Trichomonas Flashcards
T. vaginalis
human pathogen
T. TENAX
oral/gingival and tracheobroncial site; nnon-pathogenic
Peentatrichomonas hominis
intestinal tract; non pathogenic
T. FAETUS
bovine, feline, swine population
Describe T. vaginalis
- extracellular parasite; does not invade tissue’s mucosal surfaces
- microaerophilic, requires enzymes to neutralize O2 such as sulphur oxide dismutase, reductases, and thioredoxins.
- motile; jerky, rapid movements
- largest known protozoan genome = 6 chromosomes with 60 000 protein coding genes
- receptor med endocytosis to phagocytose human cells, bacteria, yeast to obtain nutrients
- iron = essential element for growth and maintain infection
striucture of T. vaginalis troph
- pyriform or pear shape
- 4 anterior flagella
- undulating membrane containing the recurrent flagellum (stops halfway down)
- pelot = chinetosomal complex at anterior of organism from which the costa, recurring flagella and undulating membrane originate
- prominent nucleus
- hydrogenosomes =mitochondria-like; double membrnae, producte ATP and have similar metbaolic activity; using H+ as e- acceptor
- axostyle (ant to posterior)
- 7-23 um long and 5-15 um wide
T or F. T. vaginalis has no cyst stage
T
life cycle of T. vaginalis
simple long binary fission every 8-12 hours
no cyst stage = vulnerable to harsh environmental conditions
can only survive 20-30 mins in air, but 6-24 hrs in urine, semen and swimming pool water
can grow at a wide pH but optimal is pH 6-6.3
epidemiology of T. vaginalis
- humans are only known natural host
- sexual contact = main mode of transmission = STI
- non-sexual transmission not common but can occur with contaminated fomites such as towels, washcloths and bath water
predominates in females (F:M 10:1)
most prevalent non-viral STI worldwide; not reportabe = neglected STI
known to increase acquisition of HIV and shedding of virus
pathogenis of T. vagnalis
- contact with host cells - adherent; mediated by surface lipoglycan and membrane proteins => cytoskeletal changed from pear shape to flattened spreading amoeboid shape
amoeboid = key player of pathogenesis
adherence = cytotoxicity; not full understood
local immune response = pro-inflammatory cytokines from urogenital cells; predominantly neutrophils in vaginal discharge; lymps and macs also present
humoral rsponse = IgA (local), M&G too but short-lived and does prevent re-nifections
mucinase allows organism to penetrate mucus barrier, coating epi surfaces of vagina and cervix
adhesins and cytolytic enzymes and proteinases (degrade Igs to make chronic infection)
T. vaginalis microbiome
2 Mycoplasma species and some have up to 4 viruses within it => contribute to its pathogenesis and virulence
host defense evasion mechanisms of T. vaginalis for chronic infection
- mucinase assists organism in penetrating mucus layer of vagna
- acidic pH of vagina helps with adhesion of organism, then it increases pH once adhered (up fro 4.5)
- T. vag also phagocytose human cells and hot defense proteins
- resistant to complement when in an iron-rich environment
- coats itself with host plasma proteins
- produces surface proteins which are homologous to host proteins
- capable of phenotypic variation
- exosomes induce IL-6 response = downregulation of IL-8 response in ectocervical cell = reduces neuts recruitment
females symptoms of T. vaginalis
50-85 % asymptomatic
infection of vagina, cervix. urethra, pelvic cavity; strawberry cervix
may have copious frothy vagina discharge = itchy and foul smelling
can have negative effect on pregnancy
associated with infection in newborn babies (neonatal pneumonia)
male symptoms T. vaginalis
70-85% asymptomatic
urethra is affected
can spread to epididymis and prostate glands
T or F. T. vaginalis has been implicated as a cause of male and female infertility
T
