Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
74 Cards in this Set
- Front
- Back
Main Bacterial STIs
|
|
|
NON-Bacterial STIs
|
|
|
The major viral STIs
|
HIV
Genital Herpes – HSV types 1 and 2 Genital warts – HPV types 6 and 11 Genital dysplasia and cancer – HPV types 16 and 18 and others Hepatitis B - HBV |
|
The major bacterial STIs
|
Gonorrhoea Neisseria gonorrhoeae
Chlamydia Chlamydia trachomatis Syphilis Treponema pallidum Mycoplasmas and Ureaplasmas Tropical infections (chancroid, LGV and Donovanosis) |
|
Other important STIs or conditions associated with sexual activity
|
Trichomoniasis – Trichomonas vaginalis
Bacterial vaginosis |
|
Early Events in Trans-mucosal
HIV-1 Infection. |
The arrows indicate the path of the virus.
The viral-envelope protein binds to the CD4 molecule on dendritic cells. Entry into the cells requires the presence of CCR5, a surface chemokine receptor. Dendritic cells, which express the viral co-receptors CD4 and CCR5, are selectively infected by R5 (macrophage-tropic) strains. Within two days after mucosal exposure, virus can be detected in lymph nodes. Within another three days, it can be cultured from plasma. |
|
HPV Immunisations
|
70% of Ca Cervix are caused by 16, 18
90% of Genital warts are caused by 6, 11 Gardasil: immunity to 6, 11, 16, 18 Cervarix: immunity to 16, 18 |
|
HPV infection
|
|
|
Dynamic relationship between HPV infection & Cervical health
|
Originally thought there was inevitable progression from low grade abnormalities to high-grade abnormalities to cervical cancer
Now recognised that LSIL cytology is a manifestation of acute HPV infection, and that most LSIL regresses over time The absolute risk of cancer associated with a high-grade abnormality difficult to determine from available observational data, but is estimated at < 1% per year |
|
Pap smear
|
Most patients with a Pap-smear report of HGSIL have CIN II or III, but some have invasive disease. Thus, the Pap smear is only a screening test, and a biopsy is required for a definitive diagnosis.
|
|
|
Panel A
shows the colposcopic appearance of the cervix in a patient with a Pap-smear report of HGSIL. The lesion surrounding the cervical os is barely visible. Panel B shows the same lesion after the application of a dilute solution of acetic acid, which highlights areas high in nucleic acid. Subsequent biopsy of this lesion revealed CIN III. |
|
Cancer & HPV infection
|
Increased risk in of anal cancer in men who have sex with men and higher if HIV positive people
Oncogenic HPV cause vulval and vaginal cancers – HPV found in 75-90% HPV is also implicated in 25% of head and neck cancers – mainly of the oropharynx |
|
Genital WartsRegression & Recurrence
|
If left untreated, 20% of patients spontaneously regress within 6 months
1 in 3 patients experience recurrence after successful treatment |
|
HSV
|
Herptic lesion on the buttock (genetia herpies)
Public toilet (atypical locations) Stay with the DRG fro the rest of the life Can be infectious even with lack of symptoms |
|
Neisseria gonorrhoeae on cells of fallopian tube
|
|
|
N. Gonorrhoeae Clinically
|
Adherence, Pinocytosis
Inhibition of ciliary function Destruction of tissue Inflammation Purulent exudate in lumen of infected organ Incubation 1 - 14 d (av. 7 days in male) Risk of acquisition from an infected contact 20% for males from females 50% for females from males |
|
Gonorrhoea urethral exudate - Gram Stain
|
Male urethera discharge
- diplococci looks similar to emningococci gram stain but M.C is plumper |
|
Neisseria gonorrhoeae (Ng)Survival
|
Ng grows in endocervix
Ng requires nutrient enriched media for growth e.g., “chocolate” agar Ng do not tolerate drying Ng do not have a true capsule Ng have an absolute requirement for iron e.g., serum glycoprotein transferrin Ng are bacteria of human beings CANT CATCH IT OFF A TOILET SEAT |
|
Neisseria gonorrhoeae (Ng) Spread and Multiplication
|
On mucosal cell surface the Ng multiply rapidly
Ng spread upwards in the urethra in the male and through the cervix in the female Ng stick to spermatozoa and hitch a ride |
|
Toll-like
Receptor 4 (TLR4) |
|
|
COMPLEMENT
|
|
|
Gonococcal infection in females is different to infection in males
|
Within minutes of infection of primary cervical epithelial cells, complement protein C3b is deposited on the lipid A portion of gonococcal lipo-oligosaccharide (LPS) and is rapidly inactivated to iC3b.
Ng inactivates C3b, stopping inflammation in the lower genital tract of females, 50-80% of whom are asymptomatic. Approximately 45% of women with gonococcal cervicitis will develop an ascending infection, the prerequisite to PID. CR3 progressively decreases in an ascending manner from the ectocervix to the fallopian tubes 70 to 90% of women with disseminated infection lack signs of genital tract involvement |
|
Gonococcal Adaptation
|
Gonococci have adapted multiple mechanisms by which they can evade the lytic action of the complement system including:
C4b inactivation & Formation of a non-functional Membrane Attack Complex (MAC) on their cell surface |
|
Hyperacute Gonococcal Conjunctivitis
|
|
|
Chlamydia Characteristics
|
Family Chlamydiaceae
Small obligate intracellular bacteria Gram-negative Range in size from 0.2 to 1.5µm in diameter There are 18 serovars of C. trachomatis |
|
Chlamydia Lifecycle
|
1. The Elementary Body (EB)
Small 0.3µm in diameter Round, tough spore like structures allowing survival outside of the host Rigid cell wall Infectious form of the organism Non-replicative 2. The Reticulate Body (RB) Larger in size – 1µm Represent the replicating stage of the cycle Synthesise DNA, RNA and proteins Non –infectious form of the organism |
|
Chlamydia trachomatis
- and ATP |
Unique growth cycle
Depends on host cell to supply ATP and essential nutrients Lacks system for electron transport No cytochromes Cannot synthesise ATP |
|
Notification of Chlamydial Infections (NSW)
|
Primarily a disease of men and women 15-35
|
|
Chlamydia trachomatis
Pathogenesis |
No latency
Elevated antibody titre Disease due in part to hypersensitivity (worse if had previous infection) Self-limiting to low-grade persistent infection for years; re-activation |
|
Ovarian tube defects
|
|
|
Chlamydia trachomatis
Immunity |
Not protective
Ct do not survive well in PMNL’s Vaccine not yet developed g - interferon can inhibit |
|
Chlamydia and blindness
|
Inflammation leads to damage and attempts at repair (fibrosis & scarring)
|
|
Treatment for Chlamydial Infections
|
Azithromycin is the preferred treatment but the down-side is that there is significant resistance in other STI agents (T.pallidum & N.gonorrhoeae) to Azithromycin.
Widespread resistance in N.gonorrhoeae to tetracyclines, but doxycycline has useful activity against syphilis. |
|
Mycoplasmataceae
|
Mycoplasmas & Ureaplasmas
First isolated in 1937 Family Mycoplasmataceae Two genera Mycoplasma and Ureaplasma Lack cell wall Smallest free living microorganism both in genome size and cellular dimension (300 nm) |
|
Mycoplasmas & Ureaplasmas
Pathogenesis |
Attach to the cell via a tip structure
Following attachment, the plasma membrane of the host appears to be forced inward, suggesting the organism must enter the cell by receptor-mediated endocytosis Ureaplasmas differ from Mycoplasmas – have enzyme urease |
|
Treponema pallidum (Tp)
- staining |
Does not stain by Gram’s method.
Not yet cultured in vitro. Not visible by light microscopy except by ‘dark-field’ or fluorescence microscopy A “silver stain” thickens the spirochaete to be seen in specimens examined by light microscopy Surface rich in lipid, Tp evades host response |
|
Treponema pallidum (Tp)Infection
|
Incubation period related to initial inoculum size :
107 organisms; lesion 5-7 days 50-100 organisms; lesion 3 weeks Spirochaete attaches by end Tp has neither LPS nor toxin Tp chemotaxic |
|
Syphilis (T. pallidum)Primary stage - chancre
|
Multiplication of Tp at site of infection
Patient highly infectious Associated host-antibody response: specific anti-Tp; IgM and IgG non-specific non-Tp (anti-cardiolipin); Veneral Disease Research Lab. (VDRL) test positive (2/3), now EIA, may take 3 mth to +ve Chancre infiltrated with lymphocytes and macrophages |
|
Dark Ground Microscopy
|
Standard bright field light microscopy light is shone onto the specimen yielding a bright background
Dark field microscopy the condenser excludes direct light allowing scattered light to focus on the specimen Bacteria appear luminous against a dark background Helical rods with Corkscrew motility 0.18microns x 6-20 microns long |
|
Syphilis (T. pallidum)Secondary stage
|
3-6 weeks after chancre when local response brings primary stage under control
Systemic infection Haematogenous spread through body Lesions in skin (where temp is less) Systemic immune response Persists for weeks or months High anti-Tp titres (no DTH) “Premunition” resists challenge unable to clear existing lesion Infection persists Formation of immune complexes Immune complexes deposited in kidneys, joints etc (Type III Hypersensitivity) Host response suppresses lesions giving “latent” period, but infection not controlled DTH uniformly positive Tp persists in spite of antibody |
|
Secondary Syphilis
|
Not itchy
Any rash especially if not itchy should include syphilis in the differential diagnosis - Classically on the palms and sole |
|
Premunition
|
able to resist challenge from re-infection but unable to clear the exisitng lesion
|
|
Syphilis (T. pallidum)Tertiary stage:
|
1 - 20 years after primary stage
Gummas (granulomatous lesions) in soft tissue Neurological involvement Syphilis & HIV |
|
|
Granulomatous response fails to kill pathogen but causes tissue damage and illness
|
|
Late syphilis:
Multiple Gummata |
|
|
Trichomonas vaginalis
|
Protozoan
Attaches to mucous membrane Anaerobic Infects sites covered by squamous but not columnar epithelium Urethra (male); vagina (female) No invasion of mucosa Frothy malodorous discharge Symptoms: nil to profound acute inflammation |
|
Trichomonas vaginalis Morphology
|
Occur in several sites in a number of animals
Commensal in GIT in man, only known human pathogen Motile protozoan, pear-shaped, ~10x7 μm Single nucleus, 5 flagella, undulating membrane, characteristic motility No cyst form recognised Capable of phagocytosis |
|
Vaginal flora
|
Multiple mixed organisms - composition varies with age, menstrual cycle, sexual experience, antimicrobials
Anaerobes predominate and lactobacillus species common - most produce H2O2 Low levels of coliforms and Gardnerella Staph aureus, haemolytic streptococci in minority |
|
Bacterial Vaginosis
|
Mixed microorganisms e.g.
Gardnerella vaginalis (+++) Prevotella spp., Mobiluncus spp. (+) Mycoplasma hominis (+) Malodorous vaginal discharge, adherent to vaginal wall “clue” cells |
|
Normal Vaginal Swab (Gram Stain)
|
|
|
Bacterial Vaginosis
|
|
|
Proposed Pathophysiology of Bacterial Vaginosis
|
The overgrowth of anaerobic microorganisms is
accompanied by the production of proteolytic enzymes that act on vaginal peptides to release several biologic products, including polyamines, which volatilize in the accompanying alkaline environment to elaborate foul-smelling trimethylamine. Polyamines act to facilitate the transudation of vaginal fluid and exfoliation of epithelial cells, creating a copious discharge. Clue cells are formed when Gardnerella vaginalis, present in high numbers, adhere in the presence of an elevated pH to exfoliated epithelial cells. |
|
Bacterial Vaginosis – Diagnosis
|
|
|
Bacterial Vaginosis is an STI
|
Sexual contact – male or female
Increased by multiple contacts Decreased by condom use Increased risk if male uncircumcised (cf other STIs) |
|
Bacterial Vaginosis – Risk Factors
|
Use of vaginal foreign bodies, perfumed soaps, or douching
Cigarette smoking Intrauterine device New male sexual partner Sex with another woman No condom use (trend toward association) |
|
Significance of Bacterial Vaginosis
|
Nuisance value, associated with obstetric syndromes, increased rate of preterm birth (usually with chorioamnionitis); postoperative wound infections
Possible increased risk of acquiring other STIs including HIV |
|
Gardnerella vaginalis
|
Gram-variable rod
Recognised by β haemolysis on blood agar Susceptible to wide range of antibiotics Normal habitat human vagina (up to 70% adult women), some girls, rectum Found in ~100% of women with BV, but causative role not clear Often in male urethra but no known significance Adheres to vaginal epithelial cells May produce cytotoxins |
|
Bacterial Vaginosis – Treatment
|
|
|
Candidiasis
|
A primary or secondary mycotic infection caused by members of the genus Candida. The clinical manifestations may be acute, subacute or chronic to episodic.
Involvement may be localized to the mouth, throat, skin, scalp, vagina, fingers, nails, bronchi, lungs, or the gastrointestinal tract, or become systemic as in septicaemia, endocarditis and meningitis. Distribution: World-wide. Aetiological Agents: Candida albicans, C. glabrata, C. tropicalis, C. krusei. C. parapsilosis, C. guilliermondii and C. pseudotropicalis. All are ubiquitous and occur naturally on humans. |
|
|
Oral candidiasis in an infant showing characteristic patches of a creamy-white to grey pseudomembrane composed of blastoconidia and pseudohyphae of C. albicans. Note the mouth of normal newborn infants has a low pH which may promote the proliferation of C. albicans. The infections are usually acquired during the birth process from mothers who had vaginal thrush during pregnancy. Clinical symptoms may persist until a balanced oral flora has been established.
|
|
Vulvo-Vaginal Candidiasis - Treatment
|
Consider other non-STI possibilities
Vaginitis – local or systemic illness Allergic vaginitis Atrophic vaginitis Chemical/irritant vaginitis Desquamative interstitial vaginitis Erosive lichen planus vaginitis Systemic illness Behçets disease |
|
Donovanosis
Calymmatobacterium granulomatis NOW KNOWN AS: Klebsiella granulomatis |
Begins as single or multiple subcutaneous nodules that soon erode through skin
Results in fleshy, beefy-red, exuberant granulation tissue which bleeds readily Genital erosion Lesions expand by direct extension and autoinoculation Haematogenous spread |
|
Lymphogranuloma venereum
|
LGV is also caused by Chlamydia trachomatis but:
Not restricted to epithelial surfaces Is invasive and causes severe inflammation Preference for lymphatic tissue Primary stage is asymptomatic small genital ulcer – self-resolving Then painful lymphadenopathy with systemic illness |
|
Genital Ulcers – Non-venereal
|
|
|
ChancroidHaemophilus ducreyi
|
Gram negative bacillus
Requires X-factor (hemin) Incubation period 4-7 days First symptom - ulcer |
|
Swab & Urine Specimen Collection - Males
|
Urethral specimens
Do not pass urine for at least 4 hours prior to specimen collection First catch urine Should not pass urine for at least 3 hours before the sample collection Collect first 10ml of urine Voiding < 30 minutes prior to collection may influence results Distal urethral swab Performed when discharge or urethritis symptoms Confirm a positive urine PCR for gonorrhoea Test a gonorrhoea contact Test of cure after treatment for gonorrhoea Proximal urethral swab Performed when chlamydia testing required and urine not taken for chlamydia PCR Other: Rectal, Pharyngeal, Ulcer/Lesion |
|
Swab & Urine Specimen Collection - Females
|
Endocervical specimens
Do not pass urine for at least 4 hours prior to specimen collection Vaginal specimens Lateral vaginal wall (Candida, Bacterial Vaginosis) Posterior fornix (Trichomonas) First catch urine As per males (if endocervical swab not available) Other: Rectal, Pharyngeal, Ulcer/Lesion |
|
Urethral Discharge Steps
|
|
|
Urethral Discharge Tx
|
|
|
Presistent/recurrent urtheral discharge in men
|
|
|
Gential Ulcers
|
|
|
Gential Ulcers Tx
|
|
|
Vaginal Discharge
|
|
|
Vaginal discharge:
Speculum |
|