Trichomonas is a parasites that inhabite the genitals

1. TRICHOMONAS
By Mr. chu Samuel n

5. Trichomonas vaginalis
• T. vaginalis, causes the disease trichomoniasis belongs to the:
• Phylum: Axostylata
• Class: Parabasalea
• Order: Trichomonadida
• Family: Trichomonadidae
• Genus: Trichomonas
• Species: Trichomonas vaginalis

6. Trichomonas vaginalis

7. Life Cycle
• Trichomonas trophozoites unlike other parasites trophozoites have a simple
life cycle. Only a trophozoite form exists.
• The organisms cannot survive for any significant period of time outside the
human body, so the parasite has no reservoirs or vectors.
• T. vaginalis colonizes either the female lower genital tract or the male
urethra and prostate.

8. Life Cycle
• It does not encyst
• Divides asexually by binary fission which is favoured by low acidity (pH > 5.9,
normal pH is 3.5 to 4.5).
• The trophozoites are transmitted from an infected person to a partner via
sexual intercourse although non-venereal infections are also possible through
fomites such as towels, toilet seats, and sauna benches.
• After an incubation period of 5-18 days, an infected person may begin to
show symptoms, although they can also remain asymptomatic.

9. • Fig 1 life cycle

10. Pathogenesis
• T. vaginalis is an obligate extracellular pathogen, adherence to epithelial
cells is critical for the establishment and maintenance of infection.
• The surface of T. vaginalis is covered with a dense glycocalyx composed
mainly of lipophosphoglycan (LPG) which is an attachment factor of the
parasite.
• It has been demonstrated that human galectin-1 expressed by cervical
epithelial cells binds to T. vaginalis LPG and crosslink parasites to host cells,
thus identifying the first host cell receptor for this parasite.

11. Pathogenesis
• The adherence that this organism illustrates is specific to vaginal epithelial
cells (VECs) and its pH, time and temperature dependent.
• A variety of virulence factors mediate this process some of` which are the
microtubules, microfilaments, adhesins and cysteine proteinases.
• The adhesins are four trichomonas enzymes called AP65, AP51, AP33, and
AP23 that mediate the interaction of the parasite to the receptor molecules
on VECs.
•

12. Pathogenesis
• Cysteine proteinases may be another virulence factor because not only do these
proteins bind to host cell surfaces but also may degrade extracellular `matrix
proteins like haemoglobin, fibronectin or collagen.
• It generally causes degeneration and desquamation of the vaginal mucosa.
• Sometimes, it is associated with small blisters or granules.
• The mucosa and superficial submucosa are infiltrated by lymphocytes, plasma
cells and polymorphonuclear leucocytes.
• Infection has been associated with an increased risk of HIV syndrome in both
sexes.`

13. Clinical manifestations
• The symptoms of T. vaginalis usually appear between 3 - 28 days after infection.
• However, many patients are asymptomatic, especially men, and serve as carriers.
• Specific symptoms seen in women include: vaginal discharge that is yellowish
green in colour and odorous; vaginal itching, soreness, and inflammation
(vaginitis); pain and/or burning during urination (urethritis); pain during sexual
intercourse (dyspareunia); punctate haemorrhages on the cervix
(colpitismacularis, or "strawberry cervix"); vulvar lesions.

14. Clinical manifestations
• Complications in women may result in cervical erosion, cervical cancer,
infertility, adnexitis, and endometritis.
• Premature rupture of the placental membranes can occur in pregnant
women, resulting in premature birth and low-birth weight.
• Acute infections are characterised by severe pruritus, vaginitis, vulvitis with
dysuria and dyspareunia, and haemorrhagic spots on the mucosa (in 2% of
patients) which results in colpitismacularis or petechiae (strawberry cervix).

15. Clinical manifestations
• Specific symptoms seen in men include: penile discharge that is thin and
whitish; pain and/or burning during urination (urethritis); testicular pain
(epididymitis); penile ulcer.
• Complications are rare in men, but can potentially lead to genitourinary
inflammation disease, sterility, scanty, clear to mucopurulent discharge,
dysuria, non-gonococcal urethritis, prostatitis, epididymitis, and urethral
disease..

16. Diagnosis
• Trichomoniasis can be diagnosed by either physical examination or
laboratory investigation.
• Normal discharge is usually clear but in trichomoniasis, it may appear yellow
to greenish in colour.
• The `discharge may then be tested for abnormal foul odour using potassium
hydroxide (KOH) ―whif test and its acidity maybe checked.

17. Diagnosis
• The following screening test can be used:
Wet mount is the most common method used to diagnose trichomoniasis
where a ―cockscrew motility is observed.
Culture - using Diamond‘s medium or Kupferberg‘sTrichosel medium for 2-
7days
Polymerase chain reaction – this is the most accurate but is mostly used in
research and not clinical settings.
OSOM Trichomonas Rapid Test (Genzyme diagnostics) – it is a new point of
care, antigen-diagnostic test for Trichomoniasis.

18. Epidemiology
• Trichomoniasis is rear among young girls and vagines usually up 14yrs
but reaches it peak between the ages of 20 and 40yrs.
• in males the highest incidents is between the ages of 21 and 30yrs
• Incidence of T. vaginalis in normal patients ranges from 2 to 15% with
an averge of 10%

19. Treatment
• oral treatment with Metronidazole (Flagyl) and Tinidazole provide
almost 100% cure rate within a few days with little or no side effect.

20. Prevention
• By reduction of sexual promisquity
• Sexual partners shoult be treat at the same time to prevent
reinfection

21. • Thank
• God is our father