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I read with great interest the article by Isenberg et al.1 The authors deserve to be commended for their pioneering interest in childhood blindness. There are certain points that I would like to clarify and supplement with regard to their study.
(1) The authors have mentioned that only babies born by a vaginal delivery were studied, since the eyes of babies delivered by caesarean section were previously proved to be nearly always sterile. This would result in a gross underestimation of the incidence of ophthalmia neonatorum in this study, for the following reason.
By convention, ophthalmia neonatorum is defined as conjunctivitis arising within 1 month after birth. Hence, some of these conjunctival infections could originate from sources other than the maternal vaginal and cervical flora. In fact, some cases of ophthalmia neonatorum, especially those caused by Staphylococcus aureus, could have originated at home, as previously reported by the authors themselves. In the same study, no significant difference in the frequency or type of infection was seen among the infants delivered vaginally or by caesarean section.2
Other authors, too have made similar observations. Krohn et al3 have found some cases of ophthalmia neonatorum to have been acquired from the infants’ nasopharyngeal passages or from their care givers after birth. Verma et al,4 in a prospective study from India, found no correlation between the microbiology of the conjunctival swabs of the infected eyes (Staph aureus was the commonest isolate) and the vaginal and cervical swabs of the mothers (Escherichia coli was the commonest isolate). They concluded that most of the cases of ophthalmia neonatorum were acquired postnatally. In the light of these previously reported studies, I feel that exclusion of cases that were delivered by caesarean section was not warranted and weakens the power of this study. The efficacy of the second drop of povidone-iodine was not tested on a significant proportion of the cases of ophthalmia neonatorum (those cases affecting the babies delivered by caesarean section).
(2) It would be relevant to note the percentage of ophthalmia neonatorum cases with neonatal dacryocystitis due to congenital nasolacrimal duct obstruction in this series. Such cases obviously would not have benefited from a second drop of povidone-iodine.
(3) The Indian study by Verma et al4 found a seasonal incidence of ophthalmia neonatorum with two peaks: in February and May-June, in most probability as a result of the monsoon and the hot tropical climate with the attendant eye seeking flies. It would be interesting to know whether any such seasonal variation was noted in this study, which was carried out in Kenya, a country with a hot tropical climate, like India. If so, the efficacy of the second drop could be investigated again during such peaks.
We greatly appreciate the inquiry of Dr Vendantham and are happy to reply to his questions.
While he is correct regarding the definition of ophthalmia neonatorum including all infections acquired by an infant during the first 30 days of life, for the purposes of our study,1 we were primarily interested in those cases resulting from neonatal exposure in the birth canal. This source of ophthalmia neonatorum is the one that would be influenced mainly by a second drop of povidone-iodine placed later on the day of birth. Infections postnatally that Dr Vendantham listed as arising, while technically still within the definition of “ophthalmia neonatorum,” would not be impacted by this second drop and therefore would not be directly affected by this study. Indeed, Dr Vendantham’s interest in neonatal dacryocystitis would also fall within the same question since the reflux from the tear duct causing this infection generally does not arise until well after the first day of life.
The proportion of ophthalmia neonatorum cases acquired postnatally compared with those acquired during the birth process probably differs by country. The difference in predominant causative organisms (Staphylococcus aureus and Enterococcus in the former situation as in India2v chlamydia and gonococcus in the latter) probably reflects the origin of the infection. Historically, in Kenya a high proportion of the infections probably arose from the birth process as reflected in the type of infecting organism. Thus, our Kenyan study, was primarily directed towards those infections acquired during birth.
The fact that ophthalmia neonatorum in some countries seems to peak in certain seasons and not in others should cause increased vigilance for this disorder in those countries. Our study, however, encompassed more than one full year of births in Kikuyu, Kenya. Therefore, the study included both the peaks and troughs of the incidence of ophthalmia neonatorum.
We thank Dr Vendantham for his interest and hope that in many countries, including India, ophthalmia neonatorum prophylaxis will either continue unabated or be initiated preferentially with the use of povidone-iodine.
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