPY IF OCULAR+ ,TREATED FOR 1 MONTH PYRIMETHAMINE+SULFADIAZINE/CLINDAMYCIN OR PREDNISONE
  • 28. IMMUNOCOMPROMISED AIDS PATIENTS SEROPOSITIVE FOR T.GONDII CD4+T LYMPHOCYTE COUNT<100/MCGL(SCREENING AIDS PATIENTS) IF CD4+T LYMPHOCYTE COUNT>200,NO NEED OF PROPHYLAXIS TRIMETHOPRIM-SULFAMETHOXAZOLE NOT TOLERATE-DAPSONE+PYRIMETHAMINE ATOVAQUONE +/_ PYRIMETHAMINE PROPHYLACTIC MONOTHERAPY- DAPSONE,PYRIMETHAMINE,AZITHROMYCIN,CLARITHROMYCIN,AEROSOLIZE D PENTAMIDINE PATIENT+HIV- CD4+T LYMPHOCYTE COUNT>200 FOR ATLEAST 6 MONTHS AFTER ART+ASYMPTOMATIC---DISCONTINUE THE PROPHYLAXIS
  • 29. CONGENITAL INFECTION NEONATES-ORAL PYRIMETHAMINE(1MG/KG) SULFADIAZINE (100 MG/KG) FOLINIC ACID FOR 1 YEAR PREDNISOLONE(1MG/KG PER DAY)-MAY BE USED PREGNANT-SPIRAMYCIN(IN ACUTE CASE EARLY IN PREGNANCY) PYRI/SULFA/FOLINIC ACID AFTER 18 WEEKS OF PREGNANCY
  • 30. PREVENTION IS BETTER THAN CURE AVOIDANCE OF HUMAN CONTACT WITH CAT FECES IS HIGHLY IMPORTANT CHANGING OF CAT LITTER AND SAFE DISPOSAL CAN PREVENT TRANSMISSION MEAT SHOULD BE COOKED TO INTERNAL TEMPERATURE OF 74-75DEGREE CELCIUS WASH YOUR HANDS AFTER HANDLING RAW MEAT PROTECT CHILDREN'S PLAY AREAS FROM CAT AND DOG DROPPINGS WASH YOUR HANDS VERY WELL AFTER BEIN G IN CONTACT WITH SOIL POSSIBLY CONTAMINATED BY ANIMAL FECES SCREENING OF IMMUNOCOMPROMISED FOR ANTIBODY TO T.GONDII PREGNANT WOMEN SHOULD AVOID CONTACT WITH KITTENS
  • 31. REFERENCES PRINCIPLES AND PRACTICES OF INFECTIOUS DISEASES,8TH EDITION- MANDELL,DOUGLAS