Parasitology

lecture: 2
Prepared by:
Dr. kholoud Baraka
Lecturer of Microbiology and Immunology.
Faculty of Pharmacy, Damanhour University.
 II- Genitourinary flagellates
TRICHOMONAS VAGINALIS

 It is the causative agent of trichomoniasis.

 It is one of the most common sexually transmitted diseases, both in
the United States and worldwide. It causes vaginitis in women and
urethritis in both men and women.
 Humans are the sole reservoir of T. vaginalis.
 Infection rates are about 5–20% in women and usually below 5% in
men. About 2–17% of female neonates born from infected mothers
contract a perinatal infection.
 T. vaginalis colonizes the mucosa of the urogenital tract and
reproduces by longitudinal binary fission.
 Trichomonads do not encyst.
 The parasite a pear-shaped about 10–20 µm long and 2–14 µm wide.
 T. vaginalis is a flagellated protozoan possessing five flagella, four of which
are located at its anterior portion. The fifth flagellum is incorporated
within the undulating membrane of the parasite.
 The nucleus in T. vaginalis is located at its anterior portion, and, a slender
hyaline, rod-like structure, called an axostyle, commences at the nucleus
and bisects the protozoan longitudinally. It protrudes through the
posterior end of the parasite, terminating in a sharp point.
 Trichomonads are anaerobic protozoa that possess hydrogenosomes;
which are specialized organelles producing H2 as a metabolite.
Life cycle
 Trichomonas vaginalis resides in the female lower genital tract and
the male urethra and prostate, where it replicates by binary fission.
The parasite does not have a cyst form, and does not survive well in
the external environment.
 Trichomonas vaginalis is transmitted among humans, its only
known host, primarily by sexual intercourse.

Transmission
 By wet bathing suits, sponges, towels, etc. as well as acquired from
non-chlorinated and poorly maintained swimming pools.
 It is possible for a pregnant woman to pass the infection to her baby
at birth.
 The infection can't be transmitted through oral contact, kissing,
hugging, sharing cups, plates or toilet seats or towels.
In women:
 T. vaginalis colonizes the vaginal mucosa, more rarely the cervix.
 In about 20–50% of cases the infection is asymptomatic.
 Vaginitis: is the inflammation of vagina which is characterized by the
production of a purulent, thin, yellowish discharge in which
trichomonads, pus cells, and bacteria are found.
 The parasites also enter the urethra in about 75–90% of cases, where
they can cause an inflammation (urethritis), but rarely infect the
urinary bladder or uterus.
In men:
 The infection is asymptomatic (50–90 %(.
 They may also cause urethritis, more rarely involving the prostate gland
(prostatitis) and seminal vesicles (reduction of sperm count) as well.
 Urethritis is characterized by scanty, clear to mucopurulent discharge,
dysuria, and mild pruritus or burning sensation immediately after sexual
intercourse.
Complications:
 Complications associated with trichomoniasis in women include
adnexitis, endometritis, infertility, low birth weight, and cervical
erosion. Trichomoniasis is also associated with increased HIV
transmission.
 In men, complications include: prostatitis, epididymitis, urethral
disease, and infertility.

• Clinical diagnosis of T. vaginalis including: a yellowish-green discharge,

pruritus, dysuria, dyspareunia, and the “strawberry” cervix (observed
only 2% of patients). However, this clinical diagnosis isn't sufficient
alone.
 Microscopic examination of fresh specimens of vaginal or urethral
secretion is for trichomonads which are recognized by their typical
tumbling movements.
 Giemsa staining to visualize T. vaginalis trophozoites.
 Immunofluorescence or ELISA test.
 PCR
 Treatment and prevention:

 Nitroimidazole oral preparations

(metronidazole or tinidazole) are given for both
sexual partners.
 Preventive measures for venereal diseases
should be used (e.g. avoid sex
with multiple partners, using condom).
 III- Blood and tissue flagellates
1. TRYPANOSOMA
 The genus Trypanosoma name is derived from the Greek trypano
(borer) and soma (body) because of their corkscrew-like motion.
 All trypanosomes are heteroxenous (requiring more than one
obligatory host to complete life cycle) and most are transmitted via a
vector.
 It is the causative agent of African trypanosomiasis (sleeping sickness)
and American trypanosomiasis (Chagas disease).
 Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense
cause African trypanosomiasis (sleeping sickness) in humans.
 Trypanosoma cruzi, the causative agent of American trypanosomiasis
(Chagas disease) occurs in humans and many vertebrate animals in
Central and South America.
 Trypanosomes are transmitted by the bites of tsetse flies.
 Antelopes and other wild or domestic animals serve as reservoir
hosts.
 There are various forms develop during the life cycle in vertebrates
and vectors (insect). The morphologically differentiated forms
include spindly, uniflagellate stages (trypomastigote, epimastigote,
promastigote) and a rounded form (amastigote). promastigote

amastigote

epimastigote trypomastigote
There are epidemiological differences between
T. gambiense and T. rhodesiense, the main one
being that:
 T. b. rhodesiense persists in wild and domestic
animals and is normally transmitted by tsetse flies
from animal to animal, more rarely to humans.
 However, T. b. gambiense, is transmitted by tsetse
flies mainly from human to human.
Transmission
 Bite of tsetse fly (genus Glossina).
 Life cycle
 Trypanosome infections follow a cyclical path between human hosts and the
insect vector. Trypanosomes reside almost exclusively in the bloodstream
and are transmitted by the bite of the tsetse fly which acquires the infection
while taking a blood meal, and returns the trypanosome to a vertebrate host
in its saliva when it takes another blood meal.
In Human
 The tsetse fly injects metacyclic trypomastigote in the human blood which
multiply by binary fission.
In Glossina flies
 Trypanosomes taken by Glossina when they suck blood from an infected
host go through a complex developmental and reproductive cycle in the
insects lasting 15–35 days.
 The ingested trypanosomes are transformed into procyclic trypomastigotes
in the midgut of the fly where they multiply by binary fission.
 In the midway between midgut & salivary gland the promastigote
transformed to epimastigote.
 In the salivary gland they transformed into metacyclic trypanomastigote
and the cycle is repeated.
 The clinical course of human African trypanosomiasis has two stages. In the
first stage, the parasite is found in the peripheral circulation, but it has not
yet invaded the central nervous system. Once the parasite crosses the blood-
brain barrier and infects the central nervous system, the disease enters the
second stage.
Stage 1 (The febrile-glandular or early hemolymphatic stage)
 Painless skin trypanosome chancre that appears about 5-15
days after the bite, resolving spontaneously after several
weeks. It is an inflammatory and edematous swelling.
 Parasitemia: within a period of approximately two weeks the trypanosomes
spread via the bloodstream and lymphatic system leading to: Fever, chills,
headache, joint and muscle pain, weight loss, generalized lymphadenopathy,
cardiac dysfunction, anemia, thrombocytopenia, raised serum IgM.
Stage 2 (The meningo-encephalitic or neurologic stage)
 Trypanosomes invade the central nervous system leading to:
Changes of behaviour, persistent headaches, confusion, convulsions, sensory
disturbances and poor coordination. Disturbance of the sleep cycle (Daytime
somnolence followed by nighttime insomnia), which gives the disease its name.
 Direct microscopic detection of the trypanosomes in the blood, lymph
node aspirate and in the cerebrospinal fluid.
 Trypanosomes can be microscopically detected in blood preparations
through Giemsa-stained smears.
 Antibodies (IgG & IgM) in the bloodstream can be detected using
various serological techniques. Elevated concentrations of protein and
IgM in CSF are indicators of stage 2 infection.
 PCR.
• The type of treatment depends on the disease stage. The drugs used
in the first stage are safer and easier to administer than those for
second stage. Also, the earlier the disease is identified, the better the
prospect of a cure.
First stage treatment:
 Pentamidine: discovered in 1940, used for the treatment of the first
stage of T. b. gambiense sleeping sickness.
 Suramin: discovered in 1920, used for the treatment of the first stage
of T. b. rhodesiense.
Second stage treatment:
 Melarsoprol: discovered in 1949, it is active in both gambiense and
rhodesiense infections. It is derived from arsenic and has many
undesirable side effects. It is currently recommended as first-line
treatment for the rhodesiense form, and as second-line for the
gambiense form.
 Eflornithine: this molecule, less toxic than melarsoprol, was
registered in 1990. It is only effective against T. b. gambiense.
Prevention and control
 Use prophylactic measures to protect against the Glossina
flies: wear clothings that cover the skin as much as possible
and treat uncovered skin with insect repellents .
 Glossina flies are targeted by insecticide sprayings in
preventive programs. More recently, the flies are being
caught in insecticide-charged traps using attractant colors
and odors.