Presentation Transcript

1. Parasitology Dr Hussien Bamashmous



2. PROTOZOA METAZOA



3. PROTOZOA Protos : first Zoon : animal Phylum of animal kingdom which includes simplest animals most are unicellular some are colonial REPROPDUCTION: usually asexual by fission some sexual reproduction



4. EXAMPLES OF PROTOZOAL DISEASE: Malaria Amebiasis Giardiasis Trichomoniasis Toxoplasmosis Visceral leishmaniasis Pneumocystis carinii



5. METAZOA META: after / beyond ZOON: animal DIVISION OF THE ANIMAL KINGDOM THAT INCLUDES ALL �MULTICELLULAR FORM� They are either NEMATODES or CESTODES



6. 1- NEMATODES NEMA: thread EIDOS: form Nematohelminthes are either : round, cylindrical, spindle shaped. Examples: ENTEROBIASIS = OXYURIASIS ( pin worm) ASCARASIS = round worm ANCYLOSTOMIASIS = hook worm TRICHINOSIS TRICHURIASIS = whip worm



7. 2- CESTODES KESTOS : GIRDLE Subclass of Cestoidae ? phylum = �PLATYHELMINTHES� EXAMPLES: TAENIASIS: tapeworms = scolex + segments (proglottidis) VISCERAL LAVAR MIGRANS FILARIASIS BILHARSIASIS (schistosomiasis)



8. MALARIAmal - aria



9. MALARIA ESSENTIALS OF DIAGNOSIS: Residence in or travel to an endemic area High fever, chills, headache Jaundice, vomiting, diarrhea Anemia, splenomegally Seizures, coma Malaria parasite in the blood smear



10. GENERAL CONSIDERATIONS: Malaria kills 1,000,000 children/ year Resurgence is observed now Female Anopheline mosquito transmits the parasite: Plasmodium Vivax (most common) P. Falciparum (most virulent) P. Ovale (similar to Vivax) P. Malariae



13. LIFE CYCLE: INFECTED HUMAN BLOOD (GAMETOCYTES) Sucked by Anopheline mosquito In its stomach wall OOKINTE ? OOCYST ? MATURE OOCYST ? rupture ? SPORPZOITE ? to its salivary glands ? bite uninfected person In the uninfected person Sporozoites disappear within 1/2 hour from the circulation and infect the hepatocytes



14. HEPATIC PHASE: ( PRE-ERYTHROCYTIC PHASE) about 2 weeks for all 3-5 weeks for P. Malarie Hypnozoites ? ONLY FOR P.VIVAX AND OVALE which is responsible for future relapses. Merozoites leave the liver thereafter to infect the RED BLOOD CELLS ERYTHROCYTIC CYCLE



15. ERYTHROCYTIC CYCLE (ASXETUAL CYCLE) ERYTHROCYTE HAEMOLYSIS METROZOITES ? TROPHOZOITES ?SCHIZONTS ? METROZOITES (which will be released by heamolysis) SYMPTOMS IMMATURE GAMETOCYTES MATURE GAMETOCYTS (male & female) Sucked by mosquito REPEAT THE CYCLE



17. P. VIVAX ? affects young red cells ? ruptures ? symptoms X 48 hours P. MALARIAE ? old red cells ? symptoms X 72 hours P. FALCIPARUM ? all cells ? NO CLASSICAL TRIAD OF SYMPTOMS SURVIVAL (especially in endemic area) ? immunity ? intensity of the cycles



18. NO HEPATIC PHASE (pre- erythrocytic phase) with: Blood transfusion Needle stick Congenital malaria Susceptibility varies genetically Partial resistance to infection with : Hemoglobin S Hemoglobin F Thalassemia G6PD deficiency Maternal immunity protects the neonate despite placental infection Clinical findings varies according to : strain host immunity



19. PRESENTATION: CLASSICAL TRIAD WITH P. VIVAX & P. OVALE COLD STAGE AFTER � HOUR ? HOT STAGE AFTER 1-6 HOURS ? SWEATING



20. OTHER SYMPTOMS AND SIGNS: Pallor and irritability Poor feeding Vomiting and diarrhea Jaundice Splenomegally Hepatomegally OLDER CHILDREN: Headache and backache Myalgia Fatigue



21. IF UNTREATED RELAPSES STOPPED: Within a year with P. Falciparum Within several years with P. Vivax May occur decades later with P. Malariae INFECTION DURING PREGNANCY: Intrauterine growth retardation Preterm Congenital malaria



22. LABORATORY FINDINGS: Multiple thick smears ? Giemsa stain Thin smear ? Wright stain In P. falciparum ? only ring form of Trophozoited & Gametocytes are seen in peripheral smear. GAMETOCYTES MAY PERSIST FOR DAYS FOLLOWING ADEQUATE THERAPY



23. Complete Blood Count: Normocytic normochromic anemia Leucopenia, leucoytosis Normal or low platelet count High retics LFT: indirect and direct hyperbilirubinaemia mild transaminase elevation hypergammaglobinaemia Occasionally: low complement positive rheumatoid factor positive ANA false positive VDRL



24. Differential diagnosis: TUBERCLUSIS BRUCELLOSIS BORRELOSIS SQUENTIAL COMMON INFECTIONS HODGKEN�S DISEASE JUVENILE RHEUMATOID ARTHERITIS RAT BITE FEVER CAT-SCRATCH FEVER IDIOPATHIC PERIODIC FEVER TYPHOID FEVER MYCOPLASA PNEUMONIA



25. COMPLICATIONS AND SEQUALAE: CHRONIC MALARIA SPECIALLY P. FALCIPARUM Anemia Deblitation Massive Splenomegaly (tropical splenomegally syndrome) MICROTHROMBOSIS AND ISCHAMIA Intestinal Tract ? bleeding and diarrhea Lung ? pneumonitis Brain ?diffuse edema, seizures, encephalopathy INTRAVASCULAR HAEMOLYSIS hemoglobinuria ? renal failure ( black water fever) CHRONIC P. MALARIAE nephrotic syndrome



26. PREVENTION SPOROZOITES ? resistant to drugs CASUAL PROPHYLAXIS = drugs which act on hepatic phase SUPPRESSION = drugs which act on erythrocytic phase CHLOROQUINE = safe in pregnancy CHLOROQUINE RESISTENCE ALL OVER EXCEPT: Central America Haiti Panama Egypt Most of the middle east



27. IN RESISTENT-FREE AREA: Cholorquine 5 m/kg of base max. 300 mg once/week. ONE WEEK BEFORE TRAVEL & FOUR WEEKS AFTER RETURN IN CHLOROQUINE RESISTENT AREA: Mefloquine (not if wt. is less than 15 kg) Maloprim = pyrimethamine + Dapsone Fansidar = pyrimethamine + Sulfdoxane FOR P.VIVAX & P. OVALE 2 week course of primaquine phosphate SCREEN FOR G6PD BEFORE PRIMAQUINE INSECT REPELLENTS & MOSQUITO NETTING (night)



28. TREATMENT: New drugs has been discovered in the treatment of Malaria . They are called the (ARTEMESSININS). They are derived from a Chinese plant. Introduced in the market since 1996. They act as internal bomb inside the Malaria parasite using its own hydrogen peroxide. The best treatment is called ACT. ACT : is combination of ARTEMESSININS and CHLOROQUINE. Unfortunately in the markets now in many countries there are mal-manufactured drugs with poor effectiveness and possibly emerging resistance.



29. Cont. TREATMENT: CHLOROQUINE PHOSPHATE Drug of choice for : Nonresistant P.Falciparum Most infections by other species Course of �3 days� ERADICATES THE ERYTHROCYTIC PHASE Give orally: 10m/kg (max 600mg) as initial dose 5 mg/kg 6 hours, 24 hrs & 48 hrs later MEFLOQUINE effective but has neuropsychiatric side effects QUINIDINE GLUCONATE (parental) 10-14 mcg/kg as a loading dose then 0.02 mg/kg/min



30. CHLOROQUINE RESISTENCE MALARIA: (P.O.) QUININE SULPHATE x 3 days + PYRIMETHAMINE x 3 days + SULPHADIAZINE x 3 days QUININE SULFATE x 3 days + TETRACYCLINE x 7 days (Parentral) QUININE DIHYDROCHLORIDE QUININE GLUCONATE



31. GENERAL MEASURES: Hydration and fever control Blood and needle precautions Hospitalization with: persistent vomiting severely ill Non-immune to P. Falciparum Iron and folate level Hepatitis and HIV screening (especially for drug users)



32. FOR CELEBRAL MALARIA: Rule out other causes Anticonvulsants Parental antimalarial Control of cerebral edema Disferoxamine Steroids = Contraindicated ( except with intravascular hemolysis)



33. Giardiasis



34. Essentials of diagnosis Chronic relapsing diarrhea Flatulence, bloating, anorexia, poor wt. gain Absence of fever and blood in stool Presence of �TROPHOZOITES� in diarrhe or stool Cysts in formed stools



35. GENERAL CONSIDERATIONS: In many areas = most common protozoan in children Caused by �GIARDIA INTESTINALS�� Water Drinking (contaminated water) in endemic areas Food-borne outbreaks do occur Incidence in � DAYCARE NURSERIES� up to 50% Incidence in mental instituations The parasite resides in the duodenum and jujenum ? Inflamation & subtotal villous atrophy



37. Clinical findings Cyst ingestion trophozoites live non-invasively in the small intestine Symptoms develop in 1-3 weeks Diarrhea (soft) Steatorrhea = mucus but no RBC / WBC Abdominal cramps anorexia, vomiting ? wt. lost The illness may last days to months or my relapse



38. Laboratory findings CBC= normal (no eosinophils) Fresh stool = +ve trophozoites Formed stool = oval cysts Duodenal aspirate & biopsy String test (Enterotest) Giardia antigen in stool



39. Differential diagnosis Toddler�s diarrhea TB enteritis Chronic amoebiasis Other causes of steatorrhea.



40. Treatment Treat symptomatic day care center cases & their contacts Drugs Furazolidine: 2mg/kg X 6h X 7-10 days Metronidazole: 5m/kg X 8h X 5-10 days Quinacrine HCL: 2mg/kg X 8h X 5-10 days



41. Leshmaniasis



42. General consideration Caused by protozoan of the genus �leishmania� Conveyed by female sand fly in which flagellate (proamistigote) develop In man ? in monocytes and macrophages ? amastigotes (leishmann-donovan bodies)



43. Visceral leishmaniasis (kala azar) In India ? man is the main host In Mediterranean ? dogs and foxes are main reservoirs Transmission by: sandflies blood transfusion Multiplication by simple fission in monocytes & macrophages in various organs ? huge hepatosplenomegally and lymphadenopathy Lishmania ? Malnutrition and Immune Suppression ? Intercurrent infections Tuberculosis



44. Clinical presentation Incubation period = 1-2 months up to 10 years Insidious onset of fever Temperature is either remittent or intermittent Hepatosplenomegally Lymphadenopathy If untreated ? severe anemia and wasting Facial hyperpigmentation After therapy: Dermal leshmaniasis, Hypopigmentaed macules, Erythematous macules, Nodular eruption



45. Diagnosis Pancytopenia: bone marrow suppression + hypersplenism Immunoglobulin (esp IgG) & albumin Aspirated and cultures from Bone marrow, liver & spleen, lymph nodes +ve Serology : immunoflourescene C.F.T Leishmania skin test ? negative using killed proamstigotes



46. Differential diagnosis Infective endocarditis Typhoid fever Brucellosis and tuberculosis Lymphomas Bilharizaisis Malaria



47. Treatment Asia (India) ? good recovery Sudan & east Africa ? more resistant Drugs used sodium stibogluconate pentavalent antimony compound IM or IV for 10 days, could be repeated after 10 days if needed days In resistant cases use: Pentamidine Isethionate 2 hydroxy Stilbamidine Amphotericin B



48. Prevention: In endemic areas ? destroy stray dogs and foxes Sandflies should be combated by insecticides & repellents No vaccine available



49. Leishmania of old world = LESHMANIA TROPICA (ORIENTAL SORE) Geographical region Asia, India, North Africa, Arabia Vector: sandfly, transmits the parasite from animal to man (ZOONOSIS) symptoms and signs incubation period 2-5 weeks up to years papule at the bite site (usually the face and limbs) ulceration of the papule ? scarring Other types of leishmaniasis



50. Diagnosis Dry needle aspirate or skin slit smear ? +ve for the organism Positive skin test Positive serology Therapy antimony compound reduces the scarring Resistant cases: pentamidine + amphotericin There is a vaccine for L.Tropica



51. Leishmania of the new world Leishmania Brazilliensis ? Espundia Leishmania Mexicana ? Chicleroulcer Leishmania peruviana ? Uta Geographical distribution: south america Vector: sandfly



52. Symptoms and signs: Painful mucocutaneous ulcers or granulomas Nasolabial lesions (common) Lips, palate ? terrible suffering and disfigurment Diagnosis: skin biopsy +ve skin test serology Therapy Antimony compound Establishing espundia ? Amphotericin



53. Brucellosis



54. IT IS A ZOONOTIC DISEASE CAUSED BY SPECIES BRUCELLA: Brucella Melitensis = goats and sheep Brucella Abortus = cattle Brucella Suis = swine Brucella Canis = dogs Routes of infection in pediatrics: Direct contact Inhalation of aerosols Ingestion of raw milk or milk products from infected animals Incidence could be decreased by: Control of the disease in domestic animals Pasteurization of milk



55. Presentation in Children: 50% acute disease Other 50% subacute disease Eitiology: Brucella named for SIR DAVID BRUCE who first isolated the organism in 1887 Epidemiology In industrialized countries ? occupational hazard In USA ? pediatric cases about 10% In Arabia ? more



56. Endemic brucellosis caused by ingestion or raw milk, cream, butter, cheese or ice cream Organism my directly invade: Eye, nasopharynx and genital tract Brucella can survive up to 3 weeks in refregerated garcass Endemic disease is maintained �In Animals� through excretion of large numbers of the organisms: in genital secretions and milk with vertical and horizontal transmission Brucella causes ? abortion in Animals



57. Human to human transmission is Rare but may be caused by: Blood transmission Bone marrow transplantation Transplacental Perinatal exposure



58. Pathology and pathogenesis BRUCELLAE ? facultative intradellular parasite Capable of surviving and multiplying within phagocytes, red blood cells and many cell lines Nonspecific host factors triggered Agglutinins Polymorphs Complements ? Opsonization & phagocytosis But Intracellular Killing Is Less Effective multiplications of the organism ? induction of immunity



59. Host responds by forming: Specific antibodies IgM appears within 1 week and comes down by 3 months IgG appears by 2-3 weeks and persists if untreated or partially treated Others like: agglutinins opsonins precepitins C.F. antibodies



60. Brucella Variants are: S. varient (smooth): more virulent resist intraleukocyte killing R. Varient (hard) : less resistant All species of brucella produce Granuloma in the liver, spleen, l.nodes, bone marrow Granulomoatous inflammation of gall bladder Interstitial orchitis Endocarditis with vegetation Granuloma in myocardium Involvement of : brain (neruobrucellosis), skin, bone



61. Clinical manifestations: Non specific: Fever, Arthralgia and arthritis, Malaise, Weakness, Neurobrucellosis ? Depression Incubation period: Few Days to Months The interval between onset of the Symptoms and Diagnosis =150 days (mean of 4 weeks Hepatosplenomegaly 30-40%



62. Uncommon manifestations Osteomeyelitis (non-suppurative) Myocarditis Endocarditis Genitourinary Neonatal brucellosis



63. Diagnosis: History Examination Investigations CBC = hemolysis, pancytopenia (hypersplenism) Bone marrow = involvement with haemophagocytosis reported Acute disease before treatment: Blood cultures = +ve up to 50% Bone marrow cultures= +ve up to 90% Serology (IgM & IgG) - high titred serum = prozone - Inhibition ? dilute with sera



64. Successful treatment Rapid decline of IgM IgG titer may persist for months or years High IgG titer ? persistent infection of relapse More sensitive test = enzyme immuno assay Tissue biopsy (liver)



65. Differential diagnosis: Acute brucllosis Influenza Typhoid fever Infectious mononucleosis Tuberculosis Tularaemia Persistent brucellosis Malignant histocycosis Lymphomas Tuberculosis



66. Prevention: Immunization of domestic herds Pasteurization of milk Periodic assessment of animals (slaughtering infected ones) Hunters should use caution in handling potentially infected animals



67. Treatment: Treatment of choice is �TETRACYCLINE� in combination : Doxycyline (orally) 5 mg/kg/day max 200m/day in 2 divided doses +(Plus) Streptomycin (IM) 30 mg/kg/day divided every 12 hours OR Gentamicin (IV) 5 - 7.5 mg/kg/day divided every 8 hours8h



68. For Children: Trimethoprim � sulfamethoxazole (orally ) 10 - 12 mg/kg/day (Trimethoprim) +(Plus) Rifampacin 15 - 20 mg/kg/day ( Duration of treatment = 3 - 6 weeks )



69. Delay in Diagnosis: High antigen load after treatment JARISH - HERXHEIMER like reaction ? Treated with Steroids if needed



70. Prognosis: Untreated cases ? case fatality rate is 3% Most deaths are due to specific organ involvement (as Endocarditis) Following treatment ? excellent prognosis Delayed diagnosis ? prolonged course Complete recovery may take up to 6 months Re-infection is uncommon Immune individuals if invadertently injected with the cattle vaccine ? local and mild systemic disease