PCOS and menopause Flashcards
Defense mechanisms in the female
Epithelial cells- mechanical barrier, Produce/secrete antimicrobial molecules, transport IgA, process and present Ag, communicate with underlying immune cells
Normal microbial flora- produce lactic acid, hydrogen peroxide to protect against foreign organisms,
Lactobacillus lowers vaginal pH to 4.2 -5
Defense mechanisms- male
Epithelial cells, normal flora, Urethral length, and urine flow
Circumcision- may decrease rates of HIV transmission in heterosexual contact, Observational studies suggest decrease in other STIs (HPV and HSV),
Health benefits> risk
The 5 ps
Partners, prevention of pregnancy, protection from STIs, practices, past history of STIs
Gonorrhea (the clap, lots of thich discharge), chlamidya (thin less discharge)
Chlamydia, goonorrhea, trichomas, ureaplasma
Test for Chlamydia and gonorrhea simultaneously, voided urine PCR probe, First urine after no urination for 1 hr, in women cervical or vaginal swab preferred
Trichomonas- culture or NAAT testing higher sensitivity not always available, elevated vaginal pH, visualization of motile trichomonads on saline microscopy (sensitivity 55-60)
Ureaplasma PCR or culture
Neisseria gonorrhea
Gram negative oxidase and catalse- positive diplococci,
Unlike N meningitidis there is no capsule, virulence factors include pili, porins and opa (opaque) proteins
Bacteria switches (mutates) surface antigens to prevent lasting immunity- reinfection is possible effective vaccine does not exist
Culture was routine for diagnosis (choc agar, non selective, Thayer martin- selective), now nucleic acid-based diagnostic approaches are routinely used
Bacteria is extracellular, but can be taken up by cells and released into subepithelial space- promotes invasion
Carriage can be asymptomatic particularly in women
historically treated with penicillin, now many strains are highly resistant, ceftriaxone is the treatment of choice
Chlamydia trachomatis
Most common STD (bacterial) in the US
Can also cause pneumonia and conjunctivitis, gram negative bacteria, very hard to see on gram stain, bugs dont have peptidoglycan layer and muramic acid, the cell wall contains LPS with weak endotoxin activity, antibiotics that target peptidoglycan cell wall (penicillins) are not effect
Chlamydia trachomatis infection
2 forms
Elementary body- metabolically inactive, cant replicate but infectious and stable in the environment
Initial body- also known as reticulate bodies, forms intracellular inclusions, metabolically active, intra cellular non infectious form, can divide and more of itself
Infects non ciliated epithelial cells of the mucosa, requires cell culture to grow- diagnosis primarily based on Nucleic acid approaches, azithromycin and doxycycline are antibiotics of choice
Trichomonas vaginalis
Urogenital Protozoa, its a parasite, Highly motile, four flagella and undulating membrane, trophozoite (replicates by binary fission), colonizes genital mucosa, mostly asymptomatic, diagnosed by direct microscopic examination of discharge, sometimes the organism is found in urine
NAAT testing- higher sensitivity and specificity
Metronidazole is the treatment of choice (pts with severe allergy to flagyl need to be desensitized)
Urea plasma urealyticum
bacteria, belongs to mycoplasma family, smallest free living bacteria, has no cell walls ( gram stain and B- lactam antibiotics are useless), very slow rate of growth (takes a long time to detect, can grow on cell free media (unlike chlamydia) nucleic acid- based diagnostic approaches are preffered
Produces urease to break down urine into ammonia- diagnositic smell, treatment of choice is erythromycin, tetracycline
Treatment pearls
For Chlamydia/gonorrhea- Azithromycin 1 gm orally, single dose, or doxycycline 100 mg orally 2xday/7days AND Ceftriaxone 250 mg IM single dose
Trichomonas- Metronidazole 2 gms orally single dose
Ureaplasma- erythromycin, doxycycline
Pelvic inflammatory disease
infection of the upper female genital tract
Ascending infection of the upper genital tract from the lower genital tract<50% women diagnosed w/PID have cultures positive for GC/chlamydia
Symptoms- pelvic or lower abdominal pain, abnormal cervical/vaginal discharge can be asymptomatic (silent)
Diagnosis- Pelvic/abdominal pain and one of the following: cervical motion tenderness, uterine tenderness, adnexal tenderness with no other cause identified
Specificity of diagnosis increased with T>101, abundant WBC on saline microscopy of vaginal fluid, elevated ESR/CRP, lab diagnosis of chlamydia and gonnorrhea
Endometrial biiopsy
PID treatment
Initiate as soon as presumptive diagnosis is made to prevent long term sequalae
Outpatient treatment- give IM ceftriaxone PLUS doxycycline BID with or without metronidazole
Inpatient treatment- surgery, Tuboovarian abcess, pregnancy severe illness with nausea/vomiting, unable to tolerate outpatient regimen no clinical response to outpt treatment
Cefotetan IV doxycycline orally or clindamycin plus gentamicin, IR drainage,
Long term complications of PID
Tubal factor infertility, increased tisk of ectopic pregnancy, chronic pelvic pain
Painful vs non painful genital sores
Painful lesions- herpes, chancroid, lymphogranuloma venereum
Non painful lesions- Syphillis, Molluscum, Genital wart
HSV 1 and 2
double stranded DNA Virus- alpha herpes virus family, DNA is encased into a capsid, which is further wrapped in a lipid bilayer, envelope, and capsid is packed with tegument proteins
Herpesvirus have 2 life cycles:
1) quiescent latent infection- limited to neurons (Sacral ganglion) not associated with clinical symptoms
2) lytic replication- active, many infectious viruses are produced, happens at the mucosa/skin at the site of initial inoculation
Reactivation- latency to lytic cycle, recurrent infection is caused by the exact virus that initiated primary infection, reactivation does not always lead to clinical symptoms, transmission can occur even if no lesions are present, infection is life long- no vaccine, majority
Neonatal herpes- can be fatal, anitviaral (acyclovir are Nucleotide analogs that specifically target viral DNA polymerase and inhibit replicaiton, there are no treatments for latent infection
Haemophilus ducreyi
disease= chancroid, pleomorphic gram negative rods (coccobacilli), erythematous papule that becomes pustular then painful ulcer with 48 hrs, lymphadenopathy in approx 50%, disease is uncommon, diagnosis- culture or nucleic acid- based detection, treated with azithromycin , ceftriaxone, ciprofloxacin
treponema pallidum
Gram negative spirochete, extra outer membrane, periplasmic flagella, very slow growth compared to other bacteria, causative agent of syphilis, primary stage: painless chncre at the inoculation site, highly infectious
Secondary - 6 weeks to 6 months after primary systemic spread to multiple organs and CNS, both systemic (fever rash - esp palms and soles) and local (conyloma latum- pink tan papules) symptoms
Latent - asymptomatic and noninfectious (except during pregnancy can relapse to secondary stage or remain asymptomatic for decades
Tertiary- may appear up to 20 yrs after 2’ syphillis, due to immune system- driven damage to multiple organs- heart, skin, bones, vessels, nerves
Congenital infection is associated high mortality rate
Diagnosis- cannot be cultured on conventional medium, not seen on light microscopy, Darkfield microscopy, serology, nucleic acid based approaches
Treated with benthazine penicillin, a modified penicillin that is slowly absorbed and has a long half life, antibiotics are not effective against tertiary stage, Jarisch herxheimer reaction- acute, self limited febrile response within 1st 24 h after treatment
Molluscum contagiosum
Very large double stranded DNA virus- pox virus family
Virion is ovoid to brick shaped complex structure with several membranes, replicates exclusively in the cytoplasm of infected cell, a unique feature for a DNA virus,
A single life cycle- lytic replication, histology of lesions includes molluscum bodies- large eosinophiilic inclusions in the cytoplasm- viral factories
Some of the nucleotide analogs used to control herpes virus replication have antiviral activity against molloscum- use is frequently limited to the immunocompromised patients
HPV
Small, double strandes DNA virus
Papovavirus
Icosahedral capsid, not enveloped, initial requires epithelial damage to access to basal epitheial layer
REplicates in the upper levels of epithelium virus DNA has to be mainted as an episome (covalently linked circle) for productive replication
Viral replication stimulates cellular division- etiology of HPV-induced genital warts
Accidental integration of broken viral DNA terminates virus replication, 2 outcomes - abortive infection or cancer, viral DNA integration that disrupts the expression of viral E2 gene increases risk of cancer along with expression of high risk viral E6 and E7 genes
No treatment specifically targeting the virus
Vaccine against high risk strain sis available
bacterial vaginosis
garderella vaginalis, part of normal vaginal flora in manyasymptomatic women, more common if sexually active but nOT an STD, disturbance of normal flora leads to overgrowth causing disease, vaginal lactobacillus keeps G vaginalis in check, can
Metronidazole, Tinidazole, Clindamycin
candida yeast infection
expands,
fluconazole
