Viral Genitourinary Infections — Questions

Specimen and test. Take a swab from the base of an ulcer or from a fresh vesicle and test by PCR, which is the diagnostic test of choice and has replaced insensitive culture. Type-specific serology can establish whether the infection is HSV-1 or HSV-2 but does not diagnose the acute lesion.

Treatment options. The aciclic nucleoside analogues aciclovir, valaciclovir or famciclovir, given either episodically at the onset of each recurrence or as daily suppressive therapy.

Treatment of choice. For a patient with recurrent disease, daily suppressive therapy is preferred, as it reduces the frequency of recurrences and asymptomatic shedding, and therefore transmission.

• HPV infection is very common in women under 30, with peak prevalence in the early twenties.
• Most of these infections are transient and clear spontaneously without ever progressing to significant disease.
• Testing younger women therefore detects many infections that would resolve on their own, leading to unnecessary follow-up and treatment; a positive test above 30 is more likely to represent a persistent infection at real risk of progression.

• Recurrent respiratory (laryngeal) papillomatosis is caused by HPV-6 and HPV-11, the same low-risk types that cause genital warts.
• The infant acquires the virus at vaginal delivery from maternal genital warts.
• The quadrivalent and nine-valent HPV vaccines include HPV-6 and HPV-11, so vaccinating girls before childbearing prevents maternal genital warts and, in turn, transmission to the infant, which is expected to reduce laryngeal papillomatosis.

A complete answer covers what the test detects, its place in screening, and the South African programme.

What it detects. Human papillomavirus cannot be cultured and serology is unhelpful, so molecular methods detecting HPV DNA or messenger RNA are the only specific tests, targeting the high-risk oncogenic types, above all HPV-16 and HPV-18.

Place in screening. High-risk HPV testing is more sensitive than cytology for detecting cervical pre-cancer, and South Africa is moving from cytology towards primary HPV testing, with positive results triaged (by cytology or directly) to colposcopy.

South African programme. Screening is offered from about age 30 in the general population and starts earlier and is repeated more often in women living with HIV, in whom HPV persists and progresses more readily. The shift supports the national goal of cervical cancer elimination.

Adenovirus types 11 and 21 cause acute haemorrhagic cystitis in young boys; BK polyomavirus causes it in the immunosuppressed.

The other viruses cause different genitourinary problems.

HSV establishes latency in the sacral dorsal root ganglia, from which it travels down the sensory nerve to cause recurrent genital lesions.

It does not persist latently in epithelium, nodes, lymphocytes or marrow.

Suppressive therapy reduces the frequency of recurrences and of asymptomatic shedding, and hence transmission; it does not cure the infection.

Latent virus is not eradicated, and the other options are not effects of the drug.

HSV-2 is the commonest cause of genital herpes, although HSV-1 accounts for an increasing proportion.

The other herpesviruses do not cause genital ulcer disease.

The low-risk types HPV-6 and HPV-11 cause over 90% of genital warts, which are benign.

Types 16 and 18 are the oncogenic types driving cancer, while the other viruses cause different genital lesions.

HPV cannot be cultured and serology is unhelpful, so detection relies on HPV DNA or messenger RNA testing.

The other methods do not reliably detect the virus.

BK polyomavirus reactivates under immunosuppression to cause an allograft nephropathy that can mimic graft rejection, as well as haemorrhagic cystitis in bone-marrow recipients.

It does not cause the other listed conditions.

Cervical screening uses cervical cytology (the Pap smear) together with, and increasingly replaced by, high-risk HPV DNA testing, with colposcopy for positive results.

Serology, culture, radiography and urine testing have no role in cervical screening.

PCR of a swab from the ulcer or vesicle is the test of choice, being far more sensitive than culture.

Serology dates past infection but not the acute lesion, and the Tzanck smear and electron microscopy are insensitive and non-specific.

The high-risk types HPV-16 and HPV-18 cause about 70% of cervical cancer and a large share of other anogenital and oropharyngeal cancers.

The other types cause benign warts (6/11, 1/2), enteric disease (40/41) or epidermodysplasia verruciformis (5).

Genital warts appear after a mean incubation of about 2 to 3 months (ranging from 3 weeks to beyond 8 months).

The other intervals are too short or too long.

Imiquimod is a Toll-like receptor 7 agonist that induces interferon and other cytokines, giving a low recurrence rate after clearance.

It is not directly cytolytic, a polymerase inhibitor, a caustic agent, or an entry blocker.

HIV is transmitted sexually but produces systemic immunodeficiency, not genital-tract disease.

Genital HSV-2, HPV warts and cancers, and genital molluscum are all organ-tropic infections of the genital tract.