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Pathogens of the Female Reproductive Site

Pathogenesis: T. vaginalis travels through urogenital areas with the assistance of flagella May also act as a carrier for other pathogenic organisms Can migrate to the fallopian tubes and peritoneal cavity Carry bacteria or viruses on their surfaces; contribute to upper genital tract infections Pear-shaped organism that propels itself with four whip-like flagella that protrude from its front end Fifth flagellum, attached to an undulating membrane, extends rearward Barbed tail (axostyle) projects from the trailing end Pathogenesis: The first step in the development of a candidal infection is colonization of the mucocutaneous surfaces The routes of candidal invasion include disruption of a colonized surface (skin or mucosa), allowing the organisms access to the bloodstream Invasion also includes persorption via the gastrointestinal wall, which may occur following massive colonization with large numbers of organisms that pass directly into the bloodstream Can cause infection via: Surface molecules that permit adherence of the organism to other structures (eg, human cells, extracellular matrix, prosthetic devices) Acid proteases and phospholipases that involve penetration and damage of cell envelopes Has the ability to convert to a hyphal form (phenotypic switching) The main populations involved in the recognition of C. albicans during the innate immune response are: monocytes, neutrophils and macrophages Dendritic cells are crucial for processing of, and antigen presentation to, T cells, and thus to activation of specific immunity

Attach themselves to tissue with the axostyles This causes some of the irritation and inflammation associated with a trichomoniasis infection

One celled protozoan parasite that causes Trichomoniasis, a sexually transmitted disease Most common place of infection for women is the vagina Symptoms: Yellow-green vaginal discharge, fishy odor, pain during urination and sexual intercourse, and genital itching or irritation Higher rate of pelvic inflammatory disease, risk factor for HIV and contributes to infertility

Most common fungal (opportunistic) fungal pathogens Diploid sexual fungus Causes vaginal yeast infections Symptoms: White vaginal discharge Burning with urination Vaginal irritation

Trichomonas vaginalis

Candida Albicans

Chlamydia trachomatis
Bacteria that causes Chlamydia, a sexually transmitted infection Can be transmitted during vaginal, anal, or oral sex; can be passed from an infected mother to baby during vaginal childbirth The bacteria initially infects the cervix and the urethra (urine canal) Symptoms:

Human papillomavirus
Sexually transmitted infection that infects genital areas Can be passed on through genital contact, most often through vaginal and anal sex Small double stranded DNA virus that infects cutaneous and mucosal epithelial tissues Non-enveloped viruses with icosahedral capsids that replicate their genomes within the nuclei of infected host cells Symptoms:

Usually appearing until 1-3 weeks after exposure Abnormal vaginal discharge or a burning sensation when urinating, lower abdominal pain, low back pain, nausea, fever, pain during intercourse, or bleeding between menstrual periods Infection of the cervix can spread to the rectum Untreated infection can spread into the uterus or fallopian tubes and cause pelvic inflammatory disease Can increase chances of becoming infected with HIV, if exposed Pathogenesis: Limited host range and infects human epithelial cells; some can also infect macrophages. Elementary bodies (EB): the small infectious form of the chlamydia Possess a rigid outer membrane which are resistant to harsh environmental conditions encountered when the chlamydia are outside of their eukaryotic host cells Bind to receptors on host cells and initiate infection; internalized by endocytosis and/or by phagocytosis EBs reorganize and become RBs in host cell endosome Reticulate bodies (RB) : the non-infectious intracellular from of the chlamydia; the metabolically active replicating form of the chlamydia Possess a fragile membrane lacking the extensive disulfide bonds characteristic of the EB. The chlamydia inhibit the fusion of the endosome with the lysosomes which resist intracellular killing RBs replicate by binary fission and reorganize into Ebs The cells and inclusions lyse (C. psittaci) or the inclusion is extruded by reverse endocytosis (C. trachomatis and C. pneumoniae)

Pathogenesis: Infection by papillomaviruses occurs through microwounds of the epithelium that expose cells in the basal layer to viral entry Cells in the basal layer consist of stem cells and transitamplifying cells that are continuously dividing and provide a reservoir of cells for the superbasal regions HPV infection of these cells leads to the activation of a cascade of viral gene expression that results in the production of approximately 20 to 100 extra-chromosomal copies of viral DNA per cell This average copy number is stably maintained in undifferentiated basal cells throughout the course of the infection HPV infected basal cells divide and viral genomes are partitioned into daughter cells, one of which detaches from the basal layer Migrates toward the stratum granulosum, and undergoes differentiation In normal uninfected epithelia, cells exit the cell cycle as they leave the basal layer As infected cells leave the basal layer, they remain active in the cell cycle Cells reenter the S phase in highly differentiated cells and activate the expression of cellular replication factors required for viral replication genital warts Certain types of HPV can cause certain cancers (i.e. cervical cancer)

References : http://www.ncbi .nl m.ni h.gov/pmc/a rti cl es /PMC419925/ http://pa thmi cro.med.s c.edu/ma yer/chl a myd.htm http://www.s ta nford.edu/cl a s s /humbi o103/ParaSi tes2005/Trichomoni asi s/l ifecycl e.htm http://www.tri chomoni a s i s .org/Trichomona s_Va gi nalis/Index.aspx http://www.na ture.com/nrmi cro/journa l /v6/n1/fig_ta b/nrmi cro1815_F2.html http://emedi ci ne.meds ca pe.com/a rti cl e/213853-overvi ew