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  1. 1. The Prokaryotes:Domains Bacteria and Archaea<br />11<br />
  2. 2. The Protozoa<br />Table 12.1<br />
  3. 3. Eukaryotic<br />Unicellular<br />Chemoheterotrophs<br />Vegetative form is a trophozoite.<br />Asexual reproduction is by fission,budding, or schizogony.<br />Sexual reproduction <br />by conjugation.<br />Some produce cysts.<br />Protozoa<br />Figure 12.16<br />
  4. 4. No mitochondria<br />Multiple flagella<br />Giardia lamblia<br />Trichomonas vaginalis (no cyst stage)<br />Archaezoa<br />Figure 12.17b–d<br />
  5. 5. No mitochondria<br />Nonmotile<br />Intracellular parasites<br />Nosema<br />Microspora<br />
  6. 6. Move by pseudopods<br />Entamoeba<br />Acanthamoeba<br />Amoebozoa<br />Figure 12.18a<br />
  7. 7. Nonmotile<br />Intracellular parasites<br />Complex life cycles<br />Plasmodium<br />Babesia<br />Cryptosporidium<br />Cyclospora<br />Apicomplexa<br />
  8. 8. 2<br />3<br />8<br />7<br />6<br />Plasmodium<br />Figure 12.19<br />
  9. 9. Cryptosporidium<br />Figure 25.19<br />
  10. 10. Move by cilia<br />Complex cells<br />Balantidium coli is the only human parasite.<br />Figure 12.20<br />Ciliophora (Ciliates)<br />
  11. 11. Move by flagella<br />Photoautotrophs<br />Euglenoids<br />Chemoheterotrophs<br />Naegleria: Flagellated and amoeboid forms; causes meningoencephalitis.<br />Trypanosoma: Undulating membrane, transmitted by vectors.<br />Leishmania: Flagellated form in sand fly vector, ovoid form in vertebrate host.<br />Euglenozoa<br />
  12. 12. Euglenozoa<br />Figure 12.21<br />
  13. 13. Why are these studied with algae and protozoa?<br />Dinoflagellates<br />Figure 12.14<br />
  14. 14.
  15. 15. INTESTINAL PROTOZOA<br />Ameba<br />Flagellates<br />Ciliates<br />Intestinal Coccidia, Microsporidia, and Blastocystis hominis<br />
  16. 16. Entamoebahistolytica<br /><ul><li>Disease:Intestinal amebiasis/amebic dysentery, extraintestinalamebiasis
  17. 17. Site in host:lumen & wall of LI
  18. 18. Portal of entry:Mouth
  19. 19. Source of infection:cysts in food & water, from feces</li></ul>AMEBA<br />
  20. 20. Causal Agent:Entamoebahistolytica<br />pathogenic ameba<br />associated with intestinal and extraintestinal infections. <br />Amoebiasis<br />
  21. 21.
  22. 22. Cysts and trophozoites are passed in feces .  <br />ingestion of mature cysts in fecally contaminated food, water, or hands. <br />Excystation occurs in the small intestine - trophozoitesare released, which migrate to the large intestine.  <br />The trophozoites multiply by binary fission - produce cysts , and both stages are passed in the feces .  <br />Pathogenecity<br />
  23. 23. Cysts and trophozoites are passed in feces . <br /> ingestion of mature cysts in fecally contaminated food, water, or hands. <br />Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine.  <br />The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces .  <br />protection by their walls, the cysts can survive days to weeks in the external environment<br />Pathogenecity<br />
  24. 24. trophozoitesremain confined to the intestinal lumen ( noninvasive infection)<br />individuals who are asymptomatic carriers, passing cysts in their stool.  <br />trophozoitesinvade the intestinal mucosa (intestinal disease)<br />through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (extraintestinal disease), <br />Pathogenecity<br />
  25. 25. E. histolytica morphologically ingested red blood cells (erythrophagocystosis)<br />  <br />Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).<br />Pathogenecity<br />
  26. 26. Worldwide, with higher incidence of amebiasis in developing countries. <br /> In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations.<br />Geographic Distribution:<br />
  27. 27. asymptomatic infection <br />("luminal amebiasis")<br />invasive intestinal amebiasis<br />(dysentery, colitis, appendicitis, toxic megacolon, amebomas)<br /> invasive extraintestinalamebiasis<br />(liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions).<br />Clinical Features:<br />
  28. 28. Fresh stool: <br />wet mounts and permanently stained preparations (e.g., trichrome)<br />Concentrates from fresh stool: <br />wet mounts, with or without iodine stain, and permanently stained preparations <br />E. histolyticatrophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.<br />Laboratory Diagnosis:<br />
  29. 29. Microscopy<br />Immunodiagnosis<br />Molecular methods for discriminating between E. histolytica and E. dispar<br />Morphologic comparison with other intestinal parasites<br />Bench aid for E. histolytica<br />Diagnostic findings:<br />
  30. 30. Trophozoite:small, usually central karyosome; finely granular chromatin<br />
  31. 31. Trophozoite with ingested RBCs<br />
  32. 32.
  33. 33. Cyst:4 nuclei in mature cyst; rod-like chromatoid bodies <br />
  34. 34. Gross pathology of liver containing amebic abscess  <br />
  35. 35. Gross pathology of amebic abscess of liver. Tube of "chocolate" pus from abscess.<br />
  36. 36.
  37. 37. Entamoeba hartmanni<br />Trophozoite: small, usually eccentric karyosome; finely granular chromatin<br />
  38. 38. Cyst:4 nuclei in mature cyst; rod-like chromatoid bodies (6-8 um, smaller than E. histolytica cysts) <br />
  39. 39. Entamoeba coli<br />Trophozoite: 1 nucleus with large eccentric karyosome; coarse, irregular peripheral chromatin<br />
  40. 40. Cyst:8 nuclei in mature cyst; splinter-like chromatoid bodies w/ pointed ends<br /> large, eccentric karyosome<br />
  41. 41.
  42. 42. Endolimax nana<br />Trophozoites:1 nucleus w/ large, irregularly shaped, blot-like karyosome; has no peripheral chromatin; cytoplasm is granular and vacuolated<br />
  43. 43. Cyst: mature cyst w/ 4 nuclei with large, blot-like karyosomes; no have chromatoid bodies<br />
  44. 44. Iodamoeba butschlii<br />Trophozoite: 1 nucleus w/ large, usually central karyosome surr by refractile, achromatic granules; cytoplasm coarsely granular, vacuolated & can contain bacteria, yeasts  <br />
  45. 45. Cyst: one nucleus with a large, usually eccentric karyosome; no chromatoid bodies but have a compact, well defined glycogen mass; shape varies from ovoidal to rounded.<br />
  46. 46. For asymptomatic infections, <br />iodoquinol, paromomycin, or diloxanidefuroate are the drugs of choice.  <br />For symptomatic intestinal disease, or extraintestinal, infections (e.g., hepatic abscess) <br />the drugs of choice are metronidazole or tinidazole, immediately followed by treatment with iodoquinol, paromomycin, or diloxanidefuroate. <br />Treatment:<br />
  47. 47. Balantidium coli<br /><ul><li>Disease:Balantidiasis;balantidiosis; balantidial dysentery
  48. 48. Site in host:LI
  49. 49. Portal of entry:Mouth
  50. 50. Source of infection:stool (cysts)
  51. 51. Lab Dx: cysts/trophs in stool</li></ul>CILIATES<br />
  52. 52.
  53. 53. Causal Agent<br />Balantidium coli, a large ciliated protozoan parasite.<br />Geographic Distribution:<br />Worldwide.  Because pigs are an animal reservoir.  Other reservoirs include rodents and nonhuman primates.<br />Balantidiasis<br />
  54. 54. cysts – infective stage<br />ingestion of contaminated food or water <br />Life cycle <br />
  55. 55. excystation occurs in the small intestine- trophozoitescolonize the large intestine <br />Trophozoites undergo encystation to produce infective cysts .  <br />Some trophozoites invade the wall of the colon and multiply. <br />Mature cysts are passed with feces .<br />Life cycle <br />
  56. 56. Most cases are asymptomatic.  <br />Clinical manifestations, when present, include <br />persistent diarrhea<br />occasionally dysentery<br />abdominal pain<br />weight loss.  <br />Symptoms can be severe in debilitated persons.<br />Clinical Features:<br />
  57. 57. trophozoites - stool specimens or in tissue<br />Cysts are less frequently encountered.  <br />Laboratory Diagnosis:<br />
  58. 58. Trophozoites: large size (50-70 µm); rows of cilia on the cell surface; a cytostome; a bean shaped macronucleus and a smaller, less conspicuous micronucleus <br />
  59. 59. Cyst: spherical to oval; cilia present in the young cyst but are absent in older forms; large, kidney-shaped macronucleus & contractile vacuoles in cytoplasm <br />
  60. 60. The drug of choice is tetracycline*, with metronidazole* and  iodoquinol* as alternatives. <br /> Tetracycline is contraindicated in pregnancy and in children less than 8 years old. <br />Treatment:<br />
  61. 61. <ul><li>May be pathogenic
  62. 62. Currently classified as an amoeba</li></ul>Blastocystis hominis<br />
  63. 63. Blastocystishominis<br />Geographic Distribution:Worldwide.<br />Causal Agent:<br />
  64. 64. thick-walled cyst present in the stools (fecal-oral route)<br />cysts infect epithelial cells of the digestive tract and multiply asexually <br />Vacuolar forms - give origin to multi vacuolar and ameboidforms<br /> multi-vacuolar -- pre-cyst -- thin-walled cyst (autoinfection)<br />ameboid-- pre-cyst --thick-walled cyst<br />Life Cycle:<br />
  65. 65.
  66. 66. can cause both asymptomatic and symptomatic<br />symptoms of illness including watery diarrhea, abdominal pain, perianalpruritus, and excessive flatulence.<br />Clinical Features:<br />
  67. 67. Cyst-like forms appear round with large, central vacuole-like body. The nuclei in the peripheral cytoplasmic rim are clearly visible, staining purple.<br />
  68. 68.
  69. 69. metronidazoleor iodoquinol<br />Treatment:<br />
  70. 70. Giardiaduodenalis (lamblia)<br /><ul><li>Disease:Giardiasis;lambliasis
  71. 71. Site in host:upper SI
  72. 72. Portal of entry:Mouth
  73. 73. Source of infection:cysts in food & water, from feces
  74. 74. Lab Dx: cysts/trophs in stool; IFA stain; Enterotest
  75. 75. Note: may be sexually transmitted</li></ul>FLAGELLATES<br />
  76. 76. Causal Agent:<br />Giardiaintestinalis<br />Giardialamblia<br />Geographic Distribution:Worldwide, more prevalent in warm climates, and in children.<br />Giardisis<br />
  77. 77.
  78. 78. Cysts for transmission<br />Both cysts and trophozoites can be found in the feces (diagnostic stages) .  <br />Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . <br />Life Cycle:<br />
  79. 79. (small intestine) excystation<br />Trophozoites multiply (lumen of the proximal small bowel )-- free or attached to the mucosa by a ventral sucking disk .<br />  Encystation(colon).  <br />cyst (nondiarrhealfeces )<br />Life Cycle:<br />
  80. 80. The spectrum varies from asymptomatic carriage to severe diarrhea and malabsorption<br /> <br /> Acute giardiasis develops after an incubation period of 1 to 14 days (average of 7 days) and usually lasts 1 to 3 weeks<br />Symptoms include diarrhea, abdominal pain, bloating, nausea, and vomiting.  <br />In chronic giardiasis the symptoms are recurrent and malabsorption and debilitation may occur.<br />Clinical Features:<br />
  81. 81. Trophozoite: pyriform shape w/ 2 nuclei & a large, central karyosome; large ventral sucking disc, 4 pairs of flagella, 2 curved median bodies<br />
  82. 82. Cysts: ellipsoid shape w/ 2 nuclei each (more mature ones will have four); lengthwise running central fibrils; short fibers laterally or obliquely across fibrils in lower half of cyst<br />
  83. 83. metronidazoleand tinidazole.  <br />Nitazoxanide(giardiasisin children)<br />Treatment:<br />
  85. 85. Cryptosporidium parvum<br /><ul><li>Disease: Cryptosporidiosis
  86. 86. Transmission: contaminated food or water by person to person contact
  87. 87. Lab Dx: Modified acid fast stain of a fecal smear; PCR; IFA</li></li></ul><li>
  88. 88. Causal Agent:Cryptosporidium parvum and Cryptosporidium hominisare (most prevalent species)<br />Geographic Distribution:first reports of human cases in 1976, worldwide.  Waterborne outbreak in Milwaukee (Wisconsin) in 1993, that affected more than 400,000 people.<br />Crytosporidiosis<br />
  89. 89.
  90. 90. Sporulatedoocysts, containing 4 sporozoites-- excreted by the infected host through feces and possibly other routes such as respiratory secretions .  <br />Transmission occurs mainly through contact with contaminated water (e.g., drinking or recreational water). <br />food sources<br />outbreaks U S -- waterparks, community swimming pools, and day care centers.  <br />Zoonotic and anthroponotictransmission<br />Life cycle<br />
  91. 91. Life cycle<br /> Following ingestion (and possibly inhalation) <br />Excystation-- sporozoitesare released --parasitize gastrointestinal AND respiratory tract.  <br />asexual multiplication (schizogony or merogony) -- sexual multiplication (gametogony) -- producing microgamonts (male) and macrogamonts (female)<br />
  92. 92. Life cycle<br /> Upon fertilization -- oocysts that sporulate in the infected host<br />Two different types of oocysts are produced<br /> thick-walled, which is commonly excreted from the host <br />thin-walled oocyst , which is primarily involved in autoinfection.  <br />
  93. 93. asymptomatic infections <br /> severe, life-threatening illness<br />incubation period is an average of 7 days (2 to 10 days).  <br />Watery diarrhea is the most frequent symptom accompanied by dehydration, wt loss, abd. pain, fever, n/v<br />immunocompetent persons, symptoms are usually short lived (1 to 2 weeks-- can be chronic and more severe in immunocompromised patients, especially those with CD4 counts <200/µl.  <br />Clinical Features:<br />
  94. 94. asymptomatic infections <br />severe, life-threatening illness<br />incubation period is an average of 7 days (but can range from 2 to 10 days).  <br />Watery diarrhea is the most frequent symptom, and can be accompanied by dehydration, weight loss, abdominal pain, fever, nausea and vomiting. <br />Clinical Features:<br />
  95. 95. Clinical Features:<br /> In immunocompetent persons, symptoms are usually short lived (1 to 2 weeks); they can be chronic <br />more severe in immunocompromised patients, especially those with CD4 counts <200/µl.  <br />also found in other digestive tract, lungs, and conjunctiva.<br />
  96. 96. Treatment:<br />Rapid loss of fluids -- fluid and electrolyte replacement.  <br />healthy, immunocompetent persons (self-limited)-- Nitazoxanide<br />  Immunocompromisedand high risk pt.-- nitazoxanide is unclear.  <br />For persons with AIDS, anti-retroviral therapyis encourage<br />
  97. 97. Laboratory Diagnosis:<br />Acid-fast staining methods<br />immunofluorescencemicroscopy <br />method of choice (followed closely by enzyme immunoassays)<br />
  98. 98. Oocysts are rounded, 4.2 µm - 5.4 µm in diameter.  Sporozoites are visible inside the oocysts, indicating that sporulation has occurred. <br />
  99. 99. Oocysts stained by the modified acid-fast method: against a blue-green background, the oocysts stand out in a bright red stain.  Sporozoites are visible inside the two oocysts to the right.<br />
  100. 100. Oocysts of C. parvum (upper left) and cysts of Giardia intestinalis (lower right) labeled with immunofluorescent antibodies.<br />
  101. 101. Cyclosporacayetanensis<br /><ul><li>Disease:Cyclosporiasis
  102. 102. Transmission: contaminated water
  103. 103. Lab Dx: Modified acid fast stain of a fecal smear</li></li></ul><li>Cyclospora oocysts from fresh stool fixed in 10% formalin and stained with modified acid-fast stain.  Compared to wet mount preparations, the oocysts are less perfectly round and have a wrinkled appearance.  Most importantly, the staining is variable among the four oocysts.<br />
  104. 104. Sporulation of Cyclospora oocysts.  The sequence shows, as observed by DIC microscopy of wet mounts: an oocyst passed in fresh stool (Day 0); sporulated oocysts at days 5 (Day 5) and 10 (Day 10), which both contain 2 sporocysts; and a ruptured oocyst (Rupture), with a sporocyst still inside the oocyst and the other sporocyst just outside ­ the coiled sporozoites are barely visible inside the sporocysts.<br /> <br />
  105. 105.
  106. 106. Causal Agent:unicellular coccidian parasite- Cyclosporacayetanensis<br />Geographic Distribution:<br />most common in tropical and subtropical areas<br />1990, foodborneoutbreaks of cyclosporiasis, 3600 persons, in the United States and Canada.<br />
  107. 107.
  108. 108. sporulation -- sporont -- two sporocysts (contains 2 sporozoites)  <br />sporulatedoocysts are ingested (in contaminated food or water) <br />oocystsexcyst in the gastrointestinal tract-- sporozoites invade the small intestine <br />asexual multiplication and sexual development -- oocysts<br />Life Cycle:<br />
  109. 109. Clinical Features:<br />incubation period of 1 week—severe watery diarrhea<br />s/sx- anorexia, wt loss, abd. pain, N/V, myalgias, low-grade fever, and fatigue. <br /> Untreated infections typically last for 10-12 weeks -- follow a relapsing course.  <br />In disease-endemic settings -- asymptomatic.<br />
  110. 110. identification of oocysts in stool specimens<br />Laboratory Diagnosis:<br />
  111. 111. combination of two antibiotics, trimethoprim-sulfamethoxazole*, also known as Bactrim, Septra, or Cotrim.  <br />Supportive measures include management of fluid and electrolyte balance, and rest.   <br />Treatment:<br />
  112. 112. Isospora belli<br /><ul><li>Disease:Isosporiasis; intestinal coccidiosis
  113. 113. Transmission: hand to mouth or through contaminated food or water
  114. 114. Lab Dx: wet mount of formalin-ethyl acetate conc. of fecal sample; modified acid fast stain</li></li></ul><li>Oocysts: large (25 to 30 µm); typical ellipsoidal shape; when excreted, they are immature and contain one sporoblast; oocyst matures after excretion: the single sporoblast divides in two sporoblasts which develop cyst walls, becoming sporocysts, which eventually contain four sporozoites each<br />
  115. 115. Causal Agent:coccidian parasite, Cystoisospora belli, is the least common of the three intestinal coccidia<br />Geographic Distribution:Worldwide, especially in tropical and subtropical areas.  <br />Infection occurs in immunodepressedpt. and outbreaks in institutionalized groups in US<br />
  116. 116.
  117. 117. infection occurs by ingestion of sporocysts-containing oocysts<br />sporocystsexcyst in the small intestine -- release their sporozoites, which invade the epithelial cells -- initiate schizogony .  <br />Life Cycle:<br />
  118. 118. acute, nonbloody diarrhea with crampyabdpain (weeks)--malabsorption& wt loss. <br />immuno-depressed patients , infants & children—severe diarrhea. <br /> Eosinophilia<br />Clinical Features:<br />
  119. 119. Microscopic <br />wet mounts by bright-field, differential interference contrast (DIC), and epifluorescence<br />modified acid-fast stain.<br />Laboratory Diagnosis:<br />
  120. 120. Trimethoprim-sulfamethoxazole is the drug of choice. <br />Treatment:<br />
  121. 121. Dientamoebafragilis<br />- NO cyst stage<br /><ul><li> not an ameba, but a flagellate!
  122. 122. may possess some pathogenicity
  123. 123. Site in host: LI
  124. 124. Portal of entry:mout
  125. 125. Source of infection: stool (trophs)</li></li></ul><li>
  126. 126. Causal Agent:Dientamoebafragilis is not an ameba but a flagellate.  <br />parasite produces trophozoites; cysts have not been identified. <br />Geographic Distribution:Worldwide.<br />
  127. 127. the trophozoite is the only stage in stools<br />Trophozoites have characteristically one or two nuclei <br />Life Cycle:<br />
  128. 128.
  129. 129. children –intermittent diarrhea, abd pain, n/v, anorexia, fatigue, malaise, poor wt gain<br />Clinical Features:<br />
  130. 130. detection of trophozoites in permanently stained fecal smears (e.g., trichrome). <br />Laboratory Diagnosis:<br />
  131. 131. Nucleus: cluster of granules, with no peripheral chromatin; size range 5-15 µm.<br />
  132. 132.
  133. 133.   The drug of choice is iodoquinol<br />Paromomycin*, tetracycline*, (contraindicated in children under age 8, pregnant and lactating women) or metronidazole can also be used.  <br />Treatment:<br />
  134. 134.
  135. 135. Microsporidia<br /><ul><li>Disease:Microsporidiosis
  136. 136. Genera found in humans:Enterocytozoon, Encephalitozoon, Pleistophora, Nosema, & Microsporidium
  137. 137. Affects immunologically compromised hosts
  138. 138. E. bieneusi: found only in humans & most frequent cause of microsporidian enteritis in AIDS patients
  139. 139. Infective form: spore
  140. 140. Lab Dx: Modified trichrome stain ; PCR</li></li></ul><li>
  141. 141. Stool smear stained with Chromotrope 2R containing Enterocytozoon bieneusi spores. Black arrows indicate E. bieneusi spores with their belt-like stripe visible.  Red arrow indicates an unidentified yeast.  The yellow arrow indicates a vacuolated spore.<br />
  142. 142. Stool smear stained with Quick-Hot Gram Chromotrope stain containing Enterocytozoon bieneusi spores. Black arrows indicate E. bieneusi spores with their belt-like stripe visible.  The red arrow indicates an unidentified yeast.  The yellow arrow indicates a vacuolated spore.<br />
  143. 143. BLOOD and TISSUE PROTOZOA<br />
  144. 144. OTHER PROTOZOA<br />BLOOD and TISSUE PROTOZOA<br />Plasmodium<br />Babesia<br />Trypanosomabrucei<br />Trypanosomacruzi<br />Toxoplasmagondii<br />Leishmania<br />
  145. 145. PROTOZOA FROM OTHER BODY SITES<br />Free-living Amebae<br />Naegleria<br />Acanthamoeba<br />Trichomonasvaginalis<br />
  146. 146. PLASMODIUM<br />Disease: Malaria<br />P. vivax: Benign tertian malaria<br />P. malariae: Quartan malaria<br />P. falciparum: Malignant tertian malaria<br />P. ovale: Ovale tertian malaria<br />Lab Dx: Giemsa stained thick and thin blood smears; IFA; PCR<br />
  147. 147. Infected RBC:<br />P. vivax and P. ovale: reticulocytes<br />P. malariae: senescent erythrocytes<br />P. falciparum: erythrocytes of all ages<br />Cyclic paroxysm of fever:<br />P. vivax and P. ovale: every 48 hours<br />P. malariae: every 72 hours<br />P. falciparum: every 36-48 hours<br />
  148. 148.
  149. 149. P. falciparum: Blood Stage Parasites<br />Thin Blood Smears<br />Fig. 1: Normal red cell; <br />Figs. 2-18: Trophozoites (among these, Figs. 2-10 correspond to ring-stage trophozoites); <br />Figs. 19-26:Schizonts (Fig. 26 is a ruptured schizont); Figs. 27, 28: Mature macrogametocytes (female); Figs. 29, 30:  Mature microgametocytes (male).<br />
  150. 150. Gametocytes of P. falciparum in thin blood smears.  Note the presence of a “Laveran’s bib”, which is not always visible.<br />
  151. 151. P. falciparum rings have delicate cytoplasm and 1 or 2 small chromatin dots.  Red blood cells (RBCs) that are infected are not enlarged; multiple infection of RBCs more common in P. falciparum than in other species.  Occasional appliqué forms (rings appearing on the periphery of the RBC) can be present.<br />
  152. 152. P. falciparum schizonts: seldom seen in peripheral blood.  Mature schizonts have 8 to 24 small merozoites; dark pigment, clumped in one mass.<br />
  153. 153. P. malariae schizonts: have 6 to 12 merozoites with large nuclei, clustered around a mass of coarse, dark-brown pigment.  Merozoites can occasionally be arranged as a rosette pattern. <br />
  154. 154. P. malariae trophozoites: have compact cytoplasm and a large chromatin dot.  Occasional band forms and/or "basket" forms with coarse, dark-brown pigment can be seen.<br />
  155. 155. P. vivax gametocytes: round to oval with scattered brown pigment and may almost fill the red blood cell (RBC).  RBCs are enlarged 1 1/2 to 2 × and may be distorted.  Under optimal conditions, Schüffner's dots may appear more fine than those seen in P. ovale.<br />
  156. 156. Rex Karl S. Teoxon, R.N, M.D<br />133<br />Vector: (night biting)<br />anopheles mosquito <br />minimus flavire<br />
  157. 157. 134<br />SIGNS AND SYMPTOMS<br />Fever, chills, profuse sweating, convulsion, Anemia and fluid and electrolytes imbalance, hepatomegaly, splenomegaly<br />Dx: blood extraction (extract blood at the height of fever) thin and thick smear. Fluorescently labeled Ab<br />
  158. 158. <ul><li>over 1 million deaths/year - mainly Africa
  159. 159. Incubation period - 8-30 days
  160. 160. influenza-like symptoms; paroxysms (fever, chills, rigors) every 36 to 48 hours, depending on species
  161. 161. sickle cell trait and P. falicparum</li></li></ul><li>136<br />COMPLICATIONS<br />P. ovale and vivax – relapse after 10 years of first exposure<br />P. falciparum – <br />Cerebral malaria – severe headache, drowsiness, seizure, delirium, coma<br />Black water fever – jaundice, ARF, hemoglobinuria, black colored urine<br />
  162. 162. 137<br />MANAGEMENT<br />P. Vivax and P. Ovale – Primaquine (relapse) <br />P. falciparum - Chloroquine <br />For chloroquine resistant plasmodium – quinine<br />* Prophylaxis – chloroquine or mefloquine, pyrimethamine/ sulfadoxine (fansidar)<br />
  163. 163. Disease:Babesiosis<br />Lab Dx:Giemsa stained thick and thin blood smears<br />BABESIA<br />
  164. 164.
  165. 165. Babesia microti infection, Giemsa stained thin smear.  The organisms resemble P. falciparum; however Babesia parasites present several distinguishing features: they vary more in shape and in size; and they do not produce pigment. <br />
  166. 166. Infection with Babesia.  Giemsa stained thin smears showing the tetrad, a dividing form pathognomonic for Babesia.  Note also the variation in size and shape of the ring stage parasites and the absence of pigment. <br />
  167. 167. TRYPANOSOMA BRUCEI<br />Disease: African trypanosomiasis<br />T. b. gambiense: Gambian trypanosomiasis, West & Mid-African sleeping sickness<br />T. b. rhodesiense: Rhodesian trypanosomiasis, East African sleeping sickness<br />Lab Dx:Giemsa stained thick and thin blood smears or lymph exudate (early stage); Giemsa stained smears of CSF (late stage)<br />
  168. 168. Site in host: lymph glands, blood stream, brain<br />Portal of entry: skin<br />Source of infection: tsetse fly<br />Winterbottom’s sign: enlargement of posterior cervical LNs<br />
  169. 169.
  170. 170. Trypomastigote: slender to fat and stumpy forms; in Giemsa stained films – C or U shaped forms NOT seen; small, oval kinetoplast located posterior to the nucleus; a centrally located nucleus, an undulating membrane, and an anterior flagellum. The trypanosomes length range is 14-33 µm <br />
  171. 171. A dividing parasite is seen at the right. Dividing forms are seen in African trypanosomiasis, but not in American trypanosomiasis (Chagas' disease)<br />
  172. 172. Tsetse fly. The vector of African trypanosomiasis<br />
  173. 173. Winterbottoms sign<br />
  174. 174. TRYPANOSOMA CRUZI<br />Disease: American trypanosomiasis, Chaga’sdisease<br />Lab Dx:Giemsa stained thick and thin blood smears for the trypomastigote; histopath exam for the amastigote<br />Site in host: Tissues – heart; blood<br />Portal of entry: skin<br />Source of infection: Kissing bug Triatomidae<br />
  175. 175. Trypomastigote: shape is short & stubby to long & slender; in Giemsa stained blood films – C or U shaped; kinetoplast is large, oval & located posterior to the nucleus; anterior long free flagellum<br />
  176. 176. Trypanosoma cruzi crithidia<br />
  177. 177. Trypanosoma cruzi: Leishmanial form <br />
  178. 178. Riduviid bug: the vector of American trypanosomiasis<br />
  179. 179. Ramana's sign: unilateral conjunctivitis and orbital edema  <br />
  180. 180. Chaga'sDisease<br /><ul><li>asymptomatic- mostly
  181. 181. acute- rash, edema on face (site of bite), </li></ul>flu-like symptoms<br /><ul><li>chronic– rare but serious
  182. 182. g.i. tract nerve damage leading to megacolon
  183. 183. heart- conductive problems and </li></ul>cardiomyopathy, sudden death<br />
  184. 184. <ul><li>"kissing bug" reduviid bug vector --(epimastigotereplicative form)</li></ul>Entry, Spread, Multiplication<br /><ul><li>bug defecates on wound releasing trypomastigotes that get rubbed into wound and vasculature
  185. 185. convert to amastigotes that invade and replicate in host cells</li></li></ul><li>
  186. 186. Diagnosis– clinical, serology, blood smear microscopy<br />Treatment- not very good, especially for late complications<br />Prevention– clear houses of bugs, use netting for sleeping<br />
  187. 187. TOXOPLASMA GONDII<br />Disease: Toxoplasmosis<br />Site in host: All organs<br />Portal of entry:<br />Ingestion of oocyst contaminated water<br />Aerosolization of oocyst contaminated dust or litter<br />Consumption of raw or undercooked cyst infected meat<br />Transplacental passage of the tachyzoite<br />
  188. 188. - Definitive host: domestic cats<br /> - Intermediate host: infected rodents<br />Accidental intermediate host: humans<br />Lab Dx: IFAT and ELISA; Giemsa-stained smears of exudates, aspirates or tissues<br />
  189. 189. Toxoplasma gondii, parasite<br />Affects birds, mammals i.e. cats<br />Infected person may carry the organism for life (reactivation is possible)<br />161<br />TOXOPLASMOSIS<br />
  190. 190. 162<br />PATHOGENESIS<br />ingestion of cyst from uncooked meat / fecal oral route from infected cats (feces)<br />Quickly multiply in the GIT<br />Distributed to CNS, lymphatic tissue, skeletal muscle, myocardium, retina and placenta<br />
  191. 191.
  192. 192. T. gondiitachyzoites:crescentic to pyriform shaped with a prominent, centrally placed nucleus.<br />
  193. 193. Toxoplasma gondii cyst in brain tissue stained with hematoxylin and eosin (100×).<br />
  194. 194. 166<br />SIGNS AND SYMPTOMS<br />Malaise, fever, myalgia, headache, fatigue, sore throat, lymphadenopathy or asymptomatic<br />FULMINANT = vomiting, cough and dyspnea, hyperpyrexia, delirium and seizures, encephalopathy, meningitis<br />INFANTS = hydrocephalus or microcephalus, seizure, jaundice later strabismus, blindness, epilepsy, mental retardation<br />
  195. 195. 167<br />DIAGNOSIS<br />Serology – high IgM or rising IgM<br />CT scan<br />Mgmt:<br />4-6 weeks of sulfadiazine + pyrimethamine (take folic acid to counteract drug’s adverse effects)<br />
  196. 196. LEISHMANIA<br /><ul><li>Disease:
  197. 197. L. tropica complex: Old Word Cutaneousleishmaniasis (oriental sore, Aleppo boil, Delhi ulcer, Baghdad boil)
  198. 198. L. mexicana complex: New Word Cutaneousleishmaniasis (chiclero ulcer, bay sore)
  199. 199. L. braziliensis complex: Mucocutaneusleishmaniasis (espundia, uta)
  200. 200. L. donovani: Visceral leishmaniasis (kala-azar or black disease, Dumdum fever)</li></li></ul><li><ul><li>Lab Dx: Giemsa stained tissue sections or impression smears
  201. 201. Site in host: Monocytes/macrophages of skin & mucosa
  202. 202. Portal of entry: Skin
  203. 203. Source of infection: Phlebotomus or Lutzomiya fly</li></li></ul><li>
  204. 204. L. tropica amastigotes: ovoid in shape; large & eccentric nucleus; small, rodlike kinetoplast positioned opposite the nucleus; rodlike axoneme perpendicular to the kinetoplast<br />
  205. 205. FREE LIVING AMEBAE<br /><ul><li>Disease:
  206. 206. Naegleria:Primary Amebic Meningoencephalitis (PAM)
  207. 207. Acanthamoeba:Chronic Granulomatous Amebic Encephalitis and keratitis
  208. 208. Lab Dx: Direct microscopic exam (Wheatley’s trichromestain)</li></ul>PROTOZOA FROM OTHER BODY SITES<br />
  209. 209. FREE LIVING AMEBAE<br /><ul><li>Portal of Entry:
  210. 210. Naegleria:nose
  211. 211. Acanthamoeba:respiratory tract or ulcers in skin or mucosa / direct invasion of eye
  212. 212. Source of infection:
  213. 213. Naegleria: warm lakes, streams, ponds or inadequately chlorinated swimming pools
  214. 214. Acanthamoeba: immunocompromised or debilitated host </li></li></ul><li>
  215. 215. N. fowleri trophozoites cultured from cerebrospinal fluid: cells have characteristically large nuclei, with a large, dark staining karyosome.  The amebae are very active and extend and retract broad pseudopods. Trichrome stain. <br />
  216. 216. Acanthamoeba spp.:the cysts are spherical, 15-20 µm in diameter, having a thick double wall. The outer wall may be spherical or wrinkled, the inner wall appear stellate or polyhedral<br />
  217. 217. Acanthamoeba spp.: cysts stained with Heidenhain’s iron alum-haematoxylin method.<br />
  218. 218. TRICHOMONAS VAGINALIS<br /><ul><li>Disease: Trichomonadvaginitis
  219. 219. Site in host: vagina & prostate
  220. 220. Portal of entry: genitalia
  221. 221. Sources of infection:trophs in vaginal & prostatic secretions
  222. 222. NO cyst stage
  223. 223. Lab Dx:trophs in vaginal & prostatic fluids</li></li></ul><li>
  224. 224. Trophozoites of T. vaginalis: large, pyriform flagellate exhibiting rapid & jerky motility. The wavelike motion of the undulating membrane is often apparent<br />
  225. 225. Trichomonas vaginalis:flagellates are 10-30 µm in lenght and 6-20 µm in breadth. Flagella, nucleus, axostyle and undullating membrane are visible. Filamentous form of Lactobacillus Döderleini is present. Giemsa-Romanowski stain.<br />
  226. 226. Trichomonas vaginalis<br />parasite<br />182<br />TRICHOMONIASIS<br />
  227. 227. 183<br />SIGNS AND SYMPTOMS<br />Females: itching, burning on urination, yellow gray frothy malodorous vaginal discharge, foul smelling<br />Males: usually asymptomatic<br />Dx: microscopic exam of vaginal discharge<br />
  228. 228. 184<br />MANAGEMENT<br />Metronidazole (Flagyl)<br />include partners<br />CX: PROM<br />
  229. 229.
  230. 230. The Helminths<br />Table 12.1<br />
  231. 231. Eukaryotic<br />Multicellular animals<br />Chemoheterotrophic<br />Kingdom: Animalia<br />Phylum: Platyhelminthes (flatworms)<br />Class: Trematodes (flukes)<br />Class: Cestodes (tapeworms)<br />Phylum: Nematodes (roundworms)<br />Helminths (Parasitic Worms)<br />
  232. 232. Trematodes<br />Figure 12.25<br />
  233. 233. Humans as Definitive Host<br />Figure 12.26<br />
  234. 234. Cestodes<br />Figure 12.27<br />
  235. 235. Humans as Intermediate Host <br />Figure 12.28<br />
  236. 236. Nematodes: Eggs Infective for Humans<br />Figure 12.29<br />
  237. 237. Nematodes: Larvae Infective for Humans<br />Figure 25.26<br />
  238. 238. Kingdom: Animalia<br />Phylum: Arthropoda (exoskeleton, jointed legs)<br />Class: Insecta (6 legs)<br />Lice, fleas, mosquitoes<br />Class: Arachnida (8 legs)<br />Mites and ticks<br />May transmit diseases (vectors)<br />Arthropods as Vectors<br />Figures 12.31a, 12.32<br />
  239. 239. HELMINTHS<br /> INTESTINAL NEMATODES<br /><ul><li>Enterobius vermicularis
  240. 240. Ascaris lumbricoides
  241. 241. Necator americanus
  242. 242. Ancylostoma duodenale
  243. 243. Trichuris trichiura
  244. 244. Strongyloides stercoralis</li></li></ul><li><ul><li>INTESTINAL CESTODES
  245. 245. Taenia saginata
  246. 246. Taenia solium
  247. 247. Hymenolepis diminuta
  248. 248. Diphyllobothrium latum
  249. 249. Dipylidium caninum</li></li></ul><li><ul><li>INTESTINAL TREMATODES
  250. 250. Clonorchis sinensis
  251. 251. Fasciola hepatica
  252. 252. Paragonimus westermani
  253. 253. Fasciolopsis buski
  254. 254. Heterophyes heterophyes
  255. 255. Metagonimus yokogawai
  256. 256. Schistosoma mansoni
  257. 257. Schistosoma haematobium
  258. 258. Schistosoma japonicum</li></li></ul><li><ul><li>TISSUE NEMATODES & CESTODES
  259. 259. Trichinella spiralis
  260. 260. Echinococcus granulosus
  261. 261. Echinococcus multilocularis
  262. 262. Spirometra species</li></li></ul><li>Causal Agents:<br />The nematode (roundworm) Capillariaphilippinensis causes human intestinal capillariasis<br />C. hepatica-- humans hepatic capillariasis<br />C. aerophila-- humans pulmonary capillariasis.<br />
  263. 263. Geographic Distribution:Capillariaphilippinensis is endemic in the Philippines and also occurs in Thailand. <br />
  264. 264.
  265. 265. Life Cycle:<br />unembryonated eggs are passed in the human stool and become embryonated<br />after ingestion by freshwater fish-- larvae hatch & penetrate the intestine-- migrate to the tissues -Ingestion of raw or undercooked fish<br />Adults worm -small intestine<br />females deposit unembryonatedeggs (autoinfection)  -- hyperinfection(a massive number of adult worms) .  <br />
  266. 266. Life Cycle:<br />Capillaria hepatica adult worms reside in the liver of various animals, especially rats. <br />Capillariaaerophila adult worms reside in the epithelium of the tracheo-bronchial tract of various animals. <br />
  267. 267. Clinical Features:<br /> Intestinal capillariasis-- pain and diarrhea<br /> autoinfection.  <br />protein-losing enteropathy-- cachexiaand death<br />Hepatic capillariasis (C. hepatica) -- acute or subacute hepatitis with eosinophilia-- dissemination -- fatal<br />Pulmonary capillariasis (C. aerophila) -- fever, cough, asthma, and pneumonia-- fatal.<br />
  268. 268. Diagnostic findings<br />Microscopy<br />Treatment:The drug of choice is mebendazole*, and albendazole* is an alternative. <br />
  269. 269. ASCARIS LUMBRICOIDES<br /><ul><li>Disease: Ascariasis; roundworm infection
  270. 270. Site in host: SI
  271. 271. Portal of entry: Mouth
  272. 272. Infective stage: ova containing second stage larva
  273. 273. Sources of infection: eggs from soil or vegetables
  274. 274. Lab Dx: eggs in stool</li></li></ul><li>Fertilized Ascaris egg (A) still at the unicellular stage. Unfertilized and fertilized eggs, (B and C, respectively).<br />
  275. 275. Adult Ascaris worm: tapered ends; length 15 to 35 cm (the females tend to be the larger ones).  This worm is a female, as evidenced by the size and genital girdle (the dark circular groove at bottom area of image).<br />
  276. 276.
  277. 277. Causal Agent:<br />Ascarislumbricoidesis the largest nematode (Adult females: 20 to 35 cm; adult male: 15 to 30 cm.)<br />Geographic Distribution:most common human helminthic infection.  Worldwide distribution.  Highest prevalence in tropical and subtropical regions, and areas with inadequate sanitation. <br />
  278. 278.
  279. 279. Life Cycle:<br />Adult worms live in the lumen of the small intestine--produce 200,000 eggs/day<br />  Fertile eggs embryonate- infective<br />eggs swallowed -- the larvae hatch &, invade the intestinal mucosa-- portal-- systemic -- lungs .  <br />lungs -- alveolar walls-- bronchial tree – throat swallowed-- small intestine-- adult worms .  <br />
  280. 280. Clinical Features:<br />adult worms usually cause no acute symptoms.  <br />High worm burdens –abd pain & obstruction.  <br />Migrating worms – occlusion of biltract or oral expulsion.  <br />lung phase of larval migration, pulmonary symptoms can occur (cough, dyspnea, hemoptysis, eosinophilicpneumonitis - Loeffler’s syndrome).<br />
  281. 281. Diagnostic findings<br />Microscopy<br />Treatment:The drugs of choice for treatment of ascariasis are albendazole* with mebendazole, ivermectin*, and nitazoxanide as alternatives.  <br /> In the United States, ascariasis is generally treated for 1-3 days with medication prescribed by a health care provider.  The drugs are effective and appear to have few side effects. <br />
  282. 282. Ascaris lumbricoides<br />In GI tract, few symptoms in light infections<br />Nausea<br />Vomiting<br />Obstruction of small bowel or common bile duct.<br />Pulmonary: symptoms due to migration<br />Alveoli (verminous pneumonia)—cough, fever wheeze, dyspnea, X-ray changes, eosinophilia<br />
  283. 283. Effects of Adult Ascaris Worms<br />Depends on worm load<br />Effects<br />Mechanical: obstruction, volvulus, intussusception, appendicitis, obstructive jaundice, liver abscesses, pancreatitis, asphyxia<br />Toxic and Metabolic<br />Malnutrition (complex)<br />
  284. 284. Ascaris lumbricoidesDiagnosis<br />Characteristic eggs on direct smear examination<br />If treating mixed infections, treat Ascaris first<br />Mebendazole<br />Pyrantel <br />Control: <br />Periodic mass treatment of children, health education, environmental sanitation<br />
  285. 285.
  286. 286. Causal Agent:The nematode (roundworm) Trichuristrichiura, also called the human whipworm.<br />Geographic Distribution:The third most common round worm of humans.  Worldwide, with infections more frequent in areas with tropical weather and poor sanitation practices, and among children.  <br />It is estimated that 800 million people are infected worldwide.  Trichuriasis occurs in the southern United States.<br />
  287. 287.
  288. 288. Life Cycle:<br />The unembryonated eggs are passed with the stool .  In the soil, the eggs develop into a 2-cell stage embryonate eggs<br /> After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine-larvae - adults in the cecum and ascending colon. <br /> Female worms in the cecum shed between 3,000 and 20,000 eggs per day. <br />
  289. 289. Clinical Features:<br />Most frequently asymptomatic.  Heavy infections, especially in small children, can cause gastrointestinal problems (abdominal pain, diarrhea, rectal prolapse) and possibly growth retardation.<br />
  290. 290. Diagnostic findings<br />microscopy<br />Examination of the rectal mucosa by proctoscopy (or directly in case of prolapses) can occasionally demonstrate adult worms.<br />Treatment:Mebendazole is the drug of choice, with albendazole as an alternative. <br />
  291. 291. Case 13<br />8-yr-old schoolgirl visiting the U.S. from Malaysia<br />1 week history of epigastric pain, flatulence, anorexia, bloody diarrhea<br />No eosinophilia noted<br />Clinical diagnosis of amoebic dysentery made <br />However, microscopy of stool prep…<br />
  292. 292.
  293. 293. Diagnosis?<br />
  294. 294. Trichuris trichiura (Whipworm)<br />Common in Southeast U.S. <br />Frequently coexists with ascaris<br />Entirely intraluminal life cycle—eggs are ingested<br />Frequently asymptomatic<br />Severe infections: diarrhea, abdominal pain and tenesmus<br />Rectal prolapse in children<br />DS-eggs in stool<br />Mebendazole 100 mg bid x 3 days<br />
  295. 295.
  296. 296.
  297. 297.
  298. 298. ENTEROBIUS VERMICULARIS<br /><ul><li>Disease: Enterobiasis; pinworm infection; seatworm infection; oxyuriasis
  299. 299. Site in host: LI, appendix
  300. 300. Portal of entry: Mouth
  301. 301. Infective stage: ova containing rhabditiform larva
  302. 302. Sources of infection: oral-fecal route; through contaminated fomites/food; inhalation ff by ingestion of airborne ova; retroinfection
  303. 303. Lab Dx: eggs in perianal region; Scotch tape swab</li></li></ul><li>Enterobius eggs: oval, asymmetric w/ one side noticeably flattened; smooth, thin-shelled, maycontain embryo <br />
  304. 304. Anterior end of Enterobius vermicularis adult worm.<br />
  305. 305.
  306. 306. Causal Agent:<br />The nematode (roundworm) Enterobiusvermicularis (previously Oxyurisvermicularis) also called human pinworm.  (Adult females: 8 to 13 mm, adult male: 2 to 5 mm.)  Humans are considered to be the only hosts of E. vermicularis. <br />Geographic Distribution:Worldwide, with infections more frequent in school- or preschool-children and in crowded conditions.  <br />Enterobiasis appears to be more common in temperate than tropical countries.  The most common helminthic infection in the United States (an estimated 40 million persons infected).<br />
  307. 307.
  308. 308. Life Cycle:<br />Eggs are deposited on perianal folds .  Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . <br /> Person-to-person transmission can also occur through handling of contaminated clothes or bed linens.  <br />Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (e.g., curtains, carpeting).  Some small number of eggs may become airborne and inhaled.  <br />.<br />
  309. 309. Life Cycle:<br />These would be swallowed and follow the same development as ingested eggs.  -larvae hatch in the small intestine -adults in the colon .<br />Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area .  The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions .  <br />Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum<br />
  310. 310. Clinical Features<br />Enterobiasis is frequently asymptomatic.  <br />The most typical symptom is perianalpruritus, especially at night, which may lead to excoriations and bacterial superinfection.  <br />Occasionally, invasion of the female genital tract with vulvovaginitis and pelvic or peritoneal granulomas can occur.  <br />Other symptoms include anorexia, irritability, and abdominal pain.<br />
  311. 311. Diagnostic findings<br />Microscopy<br />Treatment:The drug of choice is pyrantelpamoate.  <br />Measures to prevent reinfection, such as personal hygiene and laundering of bedding, should be discussed and implemented in cases where infection affects other household members. <br />
  312. 312. Case 10<br />11-year-old female<br />Doing poorly in school<br />Not sleeping well<br />Anorectic<br />Complains of itching in rectal region throughout the day<br />A Scotch-tape test reveals…<br />
  313. 313.
  314. 314.
  315. 315.
  316. 316. Diagnosis?<br />
  317. 317. Enterobius (Pinworm)<br />18 million infections in U.S.<br />Incidence higher in whites<br />Preschool and elementary school most often<br />Mostly asymptomatic<br />Nocturnal anal pruritis cardinal feature due to migration and eggs<br />May have insomnia, possible emotional symptoms<br />DS-eggs or adults on perineum {scotch tape}<br />Mebendazole 100 mg. Repeat in 2 weeks. Pyrantel pamoate 11 mg/kg; repeat 2 weeks<br />
  318. 318. NECATOR AMERICANUS<br /><ul><li>Disease: New World Hookworm Disease
  319. 319. Site in host: SI, attached
  320. 320. Portal of entry: Skin
  321. 321. Infective stage: filariform larva
  322. 322. Sources of infection: infective filariform larvae in soil
  323. 323. Lab Dx: eggs in stool</li></li></ul><li>Hookworm egg: oval or ellipsoid; thin shell; usually embryo at four cell stage<br />
  324. 324. The embryo has begun cellular division and is at an early (gastrula) developmental stage.<br />
  325. 325. Hookworm rhabditiform larva (wet preparation).<br />
  326. 326. Hookworm filariform larva (wet preparation).<br />
  327. 327.
  328. 328.
  329. 329. Anterior end of Necator americanus:oral opening of this species contains cutting "plates" . The muscular esophagus is labeled in this image (*).<br />
  330. 330. ANCYLOSTOMA DUODENALE<br /><ul><li>Disease: Old World Hookworm Disease
  331. 331. Site in host: SI, attached
  332. 332. Portal of entry: skin, usually feet
  333. 333. Infective stage: filariform larva
  334. 334. Sources of infection: infective filariform larvae in soil
  335. 335. Lab Dx: eggs in stool</li></li></ul><li>Oral opening of Ancylostoma duodenale:presence of four cutting "teeth," two on each side.<br />
  336. 336. B<br />A<br />A: Adult worm of Ancylostoma duodenale.  Anterior end is depicted showing cutting teeth.B: Adult worm of Necator americanus.  Anterior end showing mouth parts with cutting plates.<br />
  337. 337.
  338. 338.
  339. 339. Causal Agents:<br />The human hookworms include two nematode (roundworm) species, Ancylostomaduodenale and Necatoramericanus.  <br />A smaller group of hookworms infecting animals can invade and parasitize humans (A. ceylanicum) or can penetrate the human skin (causing cutaneous larva migrans), but do not develop any further (A. braziliense, A. caninum, Uncinariastenocephala).  <br />Occasionally A. caninum larva may migrate to the human intestine causing eosinophilic enteritis; this may happen when larva is ingested rather than through skin invasion.<br />
  340. 340. Geographic Distribution:<br />The second most common human helminthic infection (after ascariasis). <br /> Worldwide distribution, mostly in areas with moist, warm climate.  <br />Both N. americanus and A. duodenale are found in Africa, Asia and the Americas.  <br />Necatoramericanus predominates in the Americas and Australia, while only A. duodenale is found in the Middle East, North Africa and southern Europe.<br />
  341. 341.
  342. 342. Life Cycle:<br />Eggs are passed in the stool-released rhabditiform larvae grow in the feces and/or the soil , and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective .  <br />  On contact with the human host, the larvae penetrate the skin and are carried through the veins to the heart and then to the lungs.  They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed <br />The larvae reach the small intestine- adults.  Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host .  <br />In addition, infection by A. duodenale may probably also occur by the oral and transmammary route.  N. americanus, however, requires a transpulmonary migration phase<br />
  343. 343. Clinical Features:<br />Iron deficiency anemia is the most common symptom of hookworm infection, and can be accompanied by cardiac complications.  <br />Gastrointestinal and nutritional/metabolic symptoms can also occur.  <br />local skin manifestations ("ground itch") can occur during penetration by the filariform (L3) larvae, and respiratory symptoms can be observed during pulmonary migration of the larvae.<br />
  344. 344. Diagnostic Findings<br />Microscopy<br />between N. americanus and A. duodenale.  Larvae can be used to differentiate between N. americanus and A. duodenale, by rearing filariform larvae in a fecal smear on a moist filter paper strip for 5 to 7 days (Harada-Mori). <br />
  345. 345. Treatment:<br />In countries where hookworm is common and reinfection is likely, light infections are often not treated.  In the United States, hookworm infections are generally treated with albendazole*  Mebendazole* or pyrantelpamoate* can also be used.  <br />Eosinophilic enteritis caused by A. caninum and for cutaneous larva migrans(creeping eruption) caused by canine and feline hookworms.<br />
  346. 346. Case 12<br />57 year old farmer from Dixie County<br />Presents with profound SOB<br />Physical examination: anemic otherwise unremarkable<br />Laboratory examination reveals a profound anemia (hct 24) with aniso and poikilocytosis<br />Remainder of laboratory examination normal.<br />
  347. 347.
  348. 348. Diagnosis?<br />
  349. 349.
  350. 350. Hookworm <br />Hookworm responsible for development of USPHS<br />Caused by two different species (North American and Old World)<br />Very similar to strongyloides in life cycle<br />Attaches to duodenum, feeds on blood<br />Elaborates anticoagulant, attaches and reattaches many times<br />Loss of around 0.1 ml/d of blood per worm<br />
  351. 351.
  352. 352.
  353. 353. Case 14<br />18-year-old trailer park handyman seen in ER<br />Worked under trailers wearing shorts and no shirt<br />Developed intensely pruritic skin rash<br />Unable to sleep<br />WBC 18,000<br />65% eosinophils.<br />
  354. 354.
  355. 355. Case 15<br />An 8 year old boy<br />Presents with skin lesions and itching after spending the summer at a beach condo in St. Augustine with his family (mother, father, younger sister, dog and cat).<br />Legs show several raised, reddened, serpiginous lesions that are intensely pruritic.<br />
  356. 356.
  357. 357. Diagnosis ?<br />
  358. 358. Cutaneous Larva Migrans<br />Caused by filariform larvae of dog or cat hookworm (Ancylostoma braziliense or Ancylostoma duodenale<br />Common in Southeast U.S.<br />Red papule at entry with serpiginous tunnel<br />Intense pruritis<br />Self limiting condition<br />Diagnosis clinical<br />Topical or oral thiabendazole 25 mg/kg bid for 3-5 days<br />May use ethyl chloride topically<br />
  359. 359. Cutaneous larva migrans (creeping eruption)<br />More common in children<br />Larvae penetrate skin and cause tingling followed by intense itching.<br />Eggs shed from dog and cat bowels develop into infectious larvae outside the body in places protected from desiccation and extremes of temperature<br />Shady, sandy areas under houses, at beach, etc.<br />
  360. 360. Cutaneous larva migrans (creeping eruption)<br />Usually not associated with systemic symptoms <br />
  361. 361. Cutaneous larva migrans (creeping eruption)<br />Diagnosis and treatment<br />Skin lesions are readily recognized<br />Usually diagnosed clinically<br />Generally do not require biopsy<br />Reveal eosinophilia inflammatory infiltrate<br />Migrating parasite is generally not seen<br />Stool smear will reveal eggs<br />
  362. 362.
  363. 363.
  364. 364. Visceral Larva Migrans <br />Infection with dog or cat round worms<br />Toxocara canis; Toxocara catis<br />Underdiagnosed based on seroprevalence surveys<br />Heavy infections associated with fever, cough, nausea, vomiting, hepatomegaly, and eosinophilia<br />Uncommon in adults<br />Ocular type more common in adults<br />Diagnosis-ELISA<br />Thiabendazole: 25 mg/kg bid X 5 days<br />
  365. 365. Case 17<br />A 34 yr-old woman from Saudi Arabia<br />Radiation and cyclophosphamide, adriamycin, vincristine and prednisone for diffuse large B cell lymphoma of the neck.<br />Mild eosinophilia (AEC=500) at the time of diagnosis<br />4 months after initiation of chemo, c/o intermittent diffuse abdominal pain, bloating, constipation and occasional rectal bleeding.<br />Absolute eosinophil count: 1000<br />
  366. 366. Case 17<br />No evidence of lymphoma found on re-staging<br />Completed chemo, was deemed to be in complete remission, but had persistence of GI complaints.<br />Upper endoscopy was unrevealing.<br />Colonoscopy and biopsy revealed granulomatous inflammation, prominent eosinophilic infiltrate, surrounding a collection of eggs.<br />
  367. 367.
  368. 368. STRONGYLOIDES STERCORALIS<br /><ul><li>Disease: Strongyloidiasis, Cochin-China diarrhea or Vietnam diarrhea
  369. 369. Site in host: wall of SI
  370. 370. Portal of entry: skin
  371. 371. Infective stage: filariform larva
  372. 372. Sources of infection: larvae in soil; autoinfection
  373. 373. Lab Dx: larvae in stool</li></li></ul><li>Strongyloides stercoralis first-stage larva: The rhabditoid esophagus is clearly visible in this larva; it consists of a club-shaped anterior portion, a postmedian constriction, and a posterior bulb.<br />
  374. 374.
  375. 375. Causal Agent:<br />The nematode (roundworm) Strongyloidesstercoralis.  Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.<br />.<br />Geographic Distribution:Tropical and subtropical areas, but cases also occur in temperate areas (including the South of the United States).  More frequently found in rural areas, institutional settings, and lower socioeconomic groups<br />
  376. 376.
  377. 377. Life Cycle:<br />The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host.  Two types of cycles exist:<br />
  378. 378. Life Cycle:<br />Free-living cycle: The rhabditiform larvae passed in the stool (see "Parasitic cycle" below) can either molt twice and become infective filariform larvae (direct development) or molt four times and become free living adult males and females that mate and produce eggs from which rhabditiform larvae hatch .  <br />The latter in turn can either develop into a new generation of free-living adults (as represented in ), or into infective filariform larvae .  The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) .<br />
  379. 379. Life Cycle:<br />Parasitic cycle:Filariform larvae in contaminated soil penetrate the human skin , and are transported to the lungs where they penetrate the alveolar spaces; they are carried through the bronchial tree to the pharynx, are swallowed and then reach the small intestine . <br /> In the small intestine become adult female worms .  The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae.  The rhabditiform larvae can either be passed in the stool (see "Free-living cycle" above), or can cause autoinfection .<br /> <br />
  380. 380. Life Cycle:<br />Parasitic cycle:   In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); <br /> To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloidesstercoralis and Capillariaphilippinensis infections. <br />
  381. 381. Clinical Features<br />Frequently asymptomatic.  Gastrointestinal symptoms include abdominal pain and diarrhea.  <br />Pulmonary symptoms (including Loeffler’s syndrome) can occur during pulmonary migration of the filariform larvae.  <br />Dermatologic manifestations include urticarial rashes in the buttocks and waist areas. <br /> Disseminated strongyloidiasis occurs in immunosuppressed patients, can present with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal.  <br />Blood eosinophilia is generally present during the acute and chronic stages, but may be absent with dissemination.<br />
  382. 382. Diagnostic findings<br />Microscopy<br />Treatment:The drug of choice for the treatment of uncomplicated strongyloidiasis is ivermectin with albendazole* as the alternative.  All patients who are at risk of disseminated strongyloidiasis should be treated. <br />
  383. 383. On the day of admission…<br />Fever, confusion, and not able to get out of bed---transported to the hospital<br />Initial blood work:<br />Elevated WBC<br />Raised eosinophil count 4 times normal<br />Underwent UGI endoscopy<br />Duodenal biopsy obtained <br />
  384. 384.
  385. 385. Strongyloides: Crucial Aspects of Life Cycle<br />Infection acquired through penetration of intact skin<br />Infection may persist for many years via autoinfection<br />In immunocompromised patients, there is risk of dissemination or hyperinfection<br />Hyperinfection syndrome<br />
  386. 386. Disseminated Strongyloidiasis<br />High mortality75%<br />Penetration of gut wall by infective larvae<br />Gut organisms carried on the surface of larvae results in polymicrobial sepsis, meningitis<br />Larvae disseminate into all parts of body: CNS, lungs, bladder, peritoneum<br />
  387. 387. Summary—Clinical Findings<br />Defective cell-meditated immunity: steroids, burns, lymphomas, AIDS (?)<br />Gl symptoms in about two-thirds:<br />Abdominal pain<br />Bloating<br />Diarrhea<br />Constipation<br />Wheezing, SOB, hemoptysis<br />
  388. 388. Summary—Clinical Findings<br />Skin rash or pruritis in ~ one-third<br />Larva currens (racing larva)<br />Intensely pruritic<br />Linear or serpiginous urticaria with flare that moves 5-15 cm/hr<br />Usually buttocks, groin, and trunk<br />In dissemination, diffuse petechiae and purpura<br />
  389. 389. Summary-Clinical Findings<br />Eosinophilia 60-95%<br />Less if on steroids <br />
  390. 390. DIPHYLLOBOTHRIUM LATUM<br /><ul><li>Disease: Diphyllobothriasis; fish tapeworm infection; broad tapeworm infection
  391. 391. Site in host: SI
  392. 392. Portal of entry: mouth
  393. 393. Definitive host: human, dogs, cats
  394. 394. 1st Intermediate host: crustaceans (Cyclops or Diaptomus)
  395. 395. 2nd Intermediate host: freshwater fish
  396. 396. Infective stage: plerocercoid larvae
  397. 397. Sources of infection: plerocercoid in freshwater fish
  398. 398. Lab Dx: eggs in stool</li></li></ul><li>
  399. 399. Eggs of D. latum:oval or ellipsoidal, with at one end an operculum that can be inconspicuous.  At the opposite (abopercular) end is a small knob that can be barely discernible.  <br />
  400. 400. Eggs of Diphyllobothrium latum:are oval or ellipsoidal, with at one end an operculum (arrows) that can be inconspicuous.  The eggs are passed in the stool unembryonated. <br />
  401. 401.
  402. 402. D. latum scolex and gravid proglottids<br />
  403. 403. Proglottids of Diphyllobothrium latum.  These proglottids tend to be passed in strands of variable length in the stool.  The proglottids tend to be broader than long. <br />
  404. 404. Proglottids of D. latum:broader than it is long; size 2 to 4 mm long by 10 to 12 mm wide; uterus coiled in rosette appearance; genital pore at the center of the proglottid.<br />
  405. 405. Causal Agents:<br />The cestodeDiphyllobothriumlatum (the fish or broad tapeworm), the largest human tapeworm. <br />Geographic Distribution:Diphyllobothriasis occurs in the Northern Hemisphere <br />Freshwater fish infected with Diphyllobothrium sp. larva may be transported to and consumed in geographic areas where active transmission does not occur, resulting in human diphyllobothriasis. <br />
  406. 406.
  407. 407. Life Cycle:<br />Immature eggs are passed in feces -oncospheres -develop into a coracidia . <br /> After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae .  <br />second intermediate host, typically minnows and other small freshwater fish, the procercoid larvae are released from the crustacean and migrate into the fish flesh where they develop into a plerocercoid larvae (sparganum) <br />plerocercoid larvae are the infective stage for humans.  Because humans do not generally eat undercooked minnows and similar small freshwater fish, these do not represent an important source of infection.  <br /> <br />
  408. 408. Life Cycle:<br />  After ingestion of the infected fish, the plerocercoid develop into immature adults and then into mature adult tapeworms which will reside in the small intestine. <br /> The adults of D. latum attach to the intestinal mucosa by means of the two bilateral groves (bothria) of their scolex .  The adults can reach more than 10 m in length, with more than 3,000 proglottids. <br /> Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . <br />
  409. 409. Clinical Features:<br />Diphyllobothriasis can be a long-lasting infection (decades).  <br />Most infections are asymptomatic.  <br />Manifestations may include abdominal discomfort, diarrhea, vomiting, and weight loss.  <br />Vitamin B12 deficiency with pernicious anemia may occur.  <br />Massive infections may result in intestinal obstruction.  <br />Migration of proglottids can cause cholecystitis or cholangitis.<br />
  410. 410. Diagnostic findings<br />Microscopy<br />Treatment:Praziquantel* is the drug of choice.  Alternatively, Niclosamide can also be used to treat diphyllobothriasis.  <br />
  411. 411. DIPYLIDIUM CANINUM<br /><ul><li>Disease: Dipylidiasis; dog tapeworm infection
  412. 412. Site in host: SI
  413. 413. Portal of entry: mouth
  414. 414. Definitive host: dog & cat (or humans)
  415. 415. Intermediate host: larval flea
  416. 416. Infective stage: eggs
  417. 417. Sources of infection: flea & louse
  418. 418. Lab Dx: eggs in stool or egg sacks in stool</li></li></ul><li>Egg of Dipylidium caninum:round to oval (average size 35 to 40 µm) and contain an oncosphere that has 6 hooklets. Ovum contains hexacanth wmbryo (8-15 ova are usually enclosed within sac-like membrane) <br />
  419. 419. Egg packets of Dipylidium caninum:Proglottids of Dipylidium caninum contain characteristic egg packets that are round to ovoid and contain 5 to 15 (sometimes more) eggs each.  <br />
  420. 420. Proglottids of D. caninum: barrel-shaped proglottids (average mature size 12 mm × 3 mm) have two genital pores, one in the middle of each lateral margin.  Proglottids may be passed singly or in chains, and occasionally may be seen dangling from the anus. Proglottids are much longer than broad.<br />
  421. 421. Adult tapeworm of Dipylidium caninum.  The scolex of the worm is very narrow and the proglottids, as they mature, get larger.<br /> <br />
  422. 422. Causal Agent:<br />Dipylidiumcaninum(the double-pored dog tapeworm) mainly infects dogs and cats, but is occasionally found in humans.<br />Geographic Distribution:Worldwide.  Human infections have been reported in Europe, the Philippines, China, Japan, Argentina, and the United States<br />
  423. 423.
  424. 424. Life Cycle:<br />Gravid proglottids are passed intact in the feces or emerge from the perianal region of the host .  Subsequently they release typical egg packets . <br />ingestion of an egg by the intermediate host (larval stages of the dog or cat flea Ctenocephalides spp.), an oncosphere is released into the flea's intestine. <br /> The oncosphere penetrates the intestinal wall, invades the insect's hemocoel (body cavity), and develops into a cysticercoid larva .  The larva develops into an adult, and the adult flea harbours the infective cysticercoid . <br /> The vertebrate host becomes infected by ingesting the adult flea containing the cysticercoid .  <br />The dog is the principal definitive host for Dipylidiumcaninum.  Other potential hosts include cats, foxes, and humans (mostly children) , . <br />
  425. 425. Life Cycle:<br />Humans acquire infection by ingesting the cysticercoid contaminated flea.  This can be promulgated by close contact between children and their infected pets.  <br />In the small intestine of the vertebrate host the cysticercoid develops into the adult tapeworm (measuring up to 60 cm in length and 3 mm in width) reside in the small intestine of the host, where they each attach by their scolex.  <br />They produce proglottids (or segments) which have two genital pores (hence the name "double-pored" tapeworm).  <br />The proglottids mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool .<br />
  426. 426. Clinical Features:Most infections with Dipylidiumcaninum are asymptomatic.  Pets may exhibit behavior to relieve anal pruritis (such as scraping anal region across grass or carpeting).  Mild gastrointestinal disturbances may occur.  The most striking feature in animals and children consists of the passage of proglottids.  These can be found in the perianal region, in the feces, on diapers, and occasionally on floor covering and furniture.  The proglottids are motile when freshly passed and may be mistaken for maggots or fly larvae.<br />
  427. 427. Diagnostic findings<br />Microscopy<br />Treatment:Treatment for both animals and humans is simple and very effective.  Praziquantel is given either orally or by injection (pets only).  The medication causes the tapeworm to dissolve within the intestines.  Since the worm is usually digested before it passes, it may not be visible in the dog's stool.  These drugs are generally well tolerated. <br />
  428. 428. HYMENOLEPIS NANA<br /><ul><li>Disease: Hymenolepiasis; dwarf tapeworm infection
  429. 429. Site in host: adults & cysts in SI
  430. 430. Portal of entry: mouth
  431. 431. Definitive host: human, mice & rats
  432. 432. Intermediate host: DO NOT require an IH
  433. 433. Infective stage: eggs
  434. 434. Sources of infection: eggs fr feces in soil; autoinfection
  435. 435. Lab Dx: eggs in stool</li></li></ul><li>Egg of Hymenolepis nana: oval or subspherical and smaller than those of H. diminuta, their size being 40 - 60 µm x 30 - 50 µm.  On the inner membrane are two poles, from which 4-8 polar filaments spread out between the two membranes. The oncosphere has six hooks (seen as dark lines at 8 o'clock). <br />
  436. 436.
  437. 437.
  438. 438.
  439. 439. Three adult Hymenolepis nana tapeworms. Each tapeworm (length: 15-40 mm) has a small, rounded scolex at the anterior end, and proglottids can be distinguished at the posterior, wider end.<br />
  440. 440. HYMENOLEPIS DIMINUTA<br /><ul><li>Disease: Hymenolepiasis; rat tapeworm infection
  441. 441. Site in host: SI
  442. 442. Portal of entry: mouth
  443. 443. Definitive host: human, mice & rats
  444. 444. Intermediate host: insects (rat & mouse flea, the flour moth and flour beetle)
  445. 445. Infective stage: eggs
  446. 446. Sources of infection: cysts from insects
  447. 447. Lab Dx: eggs in stool</li></li></ul><li>Egg of Hymenolepis diminuta:round or slightly oval, size 70 - 86 µm X 60 - 80 µm, with a striated outer membrane and a thin inner membrane.  The space between the membranes is smooth or faintly granular.  The oncosphere has six hooks. <br />
  448. 448. Mature proglottids of Hymenolepis diminuta. <br />
  449. 449. Causal Agents:Hymenolepiasis is caused by two cestodes (tapeworm) species, Hymenolepis nana (the dwarf tapeworm,) and Hymenolepisdimnuta (rat tapeworm).  Hymenolepisdiminuta is a cestode of rodents infrequently seen in humans and frequently found in rodents.<br />Geographic Distribution:Hymenolepis nana is the most common cause of all cestode infections, and is encountered worldwide.  In temperate areas its incidence is higher in children and institutionalized groups.  Hymenolepisdiminuta, while less frequent, has been reported from various areas of the world.<br />
  450. 450.
  451. 451.
  452. 452. Life Cycle:<br />Eggs of Hymenolepis nana eggs are ingested by an arthropod intermediate host (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine.  <br />When eggs are ingested (in contaminated food or water or from hands contaminated with feces- oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae .  Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces , attach to the intestinal mucosa and develop into adults that reside in the ileal portion of the small intestine producing gravid proglottids .  <br />Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine <br />internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . <br />
  453. 453. Life Cycle:<br />.<br />Eggs of Hymenolepisdiminuta are passed out in the feces of the infected definitive host (rodents, man) .  The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) , and oncospheres are released from the eggs and penetrate the intestinal wall of the host , which develop into cysticercoid larvae.  Species from the genus Tribolium are common intermediate hosts for H. diminuta.  The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood.  H. diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae .  Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (e.g., oral exploration of the environment by children).  After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine.  Eversion of the scoleces occurs shortly after the cysticercoid larvae are released.  Using the four suckers on the scolex, the parasite attaches to the small intestine wall.  Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length .  Eggs are released in the small intestine from gravid proglottids that disintegrate after breaking off from the adult worms.  The eggs are expelled to the environment in the mammalian host's feces .<br />
  454. 454. Clinical Features:Hymenolepis nana and H. diminuta infections are most often asymptomatic.  Heavy infections with H. nana can cause weakness, headaches, anorexia, abdominal pain, and diarrhea.<br />
  455. 455. Clinical Features:Hymenolepis nana and H. diminuta infections are most often asymptomatic.  Heavy infections with H. nana can cause weakness, headaches, anorexia, abdominal pain, and diarrhea.<br />
  456. 456. Treatment:Diagnostic findings<br />Microscopy<br />Treatment:Praziquantel* is the drug of choice. <br />
  457. 457. TAENIA SAGINATA<br /><ul><li>Disease: Taeniasis; beef tapeworm infection
  458. 458. Site in host: SI
  459. 459. Portal of entry: mouth
  460. 460. Definitive host: human
  461. 461. Intermediate host: grazing cattle
  462. 462. Infective stage: eggs
  463. 463. Sources of infection: cysts in beef
  464. 464. Lab Dx: segments and eggs in stool; Scotch tape swab</li></li></ul><li>
  465. 465. Taeniid eggs: rounded or subspherical, diameter 31 to 43 µm, with a thick radially striated brown shell.  Inside each shell is an embryonated oncosphere with 6 hooks (hexacanth embryo).  <br />
  466. 466. Taenia egg.  Note the thick, "striated" shell and several of the larval hooks; approximate size = 40 µm. <br />
  467. 467. T. Saginata gravid proglottid:has 15 to 30 main uterine branches on each side of central stem; proglottids are much longer than wide<br />
  468. 468. TAENIA SOLIUM<br /><ul><li>Disease: Taeniasis; pork tapeworm infection
  469. 469. Site in host: SI
  470. 470. Portal of entry: mouth
  471. 471. Definitive host: human
  472. 472. Intermediate host: pig
  473. 473. Infective stage: eggs
  474. 474. Sources of infection: cysts in pork; autoinfection
  475. 475. Lab Dx: segments and eggs in stool; Scotch tape swab</li></li></ul><li>T. saginata gravid proglottid:has 15 to 30 main uterine branches on each side of central stem; proglottids are much longer than wide<br />
  476. 476.
  477. 477.
  478. 478. Scoleces of Taenia saginata and Taenia solium: Scolex of T. saginata has 4 suckers and no hooks.  T. solium has 4 suckers in addition to a double row of hooks. <br />
  479. 479. Scolex of Taenia solium:measures approximately 1 mm across.  The four suckers are numbered.  Note the presence of an armed (hooked) rostellum (*); the scolex of Taenia saginata, the beef tapeworm, does not have an armed rostellum.<br />
  480. 480. A cysticercus of Taenia in muscle.  Note the fibrous capsule (*) around the cysticercus.<br />
  481. 481. Causal Agents:<br />The cestodes (tapeworms) Taeniasaginata (beef tapeworm) and T. solium (pork tapeworm).  Taeniasolium can also cause cysticercosis.<br />Geographic Distribution:Both species are worldwide in distribution.  Taeniasolium is more prevalent in poorer communities where humans live in close contact with pigs and eat undercooked pork and is very rare in Muslim countries<br />
  482. 482.
  483. 483. Life Cycle:<br />Taeniasis is the infection of humans with the adult tapeworm of Taeniasaginata or Taeniasolium.  <br />Humans are the only definitive hosts for T. saginata and T. solium.  <br />Eggs or gravid proglottids are passed with feces ; <br />Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or gravid proglottids .  <br />Humans become infected by ingesting raw or undercooked infected meat .  In the human intestine, the cysticercus develops into an adult tapeworm<br />  The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . <br />
  484. 484. Life Cycle:<br />Length of adult worms is usually 5 m or less for T. saginata (however it may reach up to 25 m) and 2 to 7 m for T. solium.  <br />The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day).  <br />T. saginata adults usually have 1,000 to 2,000 proglottids, while T. solium adults have an average of 1,000 proglottids.  The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces.  T. saginata may produce up to 100,000 and T. solium may produce 50,000 eggs per proglottid respectively.<br />
  485. 485. Clinical Features:<br />Taeniasaginatataeniasis produces only mild abdominal symptoms.  The most striking feature consists of the passage (active and passive) of proglottids.  <br />Occasionally, appendicitis or cholangitis can result from migrating proglottids.  <br />Taeniasoliumtaeniasis is less frequently symptomatic than Taeniasaginatataeniasis.  <br />The main symptom is often the passage (passive) of proglottids.  The most important feature of Taeniasoliumtaeniasis is the risk of development of cysticercosis.<br />
  486. 486. Diagnostic findings<br />TAKE EXTREME CARE IN PROCESSING THE SAMPLES!  INGESTION OF EGGS CAN RESULT IN CYSTICERCOSIS!<br />Microscopy <br />Antibody detection may prove useful especially in the early invasive stages, when the eggs and proglottids are not yet apparent in the stools.<br />Treatment:Treatment is simple and very effective.  Praziquantel* is the drug of choice. <br />
  487. 487. Taenia saginata<br />Ingestion of raw or poorly cooked beef<br />Cows infected via the ingestion of human waste containing the eggs of the parasite<br />Cows contain viable cysticercus larvae in the muscle<br />Humans act as the host only to the adult tapeworms<br />Up to 25 meters in the lumen of intestine<br />Found all over the world, including the U.S.<br />
  488. 488. Beef Tapeworm<br />
  489. 489. Treatment<br />Praziquantel<br />Albendazole<br />Niclosamide<br />
  490. 490. Tapeworms (Cestodes)<br />Adult worms inhabit GI tract of definitive vertebrate host<br />Larvae inhabit tissues of intermediate host<br />Humans<br />Definitive for T. saginata<br />Intermediate for Echinococcus granulosus (hydatid)<br />Both definitive and intermediate for T. solium<br />Adult worms shed egg-containing segments in stool ingested by intermediate host larval form in tissues<br />
  491. 491. Cystercercosis<br />Symptoms depend on location of cysts, but frequently include motor spasms, seizures, confusion, irritability, and personality change<br />In the eye, often subretinal or in vitreous. Movement may be seen by the patient. Pain, amaurosis, and loss of vision may occur.<br />
  492. 492. Cysticercosis<br />Clinical manifestations<br />Adult worms rarely cause sxs<br />Larvae penetrate intestine, enter blood, and eventually encyst in the brain.<br />Cerebral ventircles  hydrocephalus<br />Spinal cord  compression, paraplegia<br />Subarachnoid space  chronic meningitis<br />Cerebral cortex  seizures<br />Cysts may remain asymptomatic for years, and become clinically apparent when larvae die<br />Larvae may encyst in other organs, but are rarely symptomatic<br />
  493. 493. Cysticercosis<br />Diagnosis<br />CT and MRI preferred studies<br />Discrete cysts that may enhance<br />Usually multiple lesions<br />Single lesions especially common in cases from India<br />Older lesions may calcify<br />CSF<br />Lymphs or eos, low glucose, elevated protein<br />Serology<br />Especially in cases with multiple cysts<br />
  494. 494. Cysticercosis<br />Treatment<br />Complex and controversial<br />Praziquantel and albendazole may kill cysts, but death of larvae can increase inflammation, edema and exacerbate sxs<br />When possible, surgical resection of symptomatic cyst is preferred<br />Corticosteroids vs. edema and inflammation; antiseizure meds<br />
  495. 495.
  496. 496.
  497. 497. Causal Agents:<br />Schistosomiasis is caused by digenetic blood trematodes.  The three main species infecting humans are Schistosomahaematobium, S. japonicum, and S. mansoni.  In addition, other species of schistosomes, which parasitize birds and mammals, can cause cercarial dermatitis in humans.<br />Geographic Distribution: Schistosomamansoni is found in parts of South America and the Caribbean, Africa, and the Middle East; S. haematobium in Africa and the Middle East; and S. japonicum in the Far East. <br />
  498. 498.
  499. 499. Life Cycle:<br />Eggs are eliminated with feces or urine .- eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts .  The stages in the snail include 2 generations of sporocysts and the production of cercariae .  <br />Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae .  <br />The schistosomulae migrate through several tissues and stages to their residence in the veins (, ).  Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . <br />S. japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and<br />S. mansoni occurs more often in the superior mesenteric veins draining the large intestine .  <br />  S. haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. <br />
  500. 500. Life Cycle:<br />.  Pathology of S. mansoni and S. japonicumschistosomiasis includes: Katayama fever, hepatic perisinusoidal egg granulomas, Symmers’ pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord.  <br />Pathology of S. haematobiumschistosomiasis includes: hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord.<br />Human contact with water is thus necessary for infection by schistosomes.  Various animals, such as dogs, cats, rodents, pigs, hourse and goats, serve as reservoirs for S. japonicum, and dogs for S. mekongi.<br />
  501. 501. Clinical Features<br />Many infections are asymptomatic. <br /> Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by S. mansoni and S. japonicum.  Manifestations include fever, cough, abdominal pain, diarrhea, hepatospenomegaly, and eosinophilia.  <br />Occasionally central nervous system lesions occur: cerebral granulomatous disease may be caused by ectopic S. japonicum eggs in the brain, and granulomatous lesions around ectopic eggs in the spinal cord from S. mansoni and S. haematobium infections may result in a transverse myelitis with flaccid paraplegia.  <br />.<br />
  502. 502. Clinical Features<br />Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include: colonic polyposis with bloody diarrhea (Schistosomamansoni mostly); portal hypertension with hematemesis and splenomegaly (S. mansoni, S. japonicum, S. mansoni); cystitis and ureteritis (S. haematobium) with hematuria, which can progress to bladder cancer; pulmonary hypertension (S. mansoni, S. japonicum, more rarely S. haematobium); glomerulonephritis; and central nervous system lesions.<br />
  503. 503. Diagnostic findings<br />microscopy<br />Antobodydetrectioncan be useful in both in clinical management (e.g., recent infections) and for epidemiologic surveys.<br />Treatment:Safe and effective drugs are available for the treatment of schistosomiasis.  The drug of choice is praziquantel for infections caused by all Schistosoma species.  Oxamniquine has been effective in treating infections caused by S. mansoni in some areas in which praziquantel is less effective. <br />
  504. 504.
  505. 505. FASCIOLA HEPATICA<br /><ul><li>AKA: Sheep Liver Fluke
  506. 506. Disease: Fascioliasis, “liver rot”
  507. 507. Site in host: Bile ducts
  508. 508. Portal of entry: mouth
  509. 509. Definitive host: sheep, cattle & other mammals, including humans
  510. 510. Intermediate host: snail (Lymnaea)
  511. 511. Source of infection: eating watercress, lettuce or radishes or drinking water infested with metacercariae
  512. 512. Infective stage: metacercariae
  513. 513. Lab Dx: eggs in stool </li></li></ul><li>Fasciola hepatica eggs: eggs are ellipsoidal, with small, barely distinct operculum. The operculum can be opened. The eggs have a thin shell which is slightly thicker at the abopercular end.  They are passed unembryonated.  <br />
  514. 514. Causal Agents:<br />The trematodesFasciola hepatica (the sheep liver fluke) and Fasciolagigantica, parasites of herbivores that can infect humans accidentally.<br />Geographic Distribution:Fascioliasis occurs worldwide.  Human infections with F. hepatica are found in areas where sheep and cattle are raised, and where humans consume raw watercress, including Europe, the Middle East, and Asia.  Infections with F. gigantica have been reported, more rarely, in Asia, Africa, and Hawaii.<br />
  515. 515.
  516. 516. Life Cycle:<br />Immature eggs are discharged in the biliary ducts and in the stool .  Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host , including the genera Galba, Fossariaand Pseudosuccinea.  In the snail the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ).  The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces.  Mammals acquire the infection by eating vegetation containing metacercariae.  Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress .  After ingestion, the metacercariaeexcyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults .  In humans, maturation from metacercariae into adult flukes takes approximately 3 to 4 months.  The adult flukes (Fasciola hepatica: up to 30 mm by 13 mm; F. gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host.  Fasciola hepatica infect various animal species, mostly herbivores.<br />
  517. 517. Clinical Features:During the acute phase (caused by the migration of the immature fluke through the hepatic parenchyma), manifestations include abdominal pain, hepatomegaly, fever, vomiting, diarrhea, urticaria and eosinophilia, and can last for months.  In the chronic phase (caused by the adult fluke within the bile ducts), the symptoms are more discrete and reflect intermittent biliary obstruction and inflammation.  Occasionally, ectopic locations of infection (such as intestinal wall, lungs, subcutaneous tissue, and pharyngeal mucosa) can occur.<br />
  518. 518. Diagnostic findings<br />Microscopy and antibody detection<br />Treatment:Unlike infections with other flukes, Fasciola hepatica infections may not respond to praziquantel.  The drug of choice is triclabendazole with bithionol as an alternative. <br />
  519. 519. Causal Agent:The trematodeFasciolopsisbuski, the largest intestinal fluke of humans.<br />Geographic Distribution:Asia and the Indian subcontinent, especially in areas where humans raise pigs and consume freshwater plants.<br />
  520. 520.
  521. 521. Life Cycle:<br />Immature eggs are discharged into the intestine and stool .  Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host . <br /> In the snail the parasites undergo several developmental stages (sporocysts , rediae , and cercariae ).  The cercariae are released from the snail and encyst as metacercariae on aquatic plants .<br />The mammalian hosts become infected by ingesting metacercariae on the aquatic plants.  After ingestion, the metacercariaeexcyst in the duodenum and attach to the intestinal wall. .  The  adults have a life span of about one year.<br />
  522. 522. Clinical Features:Most infections are light and asymptomatic.  In heavier infections, symptoms include diarrhea, abdominal pain, fever, ascites, anasarca and intestinal obstruction.<br />
  523. 523. Diagnostic findings<br />Microscopy<br />Treatment:Praziquantel* is the drug of choice. <br />
  524. 524. CLONORCHIS SINENSIS<br /><ul><li>AKA: Chinese or Oriental Liver Fluke
  525. 525. Disease: Clonorchiasis
  526. 526. Site in host: Bile ducts
  527. 527. Portal of entry: mouth
  528. 528. Definitive host: humans, dog & cat or other mammals
  529. 529. 1st Intermediate host: freshwater snail (Bulinus, Parafossarulus)
  530. 530. 2nd Intermediate host: freshwater fish (Cyprinidae)
  531. 531. Infective stage: metacercariae
  532. 532. Lab Dx: eggs in stool </li></li></ul><li>C. sinensis, adult: stained whole mount; approximate size = 15 mm. <br />
  533. 533.
  534. 534.
  535. 535. C. sinensis egg: small operculated eggs.  Size 27 to 35 µm by 11 to 20 µm.  The operculum, at the smaller end of the egg,  is convex and rests on a visible "shoulder".  At the opposite (larger, abopercular) end, a small knob or hooklike protrusion is often visible (as is the case here).  The miracidium is visible inside the egg.<br />
  536. 536.
  537. 537. Causal Agent:The trematodeClonorchissinensis (Chinese or oriental liver fluke).<br />Geographic Distribution:Endemic areas are in Asia including Korea, China, Taiwan, and Vietnam.  Clonorchiasis has been reported in non endemic areas (including the United States).  In such cases, the infection is found in Asian immigrants, or following ingestion of imported, undercooked or pickled freshwater fish containing metacercariae.<br />
  538. 538.
  539. 539. Life Cycle:<br />Embryonated eggs are discharged in the biliary ducts and in the stool . <br /> Eggs are ingested by a suitable snail intermediate host ; there are more than 100 species of snails that can serve as intermediate hosts.  Each egg releases a miracidia , which go through several developmental stages (sporocysts , rediae , and cercariae ).  The cercariae are released from the snail and after a short period of free-swimming time in water, they come in contact and penetrate the flesh of freshwater fish, where they encyst as metacercariae .<br />  Infection of humans occurs by ingestion of undercooked, salted, pickled, or smoked freshwater fish .  After ingestion, the metacercariaeexcyst in the duodenum and ascend the biliary tract through the ampulla of Vater .  Maturation takes approximately 1 month.  The adult flukes reside in small and medium sized biliary ducts.  In addition to humans, carnivorous animals can serve as reservoir hosts.<br />
  540. 540. Clinical Features:<br />Most pathologic manifestations result from inflammation and intermittent obstruction of the biliary ducts.  In the acute phase, abdominal pain, nausea, diarrhea, and eosinophilia can occur.  In long-standing infections, cholangitis, cholelithiasis, pancreatitis, and cholangiocarcinoma can develop, which may be fatal.<br />
  541. 541. Diagnostic findings<br />Microscopy<br />.<br />Treatment:Praziquantel or albendazole* are the drugs of choice. <br />
  542. 542. Causal Agent:<br />Trematodes (flukes) Opisthorchisviverrini (Southeast Asian liver fluke) and O. felineus (cat liver fluke).<br />Geographic Distribution:O. viverrini is found mainly in northeast Thailand, Laos, and Kampuchea.  O. felineus is found mainly in Europe and Asia, including the former Soviet Union.<br />
  543. 543.
  544. 544. Life Cycle:<br />The adult flukes deposit fully developed eggs that are passed in the feces .  <br />After ingestion by a suitable snail (first intermediate host) , the eggs release miracidia , which undergo in the snail several developmental stages (sporocysts , rediae , cercariae ).  Cercariae are released from the snail and penetrate freshwater fish (second intermediate host), encysting as metacercariae in the muscles or under the scales . <br /> The mammalian definitive host (cats, dogs, and various fish-eating mammals including humans) become infected by ingesting undercooked fish containing metacercariae.  After ingestion, the metacercariaeexcyst in the duodenum and ascend through the ampulla of Vater into the biliary ducts, where they attach and develop into adults, which lay eggs after 3 to 4 weeks .  <br />The adult flukes reside in the biliary and pancreatic ducts of the mammalian host, where they attach to the mucosa.<br />
  545. 545. Clinical Features:<br />Most infections are asymptomatic.  <br />In mild cases, manifestations include dyspepsia, abdominal pain, diarrhea or constipation.  <br />With infections of longer duration, the symptoms can be more severe, and hepatomegaly and malnutrition may be present.  <br />In rare cases, cholangitis, cholecystitis, and chlolangiocarcinoma may develop.  <br />infections due to O. felineus may present an acute phase resembling Katayama fever (schistosomiasis), with fever, facial edema, lymphadenopathy, arthralgias, rash, and eosinophilia.  <br />Chronic forms of O. felineus infections present the same manifestations as O. viverrini, with in addition involvement of the pancreatic ducts.<br />
  546. 546. Diagnostic findings<br />Microscopy<br />Treatment:Praziquantel is the drug of choice to treat opisthorchiasis. <br />
  547. 547. PARAGONIMUS WESTERMANI<br /><ul><li>AKA: Lung Fluke
  548. 548. Disease: Paragonimiasis, pulmonary distomiasis, lung fluke disease
  549. 549. Site in host: Lungs
  550. 550. Portal of entry: mouth
  551. 551. Definitive host: humans & a variety of carnivores
  552. 552. 1st Intermediate host: freshwater snail (Family Thieridae)
  553. 553. 2nd Intermediate host: freshwater crab (Eriocheir, Patamon, Sesarma, Parathelphusa) or crayfish (Cambarus, Astacus)
  554. 554. Source of infection: consumption of raw or undercooked infected freshwater crustaceans
  555. 555. Infective stage: metacercariae
  556. 556. Lab Dx: eggs in sputum & stool </li></li></ul><li>Egg of P. westermani:The average egg size is 85 µm by 53 µm (range: 68 to 118 µm by 39 to 67 µm).  They are yellow-brown, ovoidal or elongate, with a thick shell, and often asymmetrical with one end slightly flattened.  At the large end, the operculum is clearly visible.  The opposite (abopercular) end is thickened.  The eggs of P. westermani are excreted unembryonated.<br />
  557. 557.
  558. 558. Paragonimus westermani:Cross section of lung containing adult Paragonimus westermani.<br />
  559. 559.
  560. 560.
  561. 561. Causal Agent:<br />More than 30 species of trematodes (flukes) of the genus Paragonimus have been reported which infect animals and humans.  Among the more than 10 species reported to infect humans, the most common is P. westermani, the oriental lung fluke.<br />Geographic Distribution:Paragonimus spp. are distributed throughout the Americas, Africa and southeast Asia.  Paragonimuswestermani is distributed in southeast Asia and Japan.  Paragonimuskellicotti is endemic to North America.<br />
  562. 562.
  563. 563. Life Cycle:<br />The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with stool . <br /> In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues .  Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail.  The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae.  This is the infective stage for the mammalian host . <br />
  564. 564. Life Cycle:<br />Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite .  The metacercariaeexcyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (.  <br />The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively.  However, when this takes place completion of the life cycles is not achieved, because the eggs laid cannot exit these sites.  Time from infection to oviposition is 65 to 90 days. <br />Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani.<br />
  565. 565. Clinical Features:<br />The acute phase (invasion and migration) may be marked by diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia.  <br />During the chronic phase, pulmonary manifestations include cough, expectoration of discolored sputum, hemoptysis, and chest radiographic abnormalities.  <br />Extrapulmonary locations of the adult worms result in more severe manifestations, especially when the brain is involved.<br />
  566. 566. Diagnostic findings<br />Microscopy<br />Antibody detection is useful in light infections and in the diagnosis of extrapulmonaryparagonimiasis.<br />Treatment:Praziquantel* is the drug of choice to treat paragonimiasis.  Bithionol is an alternative drug for treatment of this disease. <br />
  567. 567. METAGONIMUS YOKOGAWAI<br /><ul><li>Disease: Metagonimiasis
  568. 568. Site in host: Bile ducts
  569. 569. Portal of entry: mouth
  570. 570. Definitive host: humans, dogs, cats, hogs, pelicans & other fish-eating birds
  571. 571. 1st Intermediate host: snail (Semisulcospira, Thiara and Hua)
  572. 572. 2nd Intermediate host: freshwater fish (Salmonoids & cyprinoids)
  573. 573. Infective stage: metacercariae
  574. 574. Lab Dx: eggs in stool</li></li></ul><li>M. yokogawai, adult fluke: the position of the ventral sucker is to the side of the midline with its axis in a diagonal line<br />
  575. 575. Causal Agent:<br />Metagonimusyokogawai, a minute intestinal fluke (and the smallest human fluke).<br />Geographic Distribution:Mostly the Far East, as well as Siberia, Manchuria, the Balkan states, Israel, and Spain.<br />
  576. 576.
  577. 577. Life Cycle:<br />Adults release fully embryonated eggs each with a fully-developed miracidium, and eggs are passed in the host’s feces .  <br />After ingestion by a suitable snail (first intermediate host), the eggs hatch and release miracidia which penetrate the snail’s intestine .  Snails of the genus Semisulcospira are the most frequent intermediate host for Metagonimusyokogawai.  The miracidia undergo several developmental stages in the snail, i.e. sporocysts , rediae , and cercariae .  Many cercariae are produced from each redia.  The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable fresh/brackish water fish (second intermediate host) . <br /> The definitive host becomes infected by ingesting undercooked or salted fish containing metacercariae .  After ingestion, the metacercariaeexcyst, attach to the mucosa of the small intestine and mature into adults (measuring 1.0 mm to 2.5 mm by 0.4 mm to 0.75 mm) .  In addition to humans, fish-eating mammals (e.g., cats and dogs) and birds can also be infected by M. yokogawai .<br />
  578. 578. Clinical Features:The main symptoms are diarrhea and colicky abdominal pain.  Migration of the eggs to extraintestinal sites (heart, brain) can occur, with resulting symptoms.<br />
  579. 579. Diagnostic findings<br />Microscopy<br />Treatment:Praziquantel* is the drug of choice. <br />
  580. 580. HETEROPHYES HETEROPHYES<br /><ul><li>Disease: Heterophyiasis
  581. 581. Site in host: Bile ducts
  582. 582. Portal of entry: mouth
  583. 583. Definitive host: humans, dog & cat or other fish eating mammals
  584. 584. 1st Intermediate host: brackish water snail (Pirenella, Cerithidea)
  585. 585. 2nd Intermediate host: brackish water fish (Mugil, Tilapia and Acanthogobus)
  586. 586. Infective stage: metacercariae
  587. 587. Lab Dx: eggs in stool</li></li></ul><li>Causal Agent:<br />The trematodeHeterophyesheterophyes, a minute intestinal fluke.<br />Geographic Distribution:Egypt, the Middle East, and Far East.<br />
  588. 588.
  589. 589. Life Cycle:<br />Adults release embryonated eggs each with a fully-developed miracidium, and eggs are passed in the host's feces . <br /> After ingestion by a suitable snail (first intermediate host), the eggs hatch and release miracidia which penetrate the snail’s intestine .  Genera Cerithidia and Pironella are important snail hosts in Asia and the Middle East respectively.  The miracidia undergo several developmental stages in the snail, i.e. sporocysts , rediae , and cercariae .  Many cercariae are produced from each redia.  The cercariae are released from the snail and encyst as metacercariae in the tissues of a suitable fresh/brackish water fish (second intermediate host) .  <br />The definitive host becomes infected by ingesting undercooked or salted fish containing metacercariae .  After ingestion, the metacercariaeexcyst, attach to the mucosa of the small intestine and mature into adults <br />.  In addition to humans, various fish-eating mammals (e.g., cats and dogs) and birds can be infected by Heterophyesheterophyes .<br />
  590. 590. Clinical Features:<br />The main symptoms are diarrhea and colicky abdominal pain.  <br />Migration of the eggs to the heart, resulting in potentially fatal myocardial and valvular damage, has been reported from the Philippines.  <br />Migration to other organs (e.g., brain) has also been reported.<br />
  591. 591. Laboratory Diagnosis:<br />Microscopy<br />Treatment:Praziquantel* is the drug of choice. <br />
  592. 592. FASCIOLOPSIS BUSKI<br /><ul><li>AKA: Large or giant intestinal fluke
  593. 593. Disease: Fasciolopsiasis
  594. 594. Site in host: SI
  595. 595. Portal of entry: mouth
  596. 596. Definitive host: pig & humans
  597. 597. 1st Intermediate host: snail (Segmentina / Hippeutis)
  598. 598. 2nd Intermediate host: water chestnuts & lotus
  599. 599. Infective stage: metacercariae
  600. 600. Lab Dx: eggs in stool </li></li></ul><li>
  601. 601. Adult fluke of Fasciolopsis buski.<br />
  602. 602.
  603. 603. Egg of F. buski:eggs are ellipsoidal, with a thin shell, and a usually small, indistinct operculum.  In this particular egg, the operculum is open. <br />
  604. 604.
  605. 605. SCHISTOSOMA MANSONI<br /><ul><li>Disease: Schistosomiasis, intestinal schistosomiasis, bilharziasis “snail fever”
  606. 606. Site in host: veins of LI
  607. 607. Portal of entry: skin
  608. 608. Definitive host: humans, baboons & rodents
  609. 609. Intermediate host: snail (Biomphalaria sp & Tropicorbis sp)
  610. 610. Infective stage: cercariae
  611. 611. Lab Dx: eggs in stool; rectal or liver biopsy</li></li></ul><li>
  612. 612. Biomphalaria spp.<br />
  613. 613. Schistosoma mansoni eggs: large (length 114 to 180 µm) and have a characteristic shape, with a prominent lateral spine near the posterior end.  The anterior end is tapered and slightly curved.  When the eggs are excreted, they contain a mature miracidium<br />
  614. 614.
  615. 615.
  616. 616.
  617. 617.
  618. 618. Male and female schistosomes. <br />
  619. 619. SCHISTOSOMA HAEMATOBIUM<br /><ul><l