Transcript MEDICAL PARASITOLOGY & ENTOMOLOGY

MEDICAL PARASITOLOGY
&
ENTOMOLOGY
LECTURER:
SR. NORAZSIDA RAMLI
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)
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).
G. Lamblia (trophozoite)
K= karyosome
Nu=nucleus
MB=median body
Fg=flagella
Ax=axoneme
AD=adhesive disk
G. Lamblia (cyst)
Nu=nuclues
K=karyosome
Ax=axoneme
MB=median body
CW=cyst wall
Life Cycle
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.
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.
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.
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.
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
Laboratory diagnosis
-Differentiation is based on morphological
examination of fecal preparations.
Microscopic examination
Serological assays
Immunofluoresence methods
Enzyme immunoassays
Treatment
Metronidazole
Quinacrine
Tinidazole
Furazolidone
Paromomycin
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.
UROGENITAL
FLAGELLATES
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.
T. Vaginalis trophozoite
Fg=flagella
Bb=basal body
Nu=nucleus
Ax=axostyle
um=undulating
membrane
Cy=cytostomal
groove
Cs=costa
(A) T. vaginalis
parasite as seen
in broth culture.
The axostyle,
undulating
membrane, and
flagella are
clearly visible.
5 μm
(B) T. vaginalis
on the surface of
a vaginal
epithelial cell
prior to ameboid
transformation.
5 μm
(C) Ameboid
morphology of
T. vaginalis as
seen in cell
culture.
5 μm
Life cycle
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.
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,
LABORATORY DIAGNOSIS
Clinical Presentation
Microscopic and Culture Techniques
Antibody-Based Techniques
DNA Techniques-PCR
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.
Prevention
Avoidance of unprotected sex.
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.
Questions
1) What is the name of parasite causing the
2)
3)
4)
5)
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?