PARASITIC DISEASES
BY B.M.TRISHA
2ND BPT
TOPICS TO BE COVERED
 INTRODUCTION
 CLASSES OF PARASITE
 MORPHOLOGICAL ADAPTATIONS
 BASIC TERMINOLOGIES
 MALARIA
 FILARIASIS
 AMOEBIASIS
 KALA-AZAR
 CYSTICERCOSIS
 HYDATID CYST
 SUMMARY
 QUESTIONS
INTRODUCTION
 PARASITES ARE LIVING ORGANISM WHICH DEPENDS ON HOST.
 DISEASES CAUSED BY PARASITES {PROTOZOA,HELMINTHES} ARE QUITE COMMON AND
COMPRISES A VERY LARGE GROUP OF INFECTIONS.
 PARASITES MAY CAUSE DISEASES DUE TO:
 THEIR PRESENCE IN THE LUMEN OF INTESTINE.
 INFILTRATION INTO BLOOD STREAM.
 PARASITISM MAY LEAD TO DISEASES, BUT NOT ALWAYS.
 PARASITES MAY INFECT THE GASTROINTESTINAL TRACT OR
CIRCULATORY SYSTEM AND INVADE DIFFERENT TISSUES AND
ORGANS.
 PARASITIC INFECTIONS MAY CAUSE MORTALITY OR MORBIDITY.
BASIC TERMINOLOGIES
 SYMBIOSIS : A CLOSE RELATIONSHIP BETWEEN TWO SPECIES IN WHICH BOTH
GET BENEFITTED.
 COMMENSALISM : RELATIONSHIP BETWEEN TWO SPECIES IN WHICH ONE IS
BENEFITTED AND OTHER IS NEITHER BENEFITTED NOR HARMED.
 PARASITISM : RELATIONSHIP IN WHICH ONE IS BENEFITTED AND OTHER ONE
HARMED.
MODES OF ENTRY
 INGESTION
 ARTHROPODS BITES
 PENETRATION THROUGH INTACT SKIN OR MUCOUS MEMBRANE.
CLASSES OF PARASITES
 ENDOPARASITE : CAUSES INFECTION INSIDE THE BODY.
 EXAMPLE –HOOK WORM ,ROUND WORM.
 ECTOPARASITE : CAUSES INFECTION SUPERFICIALLY ON SKIN.
 EXAMPLE - LICE ,TICKS ,MITES.
 TEMPORARY PARASITE : VISIT HOST FOR SHORT PERIOD.
 EXAMPLE - MOSQUITOES ,BUGS,MITES.
 PERMANENT PARASITE : REMAIN PARASITIC THROUGHOUT THEIR LIFE.
 EXAMPLE - TRYPANOSOMES, WUCHERERIA.
 OBLIGATE PARASITE : CAN NOT LIVE WITHOUT ITS HOST
 EXAMPLE - PLASMODIUM.
 FACULATATIVE PARASITE : LIVES PARASITIC LIFE WHEN OPPORTUNITY IS AVAILABLE
 EXAMPLE – NAEGLERIA FOWLERI
 PSEUDOPARASITISM : FREE LIVING LARVAE ACCIDENTALLY ENTERS BODY AND SURVIVE.
 EXAMPLE – LARVAE OF HOUSEFLY.
TYPES OF HOSTS
 DEFINITIVE HOST : PARASITES WHICH CAN REPRODUCE BY SEXUAL
REPRODUCTION.
 INTERMEDIATE HOST: PARASITES PRESENT IN LARVAL STAGE AS WELL AS SEXUAL
REPRODUCTION STAGE.
 PARATENIC HOST :PARASITES PRESENT IN LARVAL STAGE BUT IT DOESN’T
DEVELOP.
MORPHOLOGICAL ADAPTATION – WHEN THE
PARASITES REACHES THEIR INHABITAT THEY SLOWLY CHANGE THEIR MORPHOLOGY
FOR SURVIVAL PURPOSE.
 ECTOPARASITES : LATERALLY COMPRESSED – ESCAPE THROUGH HAIRS,
DORSOVENTRALLY FLATTENED – EASILY CLINGS ON THE HOST , PRESENCE OF
SUCKERS TO ATTACH THEMSELVES WITH HOST.
 ENDOPARASITE : ROUNDED WITH CUTICULAR SPECIALISATION- TO MACERATE
THE TISSUE, THIN FILIFORM SHAPE – PENETRATE EASILY INTO MUCOSA, RIBBON
LIKE STRUCTURE .
DISEASES CAUSITIVE AGENTS
MALARIA PLASMODIUM VIVAX, PLASMODIUM OVALE,
PLASMODIUM FALCIPARUM, PLASMODIUM
MALARIAE.
FILARIASIS WUCHERERIA BANCROFTI
AMOEBIASIS ENTAMOEBA HISTOLYTICA
KALA-AZAR [LEISHMANIASIS] LEISHMANIA TROPICA, LEISHMANIA
BRAZILIENSIS ,LEISHMANIA DONOVANI.
CYSTICERCOSIS TAENIA SOLINUM
HYDATID DISEASE [ECHINOCOCCOSIS] ECHINOCOCCUS GRANULOSUS
MALARIA
MAL – BAD ARIA - AIR
 MALARIA IS A PROTOZOAL DISEASE CAUSED BY ANY ONE OR COMBINATION OF
FOUR SPECIES: PLASMODIUM VIVAX,PLASMODIUM FALCIPARUM,PLASMODIUM
OVALE,PLASMODIUM MALARIAE.
 WHILE PLASMODIUM FALCIPARUM CAUSES MALIGNANT MALARIA,OTHER 3
PRODUCE BENIGN ILLNESS.
 THESE PARASITES ARE TRANSMITTED BY BITE OF FEMALE ANOPHELES
MOSQUITO.
 THE DISEASE IS ENDEMIC IN SEVERAL PARTS OF TROPICAL AFRICA,PARTS OF
SOUTH AND CENTRAL AMERICA,INDIA AND SOUTH-EAST ASIA.
STRUCTURE OF MALARIAL PARASITE
LIFE CYCLE OF MALARIAL PARASITE
This Photo by Unknown Author is licensed under CC BY
INCUBATION PERIOD
STAGES OF MALARIA
 COLD STAGE – CHILLS FOR 15 MINS – 1 HOUR CAUSED DUE TO RUPTURE FROM
HOST CELL
 HOT STAGE – FEVER MAY REACH UPTO 40 DEGREES, STARTS INVADING NEW
CELLS
 SWEATING STAGE-PATIENT STARTS SWEATING , ASYNCHRONOUS PAROXYSMS.
SPECIES INCUBATION PERIOD
P. FALCIPARUM 7- 14 DAYS
P. VIVAX 12- 17 DAYS
P. OVALE 9- 18 DAYS
P. MALARIAE 13- 14 DAYS
MORPHOLOGICAL FEATURES
 PARASITISATION AND DESTRUCTION OF ERYTHROCYTES ARE RESPONSIBLE FOR
MAJOR PATHOLOGICAL CHANGES
 MALARIAL PIGMENT LIBERATED BY DETROYED RBC ACCUMULATES IN PHAGOCYTIC
CELLS OF RETICULOENDOTHELIAL SYSTEM RESULTING IN ENLARGEMENT OF SPLEEN
AND LIVER {HEPATOSPLENOMEGALY}.
 IN FALCIPARUM MALARIA,THERE IS MASSIVE ABSORPTION OF HAEMOGLOBIN BY
RENAL TUBULES PRODUCING BLACKWATER FEVER {HAEMOGLOBINURIA NEPHROSIS}
 CEREBRAL MALARIA IS CHARCTERISED BY CONGESTION AND PETECHIAE ON WHITE
MATTER.
 PARASITIZED ERYTHROCYTES IN FALCIPARUM MALARIA ARE STICKY AND GET
ATTACHED TO ENDOTHELIAL CELLS RESULTING IN OBSTRUCTION OF CAPILLARIES OF
DEEP ORGANS SUCH AS OF BRAIN LEADING TO HYPOXIA AND DEATH
DIAGNOSIS OF MALARIA DONE BY DEMONSTRATION
OF MALARIAL PARASITE IN THIN OR THICK BLOOD
FILMS OR HISTOLOGICAL SECTIONS.
STAIN USED : GIEMSA STAIN
MAJOR COMPLICATIONS
 CEREBRAL MALARIA [COMA]
 RENAL IMPAIRMENT
 HYPOGLYCEMIA
 SEVERE ANEMIA
 HAEMOGLOBINURIA
 JAUNDICE
 PULMONARY OEDEMA
 ACIDOSIS FOLLOWED BY CONGESTIVE HEART FAILURE AND HYPOTENSIVE
SHOCK.
TREATMENT
 TREATMENT OF CHOICE FOR
UNCOMPLICATED MALARIA IS
COMBINATION OF TWO OR MORE
ANTIMALARIAL DRUG WITH DIFFERENT
MECHANISM OF ACTION.
 DRUG OF CHOICE IN MALARIA :
 CINCHONA ALKALOIDS : QUININE AND
QUINIDINE.
 4 AMINOQUINOLINES
 ANTIFOLATES
 ANTIBIOTICS : TETRACYCLINE,
DOXYCYCLINE
FILARIASIS
 WUCHERERIA BANCROFTI AND BRUGIA MALAYI ARE RESPOSIBLE FOR CAUSING
FILARIASIS.
 TRANSMITTED BY VECTORS LIKE MOSQUITO,CULEX.
 THE LYMPHATIC VESSELS INHABIT THE ADULTWORM,ESPECIALLY IN LYMPH
NODES,TESTIS,EPIDIDYMIS.
 MICROFILARIAE SEEN IN CIRCULATION ARE PRODUCED BY FEMALE WORM
MORPHOLOGY
 ADULT WOMRS ARE LONG HAIR LIKE TRANSPARENT NEMATODES, FILIFORM IN
SHAPE WITH TAPPERING ENDS.
 MALE MEASURES 2.5– 4CM, FEMALE MEASURES 8-10CM
 TAIL END OF MALE IS CURVED VENTRALLY WHILE FEMALE IS NARROW AND
POINTED.
LIFE CYCLE OF FILARIASIS
MORPHOLOGICAL FEATURES
 THE MOST SIGNIFICANT HISTOLOGIC CHANGES ARE DUE TO PRESENCE OF ADULT
WORMS IN LYMPHATIC VESSELS CAUSING LYMPHATIC OBSTRUCTION AND
LYMPHOEDEMA.REGIONAL LYMPH NODES ARE ENLARGED AND THEIR SINUSES
ARE DISTENDED WITH LYMPH.
 THE SURROUNDING TISSUE OF BLOCKED LYMPHATICS ARE INFILTERED BY
INFLAMATORY CELLS.
 CHRONICITY OF PROCESS CAUSES ENORMOUS THICKENING AND INDURATION OF
SKIN OF LEGS AND SCROTUM RESEMBLING A ELEPHANT HENCE NAMED
ELEPHATIASIS.
 CHYLOUS ASCITES AND CHYLURIA MAY OCCUR DUE TO RUPTURE OF ABDOMINAL
LYMPHATICS.
 MAJORITY OF INFECTED PATIENTS REMAIN ASYMPTOMATIC.
 SYMPTOMATIC CASES MAY HAVE TWO FORMS:
 ACUTE FORM: PRESENTS WITH FEVER , LYMPHANGITIS
,LYMPHADENITIS,EOSINOPHILIA, MICROFILARIAEMIA.
 CHRONIC FORM :LYMPHADENOPATHY,LYMPHOEDEMA AND
ELEPHANTIASIS.
DIAGNOSIS
 ANTIGEN DETECTION :CIRCULATING FILARIAL ANTIGEN,LYMPH NODE BIOPSY
TREATMENT
 DRUG OF CHOICE – IVERMECTIN,ALBENDAZOLE.
 TREATMENT FOR ELEPHATIASIS :
 SKIN TREATMENT – ANTIBACTERIAL CREAM.
 ELEVATE AND EXERCISE AFFECTED BODY PART.
 CDP { COMPLEX DECONGESTIVE PHYSIOTHERAPY} – LYMPH DRAINAGE,MASSAGE,
COMPRESSIVE BANDAGES.
AMBOEBIASIS
 CAUSED BY ENTAMOEBA HISTOLYTICA NAMED FOR ITS LYTIC ACTION ON TISSUE.
 MORE COMMON IN TROPICAL AND SUBTROPICAL REGION WITH POOR
SANITATION.
 TWO FORMS OF PARASITE:
 TROPHOZOITE FORM : ACTIVE ADULT FORM SEEN IN TISSUES AND DIARRHOEAL
STOOLS.
 CYSTIC FORM : SEEN IN STOOLS BUT NOT IN TISSUES.
MORPHOLOGICAL FEATURES
 THE LESIONS OF AMOEBIASIS INCLUDE AMOEBIC COLITIS,AMOEBOMA,AMOEBIC
LIVER ABSCESS AND SPREAD OF LESIONS TO OTHER SITES.
 AMOEBIC COLITIS,THE MOST COMMON TYPE OF AMOEBIC INFECTION BEGINS AS
A SMALL AREA OF NECROSIS OF MUCOSA WHICH MAY ULCERATE.THESE
ULCERATIVE LESIONS MAY ENLARGE.
 AMOEBOMA IS AN INFLAMMATORY THICKENING OF WALL OF LARGE BOWEL
RESEMBLING CARCINOMA OF COLON.
 AMOEBIC LIVER ABCESS
FORMED BY INVASION OF
RADICLE OF PORTAL VEIN BY
TROPHOZOITES.
 OTHER SITES:
 PERITONITIS :PERFORATION
OF AMOEBIC ULCER OF
COLON,EXTENSION TO LUNGS
AND PLEURA BY RUPTURE OF
AMBOEBIC LIVER
ABSCESS,HEMATOGENOUS
SPREAD TO CAUSE AMOEBIC
CARDITIS AND CEREBRAL
LESIONS,CUTANEOUS
AMEOBIASIS VIA SPREAD OF
RECTAL AMOEBIASIS OR FROM
ANAL INTERCOURSE.
DIAGNOSIS
 TROPHOZOITE FORM CAN BE STAINED POSITIVELY WITH PAS [PERIODIC ACID
SCHIFF] STAIN IN TISSUES WHILE AMOEBIC CYSTS HAVING 4 NUCLEI CAN BE
IDENTIFIED IN STOOLS.
 CYSTS ARE INFECTIVE STAGE FOUND IN CONTAMINATED WATER OR FOOD.
 TROPHOZOITES ARE FORMED FROM THE CYST STAGE IN THE INTESTINE AND
COLONIZE CAECUM .
 TRPHOZOITES AS WELL AS CYSTS ARE PASSED IN STOOLS BUT THE
TROPHOZOITES FAIL TO SURVIVE OUTSIDE OR DESTROYED BY GASTRIC
SECRETIONS.
KALA-AZAR {LEISHMANIASIS}
KALA – BLACK AZAR - FEVER
 TRANSMITTED BY SAND FLY BITES.
 ENDEMIC IN PARTS OF TROPICS AND SUBTROPICS.
 WILD AND DOMESTIC DOGS AND SMALL RODENTS ARE COMMON HOSTS.
RESPONSIBLE FOR VARIOUS SYNDROME :
 VISCERAL LEISHMANIASIS [ KALA AZAR ]
 CUTANEOUS LEISHMANIASIS
 MUCO CUTANEOUS LEISHMANIASIS
 ANTHROPONOTIC CUTANEOUS LEISHMANIASIS
 ZOONOTIC CUTANEOUS LEISHMANIASIS
 POST KALA AZAR DERMAL LEISHMANIASIS
LIFE CYCLE
CLINICAL FEATURES
 CHARATERIZED BY DARKENING OF SKIN [HENCE NAMED BLACK SICKNESS]
 IRREGULAR BOUTS OF FEVER,WEIGHT LOSS,ENLARGEMENT OF SPLEEN AND
LIVER AND ANAEMIA.
 LYMPHADENOPATHY MAY ALSO OCCUR
 POST KALA AZAR DERMAL LEISHMANIASIS – RASHES ON SKIN.
 CUTANEOUS LEISHMANIASIS CAUSES SKIN LEISONS, MAINLY ULCERS,LIFE
LONG SCARS.
 MUSCULOCUTANEOUS LEISHMANIASIS LEADS TO PARTIAL OR TOTAL
DESTRUCTION OF MUCOUS MEMBRANE OF NOSE ,MOUTH,THROAT.
DIAGNOSIS
 SEROLOGICAL TEST
 LEISHMANIN TEST
 HAEMATOLOGICAL FINDINGS
TREATMENT
 DRUG OF CHOICE
 AMPHOTERICIN
 MILTEFOSINE
 PENTAMIDINE ISETHIONATE
 CONTROL SAND FLIES
 PROPHYLAXIS
CYSTICERCOSIS
 INFECTION BY LARVAL STAGE OF TAENIA SOLIUM,PORK TAPE WORM.
 ADULT TAPE WORM RESIDES IN HUMAN INTESTINES. THE EGGS ARE PASSED IN
HUMAN FAECES WHICH ARE INJESTED BY PIGS OR THEY INFECT VEGETABLES.
 DISEASE SPREAD THROUGH ORAL ROUTE THROUGH CONTAMINATED FOOD.
 THESE EGG THEN DEVELOP INTO LARVAL STAGE IN HOST,SPREAD BY BLOOD TO
ANY SITE IN THE BODY AND FORM CYSTIC LARVAE TERMED CYSTICERCUS
CELLULOSAE.
 HUMAN BEINGS MAY ACQUIRE INFECTION BY LARVAL STAGE BY EATING
UNDERCOOKED PORK ,BY INJESTING UNCOOKED CONTAMINATED VEGETABLES.
MORPHOLOGICAL FEATURES
 THE CYSTS OCCUR ANYWHERE IN THE BODY
AND ACCORDINGLY PRODUCE SYMPTOMS.
 MOST COMMON SITES ARE BRAIN,SKELETAL
MUSCLES AND SKIN.
 CYSTICERCUS CONSISTS OF ROUND TO OVAL
WHITE CYST,CONTAINS MILKY FLUID.
 THE CYSTICERCUS MAY REMIAN VIABLE FOR
LONG TIME AND INCITE NO INFLAMMATION. BUT
WHEN EMBRYO DIES IT PRODUCES
GRANULOMATOUS REACTION WITH
EOSINOPHILS,LATER LESION MAY BECOME
SCARRED AND CALCIFIED.
DIAGNOSIS
 BIOPSY
 X –RAY
 COMPOUND TOMOGRAPHY
 MAGNETC RESONANCE IMAGING
 SEROLOGICAL TEST
TREATMENT
 EXCISION IS BEST METHOD
 DRUG OF CHOICE – ALBENDAZOLE,PRAZIQUANTEL
 SURGICAL MANAGEMENT
HYDATID CYST
 ZOONOTIC DISEASE CAUSED BY ECHINOCOCCUS GRANULOSUS,ECHINOCOCCUS
MULTILOCULARIS
 HUMANS ARE ACCIDENTAL INTERMEDIATE HOST WHEREAS ANIMALS CAN BE
BOTH INTERMEDIATE HOSTS AND DEFINITIVE HOST.
 THE TWO MAIN TYPE HYDATID DIDEASE CAUSED BY ECHINOCOCCUS
GRANULOSUS AND ECHINOCOCCUS MULTICULARIS. COMMONLY SEEN IN SOUTH
AMERICA,MIDDLE EAST AUSTRALIA.
 IN HUMANS 50-70 % CYSTS OCCUR IN LIVER, 25% IN LUNGS, 5-10% IN ARTERIAL
SYSTEM.
MORPHOLOGY
 2-8 mm LONG
 COMPRISES – SCOLEX, NECK,IMMATURE PROGLOTTID, MATURE PROGLOTTID,
GRAVID PROGLOTTID.
HYDATID CYST STRUCTURE
CLINICAL FEATURES
 MOSTLY ASYMPTOMATIC
 ABDOMINAL PAIN,VOMITTING,DYSPEPSIA
 JAUNDICE
 ANAPHYALATIC REACTION
 PULMONARY HYDATID CYST
TREATMENT
 PUNTURE,ASPIRATION,INJECTION,REASPIRATION
 SURGICAL MANAGEMENT
 ENDOSCOPY
 DRUG OF CHOICE – PRAXIQUANTEL,ALBENDAZOLE
SUMMARY
 MALARIA CAUSED BY PLASMODIUM VIVAX, P.OVALE, P.MALARIAE, P.FALCIPARUM.
 LIFE CYCLE OF MALARIA.
 FILARIASIS CAUSED BY WUCHERERIA BANCROFTI.
 AMOEBIASIS CAUSED BY ENTAMOEBA HISTOLYTICA.
 KALA AZAR CAUSED BY L. TROPICA, L. BRAZILIENSIS, L. DONOVANI.
 CYSTICERCOSIS CAUSED BY TAENIA SOLINUM.
 HYDATID DISEASE CAUSED BY ECHINOCOCCUS GRANULOSUS.
LETS TEST YOUR KNOWLEDGE
1} HEPATOSPLENOMEGALY IS SEEN IN WHICH
INFECTIOUS DISEASE ?
2} TWO FORMS OF ENTAMOEBA HISTOLYTICA ?
3} WHICH INFECTIOUS DISEASE IS ASSOCIATED WITH
ELEPHATIASIS ?
4} WHAT IS MEANT BY KALA AZAR?
PARASITIC DISEASES-1.pptx

PARASITIC DISEASES-1.pptx

  • 1.
  • 2.
    TOPICS TO BECOVERED  INTRODUCTION  CLASSES OF PARASITE  MORPHOLOGICAL ADAPTATIONS  BASIC TERMINOLOGIES  MALARIA  FILARIASIS  AMOEBIASIS  KALA-AZAR  CYSTICERCOSIS  HYDATID CYST  SUMMARY  QUESTIONS
  • 3.
    INTRODUCTION  PARASITES ARELIVING ORGANISM WHICH DEPENDS ON HOST.  DISEASES CAUSED BY PARASITES {PROTOZOA,HELMINTHES} ARE QUITE COMMON AND COMPRISES A VERY LARGE GROUP OF INFECTIONS.  PARASITES MAY CAUSE DISEASES DUE TO:  THEIR PRESENCE IN THE LUMEN OF INTESTINE.  INFILTRATION INTO BLOOD STREAM.  PARASITISM MAY LEAD TO DISEASES, BUT NOT ALWAYS.  PARASITES MAY INFECT THE GASTROINTESTINAL TRACT OR CIRCULATORY SYSTEM AND INVADE DIFFERENT TISSUES AND ORGANS.  PARASITIC INFECTIONS MAY CAUSE MORTALITY OR MORBIDITY.
  • 4.
    BASIC TERMINOLOGIES  SYMBIOSIS: A CLOSE RELATIONSHIP BETWEEN TWO SPECIES IN WHICH BOTH GET BENEFITTED.  COMMENSALISM : RELATIONSHIP BETWEEN TWO SPECIES IN WHICH ONE IS BENEFITTED AND OTHER IS NEITHER BENEFITTED NOR HARMED.  PARASITISM : RELATIONSHIP IN WHICH ONE IS BENEFITTED AND OTHER ONE HARMED. MODES OF ENTRY  INGESTION  ARTHROPODS BITES  PENETRATION THROUGH INTACT SKIN OR MUCOUS MEMBRANE.
  • 5.
    CLASSES OF PARASITES ENDOPARASITE : CAUSES INFECTION INSIDE THE BODY.  EXAMPLE –HOOK WORM ,ROUND WORM.  ECTOPARASITE : CAUSES INFECTION SUPERFICIALLY ON SKIN.  EXAMPLE - LICE ,TICKS ,MITES.  TEMPORARY PARASITE : VISIT HOST FOR SHORT PERIOD.  EXAMPLE - MOSQUITOES ,BUGS,MITES.  PERMANENT PARASITE : REMAIN PARASITIC THROUGHOUT THEIR LIFE.  EXAMPLE - TRYPANOSOMES, WUCHERERIA.  OBLIGATE PARASITE : CAN NOT LIVE WITHOUT ITS HOST  EXAMPLE - PLASMODIUM.  FACULATATIVE PARASITE : LIVES PARASITIC LIFE WHEN OPPORTUNITY IS AVAILABLE  EXAMPLE – NAEGLERIA FOWLERI  PSEUDOPARASITISM : FREE LIVING LARVAE ACCIDENTALLY ENTERS BODY AND SURVIVE.  EXAMPLE – LARVAE OF HOUSEFLY.
  • 6.
    TYPES OF HOSTS DEFINITIVE HOST : PARASITES WHICH CAN REPRODUCE BY SEXUAL REPRODUCTION.  INTERMEDIATE HOST: PARASITES PRESENT IN LARVAL STAGE AS WELL AS SEXUAL REPRODUCTION STAGE.  PARATENIC HOST :PARASITES PRESENT IN LARVAL STAGE BUT IT DOESN’T DEVELOP.
  • 7.
    MORPHOLOGICAL ADAPTATION –WHEN THE PARASITES REACHES THEIR INHABITAT THEY SLOWLY CHANGE THEIR MORPHOLOGY FOR SURVIVAL PURPOSE.  ECTOPARASITES : LATERALLY COMPRESSED – ESCAPE THROUGH HAIRS, DORSOVENTRALLY FLATTENED – EASILY CLINGS ON THE HOST , PRESENCE OF SUCKERS TO ATTACH THEMSELVES WITH HOST.  ENDOPARASITE : ROUNDED WITH CUTICULAR SPECIALISATION- TO MACERATE THE TISSUE, THIN FILIFORM SHAPE – PENETRATE EASILY INTO MUCOSA, RIBBON LIKE STRUCTURE .
  • 8.
    DISEASES CAUSITIVE AGENTS MALARIAPLASMODIUM VIVAX, PLASMODIUM OVALE, PLASMODIUM FALCIPARUM, PLASMODIUM MALARIAE. FILARIASIS WUCHERERIA BANCROFTI AMOEBIASIS ENTAMOEBA HISTOLYTICA KALA-AZAR [LEISHMANIASIS] LEISHMANIA TROPICA, LEISHMANIA BRAZILIENSIS ,LEISHMANIA DONOVANI. CYSTICERCOSIS TAENIA SOLINUM HYDATID DISEASE [ECHINOCOCCOSIS] ECHINOCOCCUS GRANULOSUS
  • 9.
    MALARIA MAL – BADARIA - AIR  MALARIA IS A PROTOZOAL DISEASE CAUSED BY ANY ONE OR COMBINATION OF FOUR SPECIES: PLASMODIUM VIVAX,PLASMODIUM FALCIPARUM,PLASMODIUM OVALE,PLASMODIUM MALARIAE.  WHILE PLASMODIUM FALCIPARUM CAUSES MALIGNANT MALARIA,OTHER 3 PRODUCE BENIGN ILLNESS.  THESE PARASITES ARE TRANSMITTED BY BITE OF FEMALE ANOPHELES MOSQUITO.  THE DISEASE IS ENDEMIC IN SEVERAL PARTS OF TROPICAL AFRICA,PARTS OF SOUTH AND CENTRAL AMERICA,INDIA AND SOUTH-EAST ASIA.
  • 10.
  • 11.
    LIFE CYCLE OFMALARIAL PARASITE This Photo by Unknown Author is licensed under CC BY
  • 12.
    INCUBATION PERIOD STAGES OFMALARIA  COLD STAGE – CHILLS FOR 15 MINS – 1 HOUR CAUSED DUE TO RUPTURE FROM HOST CELL  HOT STAGE – FEVER MAY REACH UPTO 40 DEGREES, STARTS INVADING NEW CELLS  SWEATING STAGE-PATIENT STARTS SWEATING , ASYNCHRONOUS PAROXYSMS. SPECIES INCUBATION PERIOD P. FALCIPARUM 7- 14 DAYS P. VIVAX 12- 17 DAYS P. OVALE 9- 18 DAYS P. MALARIAE 13- 14 DAYS
  • 13.
    MORPHOLOGICAL FEATURES  PARASITISATIONAND DESTRUCTION OF ERYTHROCYTES ARE RESPONSIBLE FOR MAJOR PATHOLOGICAL CHANGES  MALARIAL PIGMENT LIBERATED BY DETROYED RBC ACCUMULATES IN PHAGOCYTIC CELLS OF RETICULOENDOTHELIAL SYSTEM RESULTING IN ENLARGEMENT OF SPLEEN AND LIVER {HEPATOSPLENOMEGALY}.  IN FALCIPARUM MALARIA,THERE IS MASSIVE ABSORPTION OF HAEMOGLOBIN BY RENAL TUBULES PRODUCING BLACKWATER FEVER {HAEMOGLOBINURIA NEPHROSIS}  CEREBRAL MALARIA IS CHARCTERISED BY CONGESTION AND PETECHIAE ON WHITE MATTER.  PARASITIZED ERYTHROCYTES IN FALCIPARUM MALARIA ARE STICKY AND GET ATTACHED TO ENDOTHELIAL CELLS RESULTING IN OBSTRUCTION OF CAPILLARIES OF DEEP ORGANS SUCH AS OF BRAIN LEADING TO HYPOXIA AND DEATH
  • 15.
    DIAGNOSIS OF MALARIADONE BY DEMONSTRATION OF MALARIAL PARASITE IN THIN OR THICK BLOOD FILMS OR HISTOLOGICAL SECTIONS. STAIN USED : GIEMSA STAIN
  • 16.
    MAJOR COMPLICATIONS  CEREBRALMALARIA [COMA]  RENAL IMPAIRMENT  HYPOGLYCEMIA  SEVERE ANEMIA  HAEMOGLOBINURIA  JAUNDICE  PULMONARY OEDEMA  ACIDOSIS FOLLOWED BY CONGESTIVE HEART FAILURE AND HYPOTENSIVE SHOCK.
  • 17.
    TREATMENT  TREATMENT OFCHOICE FOR UNCOMPLICATED MALARIA IS COMBINATION OF TWO OR MORE ANTIMALARIAL DRUG WITH DIFFERENT MECHANISM OF ACTION.  DRUG OF CHOICE IN MALARIA :  CINCHONA ALKALOIDS : QUININE AND QUINIDINE.  4 AMINOQUINOLINES  ANTIFOLATES  ANTIBIOTICS : TETRACYCLINE, DOXYCYCLINE
  • 18.
    FILARIASIS  WUCHERERIA BANCROFTIAND BRUGIA MALAYI ARE RESPOSIBLE FOR CAUSING FILARIASIS.  TRANSMITTED BY VECTORS LIKE MOSQUITO,CULEX.  THE LYMPHATIC VESSELS INHABIT THE ADULTWORM,ESPECIALLY IN LYMPH NODES,TESTIS,EPIDIDYMIS.  MICROFILARIAE SEEN IN CIRCULATION ARE PRODUCED BY FEMALE WORM
  • 19.
    MORPHOLOGY  ADULT WOMRSARE LONG HAIR LIKE TRANSPARENT NEMATODES, FILIFORM IN SHAPE WITH TAPPERING ENDS.  MALE MEASURES 2.5– 4CM, FEMALE MEASURES 8-10CM  TAIL END OF MALE IS CURVED VENTRALLY WHILE FEMALE IS NARROW AND POINTED.
  • 20.
    LIFE CYCLE OFFILARIASIS
  • 21.
    MORPHOLOGICAL FEATURES  THEMOST SIGNIFICANT HISTOLOGIC CHANGES ARE DUE TO PRESENCE OF ADULT WORMS IN LYMPHATIC VESSELS CAUSING LYMPHATIC OBSTRUCTION AND LYMPHOEDEMA.REGIONAL LYMPH NODES ARE ENLARGED AND THEIR SINUSES ARE DISTENDED WITH LYMPH.  THE SURROUNDING TISSUE OF BLOCKED LYMPHATICS ARE INFILTERED BY INFLAMATORY CELLS.  CHRONICITY OF PROCESS CAUSES ENORMOUS THICKENING AND INDURATION OF SKIN OF LEGS AND SCROTUM RESEMBLING A ELEPHANT HENCE NAMED ELEPHATIASIS.  CHYLOUS ASCITES AND CHYLURIA MAY OCCUR DUE TO RUPTURE OF ABDOMINAL LYMPHATICS.
  • 22.
     MAJORITY OFINFECTED PATIENTS REMAIN ASYMPTOMATIC.  SYMPTOMATIC CASES MAY HAVE TWO FORMS:  ACUTE FORM: PRESENTS WITH FEVER , LYMPHANGITIS ,LYMPHADENITIS,EOSINOPHILIA, MICROFILARIAEMIA.  CHRONIC FORM :LYMPHADENOPATHY,LYMPHOEDEMA AND ELEPHANTIASIS.
  • 23.
    DIAGNOSIS  ANTIGEN DETECTION:CIRCULATING FILARIAL ANTIGEN,LYMPH NODE BIOPSY TREATMENT  DRUG OF CHOICE – IVERMECTIN,ALBENDAZOLE.  TREATMENT FOR ELEPHATIASIS :  SKIN TREATMENT – ANTIBACTERIAL CREAM.  ELEVATE AND EXERCISE AFFECTED BODY PART.  CDP { COMPLEX DECONGESTIVE PHYSIOTHERAPY} – LYMPH DRAINAGE,MASSAGE, COMPRESSIVE BANDAGES.
  • 24.
    AMBOEBIASIS  CAUSED BYENTAMOEBA HISTOLYTICA NAMED FOR ITS LYTIC ACTION ON TISSUE.  MORE COMMON IN TROPICAL AND SUBTROPICAL REGION WITH POOR SANITATION.  TWO FORMS OF PARASITE:  TROPHOZOITE FORM : ACTIVE ADULT FORM SEEN IN TISSUES AND DIARRHOEAL STOOLS.  CYSTIC FORM : SEEN IN STOOLS BUT NOT IN TISSUES.
  • 26.
    MORPHOLOGICAL FEATURES  THELESIONS OF AMOEBIASIS INCLUDE AMOEBIC COLITIS,AMOEBOMA,AMOEBIC LIVER ABSCESS AND SPREAD OF LESIONS TO OTHER SITES.  AMOEBIC COLITIS,THE MOST COMMON TYPE OF AMOEBIC INFECTION BEGINS AS A SMALL AREA OF NECROSIS OF MUCOSA WHICH MAY ULCERATE.THESE ULCERATIVE LESIONS MAY ENLARGE.  AMOEBOMA IS AN INFLAMMATORY THICKENING OF WALL OF LARGE BOWEL RESEMBLING CARCINOMA OF COLON.
  • 27.
     AMOEBIC LIVERABCESS FORMED BY INVASION OF RADICLE OF PORTAL VEIN BY TROPHOZOITES.  OTHER SITES:  PERITONITIS :PERFORATION OF AMOEBIC ULCER OF COLON,EXTENSION TO LUNGS AND PLEURA BY RUPTURE OF AMBOEBIC LIVER ABSCESS,HEMATOGENOUS SPREAD TO CAUSE AMOEBIC CARDITIS AND CEREBRAL LESIONS,CUTANEOUS AMEOBIASIS VIA SPREAD OF RECTAL AMOEBIASIS OR FROM ANAL INTERCOURSE.
  • 28.
    DIAGNOSIS  TROPHOZOITE FORMCAN BE STAINED POSITIVELY WITH PAS [PERIODIC ACID SCHIFF] STAIN IN TISSUES WHILE AMOEBIC CYSTS HAVING 4 NUCLEI CAN BE IDENTIFIED IN STOOLS.  CYSTS ARE INFECTIVE STAGE FOUND IN CONTAMINATED WATER OR FOOD.  TROPHOZOITES ARE FORMED FROM THE CYST STAGE IN THE INTESTINE AND COLONIZE CAECUM .  TRPHOZOITES AS WELL AS CYSTS ARE PASSED IN STOOLS BUT THE TROPHOZOITES FAIL TO SURVIVE OUTSIDE OR DESTROYED BY GASTRIC SECRETIONS.
  • 29.
    KALA-AZAR {LEISHMANIASIS} KALA –BLACK AZAR - FEVER  TRANSMITTED BY SAND FLY BITES.  ENDEMIC IN PARTS OF TROPICS AND SUBTROPICS.  WILD AND DOMESTIC DOGS AND SMALL RODENTS ARE COMMON HOSTS. RESPONSIBLE FOR VARIOUS SYNDROME :  VISCERAL LEISHMANIASIS [ KALA AZAR ]  CUTANEOUS LEISHMANIASIS  MUCO CUTANEOUS LEISHMANIASIS  ANTHROPONOTIC CUTANEOUS LEISHMANIASIS  ZOONOTIC CUTANEOUS LEISHMANIASIS  POST KALA AZAR DERMAL LEISHMANIASIS
  • 30.
  • 31.
    CLINICAL FEATURES  CHARATERIZEDBY DARKENING OF SKIN [HENCE NAMED BLACK SICKNESS]  IRREGULAR BOUTS OF FEVER,WEIGHT LOSS,ENLARGEMENT OF SPLEEN AND LIVER AND ANAEMIA.  LYMPHADENOPATHY MAY ALSO OCCUR  POST KALA AZAR DERMAL LEISHMANIASIS – RASHES ON SKIN.  CUTANEOUS LEISHMANIASIS CAUSES SKIN LEISONS, MAINLY ULCERS,LIFE LONG SCARS.  MUSCULOCUTANEOUS LEISHMANIASIS LEADS TO PARTIAL OR TOTAL DESTRUCTION OF MUCOUS MEMBRANE OF NOSE ,MOUTH,THROAT.
  • 32.
    DIAGNOSIS  SEROLOGICAL TEST LEISHMANIN TEST  HAEMATOLOGICAL FINDINGS TREATMENT  DRUG OF CHOICE  AMPHOTERICIN  MILTEFOSINE  PENTAMIDINE ISETHIONATE  CONTROL SAND FLIES  PROPHYLAXIS
  • 33.
    CYSTICERCOSIS  INFECTION BYLARVAL STAGE OF TAENIA SOLIUM,PORK TAPE WORM.  ADULT TAPE WORM RESIDES IN HUMAN INTESTINES. THE EGGS ARE PASSED IN HUMAN FAECES WHICH ARE INJESTED BY PIGS OR THEY INFECT VEGETABLES.  DISEASE SPREAD THROUGH ORAL ROUTE THROUGH CONTAMINATED FOOD.  THESE EGG THEN DEVELOP INTO LARVAL STAGE IN HOST,SPREAD BY BLOOD TO ANY SITE IN THE BODY AND FORM CYSTIC LARVAE TERMED CYSTICERCUS CELLULOSAE.  HUMAN BEINGS MAY ACQUIRE INFECTION BY LARVAL STAGE BY EATING UNDERCOOKED PORK ,BY INJESTING UNCOOKED CONTAMINATED VEGETABLES.
  • 34.
    MORPHOLOGICAL FEATURES  THECYSTS OCCUR ANYWHERE IN THE BODY AND ACCORDINGLY PRODUCE SYMPTOMS.  MOST COMMON SITES ARE BRAIN,SKELETAL MUSCLES AND SKIN.  CYSTICERCUS CONSISTS OF ROUND TO OVAL WHITE CYST,CONTAINS MILKY FLUID.  THE CYSTICERCUS MAY REMIAN VIABLE FOR LONG TIME AND INCITE NO INFLAMMATION. BUT WHEN EMBRYO DIES IT PRODUCES GRANULOMATOUS REACTION WITH EOSINOPHILS,LATER LESION MAY BECOME SCARRED AND CALCIFIED.
  • 35.
    DIAGNOSIS  BIOPSY  X–RAY  COMPOUND TOMOGRAPHY  MAGNETC RESONANCE IMAGING  SEROLOGICAL TEST TREATMENT  EXCISION IS BEST METHOD  DRUG OF CHOICE – ALBENDAZOLE,PRAZIQUANTEL  SURGICAL MANAGEMENT
  • 36.
    HYDATID CYST  ZOONOTICDISEASE CAUSED BY ECHINOCOCCUS GRANULOSUS,ECHINOCOCCUS MULTILOCULARIS  HUMANS ARE ACCIDENTAL INTERMEDIATE HOST WHEREAS ANIMALS CAN BE BOTH INTERMEDIATE HOSTS AND DEFINITIVE HOST.  THE TWO MAIN TYPE HYDATID DIDEASE CAUSED BY ECHINOCOCCUS GRANULOSUS AND ECHINOCOCCUS MULTICULARIS. COMMONLY SEEN IN SOUTH AMERICA,MIDDLE EAST AUSTRALIA.  IN HUMANS 50-70 % CYSTS OCCUR IN LIVER, 25% IN LUNGS, 5-10% IN ARTERIAL SYSTEM.
  • 37.
    MORPHOLOGY  2-8 mmLONG  COMPRISES – SCOLEX, NECK,IMMATURE PROGLOTTID, MATURE PROGLOTTID, GRAVID PROGLOTTID. HYDATID CYST STRUCTURE
  • 39.
    CLINICAL FEATURES  MOSTLYASYMPTOMATIC  ABDOMINAL PAIN,VOMITTING,DYSPEPSIA  JAUNDICE  ANAPHYALATIC REACTION  PULMONARY HYDATID CYST TREATMENT  PUNTURE,ASPIRATION,INJECTION,REASPIRATION  SURGICAL MANAGEMENT  ENDOSCOPY  DRUG OF CHOICE – PRAXIQUANTEL,ALBENDAZOLE
  • 40.
    SUMMARY  MALARIA CAUSEDBY PLASMODIUM VIVAX, P.OVALE, P.MALARIAE, P.FALCIPARUM.  LIFE CYCLE OF MALARIA.  FILARIASIS CAUSED BY WUCHERERIA BANCROFTI.  AMOEBIASIS CAUSED BY ENTAMOEBA HISTOLYTICA.  KALA AZAR CAUSED BY L. TROPICA, L. BRAZILIENSIS, L. DONOVANI.  CYSTICERCOSIS CAUSED BY TAENIA SOLINUM.  HYDATID DISEASE CAUSED BY ECHINOCOCCUS GRANULOSUS.
  • 41.
    LETS TEST YOURKNOWLEDGE 1} HEPATOSPLENOMEGALY IS SEEN IN WHICH INFECTIOUS DISEASE ? 2} TWO FORMS OF ENTAMOEBA HISTOLYTICA ? 3} WHICH INFECTIOUS DISEASE IS ASSOCIATED WITH ELEPHATIASIS ? 4} WHAT IS MEANT BY KALA AZAR?