Trichomonas vaginalis is a vaginal pathogen associated with an increased incidence of adverse outcomes of pregnancy. Data are limited regarding the effects of Trichomonas infections in the newborn. We report a symptomatic T. vaginalis infection in a 26-week premature infant and a review of the literature.
Trichomonas vaginalis during pregnancy may be associated with premature delivery and low birth weight in the newborn. Limited data suggest that maternal Trichomonas infection may also result in vaginitis, urinary tract infections, or respiratory distress in the newborn. We report a premature infant born at 26 weeks' gestation infected with T. vaginalis; an identical twin was uninfected.
A 636-g (24 weeks' gestation by maternal dating, 26 weeks' gestation by exam) twin A female infant was born to a 36-year-old woman (gravida 7, para 4, spontaneous abortion 2). The mother had no prenatal care and no known history of vaginal infections. The mother admitted to alcohol use during the pregnancy and delivered vaginally through foul smelling fluid within 30 minutes of arrival to an outside facility. No vaginal cultures were obtained from the mother and she left the facility against medical advice shortly after delivery.
The baby was reported to be active and crying with APGAR scores of 6 at 1 minute and 7 at 5 minutes. She was intubated and surfactant was administered within 8 minutes of life. Following administration of ampicillin and gentamicin for premature delivery through presumably infected amniotic fluid, the infant was transferred to the Harbor-UCLA Medical Center.
At Harbor-UCLA, the baby was extubated to nasal CPAP by 18hours of life and antibiotics were discontinued after 48 hours. On day 12, the patient was reintubated for apnea and empirically treated with ampicillin and gentamicin for possible bacterial sepsis. Blood, urine, and nasopharyngeal cultures obtained prior to initiating antibiotic therapy were negative. The infant ultimately received 7days of antibiotics and was weaned to extubation by day 20. On day of life 16, leukocytes were noted on a routine urine screening and T.vaginalis was subsequently grown from a voided urine culture. A 10-day course of metronidazole (5 mg, i.v., every 48 hours) was initiated following a 10-mg i.v. loading dose. On day 19, 24 hours after the initiation of metronidazole, the baby developed a copious white vaginal discharge. A wet mount of the vaginal discharge was negative for Trichomonas, but demonstrated moderate levels of white blood cells. A bacterial and fungal culture of the urine obtained at the time was negative. By day 25, there were no leukocytes in the urine. By day 27, no vaginal discharge was noted. The patient was discharged at 2 months of age without recrudescence of her vaginal discharge or signs consistent with a urinary tract infection. Her twin B sister was asymptomatic and had negative urine cultures and periodic tests for white blood cells (both by microscopic and leukocyte esterase methods) throughout her hospital course.
T. vaginalis is a highly contagious protozoan most commonly transmitted through sexual intercourse. Infection in adults may be asymptomatic or manifest (most commonly) as vulvovaginal itching with a malodorous vaginal discharge. Neonatal infection with T. vaginalis is infrequently reported, but has been noted to cause urinary tract infections and vaginitis in infants as premature as 28 weeks' gestation.1,2,3,4,5,6,7 In addition, infants with T. vaginalis cultured from nasopharyngeal secretions have been reported to present with significant respiratory distress,8 but its causality in this clinical setting is unclear. The precise epidemiologic and pathophysiologic features of neonatal Trichomonas infection have not been well described.
In the immediate newborn period, the vagina is sterile and alkaline.4 However, as maternal estrogens decrease postnatally, the pH falls to approximately 4.0 to 5.0. Because T. vaginalis grows best in an acidic environment, it has been proposed that the postnatal changes in pH in the newborn vagina make the infant more susceptible to the organism.9 It is likely that infants are infected through vulvovaginal contact with the organism at the time of delivery, although some have hypothesized that the organism is ingested through meconium or feces.4 Although nosocomial transmission of T. vaginalis has not been reported, this route of infection is theoretically possible. However, T. vaginalis exists only in the vegetative, trophozoite state, which is generally less hardy than cyst forms that are often implicated in the person-to-person transmission of other protozoa. In addition, T.vaginalis cannot multiply at room temperature, making nosocomial infection much less likely.10
T. vaginalis infection is associated with an increased risk of preterm delivery and low-birth-weight infants.11 Metronidazole successfully treats T. vaginalis, but its use during pregnancy is controversial because of demonstrated mutagenicity and carcinogenicity in laboratory models. Although Burtin et al.12 reported a meta-analysis of seven studies, which suggested that metronidazole does not increase the risk for birth defects in the fetus during the first trimester, metronidazole use is currently recommended only during the second and third trimesters. Treatment during pregnancy of the woman and her sexual partners can potentially prevent the complications of premature delivery as well as infection to the offspring.
In summary, we report a case of T. vaginalis grown from the urine of a very-low-birth-weight infant with clinical vaginitis. Culture of this organism in the urine likely reflects the presence of organisms in the vaginal discharge; it is doubtful that the infant had a primary urinary tract infection and clinical vaginosis. T. vaginalis may be underdiagnosed in newborns; therefore, vaginal inspection and a culture or a wet mount for T. vaginalis should be considered in the appropriate clinical context.