Uploaded on

 

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
No Downloads

Views

Total Views
3,053
On Slideshare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
65
Comments
0
Likes
1

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

  • 1. The Prokaryotes:Domains Bacteria and Archaea
    11
  • 2. The Protozoa
    Table 12.1
  • 3. Eukaryotic
    Unicellular
    Chemoheterotrophs
    Vegetative form is a trophozoite.
    Asexual reproduction is by fission,budding, or schizogony.
    Sexual reproduction
    by conjugation.
    Some produce cysts.
    Protozoa
    Figure 12.16
  • 4. No mitochondria
    Multiple flagella
    Giardia lamblia
    Trichomonas vaginalis (no cyst stage)
    Archaezoa
    Figure 12.17b–d
  • 5. No mitochondria
    Nonmotile
    Intracellular parasites
    Nosema
    Microspora
  • 6. Move by pseudopods
    Entamoeba
    Acanthamoeba
    Amoebozoa
    Figure 12.18a
  • 7. Nonmotile
    Intracellular parasites
    Complex life cycles
    Plasmodium
    Babesia
    Cryptosporidium
    Cyclospora
    Apicomplexa
  • 8. 2
    3
    8
    7
    6
    Plasmodium
    Figure 12.19
  • 9. Cryptosporidium
    Figure 25.19
  • 10. Move by cilia
    Complex cells
    Balantidium coli is the only human parasite.
    Figure 12.20
    Ciliophora (Ciliates)
  • 11. Move by flagella
    Photoautotrophs
    Euglenoids
    Chemoheterotrophs
    Naegleria: Flagellated and amoeboid forms; causes meningoencephalitis.
    Trypanosoma: Undulating membrane, transmitted by vectors.
    Leishmania: Flagellated form in sand fly vector, ovoid form in vertebrate host.
    Euglenozoa
  • 12. Euglenozoa
    Figure 12.21
  • 13. Why are these studied with algae and protozoa?
    Dinoflagellates
    Figure 12.14
  • 14.
  • 15. INTESTINAL PROTOZOA
    Ameba
    Flagellates
    Ciliates
    Intestinal Coccidia, Microsporidia, and Blastocystis hominis
  • 16. Entamoebahistolytica
    • Disease:Intestinal amebiasis/amebic dysentery, extraintestinalamebiasis
    • 17. Site in host:lumen & wall of LI
    • 18. Portal of entry:Mouth
    • 19. Source of infection:cysts in food & water, from feces
    AMEBA
  • 20. Causal Agent:Entamoebahistolytica
    pathogenic ameba
    associated with intestinal and extraintestinal infections. 
    Amoebiasis
  • 21.
  • 22. Cysts and trophozoites are passed in feces . 
    ingestion of mature cysts in fecally contaminated food, water, or hands. 
    Excystation occurs in the small intestine - trophozoitesare released, which migrate to the large intestine. 
    The trophozoites multiply by binary fission - produce cysts , and both stages are passed in the feces . 
    Pathogenecity
  • 23. Cysts and trophozoites are passed in feces . 
    ingestion of mature cysts in fecally contaminated food, water, or hands. 
    Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. 
    The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . 
    protection by their walls, the cysts can survive days to weeks in the external environment
    Pathogenecity
  • 24. trophozoitesremain confined to the intestinal lumen ( noninvasive infection)
    individuals who are asymptomatic carriers, passing cysts in their stool. 
    trophozoitesinvade the intestinal mucosa (intestinal disease)
    through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (extraintestinal disease),
    Pathogenecity
  • 25. E. histolytica morphologically ingested red blood cells (erythrophagocystosis)
     
    Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).
    Pathogenecity
  • 26. Worldwide, with higher incidence of amebiasis in developing countries. 
    In industrialized countries, risk groups include male homosexuals, travelers and recent immigrants, and institutionalized populations.
    Geographic Distribution:
  • 27. asymptomatic infection
    ("luminal amebiasis")
    invasive intestinal amebiasis
    (dysentery, colitis, appendicitis, toxic megacolon, amebomas)
    invasive extraintestinalamebiasis
    (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions).
    Clinical Features:
  • 28. Fresh stool:
    wet mounts and permanently stained preparations (e.g., trichrome)
    Concentrates from fresh stool:
    wet mounts, with or without iodine stain, and permanently stained preparations
    E. histolyticatrophozoites can also be identified in aspirates or biopsy samples obtained during colonoscopy or surgery.
    Laboratory Diagnosis:
  • 29. Microscopy
    Immunodiagnosis
    Molecular methods for discriminating between E. histolytica and E. dispar
    Morphologic comparison with other intestinal parasites
    Bench aid for E. histolytica
    Diagnostic findings:
  • 30. Trophozoite:small, usually central karyosome; finely granular chromatin
  • 31. Trophozoite with ingested RBCs
  • 32.
  • 33. Cyst:4 nuclei in mature cyst; rod-like chromatoid bodies
  • 34. Gross pathology of liver containing amebic abscess 
  • 35. Gross pathology of amebic abscess of liver. Tube of "chocolate" pus from abscess.
  • 36.
  • 37. Entamoeba hartmanni
    Trophozoite: small, usually eccentric karyosome; finely granular chromatin
  • 38. Cyst:4 nuclei in mature cyst; rod-like chromatoid bodies (6-8 um, smaller than E. histolytica cysts)
  • 39. Entamoeba coli
    Trophozoite: 1 nucleus with large eccentric karyosome; coarse, irregular peripheral chromatin
  • 40. Cyst:8 nuclei in mature cyst; splinter-like chromatoid bodies w/ pointed ends
    large, eccentric karyosome
  • 41.
  • 42. Endolimax nana
    Trophozoites:1 nucleus w/ large, irregularly shaped, blot-like karyosome; has no peripheral chromatin; cytoplasm is granular and vacuolated
  • 43. Cyst: mature cyst w/ 4 nuclei with large, blot-like karyosomes; no have chromatoid bodies
  • 44. Iodamoeba butschlii
    Trophozoite: 1 nucleus w/ large, usually central karyosome surr by refractile, achromatic granules; cytoplasm coarsely granular, vacuolated & can contain bacteria, yeasts  
  • 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.
  • 46. For asymptomatic infections,
    iodoquinol, paromomycin, or diloxanidefuroate are the drugs of choice. 
    For symptomatic intestinal disease, or extraintestinal, infections (e.g., hepatic abscess)
    the drugs of choice are metronidazole or tinidazole, immediately followed by treatment with iodoquinol, paromomycin, or diloxanidefuroate. 
    Treatment:
  • 47. Balantidium coli
    • Disease:Balantidiasis;balantidiosis; balantidial dysentery
    • 48. Site in host:LI
    • 49. Portal of entry:Mouth
    • 50. Source of infection:stool (cysts)
    • 51. Lab Dx: cysts/trophs in stool
    CILIATES
  • 52.
  • 53. Causal Agent
    Balantidium coli, a large ciliated protozoan parasite.
    Geographic Distribution:
    Worldwide.  Because pigs are an animal reservoir.  Other reservoirs include rodents and nonhuman primates.
    Balantidiasis
  • 54. cysts – infective stage
    ingestion of contaminated food or water
    Life cycle
  • 55. excystation occurs in the small intestine- trophozoitescolonize the large intestine
    Trophozoites undergo encystation to produce infective cysts . 
    Some trophozoites invade the wall of the colon and multiply. 
    Mature cysts are passed with feces .
    Life cycle
  • 56. Most cases are asymptomatic. 
    Clinical manifestations, when present, include
    persistent diarrhea
    occasionally dysentery
    abdominal pain
    weight loss. 
    Symptoms can be severe in debilitated persons.
    Clinical Features:
  • 57. trophozoites - stool specimens or in tissue
    Cysts are less frequently encountered. 
    Laboratory Diagnosis:
  • 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
  • 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
  • 60. The drug of choice is tetracycline*, with metronidazole* and  iodoquinol* as alternatives. 
    Tetracycline is contraindicated in pregnancy and in children less than 8 years old. 
    Treatment:
  • 61.
    • May be pathogenic
    • 62. Currently classified as an amoeba
    Blastocystis hominis
  • 63. Blastocystishominis
    Geographic Distribution:Worldwide.
    Causal Agent:
  • 64. thick-walled cyst present in the stools (fecal-oral route)
    cysts infect epithelial cells of the digestive tract and multiply asexually
    Vacuolar forms - give origin to multi vacuolar and ameboidforms
    multi-vacuolar -- pre-cyst -- thin-walled cyst (autoinfection)
    ameboid-- pre-cyst --thick-walled cyst
    Life Cycle:
  • 65.
  • 66. can cause both asymptomatic and symptomatic
    symptoms of illness including watery diarrhea, abdominal pain, perianalpruritus, and excessive flatulence.
    Clinical Features:
  • 67. Cyst-like forms appear round with large, central vacuole-like body. The nuclei in the peripheral cytoplasmic rim are clearly visible, staining purple.
  • 68.
  • 69. metronidazoleor iodoquinol
    Treatment:
  • 70. Giardiaduodenalis (lamblia)
    • Disease:Giardiasis;lambliasis
    • 71. Site in host:upper SI
    • 72. Portal of entry:Mouth
    • 73. Source of infection:cysts in food & water, from feces
    • 74. Lab Dx: cysts/trophs in stool; IFA stain; Enterotest
    • 75. Note: may be sexually transmitted
    FLAGELLATES
  • 76. Causal Agent:
    Giardiaintestinalis
    Giardialamblia
    Geographic Distribution:Worldwide, more prevalent in warm climates, and in children.
    Giardisis
  • 77.
  • 78. Cysts for transmission
    Both cysts and trophozoites can be found in the feces (diagnostic stages) . 
    Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . 
    Life Cycle:
  • 79. (small intestine) excystation
    Trophozoites multiply (lumen of the proximal small bowel )-- free or attached to the mucosa by a ventral sucking disk .
      Encystation(colon). 
    cyst (nondiarrhealfeces )
    Life Cycle:
  • 80. The spectrum varies from asymptomatic carriage to severe diarrhea and malabsorption
     
    Acute giardiasis develops after an incubation period of 1 to 14 days (average of 7 days) and usually lasts 1 to 3 weeks
    Symptoms include diarrhea, abdominal pain, bloating, nausea, and vomiting. 
    In chronic giardiasis the symptoms are recurrent and malabsorption and debilitation may occur.
    Clinical Features:
  • 81. Trophozoite: pyriform shape w/ 2 nuclei & a large, central karyosome; large ventral sucking disc, 4 pairs of flagella, 2 curved median bodies
  • 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
  • 83. metronidazoleand tinidazole.  
    Nitazoxanide(giardiasisin children)
    Treatment:
  • 84. INTESTINAL COCCIDIA, MICROSPORIDIA, and BLASTOCYSTIS HOMINIS
  • 85. Cryptosporidium parvum
    • Disease: Cryptosporidiosis
    • 86. Transmission: contaminated food or water by person to person contact
    • 87. Lab Dx: Modified acid fast stain of a fecal smear; PCR; IFA
  • 88. Causal Agent:Cryptosporidium parvum and Cryptosporidium hominisare (most prevalent species)
    Geographic Distribution:first reports of human cases in 1976, worldwide.  Waterborne outbreak in Milwaukee (Wisconsin) in 1993, that affected more than 400,000 people.
    Crytosporidiosis
  • 89.
  • 90. Sporulatedoocysts, containing 4 sporozoites-- excreted by the infected host through feces and possibly other routes such as respiratory secretions . 
    Transmission occurs mainly through contact with contaminated water (e.g., drinking or recreational water). 
    food sources
    outbreaks U S -- waterparks, community swimming pools, and day care centers. 
    Zoonotic and anthroponotictransmission
    Life cycle
  • 91. Life cycle
    Following ingestion (and possibly inhalation)
    Excystation-- sporozoitesare released --parasitize gastrointestinal AND respiratory tract. 
    asexual multiplication (schizogony or merogony) -- sexual multiplication (gametogony) -- producing microgamonts (male) and macrogamonts (female)
  • 92. Life cycle
    Upon fertilization -- oocysts that sporulate in the infected host
    Two different types of oocysts are produced
    thick-walled, which is commonly excreted from the host
    thin-walled oocyst , which is primarily involved in autoinfection. 
  • 93. asymptomatic infections
    severe, life-threatening illness
    incubation period is an average of 7 days (2 to 10 days). 
    Watery diarrhea is the most frequent symptom accompanied by dehydration, wt loss, abd. pain, fever, n/v
    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. 
    Clinical Features:
  • 94. asymptomatic infections
    severe, life-threatening illness
    incubation period is an average of 7 days (but can range from 2 to 10 days). 
    Watery diarrhea is the most frequent symptom, and can be accompanied by dehydration, weight loss, abdominal pain, fever, nausea and vomiting. 
    Clinical Features:
  • 95. Clinical Features:
    In immunocompetent persons, symptoms are usually short lived (1 to 2 weeks); they can be chronic
    more severe in immunocompromised patients, especially those with CD4 counts <200/µl. 
    also found in other digestive tract, lungs, and conjunctiva.
  • 96. Treatment:
    Rapid loss of fluids -- fluid and electrolyte replacement.  
    healthy, immunocompetent persons (self-limited)-- Nitazoxanide
     Immunocompromisedand high risk pt.-- nitazoxanide is unclear. 
    For persons with AIDS, anti-retroviral therapyis encourage
  • 97. Laboratory Diagnosis:
    Acid-fast staining methods
    immunofluorescencemicroscopy
    method of choice (followed closely by enzyme immunoassays)
  • 98. Oocysts are rounded, 4.2 µm - 5.4 µm in diameter.  Sporozoites are visible inside the oocysts, indicating that sporulation has occurred. 
  • 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.
  • 100. Oocysts of C. parvum (upper left) and cysts of Giardia intestinalis (lower right) labeled with immunofluorescent antibodies.
  • 101. Cyclosporacayetanensis
    • Disease:Cyclosporiasis
    • 102. Transmission: contaminated water
    • 103. Lab Dx: Modified acid fast stain of a fecal smear
  • 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.
  • 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.
     
  • 105.
  • 106. Causal Agent:unicellular coccidian parasite- Cyclosporacayetanensis
    Geographic Distribution:
    most common in tropical and subtropical areas
    1990, foodborneoutbreaks of cyclosporiasis, 3600 persons, in the United States and Canada.
  • 107.
  • 108. sporulation -- sporont -- two sporocysts (contains 2 sporozoites) 
    sporulatedoocysts are ingested (in contaminated food or water)
    oocystsexcyst in the gastrointestinal tract-- sporozoites invade the small intestine
    asexual multiplication and sexual development -- oocysts
    Life Cycle:
  • 109. Clinical Features:
    incubation period of 1 week—severe watery diarrhea
    s/sx- anorexia, wt loss, abd. pain, N/V, myalgias, low-grade fever, and fatigue. 
    Untreated infections typically last for 10-12 weeks -- follow a relapsing course. 
    In disease-endemic settings -- asymptomatic.
  • 110. identification of oocysts in stool specimens
    Laboratory Diagnosis:
  • 111. combination of two antibiotics, trimethoprim-sulfamethoxazole*, also known as Bactrim, Septra, or Cotrim. 
    Supportive measures include management of fluid and electrolyte balance, and rest.   
    Treatment:
  • 112. Isospora belli
    • Disease:Isosporiasis; intestinal coccidiosis
    • 113. Transmission: hand to mouth or through contaminated food or water
    • 114. Lab Dx: wet mount of formalin-ethyl acetate conc. of fecal sample; modified acid fast stain
  • 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
  • 115. Causal Agent:coccidian parasite, Cystoisospora belli, is the least common of the three intestinal coccidia
    Geographic Distribution:Worldwide, especially in tropical and subtropical areas. 
    Infection occurs in immunodepressedpt. and outbreaks in institutionalized groups in US
  • 116.
  • 117. infection occurs by ingestion of sporocysts-containing oocysts
    sporocystsexcyst in the small intestine -- release their sporozoites, which invade the epithelial cells -- initiate schizogony . 
    Life Cycle:
  • 118. acute, nonbloody diarrhea with crampyabdpain (weeks)--malabsorption& wt loss. 
    immuno-depressed patients , infants & children—severe diarrhea. 
     Eosinophilia
    Clinical Features:
  • 119. Microscopic
    wet mounts by bright-field, differential interference contrast (DIC), and epifluorescence
    modified acid-fast stain.
    Laboratory Diagnosis:
  • 120. Trimethoprim-sulfamethoxazole is the drug of choice.
    Treatment:
  • 121. Dientamoebafragilis
    - NO cyst stage
    • not an ameba, but a flagellate!
    • 122. may possess some pathogenicity
    • 123. Site in host: LI
    • 124. Portal of entry:mout
    • 125. Source of infection: stool (trophs)
  • 126. Causal Agent:Dientamoebafragilis is not an ameba but a flagellate. 
    parasite produces trophozoites; cysts have not been identified. 
    Geographic Distribution:Worldwide.
  • 127. the trophozoite is the only stage in stools
    Trophozoites have characteristically one or two nuclei
    Life Cycle:
  • 128.
  • 129. children –intermittent diarrhea, abd pain, n/v, anorexia, fatigue, malaise, poor wt gain
    Clinical Features:
  • 130. detection of trophozoites in permanently stained fecal smears (e.g., trichrome). 
    Laboratory Diagnosis:
  • 131. Nucleus: cluster of granules, with no peripheral chromatin; size range 5-15 µm.
  • 132.
  • 133.   The drug of choice is iodoquinol
    Paromomycin*, tetracycline*, (contraindicated in children under age 8, pregnant and lactating women) or metronidazole can also be used.  
    Treatment:
  • 134.
  • 135. Microsporidia
    • Disease:Microsporidiosis
    • 136. Genera found in humans:Enterocytozoon, Encephalitozoon, Pleistophora, Nosema, & Microsporidium
    • 137. Affects immunologically compromised hosts
    • 138. E. bieneusi: found only in humans & most frequent cause of microsporidian enteritis in AIDS patients
    • 139. Infective form: spore
    • 140. Lab Dx: Modified trichrome stain ; PCR
  • 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.
  • 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.
  • 143. BLOOD and TISSUE PROTOZOA
  • 144. OTHER PROTOZOA
    BLOOD and TISSUE PROTOZOA
    Plasmodium
    Babesia
    Trypanosomabrucei
    Trypanosomacruzi
    Toxoplasmagondii
    Leishmania
  • 145. PROTOZOA FROM OTHER BODY SITES
    Free-living Amebae
    Naegleria
    Acanthamoeba
    Trichomonasvaginalis
  • 146. PLASMODIUM
    Disease: Malaria
    P. vivax: Benign tertian malaria
    P. malariae: Quartan malaria
    P. falciparum: Malignant tertian malaria
    P. ovale: Ovale tertian malaria
    Lab Dx: Giemsa stained thick and thin blood smears; IFA; PCR
  • 147. Infected RBC:
    P. vivax and P. ovale: reticulocytes
    P. malariae: senescent erythrocytes
    P. falciparum: erythrocytes of all ages
    Cyclic paroxysm of fever:
    P. vivax and P. ovale: every 48 hours
    P. malariae: every 72 hours
    P. falciparum: every 36-48 hours
  • 148.
  • 149. P. falciparum: Blood Stage Parasites
    Thin Blood Smears
    Fig. 1: Normal red cell; 
    Figs. 2-18: Trophozoites (among these, Figs. 2-10 correspond to ring-stage trophozoites); 
    Figs. 19-26:Schizonts (Fig. 26 is a ruptured schizont); Figs. 27, 28: Mature macrogametocytes (female); Figs. 29, 30:  Mature microgametocytes (male).
  • 150. Gametocytes of P. falciparum in thin blood smears.  Note the presence of a “Laveran’s bib”, which is not always visible.
  • 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.
  • 152. P. falciparum schizonts: seldom seen in peripheral blood.  Mature schizonts have 8 to 24 small merozoites; dark pigment, clumped in one mass.
  • 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.
  • 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.
  • 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.
  • 156. Rex Karl S. Teoxon, R.N, M.D
    133
    Vector: (night biting)
    anopheles mosquito
    minimus flavire
  • 157. 134
    SIGNS AND SYMPTOMS
    Fever, chills, profuse sweating, convulsion, Anemia and fluid and electrolytes imbalance, hepatomegaly, splenomegaly
    Dx: blood extraction (extract blood at the height of fever) thin and thick smear. Fluorescently labeled Ab
  • 158.
    • over 1 million deaths/year - mainly Africa
    • 159. Incubation period - 8-30 days
    • 160. influenza-like symptoms; paroxysms (fever, chills, rigors) every 36 to 48 hours, depending on species
    • 161. sickle cell trait and P. falicparum
  • 136
    COMPLICATIONS
    P. ovale and vivax – relapse after 10 years of first exposure
    P. falciparum –
    Cerebral malaria – severe headache, drowsiness, seizure, delirium, coma
    Black water fever – jaundice, ARF, hemoglobinuria, black colored urine
  • 162. 137
    MANAGEMENT
    P. Vivax and P. Ovale – Primaquine (relapse)
    P. falciparum - Chloroquine
    For chloroquine resistant plasmodium – quinine
    * Prophylaxis – chloroquine or mefloquine, pyrimethamine/ sulfadoxine (fansidar)
  • 163. Disease:Babesiosis
    Lab Dx:Giemsa stained thick and thin blood smears
    BABESIA
  • 164.
  • 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. 
  • 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. 
  • 167. TRYPANOSOMA BRUCEI
    Disease: African trypanosomiasis
    T. b. gambiense: Gambian trypanosomiasis, West & Mid-African sleeping sickness
    T. b. rhodesiense: Rhodesian trypanosomiasis, East African sleeping sickness
    Lab Dx:Giemsa stained thick and thin blood smears or lymph exudate (early stage); Giemsa stained smears of CSF (late stage)
  • 168. Site in host: lymph glands, blood stream, brain
    Portal of entry: skin
    Source of infection: tsetse fly
    Winterbottom’s sign: enlargement of posterior cervical LNs
  • 169.
  • 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
  • 171. A dividing parasite is seen at the right. Dividing forms are seen in African trypanosomiasis, but not in American trypanosomiasis (Chagas' disease)
  • 172. Tsetse fly. The vector of African trypanosomiasis
  • 173. Winterbottoms sign
  • 174. TRYPANOSOMA CRUZI
    Disease: American trypanosomiasis, Chaga’sdisease
    Lab Dx:Giemsa stained thick and thin blood smears for the trypomastigote; histopath exam for the amastigote
    Site in host: Tissues – heart; blood
    Portal of entry: skin
    Source of infection: Kissing bug Triatomidae
  • 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
  • 176. Trypanosoma cruzi crithidia
  • 177. Trypanosoma cruzi: Leishmanial form
  • 178. Riduviid bug: the vector of American trypanosomiasis
  • 179. Ramana's sign: unilateral conjunctivitis and orbital edema 
  • 180. Chaga'sDisease
    • asymptomatic- mostly
    • 181. acute- rash, edema on face (site of bite),
    flu-like symptoms
    • chronic– rare but serious
    • 182. g.i. tract nerve damage leading to megacolon
    • 183. heart- conductive problems and
    cardiomyopathy, sudden death
  • 184.
    • "kissing bug" reduviid bug vector --(epimastigotereplicative form)
    Entry, Spread, Multiplication
    • bug defecates on wound releasing trypomastigotes that get rubbed into wound and vasculature
    • 185. convert to amastigotes that invade and replicate in host cells
  • 186. Diagnosis– clinical, serology, blood smear microscopy
    Treatment- not very good, especially for late complications
    Prevention– clear houses of bugs, use netting for sleeping
  • 187. TOXOPLASMA GONDII
    Disease: Toxoplasmosis
    Site in host: All organs
    Portal of entry:
    Ingestion of oocyst contaminated water
    Aerosolization of oocyst contaminated dust or litter
    Consumption of raw or undercooked cyst infected meat
    Transplacental passage of the tachyzoite
  • 188. - Definitive host: domestic cats
    - Intermediate host: infected rodents
    Accidental intermediate host: humans
    Lab Dx: IFAT and ELISA; Giemsa-stained smears of exudates, aspirates or tissues
  • 189. Toxoplasma gondii, parasite
    Affects birds, mammals i.e. cats
    Infected person may carry the organism for life (reactivation is possible)
    161
    TOXOPLASMOSIS
  • 190. 162
    PATHOGENESIS
    ingestion of cyst from uncooked meat / fecal oral route from infected cats (feces)
    Quickly multiply in the GIT
    Distributed to CNS, lymphatic tissue, skeletal muscle, myocardium, retina and placenta
  • 191.
  • 192. T. gondiitachyzoites:crescentic to pyriform shaped with a prominent, centrally placed nucleus.
  • 193. Toxoplasma gondii cyst in brain tissue stained with hematoxylin and eosin (100×).
  • 194. 166
    SIGNS AND SYMPTOMS
    Malaise, fever, myalgia, headache, fatigue, sore throat, lymphadenopathy or asymptomatic
    FULMINANT = vomiting, cough and dyspnea, hyperpyrexia, delirium and seizures, encephalopathy, meningitis
    INFANTS = hydrocephalus or microcephalus, seizure, jaundice later strabismus, blindness, epilepsy, mental retardation
  • 195. 167
    DIAGNOSIS
    Serology – high IgM or rising IgM
    CT scan
    Mgmt:
    4-6 weeks of sulfadiazine + pyrimethamine (take folic acid to counteract drug’s adverse effects)
  • 196. LEISHMANIA
    • Disease:
    • 197. L. tropica complex: Old Word Cutaneousleishmaniasis (oriental sore, Aleppo boil, Delhi ulcer, Baghdad boil)
    • 198. L. mexicana complex: New Word Cutaneousleishmaniasis (chiclero ulcer, bay sore)
    • 199. L. braziliensis complex: Mucocutaneusleishmaniasis (espundia, uta)
    • 200. L. donovani: Visceral leishmaniasis (kala-azar or black disease, Dumdum fever)
    • Lab Dx: Giemsa stained tissue sections or impression smears
    • 201. Site in host: Monocytes/macrophages of skin & mucosa
    • 202. Portal of entry: Skin
    • 203. Source of infection: Phlebotomus or Lutzomiya fly
  • 204. L. tropica amastigotes: ovoid in shape; large & eccentric nucleus; small, rodlike kinetoplast positioned opposite the nucleus; rodlike axoneme perpendicular to the kinetoplast
  • 205. FREE LIVING AMEBAE
    • Disease:
    • 206. Naegleria:Primary Amebic Meningoencephalitis (PAM)
    • 207. Acanthamoeba:Chronic Granulomatous Amebic Encephalitis and keratitis
    • 208. Lab Dx: Direct microscopic exam (Wheatley’s trichromestain)
    PROTOZOA FROM OTHER BODY SITES
  • 209. FREE LIVING AMEBAE
    • Portal of Entry:
    • 210. Naegleria:nose
    • 211. Acanthamoeba:respiratory tract or ulcers in skin or mucosa / direct invasion of eye
    • 212. Source of infection:
    • 213. Naegleria: warm lakes, streams, ponds or inadequately chlorinated swimming pools
    • 214. Acanthamoeba: immunocompromised or debilitated host
  • 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. 
  • 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
  • 217. Acanthamoeba spp.: cysts stained with Heidenhain’s iron alum-haematoxylin method.
  • 218. TRICHOMONAS VAGINALIS
    • Disease: Trichomonadvaginitis
    • 219. Site in host: vagina & prostate
    • 220. Portal of entry: genitalia
    • 221. Sources of infection:trophs in vaginal & prostatic secretions
    • 222. NO cyst stage
    • 223. Lab Dx:trophs in vaginal & prostatic fluids
  • 224. Trophozoites of T. vaginalis: large, pyriform flagellate exhibiting rapid & jerky motility. The wavelike motion of the undulating membrane is often apparent
  • 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.
  • 226. Trichomonas vaginalis
    parasite
    182
    TRICHOMONIASIS
  • 227. 183
    SIGNS AND SYMPTOMS
    Females: itching, burning on urination, yellow gray frothy malodorous vaginal discharge, foul smelling
    Males: usually asymptomatic
    Dx: microscopic exam of vaginal discharge
  • 228. 184
    MANAGEMENT
    Metronidazole (Flagyl)
    include partners
    CX: PROM
  • 229.
  • 230. The Helminths
    Table 12.1
  • 231. Eukaryotic
    Multicellular animals
    Chemoheterotrophic
    Kingdom: Animalia
    Phylum: Platyhelminthes (flatworms)
    Class: Trematodes (flukes)
    Class: Cestodes (tapeworms)
    Phylum: Nematodes (roundworms)
    Helminths (Parasitic Worms)
  • 232. Trematodes
    Figure 12.25
  • 233. Humans as Definitive Host
    Figure 12.26
  • 234. Cestodes
    Figure 12.27
  • 235. Humans as Intermediate Host
    Figure 12.28
  • 236. Nematodes: Eggs Infective for Humans
    Figure 12.29
  • 237. Nematodes: Larvae Infective for Humans
    Figure 25.26
  • 238. Kingdom: Animalia
    Phylum: Arthropoda (exoskeleton, jointed legs)
    Class: Insecta (6 legs)
    Lice, fleas, mosquitoes
    Class: Arachnida (8 legs)
    Mites and ticks
    May transmit diseases (vectors)
    Arthropods as Vectors
    Figures 12.31a, 12.32
  • 239. HELMINTHS
    INTESTINAL NEMATODES
    • Enterobius vermicularis
    • 240. Ascaris lumbricoides
    • 241. Necator americanus
    • 242. Ancylostoma duodenale
    • 243. Trichuris trichiura
    • 244. Strongyloides stercoralis
    • TISSUE NEMATODES & CESTODES
    • 259. Trichinella spiralis
    • 260. Echinococcus granulosus
    • 261. Echinococcus multilocularis
    • 262. Spirometra species
  • Causal Agents:
    The nematode (roundworm) Capillariaphilippinensis causes human intestinal capillariasis
    C. hepatica-- humans hepatic capillariasis
    C. aerophila-- humans pulmonary capillariasis.
  • 263. Geographic Distribution:Capillariaphilippinensis is endemic in the Philippines and also occurs in Thailand. 
  • 264.
  • 265. Life Cycle:
    unembryonated eggs are passed in the human stool and become embryonated
    after ingestion by freshwater fish-- larvae hatch & penetrate the intestine-- migrate to the tissues -Ingestion of raw or undercooked fish
    Adults worm -small intestine
    females deposit unembryonatedeggs (autoinfection)  -- hyperinfection(a massive number of adult worms) . 
  • 266. Life Cycle:
    Capillaria hepatica adult worms reside in the liver of various animals, especially rats. 
    Capillariaaerophila adult worms reside in the epithelium of the tracheo-bronchial tract of various animals. 
  • 267. Clinical Features:
    Intestinal capillariasis-- pain and diarrhea
    autoinfection. 
    protein-losing enteropathy-- cachexiaand death
    Hepatic capillariasis (C. hepatica) -- acute or subacute hepatitis with eosinophilia-- dissemination -- fatal
    Pulmonary capillariasis (C. aerophila) -- fever, cough, asthma, and pneumonia-- fatal.
  • 268. Diagnostic findings
    Microscopy
    Treatment:The drug of choice is mebendazole*, and albendazole* is an alternative. 
  • 269. ASCARIS LUMBRICOIDES
    • Disease: Ascariasis; roundworm infection
    • 270. Site in host: SI
    • 271. Portal of entry: Mouth
    • 272. Infective stage: ova containing second stage larva
    • 273. Sources of infection: eggs from soil or vegetables
    • 274. Lab Dx: eggs in stool
  • Fertilized Ascaris egg (A) still at the unicellular stage. Unfertilized and fertilized eggs, (B and C, respectively).
  • 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).
  • 276.
  • 277. Causal Agent:
    Ascarislumbricoidesis the largest nematode (Adult females: 20 to 35 cm; adult male: 15 to 30 cm.)
    Geographic Distribution:most common human helminthic infection.  Worldwide distribution.  Highest prevalence in tropical and subtropical regions, and areas with inadequate sanitation. 
  • 278.
  • 279. Life Cycle:
    Adult worms live in the lumen of the small intestine--produce 200,000 eggs/day
     Fertile eggs embryonate- infective
    eggs swallowed -- the larvae hatch &, invade the intestinal mucosa-- portal-- systemic -- lungs .  
    lungs -- alveolar walls-- bronchial tree – throat swallowed-- small intestine-- adult worms .  
  • 280. Clinical Features:
    adult worms usually cause no acute symptoms. 
    High worm burdens –abd pain & obstruction. 
    Migrating worms – occlusion of biltract or oral expulsion. 
    lung phase of larval migration, pulmonary symptoms can occur (cough, dyspnea, hemoptysis, eosinophilicpneumonitis - Loeffler’s syndrome).
  • 281. Diagnostic findings
    Microscopy
    Treatment:The drugs of choice for treatment of ascariasis are albendazole* with mebendazole, ivermectin*, and nitazoxanide as alternatives. 
    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. 
  • 282. Ascaris lumbricoides
    In GI tract, few symptoms in light infections
    Nausea
    Vomiting
    Obstruction of small bowel or common bile duct.
    Pulmonary: symptoms due to migration
    Alveoli (verminous pneumonia)—cough, fever wheeze, dyspnea, X-ray changes, eosinophilia
  • 283. Effects of Adult Ascaris Worms
    Depends on worm load
    Effects
    Mechanical: obstruction, volvulus, intussusception, appendicitis, obstructive jaundice, liver abscesses, pancreatitis, asphyxia
    Toxic and Metabolic
    Malnutrition (complex)
  • 284. Ascaris lumbricoidesDiagnosis
    Characteristic eggs on direct smear examination
    If treating mixed infections, treat Ascaris first
    Mebendazole
    Pyrantel
    Control:
    Periodic mass treatment of children, health education, environmental sanitation
  • 285.
  • 286. Causal Agent:The nematode (roundworm) Trichuristrichiura, also called the human whipworm.
    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. 
    It is estimated that 800 million people are infected worldwide.  Trichuriasis occurs in the southern United States.
  • 287.
  • 288. Life Cycle:
    The unembryonated eggs are passed with the stool .  In the soil, the eggs develop into a 2-cell stage embryonate eggs
     After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine-larvae - adults in the cecum and ascending colon. 
    Female worms in the cecum shed between 3,000 and 20,000 eggs per day. 
  • 289. Clinical Features:
    Most frequently asymptomatic.  Heavy infections, especially in small children, can cause gastrointestinal problems (abdominal pain, diarrhea, rectal prolapse) and possibly growth retardation.
  • 290. Diagnostic findings
    microscopy
    Examination of the rectal mucosa by proctoscopy (or directly in case of prolapses) can occasionally demonstrate adult worms.
    Treatment:Mebendazole is the drug of choice, with albendazole as an alternative. 
  • 291. Case 13
    8-yr-old schoolgirl visiting the U.S. from Malaysia
    1 week history of epigastric pain, flatulence, anorexia, bloody diarrhea
    No eosinophilia noted
    Clinical diagnosis of amoebic dysentery made
    However, microscopy of stool prep…
  • 292.
  • 293. Diagnosis?
  • 294. Trichuris trichiura (Whipworm)
    Common in Southeast U.S.
    Frequently coexists with ascaris
    Entirely intraluminal life cycle—eggs are ingested
    Frequently asymptomatic
    Severe infections: diarrhea, abdominal pain and tenesmus
    Rectal prolapse in children
    DS-eggs in stool
    Mebendazole 100 mg bid x 3 days
  • 295.
  • 296.
  • 297.
  • 298. ENTEROBIUS VERMICULARIS
    • Disease: Enterobiasis; pinworm infection; seatworm infection; oxyuriasis
    • 299. Site in host: LI, appendix
    • 300. Portal of entry: Mouth
    • 301. Infective stage: ova containing rhabditiform larva
    • 302. Sources of infection: oral-fecal route; through contaminated fomites/food; inhalation ff by ingestion of airborne ova; retroinfection
    • 303. Lab Dx: eggs in perianal region; Scotch tape swab
  • Enterobius eggs: oval, asymmetric w/ one side noticeably flattened; smooth, thin-shelled, maycontain embryo 
  • 304. Anterior end of Enterobius vermicularis adult worm.
  • 305.
  • 306. Causal Agent:
    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. 
    Geographic Distribution:Worldwide, with infections more frequent in school- or preschool-children and in crowded conditions. 
    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).
  • 307.
  • 308. Life Cycle:
    Eggs are deposited on perianal folds .  Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area . 
    Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. 
    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. 
    .
  • 309. Life Cycle:
    These would be swallowed and follow the same development as ingested eggs.  -larvae hatch in the small intestine -adults in the colon .
    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 . 
    Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum
  • 310. Clinical Features
    Enterobiasis is frequently asymptomatic. 
    The most typical symptom is perianalpruritus, especially at night, which may lead to excoriations and bacterial superinfection. 
    Occasionally, invasion of the female genital tract with vulvovaginitis and pelvic or peritoneal granulomas can occur. 
    Other symptoms include anorexia, irritability, and abdominal pain.
  • 311. Diagnostic findings
    Microscopy
    Treatment:The drug of choice is pyrantelpamoate. 
    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. 
  • 312. Case 10
    11-year-old female
    Doing poorly in school
    Not sleeping well
    Anorectic
    Complains of itching in rectal region throughout the day
    A Scotch-tape test reveals…
  • 313.
  • 314.
  • 315.
  • 316. Diagnosis?
  • 317. Enterobius (Pinworm)
    18 million infections in U.S.
    Incidence higher in whites
    Preschool and elementary school most often
    Mostly asymptomatic
    Nocturnal anal pruritis cardinal feature due to migration and eggs
    May have insomnia, possible emotional symptoms
    DS-eggs or adults on perineum {scotch tape}
    Mebendazole 100 mg. Repeat in 2 weeks. Pyrantel pamoate 11 mg/kg; repeat 2 weeks
  • 318. NECATOR AMERICANUS
    • Disease: New World Hookworm Disease
    • 319. Site in host: SI, attached
    • 320. Portal of entry: Skin
    • 321. Infective stage: filariform larva
    • 322. Sources of infection: infective filariform larvae in soil
    • 323. Lab Dx: eggs in stool
  • Hookworm egg: oval or ellipsoid; thin shell; usually embryo at four cell stage
  • 324. The embryo has begun cellular division and is at an early (gastrula) developmental stage.
  • 325. Hookworm rhabditiform larva (wet preparation).
  • 326. Hookworm filariform larva (wet preparation).
  • 327.
  • 328.
  • 329. Anterior end of Necator americanus:oral opening of this species contains cutting "plates" . The muscular esophagus is labeled in this image (*).
  • 330. ANCYLOSTOMA DUODENALE
    • Disease: Old World Hookworm Disease
    • 331. Site in host: SI, attached
    • 332. Portal of entry: skin, usually feet
    • 333. Infective stage: filariform larva
    • 334. Sources of infection: infective filariform larvae in soil
    • 335. Lab Dx: eggs in stool
  • Oral opening of Ancylostoma duodenale:presence of four cutting "teeth," two on each side.
  • 336. B
    A
    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.
  • 337.
  • 338.
  • 339. Causal Agents:
    The human hookworms include two nematode (roundworm) species, Ancylostomaduodenale and Necatoramericanus. 
    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). 
    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.
  • 340. Geographic Distribution:
    The second most common human helminthic infection (after ascariasis). 
    Worldwide distribution, mostly in areas with moist, warm climate. 
    Both N. americanus and A. duodenale are found in Africa, Asia and the Americas. 
    Necatoramericanus predominates in the Americas and Australia, while only A. duodenale is found in the Middle East, North Africa and southern Europe.
  • 341.
  • 342. Life Cycle:
    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 . 
      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
    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 . 
    In addition, infection by A. duodenale may probably also occur by the oral and transmammary route.  N. americanus, however, requires a transpulmonary migration phase
  • 343. Clinical Features:
    Iron deficiency anemia is the most common symptom of hookworm infection, and can be accompanied by cardiac complications. 
    Gastrointestinal and nutritional/metabolic symptoms can also occur. 
    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.
  • 344. Diagnostic Findings
    Microscopy
    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). 
  • 345. Treatment:
    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. 
    Eosinophilic enteritis caused by A. caninum and for cutaneous larva migrans(creeping eruption) caused by canine and feline hookworms.
  • 346. Case 12
    57 year old farmer from Dixie County
    Presents with profound SOB
    Physical examination: anemic otherwise unremarkable
    Laboratory examination reveals a profound anemia (hct 24) with aniso and poikilocytosis
    Remainder of laboratory examination normal.
  • 347.
  • 348. Diagnosis?
  • 349.
  • 350. Hookworm
    Hookworm responsible for development of USPHS
    Caused by two different species (North American and Old World)
    Very similar to strongyloides in life cycle
    Attaches to duodenum, feeds on blood
    Elaborates anticoagulant, attaches and reattaches many times
    Loss of around 0.1 ml/d of blood per worm
  • 351.
  • 352.
  • 353. Case 14
    18-year-old trailer park handyman seen in ER
    Worked under trailers wearing shorts and no shirt
    Developed intensely pruritic skin rash
    Unable to sleep
    WBC 18,000
    65% eosinophils.
  • 354.
  • 355. Case 15
    An 8 year old boy
    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).
    Legs show several raised, reddened, serpiginous lesions that are intensely pruritic.
  • 356.
  • 357. Diagnosis ?
  • 358. Cutaneous Larva Migrans
    Caused by filariform larvae of dog or cat hookworm (Ancylostoma braziliense or Ancylostoma duodenale
    Common in Southeast U.S.
    Red papule at entry with serpiginous tunnel
    Intense pruritis
    Self limiting condition
    Diagnosis clinical
    Topical or oral thiabendazole 25 mg/kg bid for 3-5 days
    May use ethyl chloride topically
  • 359. Cutaneous larva migrans (creeping eruption)
    More common in children
    Larvae penetrate skin and cause tingling followed by intense itching.
    Eggs shed from dog and cat bowels develop into infectious larvae outside the body in places protected from desiccation and extremes of temperature
    Shady, sandy areas under houses, at beach, etc.
  • 360. Cutaneous larva migrans (creeping eruption)
    Usually not associated with systemic symptoms
  • 361. Cutaneous larva migrans (creeping eruption)
    Diagnosis and treatment
    Skin lesions are readily recognized
    Usually diagnosed clinically
    Generally do not require biopsy
    Reveal eosinophilia inflammatory infiltrate
    Migrating parasite is generally not seen
    Stool smear will reveal eggs
  • 362.
  • 363.
  • 364. Visceral Larva Migrans
    Infection with dog or cat round worms
    Toxocara canis; Toxocara catis
    Underdiagnosed based on seroprevalence surveys
    Heavy infections associated with fever, cough, nausea, vomiting, hepatomegaly, and eosinophilia
    Uncommon in adults
    Ocular type more common in adults
    Diagnosis-ELISA
    Thiabendazole: 25 mg/kg bid X 5 days
  • 365. Case 17
    A 34 yr-old woman from Saudi Arabia
    Radiation and cyclophosphamide, adriamycin, vincristine and prednisone for diffuse large B cell lymphoma of the neck.
    Mild eosinophilia (AEC=500) at the time of diagnosis
    4 months after initiation of chemo, c/o intermittent diffuse abdominal pain, bloating, constipation and occasional rectal bleeding.
    Absolute eosinophil count: 1000
  • 366. Case 17
    No evidence of lymphoma found on re-staging
    Completed chemo, was deemed to be in complete remission, but had persistence of GI complaints.
    Upper endoscopy was unrevealing.
    Colonoscopy and biopsy revealed granulomatous inflammation, prominent eosinophilic infiltrate, surrounding a collection of eggs.
  • 367.
  • 368. STRONGYLOIDES STERCORALIS
    • Disease: Strongyloidiasis, Cochin-China diarrhea or Vietnam diarrhea
    • 369. Site in host: wall of SI
    • 370. Portal of entry: skin
    • 371. Infective stage: filariform larva
    • 372. Sources of infection: larvae in soil; autoinfection
    • 373. Lab Dx: larvae in stool
  • 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.
  • 374.
  • 375. Causal Agent:
    The nematode (roundworm) Strongyloidesstercoralis.  Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.
    .
    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
  • 376.
  • 377. Life Cycle:
    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:
  • 378. Life Cycle:
    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 . 
    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) .
  • 379. Life Cycle:
    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 . 
    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 .
     
  • 380. Life Cycle:
    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);
    To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloidesstercoralis and Capillariaphilippinensis infections. 
  • 381. Clinical Features
    Frequently asymptomatic.  Gastrointestinal symptoms include abdominal pain and diarrhea. 
    Pulmonary symptoms (including Loeffler’s syndrome) can occur during pulmonary migration of the filariform larvae. 
    Dermatologic manifestations include urticarial rashes in the buttocks and waist areas. 
    Disseminated strongyloidiasis occurs in immunosuppressed patients, can present with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal. 
    Blood eosinophilia is generally present during the acute and chronic stages, but may be absent with dissemination.
  • 382. Diagnostic findings
    Microscopy
    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. 
  • 383. On the day of admission…
    Fever, confusion, and not able to get out of bed---transported to the hospital
    Initial blood work:
    Elevated WBC
    Raised eosinophil count 4 times normal
    Underwent UGI endoscopy
    Duodenal biopsy obtained
  • 384.
  • 385. Strongyloides: Crucial Aspects of Life Cycle
    Infection acquired through penetration of intact skin
    Infection may persist for many years via autoinfection
    In immunocompromised patients, there is risk of dissemination or hyperinfection
    Hyperinfection syndrome
  • 386. Disseminated Strongyloidiasis
    High mortality75%
    Penetration of gut wall by infective larvae
    Gut organisms carried on the surface of larvae results in polymicrobial sepsis, meningitis
    Larvae disseminate into all parts of body: CNS, lungs, bladder, peritoneum
  • 387. Summary—Clinical Findings
    Defective cell-meditated immunity: steroids, burns, lymphomas, AIDS (?)
    Gl symptoms in about two-thirds:
    Abdominal pain
    Bloating
    Diarrhea
    Constipation
    Wheezing, SOB, hemoptysis
  • 388. Summary—Clinical Findings
    Skin rash or pruritis in ~ one-third
    Larva currens (racing larva)
    Intensely pruritic
    Linear or serpiginous urticaria with flare that moves 5-15 cm/hr
    Usually buttocks, groin, and trunk
    In dissemination, diffuse petechiae and purpura
  • 389. Summary-Clinical Findings
    Eosinophilia 60-95%
    Less if on steroids
  • 390. DIPHYLLOBOTHRIUM LATUM
    • Disease: Diphyllobothriasis; fish tapeworm infection; broad tapeworm infection
    • 391. Site in host: SI
    • 392. Portal of entry: mouth
    • 393. Definitive host: human, dogs, cats
    • 394. 1st Intermediate host: crustaceans (Cyclops or Diaptomus)
    • 395. 2nd Intermediate host: freshwater fish
    • 396. Infective stage: plerocercoid larvae
    • 397. Sources of infection: plerocercoid in freshwater fish
    • 398. Lab Dx: eggs in stool
  • 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. 
  • 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. 
  • 401.
  • 402. D. latum scolex and gravid proglottids
  • 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. 
  • 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.
  • 405. Causal Agents:
    The cestodeDiphyllobothriumlatum (the fish or broad tapeworm), the largest human tapeworm. 
    Geographic Distribution:Diphyllobothriasis occurs in the Northern Hemisphere 
    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. 
  • 406.
  • 407. Life Cycle:
    Immature eggs are passed in feces -oncospheres -develop into a coracidia . 
    After ingestion by a suitable freshwater crustacean (the copepod first intermediate host) the coracidia develop into procercoid larvae . 
    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)
    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. 
     
  • 408. Life Cycle:
      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. 
    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. 
    Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces . 
  • 409. Clinical Features:
    Diphyllobothriasis can be a long-lasting infection (decades). 
    Most infections are asymptomatic. 
    Manifestations may include abdominal discomfort, diarrhea, vomiting, and weight loss. 
    Vitamin B12 deficiency with pernicious anemia may occur. 
    Massive infections may result in intestinal obstruction. 
    Migration of proglottids can cause cholecystitis or cholangitis.
  • 410. Diagnostic findings
    Microscopy
    Treatment:Praziquantel* is the drug of choice.  Alternatively, Niclosamide can also be used to treat diphyllobothriasis.  
  • 411. DIPYLIDIUM CANINUM
    • Disease: Dipylidiasis; dog tapeworm infection
    • 412. Site in host: SI
    • 413. Portal of entry: mouth
    • 414. Definitive host: dog & cat (or humans)
    • 415. Intermediate host: larval flea
    • 416. Infective stage: eggs
    • 417. Sources of infection: flea & louse
    • 418. Lab Dx: eggs in stool or egg sacks in stool
  • 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) 
  • 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. 
  • 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.
  • 421. Adult tapeworm of Dipylidium caninum.  The scolex of the worm is very narrow and the proglottids, as they mature, get larger.
     
  • 422. Causal Agent:
    Dipylidiumcaninum(the double-pored dog tapeworm) mainly infects dogs and cats, but is occasionally found in humans.
    Geographic Distribution:Worldwide.  Human infections have been reported in Europe, the Philippines, China, Japan, Argentina, and the United States
  • 423.
  • 424. Life Cycle:
    Gravid proglottids are passed intact in the feces or emerge from the perianal region of the host .  Subsequently they release typical egg packets . 
    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. 
    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 . 
    The vertebrate host becomes infected by ingesting the adult flea containing the cysticercoid . 
    The dog is the principal definitive host for Dipylidiumcaninum.  Other potential hosts include cats, foxes, and humans (mostly children) , . 
  • 425. Life Cycle:
    Humans acquire infection by ingesting the cysticercoid contaminated flea.  This can be promulgated by close contact between children and their infected pets. 
    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. 
    They produce proglottids (or segments) which have two genital pores (hence the name "double-pored" tapeworm). 
    The proglottids mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool .
  • 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.
  • 427. Diagnostic findings
    Microscopy
    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. 
  • 428. HYMENOLEPIS NANA
    • Disease: Hymenolepiasis; dwarf tapeworm infection
    • 429. Site in host: adults & cysts in SI
    • 430. Portal of entry: mouth
    • 431. Definitive host: human, mice & rats
    • 432. Intermediate host: DO NOT require an IH
    • 433. Infective stage: eggs
    • 434. Sources of infection: eggs fr feces in soil; autoinfection
    • 435. Lab Dx: eggs in stool
  • 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). 
  • 436.
  • 437.
  • 438.
  • 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.
  • 440. HYMENOLEPIS DIMINUTA
    • Disease: Hymenolepiasis; rat tapeworm infection
    • 441. Site in host: SI
    • 442. Portal of entry: mouth
    • 443. Definitive host: human, mice & rats
    • 444. Intermediate host: insects (rat & mouse flea, the flour moth and flour beetle)
    • 445. Infective stage: eggs
    • 446. Sources of infection: cysts from insects
    • 447. Lab Dx: eggs in stool
  • 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.
  • 448. Mature proglottids of Hymenolepis diminuta.
  • 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.
    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.
  • 450.
  • 451.
  • 452. Life Cycle:
    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. 
    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 . 
    Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine
    internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment . 
  • 453. Life Cycle:
    .
    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 .
  • 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.
  • 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.
  • 456. Treatment:Diagnostic findings
    Microscopy
    Treatment:Praziquantel* is the drug of choice. 
  • 457. TAENIA SAGINATA
    • Disease: Taeniasis; beef tapeworm infection
    • 458. Site in host: SI
    • 459. Portal of entry: mouth
    • 460. Definitive host: human
    • 461. Intermediate host: grazing cattle
    • 462. Infective stage: eggs
    • 463. Sources of infection: cysts in beef
    • 464. Lab Dx: segments and eggs in stool; Scotch tape swab
  • 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). 
  • 466. Taenia egg.  Note the thick, "striated" shell and several of the larval hooks; approximate size = 40 µm. 
  • 467. T. Saginata gravid proglottid:has 15 to 30 main uterine branches on each side of central stem; proglottids are much longer than wide
  • 468. TAENIA SOLIUM
    • Disease: Taeniasis; pork tapeworm infection
    • 469. Site in host: SI
    • 470. Portal of entry: mouth
    • 471. Definitive host: human
    • 472. Intermediate host: pig
    • 473. Infective stage: eggs
    • 474. Sources of infection: cysts in pork; autoinfection
    • 475. Lab Dx: segments and eggs in stool; Scotch tape swab
  • T. saginata gravid proglottid:has 15 to 30 main uterine branches on each side of central stem; proglottids are much longer than wide
  • 476.
  • 477.
  • 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.
  • 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.
  • 480. A cysticercus of Taenia in muscle.  Note the fibrous capsule (*) around the cysticercus.
  • 481. Causal Agents:
    The cestodes (tapeworms) Taeniasaginata (beef tapeworm) and T. solium (pork tapeworm).  Taeniasolium can also cause cysticercosis.
    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
  • 482.
  • 483. Life Cycle:
    Taeniasis is the infection of humans with the adult tapeworm of Taeniasaginata or Taeniasolium. 
    Humans are the only definitive hosts for T. saginata and T. solium. 
    Eggs or gravid proglottids are passed with feces ;
    Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or gravid proglottids . 
    Humans become infected by ingesting raw or undercooked infected meat .  In the human intestine, the cysticercus develops into an adult tapeworm
      The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine . 
  • 484. Life Cycle:
    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. 
    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). 
    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.
  • 485. Clinical Features:
    Taeniasaginatataeniasis produces only mild abdominal symptoms.  The most striking feature consists of the passage (active and passive) of proglottids. 
    Occasionally, appendicitis or cholangitis can result from migrating proglottids.  
    Taeniasoliumtaeniasis is less frequently symptomatic than Taeniasaginatataeniasis. 
    The main symptom is often the passage (passive) of proglottids.  The most important feature of Taeniasoliumtaeniasis is the risk of development of cysticercosis.
  • 486. Diagnostic findings
    TAKE EXTREME CARE IN PROCESSING THE SAMPLES!  INGESTION OF EGGS CAN RESULT IN CYSTICERCOSIS!
    Microscopy
    Antibody detection may prove useful especially in the early invasive stages, when the eggs and proglottids are not yet apparent in the stools.
    Treatment:Treatment is simple and very effective.  Praziquantel* is the drug of choice. 
  • 487. Taenia saginata
    Ingestion of raw or poorly cooked beef
    Cows infected via the ingestion of human waste containing the eggs of the parasite
    Cows contain viable cysticercus larvae in the muscle
    Humans act as the host only to the adult tapeworms
    Up to 25 meters in the lumen of intestine
    Found all over the world, including the U.S.
  • 488. Beef Tapeworm
  • 489. Treatment
    Praziquantel
    Albendazole
    Niclosamide
  • 490. Tapeworms (Cestodes)
    Adult worms inhabit GI tract of definitive vertebrate host
    Larvae inhabit tissues of intermediate host
    Humans
    Definitive for T. saginata
    Intermediate for Echinococcus granulosus (hydatid)
    Both definitive and intermediate for T. solium
    Adult worms shed egg-containing segments in stool ingested by intermediate host larval form in tissues
  • 491. Cystercercosis
    Symptoms depend on location of cysts, but frequently include motor spasms, seizures, confusion, irritability, and personality change
    In the eye, often subretinal or in vitreous. Movement may be seen by the patient. Pain, amaurosis, and loss of vision may occur.
  • 492. Cysticercosis
    Clinical manifestations
    Adult worms rarely cause sxs
    Larvae penetrate intestine, enter blood, and eventually encyst in the brain.
    Cerebral ventircles  hydrocephalus
    Spinal cord  compression, paraplegia
    Subarachnoid space  chronic meningitis
    Cerebral cortex  seizures
    Cysts may remain asymptomatic for years, and become clinically apparent when larvae die
    Larvae may encyst in other organs, but are rarely symptomatic
  • 493. Cysticercosis
    Diagnosis
    CT and MRI preferred studies
    Discrete cysts that may enhance
    Usually multiple lesions
    Single lesions especially common in cases from India
    Older lesions may calcify
    CSF
    Lymphs or eos, low glucose, elevated protein
    Serology
    Especially in cases with multiple cysts
  • 494. Cysticercosis
    Treatment
    Complex and controversial
    Praziquantel and albendazole may kill cysts, but death of larvae can increase inflammation, edema and exacerbate sxs
    When possible, surgical resection of symptomatic cyst is preferred
    Corticosteroids vs. edema and inflammation; antiseizure meds
  • 495.
  • 496.
  • 497. Causal Agents:
    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.
    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. 
  • 498.
  • 499. Life Cycle:
    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 . 
    Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . 
    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 . 
    S. japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and
    S. mansoni occurs more often in the superior mesenteric veins draining the large intestine . 
      S. haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. 
  • 500. Life Cycle:
    .  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. 
    Pathology of S. haematobiumschistosomiasis includes: hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord.
    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.
  • 501. Clinical Features
    Many infections are asymptomatic. 
    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. 
    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. 
    .
  • 502. Clinical Features
    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.
  • 503. Diagnostic findings
    microscopy
    Antobodydetrectioncan be useful in both in clinical management (e.g., recent infections) and for epidemiologic surveys.
    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. 
  • 504.
  • 505. FASCIOLA HEPATICA
    • AKA: Sheep Liver Fluke
    • 506. Disease: Fascioliasis, “liver rot”
    • 507. Site in host: Bile ducts
    • 508. Portal of entry: mouth
    • 509. Definitive host: sheep, cattle & other mammals, including humans
    • 510. Intermediate host: snail (Lymnaea)
    • 511. Source of infection: eating watercress, lettuce or radishes or drinking water infested with metacercariae
    • 512. Infective stage: metacercariae
    • 513. Lab Dx: eggs in stool
  • 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. 
  • 514. Causal Agents:
    The trematodesFasciola hepatica (the sheep liver fluke) and Fasciolagigantica, parasites of herbivores that can infect humans accidentally.
    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.
  • 515.
  • 516. Life Cycle:
    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.
  • 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.
  • 518. Diagnostic findings
    Microscopy and antibody detection
    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. 
  • 519. Causal Agent:The trematodeFasciolopsisbuski, the largest intestinal fluke of humans.
    Geographic Distribution:Asia and the Indian subcontinent, especially in areas where humans raise pigs and consume freshwater plants.
  • 520.
  • 521. Life Cycle:
    Immature eggs are discharged into the intestine and stool .  Eggs become embryonated in water , eggs release miracidia , which invade a suitable snail intermediate host . 
    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 .
    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.
  • 522. Clinical Features:Most infections are light and asymptomatic.  In heavier infections, symptoms include diarrhea, abdominal pain, fever, ascites, anasarca and intestinal obstruction.
  • 523. Diagnostic findings
    Microscopy
    Treatment:Praziquantel* is the drug of choice. 
  • 524. CLONORCHIS SINENSIS
    • AKA: Chinese or Oriental Liver Fluke
    • 525. Disease: Clonorchiasis
    • 526. Site in host: Bile ducts
    • 527. Portal of entry: mouth
    • 528. Definitive host: humans, dog & cat or other mammals
    • 529. 1st Intermediate host: freshwater snail (Bulinus, Parafossarulus)
    • 530. 2nd Intermediate host: freshwater fish (Cyprinidae)
    • 531. Infective stage: metacercariae
    • 532. Lab Dx: eggs in stool
  • C. sinensis, adult: stained whole mount; approximate size = 15 mm.
  • 533.
  • 534.
  • 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.
  • 536.
  • 537. Causal Agent:The trematodeClonorchissinensis (Chinese or oriental liver fluke).
    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.
  • 538.
  • 539. Life Cycle:
    Embryonated eggs are discharged in the biliary ducts and in the stool . 
    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 .
      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.
  • 540. Clinical Features:
    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.
  • 541. Diagnostic findings
    Microscopy
    .
    Treatment:Praziquantel or albendazole* are the drugs of choice. 
  • 542. Causal Agent:
    Trematodes (flukes) Opisthorchisviverrini (Southeast Asian liver fluke) and O. felineus (cat liver fluke).
    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.
  • 543.
  • 544. Life Cycle:
    The adult flukes deposit fully developed eggs that are passed in the feces . 
    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 . 
    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 . 
    The adult flukes reside in the biliary and pancreatic ducts of the mammalian host, where they attach to the mucosa.
  • 545. Clinical Features:
    Most infections are asymptomatic. 
    In mild cases, manifestations include dyspepsia, abdominal pain, diarrhea or constipation. 
    With infections of longer duration, the symptoms can be more severe, and hepatomegaly and malnutrition may be present. 
    In rare cases, cholangitis, cholecystitis, and chlolangiocarcinoma may develop. 
    infections due to O. felineus may present an acute phase resembling Katayama fever (schistosomiasis), with fever, facial edema, lymphadenopathy, arthralgias, rash, and eosinophilia. 
    Chronic forms of O. felineus infections present the same manifestations as O. viverrini, with in addition involvement of the pancreatic ducts.
  • 546. Diagnostic findings
    Microscopy
    Treatment:Praziquantel is the drug of choice to treat opisthorchiasis. 
  • 547. PARAGONIMUS WESTERMANI
    • AKA: Lung Fluke
    • 548. Disease: Paragonimiasis, pulmonary distomiasis, lung fluke disease
    • 549. Site in host: Lungs
    • 550. Portal of entry: mouth
    • 551. Definitive host: humans & a variety of carnivores
    • 552. 1st Intermediate host: freshwater snail (Family Thieridae)
    • 553. 2nd Intermediate host: freshwater crab (Eriocheir, Patamon, Sesarma, Parathelphusa) or crayfish (Cambarus, Astacus)
    • 554. Source of infection: consumption of raw or undercooked infected freshwater crustaceans
    • 555. Infective stage: metacercariae
    • 556. Lab Dx: eggs in sputum & stool
  • 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.
  • 557.
  • 558. Paragonimus westermani:Cross section of lung containing adult Paragonimus westermani.
  • 559.
  • 560.
  • 561. Causal Agent:
    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.
    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.
  • 562.
  • 563. Life Cycle:
    The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with stool . 
    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 . 
  • 564. Life Cycle:
    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 (. 
    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. 
    Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani.
  • 565. Clinical Features:
    The acute phase (invasion and migration) may be marked by diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia. 
    During the chronic phase, pulmonary manifestations include cough, expectoration of discolored sputum, hemoptysis, and chest radiographic abnormalities. 
    Extrapulmonary locations of the adult worms result in more severe manifestations, especially when the brain is involved.
  • 566. Diagnostic findings
    Microscopy
    Antibody detection is useful in light infections and in the diagnosis of extrapulmonaryparagonimiasis.
    Treatment:Praziquantel* is the drug of choice to treat paragonimiasis.  Bithionol is an alternative drug for treatment of this disease. 
  • 567. METAGONIMUS YOKOGAWAI
    • Disease: Metagonimiasis
    • 568. Site in host: Bile ducts
    • 569. Portal of entry: mouth
    • 570. Definitive host: humans, dogs, cats, hogs, pelicans & other fish-eating birds
    • 571. 1st Intermediate host: snail (Semisulcospira, Thiara and Hua)
    • 572. 2nd Intermediate host: freshwater fish (Salmonoids & cyprinoids)
    • 573. Infective stage: metacercariae
    • 574. Lab Dx: eggs in stool
  • M. yokogawai, adult fluke: the position of the ventral sucker is to the side of the midline with its axis in a diagonal line
  • 575. Causal Agent:
    Metagonimusyokogawai, a minute intestinal fluke (and the smallest human fluke).
    Geographic Distribution:Mostly the Far East, as well as Siberia, Manchuria, the Balkan states, Israel, and Spain.
  • 576.
  • 577. Life Cycle:
    Adults release fully embryonated eggs each with a fully-developed miracidium, and eggs are passed in the host’s feces . 
    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) . 
    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 .
  • 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.
  • 579. Diagnostic findings
    Microscopy
    Treatment:Praziquantel* is the drug of choice. 
  • 580. HETEROPHYES HETEROPHYES
    • Disease: Heterophyiasis
    • 581. Site in host: Bile ducts
    • 582. Portal of entry: mouth
    • 583. Definitive host: humans, dog & cat or other fish eating mammals
    • 584. 1st Intermediate host: brackish water snail (Pirenella, Cerithidea)
    • 585. 2nd Intermediate host: brackish water fish (Mugil, Tilapia and Acanthogobus)
    • 586. Infective stage: metacercariae
    • 587. Lab Dx: eggs in stool
  • Causal Agent:
    The trematodeHeterophyesheterophyes, a minute intestinal fluke.
    Geographic Distribution:Egypt, the Middle East, and Far East.
  • 588.
  • 589. Life Cycle:
    Adults release embryonated eggs each with a fully-developed miracidium, and eggs are passed in the host's feces . 
    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) . 
    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
    .  In addition to humans, various fish-eating mammals (e.g., cats and dogs) and birds can be infected by Heterophyesheterophyes .
  • 590. Clinical Features:
    The main symptoms are diarrhea and colicky abdominal pain. 
    Migration of the eggs to the heart, resulting in potentially fatal myocardial and valvular damage, has been reported from the Philippines. 
    Migration to other organs (e.g., brain) has also been reported.
  • 591. Laboratory Diagnosis:
    Microscopy
    Treatment:Praziquantel* is the drug of choice. 
  • 592. FASCIOLOPSIS BUSKI
    • AKA: Large or giant intestinal fluke
    • 593. Disease: Fasciolopsiasis
    • 594. Site in host: SI
    • 595. Portal of entry: mouth
    • 596. Definitive host: pig & humans
    • 597. 1st Intermediate host: snail (Segmentina / Hippeutis)
    • 598. 2nd Intermediate host: water chestnuts & lotus
    • 599. Infective stage: metacercariae
    • 600. Lab Dx: eggs in stool
  • 601. Adult fluke of Fasciolopsis buski.
  • 602.
  • 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. 
  • 604.
  • 605. SCHISTOSOMA MANSONI
    • Disease: Schistosomiasis, intestinal schistosomiasis, bilharziasis “snail fever”
    • 606. Site in host: veins of LI
    • 607. Portal of entry: skin
    • 608. Definitive host: humans, baboons & rodents
    • 609. Intermediate host: snail (Biomphalaria sp & Tropicorbis sp)
    • 610. Infective stage: cercariae
    • 611. Lab Dx: eggs in stool; rectal or liver biopsy
  • 612. Biomphalaria spp.
  • 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
  • 614.
  • 615.
  • 616.
  • 617.
  • 618. Male and female schistosomes.
  • 619. SCHISTOSOMA HAEMATOBIUM
    • Disease: Urinary schistosomiasis, schistosomal hematuria, urinary bilharziasis
    • 620. Site in host: veins of urinary bladder
    • 621. Portal of entry: skin
    • 622. Definitive host: humans, monkeys & baboons
    • 623. Intermediate host: snail (Bulinus, Physopsis, and Biomphalaria sp)
    • 624. Infective stage: cercariae
    • 625. Lab Dx: eggs in stool; cystoscopy
  • Bulinus spp.
  • 626. S. haematobium eggs: large and have a prominent terminal spine at the posterior end
  • 627.
  • 628. S.haematobium: adult schistosomes live in pairs in the pelvic veins (especially in the venous plexus surrounding the bladder); males are 10-15 mm in lenght by 0,8-1 mm in diameter, and have a ventral infolding from the ventral sucker to the posterior end forming the gynecophoric canal. Adult male with female in the copulatory groove.
  • 629. SCHISTOSOMA JAPONICUM
    • Disease: Schistosomiasis, Katayama fever
    • 630. Site in host: veins of SI
    • 631. Portal of entry: skin
    • 632. Definitive host: humans, dogs, cats, horses, pigs, cattle, deer, caribou & rodents
    • 633. Intermediate host: snail (Oncomelania)
    • 634. Infective stage: cercariae
    • 635. Lab Dx: eggs in stool; liver biopsy
  • Onchomelania, hupensis spp.
  • 636. S. japonicum egg: typically oval or subspherical, and has a vestigial spine (smaller than those of the other species)
  • 637.
  • 638. Cercaria
  • 639.
  • 640.
  • 641.
  • 642. TISSUE NEMATODES and CESTODES
    TRICHINELLA SPIRALIS
    • Disease: Trichinosis, trichiniasis, trichinelliasis
    • 643. Site in host: Adult – SI wall; Encysted larvae – striated muscle
    • 644. Portal of entry: Mouth
    • 645. Definitive Host: human, pig, bear & other carnivorous/omnivorous animals
    • 646. Sources of infection: encysted larvae in pork
    • 647. Lab Dx: skin test, serology (slide flocculation/ ELISA), muscle biopsy
  • 648. Encysted larvae of Trichinellain pressed muscle tissue. The coiled larvae can be seen inside the cysts.
  • 649. Larvae of Trichinella, freed from their cysts, typically coiled; length: .8 to 1 mm.
  • 650.
  • 651. ECHINOCOCCUS GRANULOSUS
    • Disease: Echinococcosis, hydatid disease, hydatid cyst
    • 652. Site in host: liver, lungs, brain, bones
    • 653. Portal of entry: Mouth
    • 654. Definitive Host: dogs, wolves & other Canidae
    • 655. Sources of infection: eggs from dog feces in soil
    • 656. Lab Dx: skin test, X-ray, CAT scan, serology
  • 657.
  • 658.
  • 659. "Hydatid sand". Fluid aspirated from a hydatid cyst shows multiple protoscolices (size approximately 100 µm), each of which has typical hooklets. The protoscolices are normally invaginated (left), and evaginate (middle, then right) when put in saline.
  • 660.
  • 661.
  • 662. Echinococcus granulosus:the protoscolices then become invaginated and measure 90-140 by 70-120 µm. They can transform into daughter cysts.These cysts can proliferate both internally and externally giving exogenous cysts. Spontaneous or surgical rupture of the cyst can originate a secondary hydatidosis.
  • 663. Histopathology of hydatid cyst.
  • 664. Echinococcus granulosus:the presence of isolated hooklets is diagnostic for hydatidosis. Hooklets can be observed in hydatid fluid and must be searched in sputum after a vomica .
  • 665. Hydatid cysts
  • 666. ECHINOCOCCUS MULTILOCULARIS
    • Disease: Alveolar Echinococcosis
    • 667. Site in host: liver, lungs, brain, bones
    • 668. Portal of entry: Mouth
    • 669. Definitive Host: foxes, cats, dogs, & other carnivores
    • 670. Intermediate Host: mouse, vole, & lemming (human is an accidental host)
    • 671. Sources of infection: eggs from dog/cat feces in soil
    • 672. Lab Dx: serologic tests (ELISA, IHA)
  • MICROFILARIAE
    WUCHERERIA BANCROFTI
    • Disease: Bancroftian filariasis, wuchereriasis
    • 673. Site in host: Lymphatics
    • 674. Portal of entry: Skin
    • 675. Definitive Host: human
    • 676. Intermediate Host: mosquito (Culex, Aedes, Anopheles species)
    • 677. Sources of infection: Mosquitoes
    • 678. Lab Dx: Blood smear
    Periodic form: between 10 am and 2am
    Subperiodic form: between 2 and 5 pm
    - Microfilariae: sheathed; nuclei do not extend to tip of tail
  • 679.
  • 680. Brugia malayi /Wuchereria bancrofti: B.malayi is transmitted by mosquitoes of the genus Mansonia, Anopheles and Aedes. W.bancrofti is transmitted by mosquitoes of the genus Culex, Anopheles and Aedes.
  • 681. Microfilaria of Wuchereria bancrofti: sheathed, its body is gently curved, and the tail is tapered to a point. The nuclear column (the cells that constitute the body of themicrofilaria) is loosely packed, the cells can be visualized individually and do not extend to the tip of the tail.
  • 682. Wuchereria bancrofti adults in section of lymph node
  • 683.
  • 684.
  • 685. BRUGIA MALAYI
    • Disease: Malayan filariasis
    • 686. Site in host: Lymphatics
    • 687. Portal of entry: Skin
    • 688. Definitive Host: human, monkey & cat
    • 689. Intermediate Host: mosquito (Mansonia, Aedes, Anopheles species)
    • 690. Sources of infection: Mosquitoes
    • 691. Lab Dx: Blood smear
    Periodic (nocturnal) form: between 10 am and 2am
    Subperiodic form: between 9 and 11 pm
    - Microfilariae: sheathed; nuclei exted to tip of tail w/ 2 separated & swollen terminal nuclei
  • 692.
  • 693. Microfilaria of Brugia malayi:has a sheath, are more tightly coiled, and the nuclear column is more tightly packed, preventing the visualization of individual cells.
  • 694. Microfilaria of Brugia malayi, collected by the Knott (centrifugation) concentration technique, in 2% formalin wet preparation.  Note the clearly visible sheath that extends beyond the anterior and posterior ends of the microfilaria.  (There are four sheathed species: Wuchereria bancrofti, Brugia malayi, Brugia timori, and Loa loa.)
  • 695. Detail from the microfilaria of Brugia malayi showing the tapered tail, with a subterminal and a terminal nuclei, separated by a gap without nuclei. 
  • 696. LOA LOA
    • Disease: Loiasis, eye worm, fugitive swellings, Calabar swellings
    • 697. Site in host: Subcutaneous
    • 698. Portal of entry: Skin
    • 699. Definitive Host: human and monkey
    • 700. Intermediate Host: fly (Chrysops)
    • 701. Sources of infection: fly
    • 702. Lab Dx: Blood smear
    Diurnal periodicity: between 11 am and 1 pm
    - Microfilariae: sheathed; nuclei extend to tip of tail
  • 703.
  • 704.
  • 705. Microfilariae of Loa loa  (right) and Mansonella perstans (left). L. loa is sheathed, with a relatively dense nuclear column; its tail tapers and is frequently coiled, and nuclei extend to the end of the tail.  M. perstans is smaller, has no sheath, and has a blunt tail with nuclei extending to the end of the tail.
  • 706. MANZONELLA OZZARDI and MANSONELLA PERSTANS
    • Disease: Ozzardi filariasis/Perstan filariasis
    • 707. Site in host: body cavities
    • 708. Portal of entry: Skin
    • 709. Definitive Host: human
    • 710. Intermediate Host: midge (Culicoides & Simulium)
    • 711. Sources of infection: midge
    • 712. Lab Dx: Blood smear
    • 713. Microfilariae found in blood: No periodicity; unsheathed; nuclei do not extend to tip of tail (M. ozzardi)/extend to tip of tail (M. perstan)
  • 714.
  • 715. MANZONELLA STREPTOCERCA
    • Disease: Ozzardi filariasis/Perstan filariasis
    • 716. Site in host: body cavities
    • 717. Portal of entry: Skin
    • 718. Definitive Host: human
    • 719. Intermediate Host: midge (Culicoides & Simulium)
    • 720. Sources of infection: midge
    • 721. Lab Dx: Blood smear
    • 722. Microfilariae found in skin: No periodicity; unsheathed; nuclei extend to tip of tail
  • 723. Microfilaria of Mansonella streptocerca from a skin snip: unsheathed, has a nearly straight body attitude, the tail is typically coiled into a “shepherd’s crook”, and terminal nuclei extend as a single row to the end of the tail.
  • 724. ONCHOCERCA VOLVULUS
    • Disease: Onchocerciasis, onchocercosis, river blindness, “Sowda”
    • 725. Site in host: Subcutaneous
    • 726. Portal of entry: Skin
    • 727. Definitive Host: human
    • 728. Intermediate Host: fly (Simulium)
    • 729. Sources of infection: fly
    • 730. Lab Dx: skin biopsy or snips, nodule aspirate
    • 731. Microfilariae found in skin: No periodicity; unsheathed; nuclei do not extend to tip of tail
  • 732. Microfilaria of Onchocerca volvulus: tail is sharply and is s sharply angled at the end
  • 733.
  • 734. Onchocerca volvulus, posterior end
  • 735.
  • 736. Histopathology of Onchocerca volvulus nodule.
  • 737. DRACUNCULUS MEDINENSIS, THE GUINEA WORM
    • Disease: Dracontiasis, dracunculosis, guinea worm disease
    • 738. Site in host: Subcutaneous
    • 739. Portal of entry: Mouth
    • 740. Definitive Host: human & domesticated and wild fur bearing animals
    • 741. Intermediate Host: water flea (Cyclops)
    • 742. Sources of infection: fly
    • 743. Lab Dx: skin biopsy or snips, nodule aspirate
    • 744. Microfilariae found in skin: No periodicity
  • 745. The female guinea worm induces a painful blister (A); after rupture of the blister, the worm emerges as a whitish filament (B) in the center of a painful ulcer which is often secondarily infected. 
  • 746. D. medinensis worm wound around matchstick.This helminth is gradually withdrawn from the body by winding the stick.