Co-infections with Ureaplasma parvum and Herpes simplex virus in an acquired immunodeficiency syndrome patient

Sir,

Coexisting sexually transmitted infections (STI's) facilitate acquisition and transmission of other STI's including human immunodeficiency virus (HIV). Ulcerative STI's including syphilis, chancroid, Herpes simplex virus (HSV) increase the host susceptibility to HIV by disruption of mucosal barriers. The nonulcerative STI's caused by Chlamydia trachomatis, Ureaplasma spp., genital mycoplasmas have also been reported to potentially increase the susceptibility of acquiring and transmitting HIV.[1]

A 33-year-old man, presented with chief complaints of urethral discharge with burning micturition of 20 days duration and eruption of recurrent ulcers around genitals since 1-year. He was diagnosed seropositive for HIV-1 1-year back and was on antiretroviral therapy since then. Sexual history revealed he had multiple heterosexual and homosexual partners.

On examination, he had scanty mucoid to mucopurulent urethral discharge. In addition, he had multiple polycylic tender erosions covered with yellow slough on the glans and prepuce. The perineal and perianal area was normal on examination. On palpation, there was no inguinal lymphadenopathy or suprapubic tenderness. The patient was diagnosed clinically as a case of recurrent genital herpes.

On investigation, his CD4⁺ lymphocyte count was 88/µl. He was nonreactive for Venereal Disease Research Laboratory and seronegative for both hepatitis B surface antigen and antihepatitis C antibodies. Gram-stained smear of urethral discharge revealed 20–30 pus cells/high powered field. Culture of discharge was negative for Neisseria gonorrhoeae. Three Dacron swab specimens of the discharge were collected. Two swabs were inoculated into pleuropneumonia like organisms broth containing urea and arginine for isolation of Ureaplasma spp. and Mycoplasma hominis, respectively. The semi quantitative cultures were positive for Ureaplasma spp. at a concentration of >10⁵ color changing units per ml within 48 h of incubation. The Ureaplasma spp. was susceptible to azithromycin, doxycycline, ofloxacin, ciprofloxacin, levofloxacin and josamycin by microbroth dilution method.[2] Third swab was subjected to multiplex polymerase chain reaction (PCR) for Ureaplasma spp. and M. hominis. In addition, PCR's for Mycoplasma genitalium, and C. trachomatis were performed. The sample was positive for Ureaplasma spp., which was further biotyped. It belonged to biovar 1 (Ureaplasma parvum).

The patient was diagnosed with acquired immunodeficiency syndrome having co-infections with U. parvum [Figure 1] and HSV. He was treated with azithromycin and acyclovir and evaluated 1-week after treatment. He reported cessation of urethral discharge with healing of ulcers. Post-treatment, first-void urine sample of the patient was negative for Ureaplasma spp. both by culture and PCR. The patient was counseled for safe sex practices and advised for regular follow-ups at a interval of 2 weeks.

Figure 1.

Gel electrophoresis image, showing results of polymerase chain reaction amplification for identification of Ureaplasma serovars

Risk of retroviral transmission is increased in the presence of co-infections with organisms such as HSV, syphilis, chancroids and genital mycoplasmas.[4] To the best of our knowledge, this is the first report of co-infection with U. parvum and HSV in HIV-infected individual.

Because of the frequency with which ureaplasmas occur in healthy asymptomatic individuals, it has been suggested that only certain subgroups of the species are pathogenic. The majority of human Ureaplasma isolates belong to U. parvum (biovar 1). Ureaplasma urealyticum (biovar 2) is isolated less often.[3] Ureaplasma consists of 14 serovars. Among the different serovars of U. parvum, serovar 3/14 is the most frequent serovar detected and suggests a possible pathogenic role of U. parvum serovar 3/14.[3] Our patient was also infected with U. parvum serovar 3/14, thereby supporting its pathogenic potential.

Our patient had a CD4⁺ count of 88/µl. Previous studies have shown an association of HSV with CD4⁺ counts, but no such definitive association with genital mycoplasmas is known.[4] Hence, screening of all HIV patients for genital mycoplasmas, irrespective of their CD4⁺ counts should be done. This case highlights the importance of screening of all patients with high risk behavior, for multiple co-pathogens infecting the genital tract. Early detection and treatment of sexually transmitted pathogens in HIV-infected patients would prove prudent to control retroviral transmission.