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There has been a dramatic decline in the prevalence of trichomoniasis in Australia over the past 30 years. In 1979, 17.8% of women attending a Sydney STI clinic had Trichomonas vaginalis infection.1 By 1998 less than 1% of non-Indigenous women presenting to family planning and STI clinics in another jurisdiction were diagnosed with the condition2 and most Australian urban pathology laboratories do not diagnose a case from one year to the next. Similar observations have been reported elsewhere: the rate of detection of trichomoniasis in Papanicolaou (Pap) smears in Denmark fell from 19% in 1967 to <2% in 1997,3 and a study in Brazil found similar results (a peak of 17.3% in 1978, falling to 3.4% in 1998).4
In the absence of any health promotional activities relating to trichomoniasis and in a setting where the prevalence of another STI, Chlamydia trachomatis, has shown a fourfold increase in notifications in the past 10 years (Communicable Diseases Network Australia, National Notifiable Diseases Surveillance System, personal communication), what can explain the decline and fall of T vaginalis?
I propose that the change in prevalence is an unintended consequence of the introduction of coordinated Pap smear screening programmes in the 1970s and 1980s. As the Pap screening programmes gained momentum in the urban areas, a positive finding on the Pap smear, which has a sensitivity for the diagnosis of T vaginalis of around 50–60%, would have been conveyed to the referring medical practitioner who would treat the woman with metronidazole or tinidazole. In addition, the increasing use of these antibiotics for the treatment of other conditions, in particular bacterial vaginosis, may have further reduced the prevalence during the same period. As there are no cytological changes that are diagnostic of C trachomatis, Pap screening would be expected to have no effect on chlamydia prevalence.
In Australian urban populations the proportion of women undergoing Pap screening in the 20–40 year age group is approaching 70%. On the other hand, in some remote Aboriginal populations the introduction of coordinated screening has lagged behind urban areas5 and trichomoniasis remains hyperendemic (prevalence of approximately 25%).6
(Of course these observations could be confounded by a number of factors: Pap screening rates correlate with socioeconomic status and the rate of partner change could be different between these groups. However, it has been shown that access to services is more important than differences in the rate of partner change when comparing STI rates in Indigenous and non-Indigenous populations in Australia.2)
The Pap smear hypothesis could be tested by correlating the prevalence of trichomoniasis with the rate of cervical cancer screening in selected populations and through clinic based case-control studies. (The virtual absence of trichomoniasis in urban Australia means that this work must be performed in other populations.) If the prevalence of T vaginalis is related to Pap screening, a similar approach to chlamydia control—that is, routinely linking nucleic acid amplification testing for C trachomatis with the Pap smear, could also be considered.
Conflict of interest: None.
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