Although there continues to be some controversy about the safety of metronidazole in pregnancy, there has never been a documented case of fetal malformation attributed to its use, even when it is used in the first trimester. Recently, controversy has also developed concerning the treatment of trichomoniasis in pregnancy and its relationship to preterm birth.
Trichomoniasis treatment on pregnant women. Two studies have recently been published which suggest that treatment of trichomoniasis in pregnancy may actually increase the risk of preterm birth
rather than decrease the risk as predicted. However, there
are limitations to both of these studies. One of the studies used
much higher doses of metronidazole than are recommended.
In addition, the study was stopped prematurely because of the
trend toward preterm birth that was seen, and so the number
of women enrolled fell short of the number needed for a
definitive analysis. The second study was a subanalysis of
a study designed to answer questions relating to STD (sexual transmition diseases) and HIV
risk, therefore, it was not designed primarily to answer questions regarding the risks of preterm birth associated with treatment of trichomoniasis in pregnancy.
Since the publication of these papers, the Centers for Disease Control and
Prevention has not revised recommendations for treatment
during pregnancy. Pregnant women may be treated with the
2-g single dose of metronidazole. Occasionally patients
are allergic to metronidazole. Since there is no effective alternative, desensitization is the only option. Another
therapeutic dilemma involves metronidazole resistance in Trichomoniasis vaginalis. The mechanism of development of anaerobic resistance to metronidazole also is controlled by hydrogenosomes,
in that metronidazole competes for H as an electron acceptor. In metronidazole-resistant trichomoniasis vaginalis, the expression levels of the hydrogenosomal enzymes pyruvateferredoxin oxidoreductase, ferridoxin, malic enzyme, and hydrogenase are
reduced dramatically, which probably eliminates the ability of
the parasite to activate metronidazole.