1. MEDICAL PARASITOLOGY & ENTOMOLOGY
LECTURER:
Mdm. NORAZSIDA RAMLI

2. 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)

4. 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).

5. G. Lamblia (trophozoite)
K= karyosome
Nu=nucleus
MB=median body
Fg=flagella
Ax=axoneme
AD=adhesive disk

8. G. Lamblia (cyst) Nu=nuclues K=karyosome Ax=axoneme MB=median body
CW=cyst wall

12. Life Cycle

13. 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.

14. 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.

15. 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.

16. 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.

18. 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

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

20. Treatment
Metronidazole
Quinacrine
Tinidazole
Furazolidone
Paromomycin

21. 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.

22. UROGENITAL FLAGELLATES

23. 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.

24. T. Vaginalis trophozoite
Fg=flagella
Bb=basal body
Nu=nucleus
Ax=axostyle
um=undulating membrane
Cy=cytostomal groove
Cs=costa

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

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

28. (C) Ameboid morphology of T. vaginalis as seen in cell culture.

29. Life cycle

30. 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.

31. 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,

32. LABORATORY DIAGNOSIS Clinical Presentation
Microscopic and Culture Techniques
Antibody-Based Techniques
DNA Techniques-PCR

33. 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.

34. Prevention
Avoidance of unprotected sex.

35. 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.

36. Questions
What is the name of parasite causing the patient’s illness? What is the infectious stage of this parasite?
How does this parasite sometimes result in malabsorption?
How does this parasite avoid being dislodged by intestinal peristalsis?
How is this parasite transmitted? How can transmission be prevented?
How is this illness treated?