MEDICAL PARASITOLOGY

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MEDICAL PARASITOLOGY ENTOMOLOGY

• LECTURER
• SR. NORAZSIDA RAMLI

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INTESTINAL FLAGELLATES

• Giardia lamblia (pathogenic)
• Chilomastix mesnili (non-pathogenic)
• Enteromonas hominis (non-pathogenic)
• Retortamonas intestinalis (non-pathogenic)
• Trichomonas hominis (non-pathogenic)
• Dientamoeba fragilis (non-pathogenic)

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Giardia lamblia

• Also known as G. intestinalis or G. duodenalis.
• Diseases Giardiasis, lambliasis, flagellate
  diarrhea.
• Geographic distribution world wide, more
  prevalence in warm climates.
• Consist of 2 stages 1)trophozoite 2)cyst
• Trophozoite 9-20µm in length, 5-15µm in width,
  oval to pear shaped, 2 nucleus,
• Cyst 8-18µm in length, 7-10µm in width, oval,
  more eccentric karyosome, 4 median bodies (mature
  cyst), 4 nucleus (mature cyst).

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G. Lamblia (trophozoite)

• K karyosome
• Nunucleus
• MBmedian body
• Fgflagella
• Axaxoneme
• ADadhesive disk

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G. Lamblia (cyst)

• Nunuclues
• Kkaryosome
• Axaxoneme
• MBmedian body
• CWcyst wall

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• Life Cycle

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• Infective stage cyst
• Acquired by ingestion? passage through stomach?
  small intestine ? duodenum ? large intestine ?
  pass in stool ? environment.
• Duodenum excystation occurs ? trophozoite
  multiply itself by longitudinal binary fission
  (approximately 8 hours intervals).
• Large intestine encystation occurs.
• Both trophozoite and cyst can be found in the
  feces.

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Transmission Pathogenesis

• The most pathogenic intestinal flagellate.
• Distribution world wide
• Found in the gastrointestinal tracts of a variety
  of mammals, including man.
• Habitat ponds, lakes, stream.
• Resistant to chlorine.
• Filtration is necessary to eliminate
  contamination.

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• Transmitted via water, foods (fruits and raw
  vegetables), person to person contact (oral-anal
  sexual practices).
• Incubation period bout 2-3 weeks ? get symptoms
  watery foul-smelling diarrhea, abdominal cramps,
  flatulence, anorexia, and nausea.
• Also have fat-soluble deficiencies, folic acid
  deficiencies, hypoproteinemia with
  hypogammaglobulinemia and structural changes in
  intestinal villi.

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• Severe cases get malabsorption syndrome and
  steatorrhea, and weight loss.
• Patient r often, however asymptomatic.
• How d parasite attaches to the intestinal mucosa?
  By the sucking disc/adhesive disc located on the
  ventral side of the cell.

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Severe cases

• Attachment of trophozoites to the brush border
  could produce a mechanical irritation or mucosal
  injury. In addition, normal villus structure is
  affected in some patients. For example, villus
  blunting (atrophy) and crypt cell hypertrophy and
  an increase in crypt depth have been observed to
  varying degrees. The increase in crypt cells will
  lead to a repopulation of the intestinal
  epithelium by relatively immature enterocytes
  with reduced absorptive capacities. An increased
  inflammatory cell infiltration in the lamina
  propria has also been observed and this
  inflammation may be associated with the
  pathology. Giardia infection can also lead to
  lactase deficiency as well as other enzyme
  deficiencies in the microvilli. This reduced
  digestion and absorption of solutes may lead to
  an osmotic diarrhea and could also explain the
  malabsorption syndromes. Thus far, no single
  virulence factor or unifying mechanism explains
  the pathogenesis of giardiasis

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Laboratory diagnosis

• -Differentiation is based on morphological
  examination of fecal preparations.
• Microscopic examination
• Serological assays
• Immunofluoresence methods
• Enzyme immunoassays

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Treatment

• Metronidazole
• Quinacrine
• Tinidazole
• Furazolidone
• Paromomycin

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Prevention

• By avoidance of contaminated water.
• Filtration (this parasite resistant to chemicals
  such as chlorine).
• Protecting water supplies from reservoir hosts
  such as beavers, muskrats and voles.
• Exercising good personal hygiene.
• Safe sexual practices.

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UROGENITAL FLAGELLATES
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Trichomonas vaginalis

• Caused a sexually transmitted disease.
• Have only trophozoite stage.
• Trophozoite 8-23µm in length, 5-12µm in width,
  rounded anterior end, tapered posterior end, 4-6
  flagella (originate from the anterior end),
  undulating membrane shorter than T. hominis,
  usually with visible axostyle, granules near the
  axostyle, chromatin is evenly distributed, single
  nucleus.
• In wet preps? exhibit a rapid, jerky motion.

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T. Vaginalis trophozoite

• Fgflagella
• Bbbasal body
• Nunucleus
• Axaxostyle
• umundulating membrane
• Cycytostomal groove
• Cscosta

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• (A) T. vaginalis parasite as seen in broth
  culture. The axostyle, undulating membrane, and
  flagella are clearly visible.

5 µm
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• (B) T. vaginalis on the surface of a vaginal
  epithelial cell prior to ameboid transformation.

5 µm
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• (C) Ameboid morphology of T. vaginalis as seen in
  cell culture.

5 µm
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Life cycle
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LIFE CYCLE

• Women Reside on the mucous membranes of the
  vagina.
• Feed on bacteria and white blood cells.
• Men reside in the prostate gland or the urethral
  epithelium.
• Multiplication occurs by longitudinal binary
  fission.

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Transmission/pathogenesis

• Transmitted by sexual contact.
• Infected person may be asymptomatic or,
• Women burning, itching, irritation and produce o
  profuse foul-smelling, yellowish discharge, and
  also red lesions on the vaginal mucosa.
• Men urethritis, severe cases? prostate
  tenderness and swelling,

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LABORATORY DIAGNOSIS

• Clinical Presentation
• Microscopic and Culture Techniques
• Antibody-Based Techniques
• DNA Techniques-PCR

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Treatment

• Metronidazole, oral antibiotics for both
  partners.
• To avoid re-infection, any sexual partners must
  also be treated.
• Once successfully treated, T. vaginalis doesn't
  come back unless a new infection is acquired.

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Prevention

• Avoidance of unprotected sex.

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CASE STUDY

• A 24-year old hiker had recently returned from a
  camping trip to Colorado. While camping, she had
  obtained drinking water from an untreated stream.
  Several weeks after returning home, she presented
  to her family physician with profuse, watery
  diarrhea, cramphy abdominal pain, and
  foul-smelling flatulence.
• Stool specimens were negative for enteric
  bacterial pathogen, but wet mounts demonstrated
  binucleate pear-shaped trophozoites showing a
  falling leaf type of motility. A permanent
  trichrome stain confirmed the diagnosis.

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Questions

1. What is the name of parasite causing the
   patients illness? What is the infectious stage
   of this parasite?
2. How does this parasite sometimes result in
   malabsorption?
3. How does this parasite avoid being dislodged by
   intestinal peristalsis?
4. How is this parasite transmitted? How can
   transmission be prevented?
5. How is this illness treated?