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Lecture 25 - Intestinal Protozoa
Author: Amelia Virostko

1. Entamoeba histolytica

1.1. Introduction

  1. Causes dysentery and liver abscesses
  2. Cyst form enables survival in rugged external environments, trophozoite form invades and obtains nutrients once inside the host

1.2. Encounter

  1. Prevalent in developing countries in Africa, Asia, and South America
  2. Found in feces of infected humans and transmitted through the fecal-oral route via ingestion of contaminated food or water

1.3. Entry

  1. After entry into the GI tract, cysts undergo excystation to release trophozoites, which attach to colonic epithelial cells and cause contact-dependent lysis and phagocytosis of the cells

1.4. Spread/Multiplication

  1. Trophozoites multiply through binary fission
  2. Disseminate via portal tract to extraintestinal sites

1.5. Damage and Clinical Manifestations

  1. Intestinal amebiasis
    1. Asymptomatic infection
    2. Amebic colitis with inflammatory neutrophil infiltrate, followed by tissue necrosis and flask-shaped ulcers
    3. Presents with bloody diarrhea and abdominal pain and occasional fever
  2. Extraintestinal amebiasis
    1. Liver abscesses, or occasional pleuropulmonary, peritoneal, pericardial, or cerebral abscesses

1.6. Pathogenesis

  1. Galactose/N-acetylgalactosame lectin involved in adherence and contact-dependent lysis
  2. Amebapore important for cell lysis
  3. Infection induces expression of pro-inflammatory cytokines such as IL-1, IL-8, TNF-alpha, and GRO-alpha

1.7. Diagnosis and Identification

  1. Clinical symptoms: bloody diarrhea, abdominal pain, upper right quadrant pain, and fever
  2. Microscopic identification of cysts or trophozoites
  3. Serologic tests to detect antibodies again E. histolytica
  4. ELISA to detect amebic antigens in feces or PCR to detect parasite DNA

1.8. Treatment

  1. Cysticidal agents such as diiodohydroxyquin or diloxanide fluroate for asymptomatic cyst passers
  2. Metronidazole plus cysticidal agent for acute amebic colitis

1.9. Outcome

  1. Exposure provides some protective immunity, but not always complete
  2. Some patients develop chronic colitis, or life-threatening complications such as fulminant colitis or intestinal perforation
  3. Extraintestinal amebiasis can be fatal, particularly if pulmonary abscesses form

2. Cryptosporidium spp.

2.1. Introduction

  1. Mild and self-limiting watery diarrhea in immunocompetent hosts, but potential severe and chronic infection in AIDS patients
  2. Complicated life cycle with the following forms
    1. Oocysts: infectious form containing 4 motile sporozoites
    2. Sporozoites: invasive form released from oocysts that attach to and invade intestinal and epithelial cells and eventually develop into trophozoites
    3. Trophozoites: develop in a parasitophorus vaculoe within epithelial cells to form Type I meronts that divide into 8 Type I merozoites
    4. Merozoites: invasive form that reinvade adjacent cellsor develop into Type II meronts
    5. Macro and micro gamonts: sexual stages that form microgametes to form zygotes and oocysts

2.2. Encounter

  1. More prevalent in developing countries
  2. Found in feces as oocyst
  3. Acquire through contact with infected animals or humans, ingestion of contaminated food or water

2.3. Entry

  1. In the GI tract, oocyst excysts to release sporozoites, which are motile and attach to and invade small intestinal epithelial cells

2.4. Spread

  1. Usually localized to small intestine in immunocompetent hosts
  2. Infects biliary and pancreatic ducts, as well as respiratory tract in immunocompromised hosts

2.5. Multiplication

  1. Sporozoites dvelop into trophozoites, which form Type I meronts
  2. Type I meronts undergo asexual division into Type I merozoites, which develop into Type II meronts or divide into 4 Type II merozoites
  3. Type II merozoites develop into macro and micro gamonts
  4. Zygotes develop into oocysts which sporulate

2.6. Damage and Clinical Manifestations

  1. Villous atrophy and inflammation often develop
  2. Intestinal crypts may undergo hypertrophy
  3. Most patients develop watery diarrhea, abdominal cramps, anorexia, weight loss, and occasional fever and vomiting

2.7. Pathogenesis

  1. Surface adhesions and proteases
  2. Induces expression of pro-inflammatory cytokines that produce further inflammation

2.8. Diagnosis and Identification

  1. Microscopic identification
  2. Oocysts in fecal samples using a modified acid-fast stain or immunofluoresence assay
  3. ELISA to detect stool antigens
  4. Intestinal biopsies

2.9. Treatment

  1. Nitazoxanide
  2. Oral or parenteral rehydration, supplemental nutrition, and anti-gut motility drugs

2.10. Outcome

  1. No symptoms or mild self-limiting diarrhea in immunocompetent hosts
  2. Immunocompromised hosts may develop severe persistent and potentially fatal diarrhea and wasting

3. Giardia Lamblia

3.1. Introduction

  1. Pear-shaped binucleated organism with 4 pairs of flagella
  2. Cysts are infective form, trophozoites are vegetative active motile form

3.2. Encounter

  1. Found in feces in cyst form and transmitted through fecal-oral route from person-to-person contact or ingestion of contaminated food or water
  2. Hiker's diarrhea from ingesting water from mountain streams

3.3. Entry

  1. Once ingested, acid from stomach and trypsin in duodenum transform G. lamblia into vegetative trophozoite form

3.4. Spread/Multiplication

  1. Trophozoites divide by binary fission, attach to small intestinal epithelium, and exert pathogenic effects
  2. Infection localized to small intestine, and parasite does not invade or disseminate
  3. Trophozoites encyst on exposure to bile acid and higher pH and cysts are excreted via feces

3.5. Damage and Clinical Manifestations

  1. Villous atrophy and crypt hyperplasia can occur in the intestinal mucosa
  2. Increased inflammatory cell infiltrate and increased intraepithelial lymphocytes
  3. Asymptomatic to mild self-limiting diarrhea to severe chronic infection with malabsorption and weight loss

3.6. Pathogenesis

  1. Surface proteins and proteases
  2. Mucosal inflammation resulting in structural and functional abnormalities

3.7. Diagnosis and Identification

  1. Microscopic identification of cyst or trophozoites
  2. Detection of stool antigen through ELISA or immunofluoresence assay

3.8. Treatment

  1. Metronidazole is 1st line agent
  2. Furazolidone may be used in younger children

3.9. Outcome

  1. Usually mild and self-limiting
  2. Patients with humoral immunodeficiency or selective IgA deficiency may develop chronic or recurrent disease
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