Week 3 - STI, Scotum, Testes & Penis Disorders Flashcards
Outline syphilis.
• Treponema pallidum (spirochete), global, endemic, incidence increasing.
• Body fluids → skin/mucosa or placenta to new born.
- Transmitted by body fluids directly to skin/mucosa or mother to foetus via placenta.
- Bacteria cannot survive outside the body so direct contact is important.
• Widespread dissemination through lymphatics.
- Occurs early in the disease.
• Proliferative endarteritis - chronic inflam. plasma cells*
- Characteristic lesions of syphilis is proliferative endarteritis - vascular damage. Chronic inflammation with plenty of plasma cells.
- Microscopy - plenty of plasma cells around blood vessel. Endarteritis with plasma cells.
• Congenital - abortion → rash, liver and lung fibrosis, 8th nerve deafness, interstitial keratitis, hutchison teeth (notching of the incisors).
- When baby acquires syphilis. Ranges from intrauterine death (abortion) to mild rash with above features.
*See diagram.
Describe the 3 stages of syphilis.
• Primary (3wk) - chancre: ulcerated papule, resolve* spontaneously. Highly infectious*
- Clinically, it occurs in 3 stages.
- Primary - first 3 weeks. Phase where person is highly infectious. Chancre - ulcerated papule that resolves spontaneously.
- Although syphilis produces lots of antibodies, they are not protective.
• Secondary (months) - recurrent lymphadenopathy, palmar rash, Condyloma lata (painless, moist, plaques). Highly infectious etc. Resolve*
- Following healing of chancre, present months later with above features.
- Highly infectious and usually resolve without any treatment.
• Tertiary (years) - Gumma-Necrotising granuloma CVS, CNS. Tabes dorsalis, general paresis, aneurysms 80%.
- Most damage - usually after 5-20 years.
- Known as Gumma - necrotising granulomas in the cardiovascular system mainly but also in the CNS and other organs.
- Aortic aneurysms 80% of cases.
Describe the diagnosis of syphilis.
Non Treponemal Ab (to cardiolipin):
• Only early phase, non specific, false positive. Common tests:
- VDRL (Venereal Disease Research Lab).
- RPR (Rapid plasma regain).
• Cardiolipin present on bacteria and in the body.
• Usually in the early phase, not the tertiary phase.
• False positive - not specific to bacteria, can be positive in other diseases.
• Good for screening only, need to confirm. Confirmed with specific antibodies to Treponema.
Treponemal Ab: • Usually positive in all stages. False positive* • FTA-ABS (fluorescent Trepo. Ab) - Fluorescent Treponema antibody absorption test. • TP-PA (TP particle agglutination) - Particle agglutination test. • MHA-TP (Microhaemagglutinin Assay). - Microhaemagglutinin test.
• Direct detection: darkfield microscopy, PCR, culture?
Outline gonorrhoea.
• Common, second to Chlamydia, incidence increasing, resistant to many drugs. Suppurative, only humans. Person to person and to fetus on birth (passage).
- Common pyogenic infection (pus forming).
- Direct contact or mother to foetus.
• Produces dysuria, mucupurulent discharge → PID.
- Ascending infection leading to pelvic inflammatory disease.
• Neisseria gonorrhoeae, gram neg. diplococci.
• Stick to epithelia, 1-14 day incubation.
- Penetrate through epithelia and disseminate through body.
• Fever, pain, inflammation, dysuria, discharge - white pus.
• Urethra, cx, rectum, pharynx, or eyes.
- Causes all itis - urethritis, cervicitis, proctitis, pharyngitis.
• Intracellular, gram neg diplococci.
- Organisms within cytoplasm of neutrophils.
• Complications: stricture, PID, spread.
- PID with fibrosis - frozen pelvis.
• Ocular, neonatal conjunctivitis.
Outline nongonococcal urethritis (NGU).
• Most common STI. Chlamydia*, trichomonas vaginalis (protozoa), ureaplasma, Mycoplasma genitalium etc.
- Commonly due to Chlamydia but also other organisms.
Outline chlamydia.
• Chlamydia trachomatis (pathology similar to gonococci - less pus in chlamydia infections).
• Gram -ve, elementary body → reticulate body in cell.
- Gram negative bacteria. 2 forms - elementary body outside, reticulate body within cells.
• ~50% are asymptomatic.
• Major cause of infertility in men and women.
- Causes extensive fibrosis → infertility.
- Can be asymptomatic and infecting other people through sexual activity.
• 40% PID, 20% infertility, 9% ectopic pregnancy.
- 40% of cases present with PID.
• In men - urethritis, epididymo-orchitis, prostatitis.
• In patients with HLAB27 → reactive arthritis (Reiter’s syndrome).
• Children - seasonal purulent conjunctivitis. Repeated, untreated → scarring of cornea and eyelids → visual impairment/blindness.
- Children present with seasonal purulent conjunctivitis. Repeated/untreated cases can lead to scarring of cornea and eyelids.
Describe the diagnosis of chlamydia.
• Nucleic acid amplification Test (NAAT). Sensitive test.
• In combination with tests for Neisseria gonorrhoeae (also HIV).
- Patients usually tested for chlamydia, gonorrhea and HIV.
Outline Reiter’s syndrome.
• Common inflammatory polyarthritis in young men.
- Reactive immune polyarthritis secondary to Chlamydia.
• Chlamydia trachomatis (rarely salmonella and shigella).
• HLA-B27 - risk factor in 70%.
- Patients with HLAB27 more at risk.
• Fever, malaise, myalgia.
• Reactive asymmetric arthritis.
• Conjunctivitis.
• Knee, ankle and feet common e.g. sausage toe, inflammed ankle.
• Chronic, recurrent.
• Disability in ~20% cases.
Differentiate GU and Non-GU.
- Major difference is in gonococcal - intracellular diplococci present.
- In non-GU - may not be any organisms present, just neutrophils.
- More pus in gonococcal than non-GU.
Outline lymphogranuloma venereum.
• LGV - Chlamydia trachomatis, serotypes L1-L3.
- Also caused by Chlamydia trachomatis but different serotypes (L1-L3).
- Produce ulcerative lesions of the penis and lymph nodes. Initially lymphadenitis then ulcerates.
• Chronic ulcerative, lymphedema, procto-colitis.
• Genital painless papule 2-5 days.
• 1-4 wk suppurative necrotic inguinal lymphadenitis.
• Suppurative granuloma (neutrophil abscess) and chlamydial inclusions in microscopy.
- Also causes extensive granulomas and fibrosis → PID.
Complications:
• Rectal strictures. Pelvic inflammatory disease, frozen pelvis - extensive fibrosis.
Outline chancroid.
Chancroid (soft chancre):
• AKA third venereal disease (Syphilis, Gonorrhoea).
- Also produces ulcers similar to LGV but caused by different organism.
• Haemophilus ducreyi.
• Gram -ve coccobacillus.
• Tropical. HIV common, prostitution risk factor*
- Common in prostitution and HIV infected people.
• Erythematous papule → painful ulcer, yellow pus.
- Characteristic feature is painful ulcer and yellowish pus, both male/female genitalia.
• Inguinal lymphadenopathy → buboes → pus draining ulcers.
- Marked lymphadenopathy known as buboes with pus discharging ulcers - typical in chancroid.
Outline granuloma inguinale.
• Chronic fibrosing STD by Klebsiella granulomatis. AKA Granuloma venereum/donovansis.
- Not very common, also produces ulcer.
- Klebsiella granulomatis within macrophage bacilli.
• The initial papules on genitalia → ulcers → urethral, vulvar or anal strictures.
• Granulation tissue and intense epithelial hyperplasia that can mimic squamous cell carcinoma.
• Intracellular coccobacilli within vacuolated macrophages (known as Donovan bodies).
• Note: Leishmania donovani (protozoa) - Donovan bodies* is different.
Outline genital herpes.
• STD - Herpes Simplex Virus HSV1 and HSV2*
- HSV2 most common.
• 95% of HIV +ve are also positive for HSV.
• Direct contact only - not fomites.
- Mucosa to mucosa.
• 4 day incubation, produces itchy, painful, closely grouped vesicles surrounded by erythema.
• Vesicles burst to form painful ulcers.
• Multinucleate giant cells with viral inclusion.
- Viral inclusions are characteristic on microscopy. Positive by anti herpes virus antibodies.
• Painful inguinal lymphadenopathy.
• Self limited mild in normal.
• Severe infection in immunocompromised.
• Neonatal herpes encephalitis - severe and fatal.
Identify the structure, origin and lymphatics of the testes.
- The testes develop in the abdomen (para-aortic region) - testicular lymphatics is para-aortic lymph nodes. Penis and scrotum - inguinal lymph nodes.
- Testes are packed with seminiferous tubules. Each of these tubules are lined by germ cells which gradually mature towards the centre to form sperm. (spermatogonia → primary spermatocyte → secondary spermatocyte → spermatid → sperm cell).
Outline epididymo-orchitis.
Aetiology:
• Gonococcal - Neisseria gonorrhoeae
• Non Gonococcal - chlamydia, mycoplasma
- Commonest - NG chlamydia.
Clinical features:
• Testicular pain - unilateral
• Erythema/oedema of the scrotum.
• Uretheritis, dysuria/urethral discharge.
Morphology:
• Gross - swollen, hot, acute inflammation, oedema.
• Microscopy - oedema, neutrophils (acute inflammation), necrosis.
Investigations:
• Exclude torsion/trauma in <30 years.
• Serology, microbiology: C/S, PCR.
Describe gonococcal epididymo-orchitis.
- Formation of pus, huge abscess in epididymis and pus in the testes.
- Microscopy - gram negative diplocci.
- Investigations - first pass urine and NAAT. Culture - urethral swab.
Outline mumps orchitis.
• Paramyxovirus, respiratory tract spread.
- Commonly epidemics in school children.
• Acute, febrile, bilateral parotitis - children and orchitis in adults (25%) and viral meningitis (15%).
- Bilateral parotitis typical in children.
- Orchitis in 25% patients particularly teenagers.
- Rarely meningitis.
• Orchitis - unilateral, enlarged, painful and tender.
• Patchy inflammation, neutrophils and lymphocytes.
• Increasing pressure → ischaemia, necrosis.
- Increasing pressure due to tough capsule causes ischaemia and necrosis.
• If mild → complete resolution.
• If severe → patchy atrophy → infertility.
- Severe - infertility due to atrophy.
• Microscopy - gradually there is oedema formation and plenty of inflammatory cells filling the tubule damaging the spermatogonia. Patchy areas of inflammation within tubule.
Outline cryptorchidism.
Cryptorchidism: “undescended testes”
• Normal descent: 3m to pelvis, 9m to scrotum.
- Usually descends by time of delivery to scrotum (9 months) from the para-aortic region.
• Non descent 5% at birth, 1% at 1y (10% bilateral).
- 5% don’t descend before birth. 1% remain after 1 year. If left undescended in inguinal canal → testes undergo atrophy.
• Cause: Hormonal, intrinsic and mechanical.
• Common in Patau, Prader willi syndrome etc.
• Atrophy - sertoli and Leydig cell hyperplasia.
- Complication = atrophy. Due to temperature increase, spermatogonia undergo atrophy leaving behind only sertoli and Leydig cell hyperplasia.
• 3-5 fold increase in Germ cell malignancy - even in the other testes.
- Increased incidence of germ cell malignancy.
• Orchiopexy - surgical fixing (of testes back into scrotum), reduces risk of sterility and cancer (when done early).
Describe the morphology of testicular atrophy.
- When there is atrophy, initially there are only sertoli and Leydig cells remaining within the tubules. All the spermatogonia disappear, testes shrink in size.
- Later, in case of mumps, there will be total atrophy. Patchy atrophy, some normal tubules and totally atrophic tubules.
Outline torsion of the testes.
• Twisting of spermatic cord on its axis.
• 1y or 13-16y, swollen, hard, painful.
- Common in infants and teenagers.
- Very painful, sudden, swollen.
• Precipitated by exertion/contraction of cremaster muscle.
Risk factors:
• Maldescent (of testes), long spermatic cord/mesorchium.
2 types:
• Within tunica vaginalis - common, testis and epididymis involvement only.
- Most common, testes turn within tunica vaginalis. Only testes and epididymis involved.
• Above tunica - all structures in that side of the scrotum (includes tunica vaginalis).
- All structures are involved.
Pathogenesis:
• Venous stasis → venous infarction.
- Due to twisting, there is obstruction to venous outflow. However, the thick walled arteries still continue to supply. Results in obstruction to venous outflow → causing venous infarction.
• Surgical emergency → correction/orchidectomy.
- If not performed within a few hours, undergoes total infarction.
Describe inflammatory accumulations of the testes.
- Hydrocele: common, clear fluid in tunica vaginalis. Congenital/acquired (inflammation).
• Collection of clear fluid in tunica vaginalis. Can be congenital or acquired due to inflammation. - Varicocele: engorged spermatic cord veins (pampiniform plexus). Common cause of infertility oligospermia. Primary/secondary.
• Engorged spermatic cord veins. - Spermatocele: epididymis dilatation, trauma/infection, multilocular, sperms.
• Trauma to epididymis (one of the tubules) causing dilated cysts containing semen. - Haematocele: blood in tunica vaginalis. Trauma, tumours.
• Blood accumulating in tunica vaginalis. Trauma or tumours. Accumulation of blood results in atrophy of the testes due to compression and increased temperature.
Outline hydrocele.
- Marked swelling of the scrotum.
- Transilluminant due to the clear fluid (no inflammation).
- Can be non-communicating, communicating (communicates with abdominal cavity) or hydrocele of spermatic cord (rare).
Outline disorders of sexual development.
• Ambiguous genitalia → transgender.
• By default all are female.
- All female unless someone has a SRY gene functioning on short arm of Y chromosome → produce androgens → give male characteristic.
- If no gene or mutated gene or testes not functioning, phenotypically will be female (even if have XY genes).
• SRY gene on short arm of Y androgens → male.
• Congenital Adrenal Hyperplasia (CAH) is the most common cause.
- Most common cause of transgender sex. AKA female pseudohermaphrodite. Rarely caused by drugs and hormone therapy during pregnancy (excess androgenic hormones).
- Opposite is male pseudohermaphrodite - genetically male but with female sexual characteristics due to gonadal dysgenesis.
- True hermaphrodite rare - both ova and testes in single person.
• Mixed gonadal dysgenesis (MGD) is the second common cause of DSD.
• Sex chromosome DSD: Turner’s, Klinefelters etc.
- Female pseudohermaphrodite*** - XX male - CAH.
- Male pseudohermaphrodite** - XY female - gonadal dysgenesis.
- True hermaphrodite (rare) - XX/XY - both gonads.
- Mixed gonadal dysgenesis* - Male Turner - streak and testes.
Outline tumours of the testes.
• Commonest tumour of young males, painless swelling.
Aetiology:
• Idiopathic, undescended testes (10%, 10 times).
- Idiopathic most common, 10% related to undescended testes (10x more chance of developing tumour).
Classification:
95% Germ cell tumours
• Seminoma 45% - good prognosis (more local). Most common.
• Non seminoma (NSGT) 45% - poor prognosis. Embryonal ca, Teratoma, Chriocarcinoma, mixed - common.
- 60% of cases, microscopically will find more then one type of germ cell tumour - multipotent nature, can differentiate into any type of cell. Mixed patterns common.
5% Sertoli/Leydig cell tumours.
Clinical features: • Adults 20-40y - Seminoma. • Children <10y - NSGT - Yolksac tumour. • Painless, dragging, unilateral, solid. - Sensation of dragging, solid swelling. • Metastases - para aortic LN* - Metastases goes to the para aortic nodes because of its embryologic origin.
