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Parasitology Review 2017

  1. 1. Parasitology Review 2017 MARGIE MORGAN
  2. 2. Clinical presentation Travel history or poor sanitation put you at the highest risk for parasitic infection Infections associated with sporadic symptoms Poor immune status higher risk Dysentery not common (amebiasis) Most usual symptoms: ◦Abdominal pain, cramping, long term nausea, and malaise, mucous in stool, and +/- fever
  3. 3. Laboratory Diagnosis Currently based on microscopic exam, and molecular panels for the most common (select) parasites ◦Stool (PCR applicable) ◦Non-stool ◦ Perianal specimen ◦ Sigmoidoscopic specimen ◦ Duodenal aspirates ◦ Liver abscess ◦ Sputum ◦ Urine ◦ Urogenital ◦Blood ◦Tissue Alternative methods: ◦Serology ◦Fluorescent stains
  4. 4. Two-vial collection kit for Stool 10% formalin Concentration with ethyl acetate to eliminate fecal debris Wet mount, DFA staining and NAAT Helminth eggs, larvae, microsporidia, and protozoan cysts PVA with fixative Polyvinyl alcohol Permanent stained smear ◦Trichrome stain Protozoan trophozoites and cysts Mercury based fixatives phased out for safety – Zinc fixatives are now used
  5. 5. Most Common Pathogens Protozoa ◦Intestinal & urogenital ◦ E histolytica, Blastocystis hominis, Giardia lamblia, Dientamoeba fragilis, Balantidium coli, Cryptosporidium sp., Cyclospora sp, Cyclospora, Cytoisospora(Isospora) belli, and Microsporidia ◦Blood & tissue ◦ Plasmodium, Babesia, Trypanosomes ◦ Toxoplasma gondii, Leishmania ◦ Naegleria, Acanthamoeba, Balamuthia Helminths ◦Nematodes ◦ Ascaris, Trichuris, hookworm, pinworm, and Strongyloides ◦Cestodes ◦ Taenia, Hymenolepis, Diphyllobothrium ◦Trematodes ◦ Fasciola, Fasciolopsis, Schistosoma, Paragonimus, Clonorchis
  6. 6. PROTOZOA Amebae (found in stool) ◦ Entamoeba coli ◦ Entamoeba histolytica ◦ Endolimax nana ◦ Iodamoeba butschlii ◦ Dientamoeba fragilis Flagellates (found in stool) ◦ Giardia lamblia ◦ Chilomastix mesnili Ciliates, Coccidia, Blastocystis ◦ Balantidium ◦ Cryptosporidium ◦ Cystoisospora (Isospora) belli ◦ Sarcocystis ◦ Cyclospora ◦ Microsporidium ◦ Blastocystis hominis Blood-Borne Protozoa ◦ Babesia ◦ Leishmania ◦ Trypanosoma brucei ◦ T. cruzi ◦ Plasmodium Other ◦ Toxoplasma ◦ Naegleria fowleri ◦ Acanthamoeba
  7. 7. Protozoa Found in Stool: Amebae pathogen
  8. 8. Intestinal amoeba Entamoeba coli Entamoeba histolytica/dispar Entamoeba hartmanni Endolimax nana Iodamoeba butschlii
  9. 9. Entamoeba histolytica/dispar E. histolytica is a pathogen and E. dispar is a nonpathogenic species that can also occur in the large intestine. Morphologically indistinguishable ◦Antigen testing or molecular methods to distinguish the two species E histolytica ◦Cysts = infectious form ◦Trophozoites = invasive form ◦Cysts found in contaminated water and poor sanitation ◦Colon biopsy shows “flask-shaped” ulcer with Trophs ◦Non-intestinal disease = extra-intestinal amebiasis (liver abscess) with Trophs ◦Serology can be useful
  10. 10. Entamoeba histolytica/dispar Cysts @10-12 um In diameter Up to 4 nuclei in the cyst Peripheral chromatin is evenClean chromatin Bulls-eye nucleoli
  11. 11. Entamoeba histolytica/dispar Trophozoites & Cysts Trophozoite with ingested rbcs Elongated chromatoid body
  12. 12. Amebic abscess Flask-shaped ulcer of intestinal amebiasis Amebic liver abscess Entamoeba histolytica Serology – high % positive in extra- intestinal cases
  13. 13. Entamoeba coli cyst and trophozoite Considered a commensal in the intestine Cyst @ 20 – 25µm Up to 8 nuclei Shed from host Lives in environment Trophozoite is the invasive form that invades the intestine Single nucleus with a large karyosome located eccentrically irregular chromatin ring. The cytoplasm appears dirty and vacuolated
  14. 14. Entamoeba coli – important to differentiate from the pathogen E. histolytica Trophozoites & Cysts Cysts usually 15-25µm, with 5 or more nuclei visible.
  15. 15. Endolimax nana trophozoite Cysts – 8-10 µm in size, one nucleus Mostly thought to be a non-pathogen, seen in stool specimens from HIV/AIDS patients, some literature suggesting it can cause intermittent or chronic diarrhea
  16. 16. Iodamoeba butschlii cysts, 10 – 12 µm in size with starch inclusion (glycogen mass) Iodine preparation – glycogen inclusion stains with iodine
  17. 17. Flagellates Giardia lamblia Dientamoeba fragilis Trichomonas vaginalis
  18. 18. Protozoa Found in Stool: Flagellates Pathogen
  19. 19. Giardia lamblia Contaminated water, undercooked foods Mild diarrhea to severe malabsorption Foul, watery diarrhea Day-care center outbreaks reported, traveler’s diarrhea Cysts/trophozoites may be seen in stool, but can be hard to find; Fluorescent stains and NAAT for more sensitive detection Duodenal aspirations can be used if stool specimens are negative TROPHOZOITE “falling leaf” motility CYSTS
  20. 20. Giardia lamblia trophozoite Waxing and waning symptoms Can be irregularly shed in stool material making antigen and molecular methods necessary for detection Russia & Mexico -Hot beds of infection Confined to intestine Flagyl (Metronidazole) is drug of choice
  21. 21. Giardia lamblia cysts Clearing between the cell wall and the cell membrane
  22. 22. Giardia lamblia cysts
  23. 23. Giardia lamblia only invades intestinal tissue
  24. 24. Chilomastix mesnili cyst Nonpathogen Mimics Giardia lamblia cyst – except for clear space at end of cyst Internal structure looks like “shepherd’s crook” or safety pin C. mesnili trophozoite
  25. 25. Dientamoeba fragilis Diarrhea, anal pruritus Only a trophozoite stage 5 – 15 µm (No cyst) Usually two nuclei visible in the trophozlite Can occur in Co-infection with Enterobius (pinworm)
  26. 26. Trichomonas vaginalis Urogenital protozoan Scant, watery vaginal discharge Four flagella, short undulating membrane
  27. 27. Protozoa Found in Stool: Ciliates, Coccidia, Blastocystis
  28. 28. Ciliates Balantidium coli ◦Mainly in swine ◦Contact with swine & poor hygiene ◦Only ciliate that’s pathogenic to humans ◦Similar disease as amebiasis, but extraintestinal invasion rare ◦Largest (50-200 um) trophozoite; surface covered with cilia; macronucleus ◦Cyst 40-60 um ◦Readily identified in fresh, wet mounts ◦Can cause flask shaped ulcer in intestine
  29. 29. Intestinal Sporozoa (coccidia) Isospora (Cystoisospora) Cryptosporidium Cyclospora Sarcocystis
  30. 30. Isospora(Cystoisospora) belli Contaminated food/water, oral-anal Found most commonly in HIV/AIDS Infects intestinal epithelium Malabsorption syndrome mimicking giardiasis Positive Modified acid fast stain
  31. 31. Cryptosporidium spp C. parvum and C. hominis Contaminated water Resistant to usual water-purification procedures (chlorination, ozone) Daycare center outbreaks (fecal-oral), swimming pools Watery diarrhea; more severe in AIDS
  32. 32. Cryptosporidiosis: Diagnosis Partial Acid Fast Stain Positive Not detected in routine O & P exams (left) Requires modified acid-fast stains for detection, oocysts measure 4-6 µm , Antigen, DFA and Molecular assays aid detection. PAF stain Positive
  33. 33. Direct Fluorescence Antibody stain – Cryptosporidium spp Molecular assays (PCR) and Enzyme immunoassay for antigen available. Giardia Cryptosporidium Combo stain for Cryptosporidium and Giardia lamblia
  34. 34. Cryptosporidia in intestine Cryptosporidia in the intestine - located just below the plasma membrane
  35. 35. Cyclospora cayetanensis Contaminated fruits and vegetables – particularly ones with plant hairs Watery diarrhea; fatigue, anorexia, weight loss, flu like symptoms. More severe in immune suppressed, can last for months Infects upper small bowel Treatment Oral Trimethoprim/sulfamethoxazole Found in vacuoles in cytoplasm of jejunal epithelium, villous atrophy, crypt hyperplasia
  36. 36. Cyclospora cayetanensis Modified acid fast positive 8-10 microns UV autofluorescence Also positive on Calcofluor white stain
  37. 37. Microsporidia Obligate intracellular fungal parasite Enterocytozoon and Encephalitozoon species most common genera Primitive eukaryotic organism (fungi) Infection by ingestion of spores Chronic diarrhea in AIDS patients Myositis, hepatitis, peritonitis, keratitis, gastrointestinal and biliary tract
  38. 38. Microsporidia -Diagram of detailed internal spore structures Positive on modified Trichrome and Calcofluor white stains -Longer staining times will eventually allow for it to work its way into the spore
  39. 39. Blastocystis hominis (algae) Small #s: can be commensal Large #s: may be pathogenic Contaminated food and H20  Traveler’s diarrhea Iodine wet mount Nuclear blobs Around the periphery Trichrome stain
  40. 40. None;None; self resolving.self resolving. Maltese cross in rbcMaltese cross in rbcHemolytic anemia,Hemolytic anemia, Jaundice, fever,Jaundice, fever, hepatomegalyhepatomegaly Ixodes tickIxodes tickBabesia microtiBabesia microti Pentosam;Pentosam; PentamidinePentamidine isethionate.isethionate. IntracellularIntracellular (macrophages)(macrophages) leishmanial bodiesleishmanial bodies with kinetoplastwith kinetoplast Visceral leishmaniasisVisceral leishmaniasis (Kala-azar),(Kala-azar), granulomatous skingranulomatous skin lesionslesions Iraq/Iran/AfghanistanIraq/Iran/Afghanistan Phlebotomine sandflyPhlebotomine sandflyLeishmania donovaniLeishmania donovani CNS:CNS: melarsoperolmelarsoperol Nifurtimox andNifurtimox and Benzonidazole.Benzonidazole. Hemoflagellate inHemoflagellate in blood or tissue.blood or tissue. C- or comma-shapedC- or comma-shaped AmericanAmerican trypanosomiasis;trypanosomiasis; Chagas disease:Chagas disease: megacolon, cardiacmegacolon, cardiac failure.failure. Reduvid (kissing) bugReduvid (kissing) bugT. cruziT. cruzi Blood stage:Blood stage: Suramin orSuramin or petamidinepetamidine isethionateisethionate Hemoflagellate inHemoflagellate in blood or lymph nodeblood or lymph node AfricanAfrican trypanosomiasis;trypanosomiasis; Sleeping sicknessSleeping sickness Encephalitis; cardiacEncephalitis; cardiac failurefailure Tsetse flyTsetse flyTrypanosoma bruceiTrypanosoma brucei TreatmentTreatmentDiagnosisDiagnosisDisease/SymptomsDisease/SymptomsTransmissionTransmissionOrganismOrganism BLOOD BORNE PROTOZOA
  41. 41. Trypanosomes 2 Diseases ◦Chagas disease (American trypanosomiasis) ◦Trypanosoma cruzi ◦Vector: Reduviid / Triatome (kissing) bug ◦African sleeping sickness (African trypanosomiasis) ◦T. brucei (gambiense and rhodesiense) ◦Vector: Tsetse fly
  42. 42. Trypanosoma cruzi  Chagas (American trypanosomiasis) Vector: Reduvid/Triatoma (kissing) bug Trypomastigotes are the only stage found in the blood of an infected person; may be seen in CSF in CNS infections Motile circulating trypomastigotes are readily seen on slides of fresh anticoagulated blood in acute infection but are rarely detectable by microscopy in chronic T. cruzi infection. A typical trypomastigote has: ◦ A large, subterminal or terminal kinetoplast, ◦ A centrally located nucleus, ◦ An undulating membrane, and ◦ A flagellum running along the undulating membrane, leaving the body at the anterior end. ◦ 12 to 30 µm in length. Amastigote stage parasite may be seen in histopathology specimens from affected organs. C-shape
  43. 43. Trypanosoma cruzi – Trypomastigote Peripheral blood – Giemsa stain Reduvid bug Amastigote of T. cruzi in cardiac tissue
  44. 44. Trypanosoma brucei  Sleeping sickness (African trypanosomiasis) The two T. brucei species that cause African trypanosomiasis are indistinguishable morphologically ◦ T. brucei gambiense ◦ T. brucei rhodesiense A typical trypomastigote has: ◦ A small kinetoplast located at the posterior end ◦ A centrally located nucleus ◦ An undulating membrane, and ◦ A flagellum running along the undulating membrane, leaving the body at the anterior end ◦ 14 to 33 µm in length Trypomastigotes are the only stage found in patients. kinetoplast nucleus
  46. 46. Leishmania Obligate intracellular parasite Vector: female sand fly bite Two forms of disease ◦Visceral leishmaniasis (kala azar) ◦L. donovani ◦Cutaneous leishmaniasis ◦L. tropica ◦L. braziliensis
  47. 47. Leishmania
  48. 48. Leishmania – Clinical Disease Cutaneous ◦Single or few chronic, ulcerating lesions; many species ◦Latin America, southern Europe, Middle east, southern Asia, Africa ◦Mucocutaneous in Latin America Visceral ◦primarily L. donovani complex (Asia), L. infantum/chagasi (Africa and Latin America), others ◦Hepatosplenomegaly, anemia, cytopenias, systemic symptoms ◦India, Bangladesh, Nepal, Sudan, and Brazil ◦Important OI in HIV infection
  49. 49. Leishmania Diagnosis ◦Biopsy of infected tissue (skin, bone marrow) ◦Multiple, tiny 2-5 um amastigotes within histiocytes ◦Distinct kinetoplast (bar-like structure adjacent to nucleus) ◦PCR methods ◦Urinary antigens (visceral) DDx of multiple tiny intracellular organisms ◦Leishmania – kinetoplast ◦Histoplasma – budding ◦Toxoplasma – somewhat curved, mostly extracellular
  50. 50. Leishmania amastigotes ◦Macrophages filled with amastigotes (arrows), several of which have a clearly visible nucleus and kinetoplast Nucleus Kinetoplast
  51. 51. Babesia Protozoan: B. microti, B. divergens Zoonosis (deer, cattle, rodents; humans accidental host) Transmission vector: Ixodes tick bite Infects red blood cells Found world-wide B. microti along the Northeast US ◦ Nantucket Island, Martha’s vineyard, Shelter Island Malaria-like syndrome ◦ Fever but without periodicity, “B-symptoms”, hemolytic anemia, hemoglobinuria, renal failure Dx: ◦ Blood smear examination ◦ Ring form only (mimics P. falciparum) ◦ Tetrads (unlike P. falciparum) Maltese cross (tetrads) Ixodes tick
  52. 52. Babesia Maltese cross forms
  53. 53. MALARIA Protozoan parasite Transmitted by the anopheles mosquito Endemic in tropical areas
  54. 54. Malaria Symptoms Fever pattern ParasiteParasite DiseaseDisease PlasmodiumPlasmodium falciparumfalciparum MalignantMalignant tertiantertian malariamalaria P. vivaxP. vivax BenignBenign tertiantertian malariamalaria P. ovaleP. ovale BenignBenign tertiantertian malariamalaria P. malariaeP. malariae QuartanQuartan malariamalaria Tertian = q 48 hours (every other day) Quartan = q 72 hours
  55. 55. Malaria Physical exam findings ◦Fever ◦Splenomegaly ◦P. falciparum - most pathogenic species ◦Jaundice ◦Hepatomegaly ◦Increase in respiratory rate ◦CNS involvement ◦Blackwater fever – hemolysis, renal failure Diagnosis: peripheral blood smear Antigen screen (EIA) and NAAT
  56. 56. Malaria Primary distinction is P. falciparum and non-falciparum disease ◦P. falciparum = rapidly progressive and LETHAL (malignant tertian fever), often chloroquine-resistant ◦Non-falciparum = rarely cause severe manifestations, often chloroquine sensitive Relapsing malaria ◦Dormant hepatic phase can recur from liver ◦Occurs only with P. vivax and P. ovale
  57. 57. MALARIA Life Cycle of Plasmodium Species
  58. 58. Progression of the RBC forms of Malaria Ring form  Trophozoite Schizont Gametocyte Merozoites (ruptured schizont)
  59. 59. Plasmodium species Plasmodium falciparum Plasmodium vivax Plasmodium ovale Plasmodium malariae Plasmodium knowlesi – primates only
  60. 60. ovaleovale VectorVector MosquitoMosquito MosquitoMosquito MosquitoMosquito Ixodes tickIxodes tick RBCRBC Any RBCAny RBC Young RBC;Young RBC; enlargedenlarged Mature RBC;Mature RBC; Not enlargedNot enlarged RingRing Multiple canMultiple can be seen;be seen; delicate;delicate; “appliqu锓appliqué” Rarely >1;Rarely >1; thickenedthickened 1-121-12 TetradsTetrads ((MalteseMaltese crosscross)) DelicateDelicate Rings onlyRings only SchizontSchizont Rarely seenRarely seen Commonly seenCommonly seen ““rosette”rosette” nonenone GametocyteGametocyte Banana-Banana- shapedshaped RoundRound nonenone Extra-RBCExtra-RBC formform NoneNone NoneNone PresentPresent Schüffner dotsSchüffner dots NoNo YesYes NoNo PigmentationPigmentation BrownBrown NoNo Infection rateInfection rate >2%>2% <2%<2% 5-10%5-10% ProtectiveProtective polymorphismpolymorphism ss Hemoglobin S,Hemoglobin S, C,E, alpha andC,E, alpha and beta thal, G6PDbeta thal, G6PD Duffy negativeDuffy negative (P. vivax)(P. vivax) DormantDormant hepatic phasehepatic phase (relapse)(relapse) NoNo YesYes NoNo
  61. 61. Malarial Preparations Thick smear Drop of blood on slide Water rinse to eliminate rbc’s Stain with Giemsa stain (not Wright-Giemsa) proper pH Need the proper pH to stain the Schuffner’s granules Concentrated to spot malaria parasites Thin smear Feather edge smear For optimal morphology, stain with Giemsa (not Wright- Giemsa) stain with proper pH Speciation of malaria Parasitemia (%)
  62. 62. Schuffner’s granules
  63. 63. P. ovale Fimbriated edge
  64. 64. “Rosette” schizont
  65. 65. P. malariae
  66. 66. P. vivax Amoeboid ring form P.vivax – benign tertian malaria (fever every 48 hours), Duffy negative Red blood cell protects from Plasmodium invasion- African natives lack Duffy rbc antigen and this prevents them from P. vivax. Untreated infections last several years remaining dormant in the liver. Patients can survive years without treatment, but recurrent and chronic infection can lead to brain, kidney and liver damage
  67. 67. • P. falciparum -multiple ring forms per cell -accolade forms(ring forms on the edge of cell. -Banana gametocyte
  68. 68. Malignant tertian malaria Black water fever P. falciparum High % parasitism Accolade form Banana gametocyte
  69. 69. P. falcipriumP. falciprium Non-Non- FalciparumFalciparum BabesiaBabesia VectorVector MosquitoMosquito MosquitoMosquito Ixodes tickIxodes tick RBCRBC All RBCAll RBC Young RBCYoung RBC RingRing 1-31-3 delicatedelicate Rarely >1Rarely >1 thickenedthickened 1-121-12 TetradsTetrads DelicateDelicate Rings onlyRings only GametocyteGametocyte Banana shapedBanana shaped roundround nonenone Extra-RBCExtra-RBC formform NoneNone NoneNone PresentPresent PigmentationPigmentation BlackBlack brownbrown nonenone InfectionInfection raterate >2%>2% <2%<2% 5-10%5-10% ProtectiveProtective polymorphispolymorphis msms Hemoglobin S,Hemoglobin S, C,E, alpha andC,E, alpha and beta thal, G-6-beta thal, G-6- PDPD Duffy negativeDuffy negative
  70. 70. OrganismOrganism TransmissionTransmission Disease/SymptoDisease/Sympto msms DiagnosisDiagnosis TreatmentTreatment ToxoplasmaToxoplasma gondiigondii Oral from cat fecalOral from cat fecal materialmaterial or meator meat Adult: flu like;Adult: flu like; congenital:congenital: abortion, neonatalabortion, neonatal blindness andblindness and neuropathiesneuropathies Intracellular (inIntracellular (in macrophages)macrophages) tachyzoitestachyzoites SulphonamidesSulphonamides ,, pyemethaminepyemethamine , possibly, possibly spiramycinspiramycin (non-FDA)(non-FDA) Other Protozoa - Toxoplasma
  71. 71. Toxoplasma gondii Coccidian protozoan House cat (kittens) = definitive host Infection from: ◦Ingestion of infective oocysts from contaminated cat feces ◦Ingestion of improperly cooked meat from animals that serve as intermediate hosts Symptoms ◦Predilection for lung, heart, lymphoid organs, CNS/eye ◦Infectious mono-like; lymphadenitis, hepatitis, rash, encephalomyelitis, myocarditis, chorioretinitis ◦Transplacental infection ◦ 1st trimester  spontaneous abortion, stillbirth or severe disease ◦ 2nd /3rd trimester  CNS infections (epilepsy, encephalitis, intracranial calcifications, MR, chorioretinitis, blindness, hearing loss), jaundice, rash ◦AIDS - Encephalitis; mass lesions in brain
  72. 72. Toxoplasma gondiiDiagnosis ◦Serology EIA ◦Anti-toxo IgM – congenital and acute infection; may persist for months ◦Anti-toxo IgG – common; if positive, gestations safe from intrauterine toxoplasmosis infection ◦PCR
  73. 73. Toxoplasma gondii Toxoplasma gondii cyst Toxoplasma in brain tissue stained tachyzoites with hematoxylin and eosin
  74. 74. Free-living Amoeba Naegleria fowleri Acanthamoeba Balamuthia
  75. 75. Amoebic meningoencephalitis Most common cause: Naegleria fowleri Granulomatous amoebic encephalitis or brain abscess: Acanthamoeba and Balamuthia Clinical scenario: swimming or diving into fresh- water pools
  76. 76. Contact-lens keratitis Caused by Acanthamoeba Can be cultured on a “lawn of E. coli” ◦Take corneal scrapings ◦Visible trail of ameba moving across plate ingesting E. coli Wright’s stain
  77. 77. HELMINTHS Nematodes (roundworms) Trematodes (flukes) Cestodes (tapeworms)
  78. 78. Nematodes Enterobius Ascaris Trichuris Necator and Ancylostoma (Hookworm) Microfilaria – Wucheria, Brugia, Loa loa, Mansonella, and Onchocerca
  79. 79. Enterobius vermicularis (pinworm) Humans considered only host Females 8-13mm, males 2-5 mm Dwell in the cecum ¼-1/2 inch in thickness, white, lloks like string in stool Lay up to 15,000 eggs ◦Oval with a flattened side: 50-60um by 20-30um Diagnosis- Scotch tape test or anal swab Most common helminth in US
  80. 80. Enterobius vermicularis (pinworm) eggs Asymmetrical eggs
  81. 81. Pinworm larvae - may be seen in stool specimens examined for pinworm Eggs
  82. 82. Ascaris lumbricoides (roundworm) 1-1.2 billion people infected ◦More common in children 20,000 death Largest helminth to affect humans Females 20-35cm long, males 15-30cm with a curved tale ◦Can cause intestinal obstruction
  83. 83. Ascaris lumbricoides
  84. 84. Trichuris Trichiura (whipworm) Soil transmitted Disease can can be similar to amebiasis PVA preserved samples inferior to formalin Adults attach to large intestine and are rarely recovered – diagnosis by detecting egg in stool specimens Thinnest part- head Males are smaller than females
  85. 85. Trichuris trichiura tail Head
  86. 86. Necator americanus, Ancylostoma duodenale (Hookworms) Soil transmitted 2nd most common helminth infection Enter via exposed skin Necator or Ancylostoma – Hookworm egg
  87. 87. Strongyloides stercoralis Soil transmitted Larval form only Presence of internal structures can separate from artifact In immune suppressed - massive intestinal infection and migration to the respiratory tract (eosinophilic pneumoniae) possible Strongyloides larvae
  88. 88. Strongyloides stercoralis Can be found in intestines or stools In real sick can go to lung and cause pneumonia
  89. 89. Trichinella spiralis -Tissue nematode -All stages occur in single host -usually an incidental finding in muscle
  90. 90. Microfilariae Sheathed ◦Wucheria bancrofti and Brugia malayi ◦Elephantiasis (lymphangitis/lymphedema) ◦Loa loa ◦Calabar swellings & migrating worms in the conjunctiva Not sheathed ◦Onchocerca volvulus ◦Mansonella species ◦Allergic skin reactions, edema, Calabar swellings
  91. 91. Identification of microfilariae is based on the presence of a sheath covering the larvae, as well as the distribution of nuclei in the tail region A, W. bancrofti. B, B. malayi. C, L. loa. D, O. volvulus. E, Mansonella perstans. F, Mansonella streptocerca. G, Mansonella ozzardi.
  92. 92. Filaria Identification a. W. bancrofti ◦ Sheathed, nuclei stop short of end of tail a. B. malayi ◦ Sheathed, two small nuclei in tail a. O. volvulus ◦ Unsheathed, from skin, not blood a. Loa loa ◦ Sheathed, nuclei to continue to end of tail
  93. 93. Wucheria bancrofti
  94. 94. Brugia malayi
  95. 95. Loa loa
  96. 96. Mansonella perstans
  97. 97. Onchocerciasis Black fly
  98. 98. Onchocerciasis
  99. 99. Trematodes (Flatworms) Intestinal and Liver flukes ◦Fasciolopsis buski ◦Fasciola hepatica Liver flukes ◦Clonorchis sinensis (Chinese liver fluke) Paragonimus westermani – oriental lung fluke Schistosomes ◦S mansoni – intestinal bilharziasis ◦S haematobium - urinary ◦S japonicum – blood fluke, found in intestines
  100. 100. Intestinal and liver flukes
  101. 101. Fasciolopsis buski Fasciola hepatica The two most common intestinal flukes
  102. 102. Fasciola hepatica Distinct nose Fascioliasis is a parasitic infection typically caused by Fasciola hepatica, also known as "the common liver fluke" or "the sheep liver fluke. Fascioliasis is found in all 5 continents, especially where sheep or cattle are reared. Infected by eating raw watercress or other water plants contaminated with immature parasite larvae. The immature larval flukes migrate through the intestinal wall, the abdominal cavity, and the liver tissue, into the bile ducts, where they develop into mature adult flukes, which produce eggs. The pathology typically is most pronounced in the bile ducts and liver. Fasciola infection is both treatable and preventable
  103. 103. Intestinal fluke Fasciolopsis buski, causes fasciolopsiasis, is the largest intestinal fluke of humans. Prevented by cooking aquatic plants well before eating them. Found in south and southeastern Asia. Fasciolopsiasis is treatable. Many people do not have symptoms from Fasciolopsis infection. However, abdominal pain and diarrhea can occur 1 or 2 months after infection. With heavy infections Fasciolopsis flukes can cause intestinal obstruction, abdominal pain, nausea, vomiting, and fever.
  104. 104. Clonorchis sinensis knobbin Shoulders operculates Clonorchis is a liver fluke that can infect the liver, gallbladder and bile duct. Found across parts of Asia, it is also known as the Chinese or oriental liver fluke.
  105. 105. Egg is operculate, not embryonated, thick shell, asymmetrical and large Paragonimus westermani Paragonimus is a parasitic lung fluke (flat worm). Infections occur after a person eats raw or undercooked infected crab or crayfish. The illness is known as paragonimiasis. Paragonimus infection also can be very serious if the fluke travels to the central nervous system, where it can cause symptoms of meningitis.
  106. 106. Schistosoma mansonii
  107. 107. Schistosomiasis, also known as bilharzia, more than 200 million people are infected worldwide. In terms of impact this disease is second only to malaria as the most devastating parasitic disease. The parasites that cause schistosomiasis live in certain types of freshwater snails. The infectious form of the parasite, known as cercariae, emerge from the snail, hence contaminating water. You can become infected when your skin comes in contact with contaminated freshwater. Most human infections are caused by Schistosoma mansoni, S. haematobium, or S. japonicum. Stool or urine samples can be examined microscopically for parasite eggs (stool for S. mansoni or S. japonicum eggs and urine for S. haematobium eggs).
  108. 108. Cestodes (Tapeworms) Examples Diphyllobothrium latum Taenia saginata Taenia solium Hymenolepis nana Hymenolepis diminuta Echinococcus granulosis Flattened dorsoventrally, segmented Head with armed or unarmed scolex Proglottids immature, mature (sex organs) Gravid (with eggs) Internal structure of proglottids Hermaphroditic-ovary, testes, vitellaria, uterus, genital pore and ducts Lateral excretory and nervous system No gut-tegument absorbs nutrients Muscles-longitidinal and horizontal
  109. 109. Diphyllobothrium latum
  110. 110. Diphyllobothrium latum Poorly-cooked fresh-water fish (salmon) Scandinavian, Russia, Canada, N. USA, Alaska Broad fish tapeworm Longitudinal sucker Eggs have non-shouldered operculum and knob ◦They are not embryonated Infection causes VitaminB12 deficiency
  111. 111. Diphyllobothrium latum
  112. 112. Sucking plate Diphyllobothrium latum
  113. 113. Taenia saginata  Beef tapeworm  4 suckers on scolex  >13 uterine branches in proglottids Ingestion of cysticerci in beef Intestinal infestation Ingestion of eggs -> Non-human pathogen Taenia Solium Pig tapeworm Ring of thorns/crown on scolex <13 uterine branches in proglottids Ingestion of cysticerci in pork Intestinal infestation Ingestion of eggs -> Cysticercosis Taenia Species – two species Outstanding characteristics
  114. 114. Taenia species
  115. 115. Taenia eggs Identical eggs for the two species
  116. 116. Taenia saginata Proglottid > 12 uterine branches
  117. 117. Taenia solium Proglottis – fewer uterine branches (<=12 uterine branches) Scolex - Ring of thorns
  118. 118. Cysticercosis Caused by the ingestion of T. solium eggs Not by eating infected pork
  119. 119. Hymenolepis nana
  120. 120. Hymenolepis nana Most common cestode recovered in USA Worm is 2-4 cm Egg has inner & outer shell separated space Water /food contaminated by rodent droppings Hooklets inside Larger outer shell No radial striations
  121. 121. Hymenolepis diminuta Uncommon tapeworm Big egg @ 80 microns in diameter
  122. 122. Echinococcus – hydatid cyst disease found in Africa, Europe, Asia, the Middle East, and Central and South America. Highest prevalence is found in populations that raise sheep. Infection ingestion of egg found in animal feces.
  123. 123. Echinococcus – hydatid cyst Short tapeworm Sand like material contained in the Cyst, due to inverted folded tapeworms
  124. 124. Relative size of Helminth eggs
  125. 125. Additional Insects of interest
  126. 126. Maggots House fly larvae Bot fly larvae Bot fly bites human, Larvae develops and extrudes from the skin
  127. 127. Ticks of importance Soft tick - Expands with blood engorgement Hard Ticks
  128. 128. Black Widow spider Hour glass On tummy
  129. 129. Flea Body louse Crab louse Hair nit
  130. 130. Scabies Tinyeggsunderskin Mite

Editor's Notes

  • Particularly difficult to differentiate from falciprium
  • Hallmark of babesiosis is the tetrad (Maltese cross; cruciform body)
  • Blackwater fever (falciprium and think black pee)
  • Microscopic examination
  • Exception for non-falcirpium is P. vivax where chlorquine resistance is seen in Papua New Guinea and Indonesia
  • The malaria parasite life cycle involves two hosts.  During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host.  Sporozoites infect liver cells and mature into schizonts, which rupture and release merozoites.  (Of note, in P. vivax and P. ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.)  After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ).  Merozoites infect red blood cells .  The ring stage trophozoites mature into schizonts, which rupture releasing merozoites.  Some parasites differentiate into sexual erythrocytic stages (gametocytes).  Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal .  The parasites’ multiplication in the mosquito is known as the sporogonic cycle .  While in the mosquito&amp;apos;s stomach, the microgametes penetrate the macrogametes generating zygotes .  The zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts .  The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito&amp;apos;s salivary glands.  Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle . 
  • Presence of absence of various stages in the blood
    Morphology of the gametocyte
    Size of the infected RBC
  • Most prevalent
    Widest geographical distribution
  • Enlarged RBC; fimbriated/ragged rbc
  • Fever cycle every 72 hours (quartan), can remain dormant in the blood for years.
    Untreated infections may last as long as 20 years
  • P