Letters to the Editor
Indian Pediatrics 2000;37: 219-221
|Epidemiology of Poliomyelitis in Delhi, 1997|
Jagvir Singh and colleagues deserve our appreciation and gratitude for the timely publication of the epidmiology of poliomyelitis in Delhi in 1997, after three cycles of national immunization days (NIDs) starting in the last quarter of 1994(1). In addition to the lessons highlighted by them, there are others which show that the tactics chosen by the Ministry of Health and Family Welfare (MoHFW) for the elimination of polio has been deficient or faulty from scientific and managerial viewpoints. I shall enumerate them below.
1. Low Efficiency of Surveillance and Virological Investigations
Of the 158 reported cases of acute flaccid paralysis (AFP), 2 samples of stool were collected only from 97, and sample collection within 14 days of onset was recorded in only 91 children. In other words, surveillance and sample collection had not been fully established even in Delhi and even as late as in 1997, 3 years after commencing NIDs. As pointed out earlier, it was an error in tactics to have begun with NIDs before establishing an adequate level and quality of surveillance and virology(2). While surveillance and virology are confined to the health system, NIDs require total public cooperation, which was obtained by the promise that polio would be eliminated by NIDs. If the MoHFW had wanted to rapidly eliminate polio as the surveillance and virology were built up, they should not have chosen the tactic of NIDs which had failed to eliminate polio even after 8 consecutive years of attempts in Brazil, but on the other hand they should have chosen the tactic of 3-dose pulse, which has a better documented efficeincy and efficacy to rapidly eliminate polio(2). That the public might develop fatigue after repeated but unproductive NIDs was a needless risk taken by the MoHFW. As it turns out, the MoHFW had to revise the tactic to 4-dose NIDs in parts of India and 6-dose NIDs in 8 States in an attempt to make up for lost time. In order to sustain public cooperation they should have started with such massive efforts first, achieved success and then maintained elimination status by 2-dose NIDs, rather than conducting several `dress rehearsals' and giving false hopes first and enacting the full drama last.
Of the 158 cases of AFP, only 53 (34%) yielded wild polioviruses. There are 3 reasons to indicate that the majority of virus-negative cases were also actually polio. They are the close similarities of seasonality, age distribution and vaccine coverage between the virus positive and negative cases. Of these, seasonality is the most important. The peak prevalence of clinical polio (read AFP) was in July-August in the pre-NIDs era. The shifting of the peak prevalence of true polio cases to November-December, the period immediately prior to the next NIDs, is understandable. Logically, AFP of which the peak prevalence had been shifted along with polio, is also polio. Had the etiology been different, the dichotomy of seasonality should have become visible. In summary, the efficiency of surveillance and virology was inadequate in 1997. Let us hope that it has substantially improved in 1998 and 1999.
2. Low Efficiency of Oral Polio Vaccine (OPV) for Polio Elimination.
The authors have stated that after about 15 years of national polio immunization and reaching a reported 3-dose OPV coverage level higher than that required under the Expanded Programme on Immunization, the incidence of reported polio had declined from 25 to only 6 per 100,000 population(1). That amounts to 76% reduction in incidence, a highly unsatis-factory vaccine performance. However, this degree of decline actually corresponds to the 3-dose vaccine efficacy of OPV (i.e., the expected reduction if 100% are immunized). Thus , we had achieved extremely high 3-dose coverage already, but no additional benefit from "herd effect" was evident. In other words, there was evidence as early as in 1992 (and indeed even earlier) that the herd effect of OPV was unreliable for polio control. Further evidence for this conclusion is present in the paper under review(1). The authors have justifiably assumed that most of the cases of reported AFP in Delhi were polio and that its incidence was 1.34 per 100,000 in 1997, as mentioned earlier(1). The pre-NIDs incidence of polio was 5.9 and after 3 years of NIDs it had declined only by some 77%. If OPV given in 2-dose NIDs had induced high herd effect, the decline should have been steeper and transmission should have ceased. This decline (77%) could be attributed to the effect of additional doses of OPV given to a majority of children, rather than due to giving them in campaigns of NIDs. At the end of 3 years of NIDs, a majority of infants would have received 5 doses, most of one-year-olds would have got 7-8 doses, and a majority of children 2-4 years would have received 9-10 doses. Yet, polio prevalence continued.
One of the hallmarks of vaccine herd effect is the increase in the median age of children with disease, consequent to the slowing down of the circulation of the pathogen. It has not happened to polio in Delhi(1). The authors point out that "the age distribution of cases in 1997 did not differ from that observed in the prevaccination era in Delhi or other parts of the country", once again confirming the lack of sufficient herd effect of OPV given routinely and even if given as 2-dose NIDs(1). It takes a minimum of 3 doses by campaign, termed pulse immunization, for adequate herd effect and break in transmission of polioviruses(2).
Even in 1997, over a third of cases, both virus positive and virus negative, were in children defined as "fully immunized" with 3 or more doses of OPV(1). That itself is clear evidence for poor vaccine efficacy. It had been found earlier that the vaccine efficacy of 3 doses of OPV is in the range of about 70-75%. Therefore, when 100% of children are given 3 doses of OPV, some 25-30% of cases will occur in "fully vaccianted" children. This level had been reached in Delhi. In other words, 3-dose coverage had already reached near saturation point before 1997, inspite of the unpublished estimated data of only 70% coverage in 12-23 months old children in East Delhi(1). On the other side of the coin, about a quarter of cases were in unvaccinated children. When poliovirus type 1 continues to circulate, as has been the case in Delhi in 1997 with 72% of isolates being type 1, about 1 in 160 unvaccinated children will develop polio(3). Thus, 54 cases represent less than 9000 unvaccinated children. In a population of some 900,000 under-five children, they constitute a mere 1%, once again showing that vaccine coverage had been excellent in Delhi. Low immunization coverage, pockets of unimmunized children and low potency of OPV due to problems in cold chain and so forth are not the real reasons for poor vaccine performance, although each of them would add to the problem. Several circumstantial evidences have been shown above to disprove low coverage. The absence of clustering of polio cases, as reported by the authors prove that cases were not among unimmunized pockets, but widely distributed. The potency of OPV has been under close scrutiny every year since 1988 and except in 2 years, in all other years over 83% samples had satisfactory potency(1). Even if perfect OPV had been used, the results would not have been much better(4).
3. Are the Present Tactics of Surveillance and Virology Adequate?
The study showed a shift in the seasonality, with the peak prevalence of polio delayed from July-August to November-December(1). Is this evidence for the slowing down of wild virus circulation, indicating even a small degree of herd effect? I do not believe so. Polio is the result of wild virus and sufficient numbers of susceptible children coming into close encounter. The absence or very low incidence of polio in July-August may mean either very little wild virus circulation or very few susceptible children available. Since we have already seen that immunization coverages with 5-10 doses of OPV were very high, the more likely explanation for low polio prevalence is the lack of sufficient numbers of susceptible children. Those who were born after the last NIDs would be the major segment of susceptible subjects, and their number would be the maximum in November-December. The shift of seasonality and the fact that 50% of cases were in infants would support this interpretation. In that case we have no clear evidence that wild virus circulation had actually declined in July-August; it could have just remained silent without causing polio. It had earlier been shown that OPV may protect from disease as children seroconvert, but they could still fully participate in wild virus circulation(3). This is a consequence of poor mucosal immunity and poor herd effect of routine OPV immunization as well as 2-dose NIDs.
The crucial importance of the above reasoning is to strongly suggest that the present approach of surveillance of AFP and its virological diagnosis may be inadequate to ensure the absence of silent virus circulation among well children. It would be prudent to design investigations to test this hypothesis, as both the MoHFW and one major donor agency have been advised (unpublished). If studies show the hypothesis incorrect, nothing is lost; if proven right, then we will be able to avoid an embarassing scene of the reappearance of poliovirus after AFP surveillance and virology give negative results.
If the 4-dose and 6-dose OP campaigns are conducted well in 1999-2000, there should be no more poliovirus circulation in India. However, the false promise of the earlier 2-dose NIDs had created skepticism in the minds of professionals and the public, as in the story of the shepherd boy crying wolf. The MoHFW should conduct the intensified campaigns diligently to ensure success in eliminating the circulation of wild viruses. No one should underestimate the enemy. Let us hope that the OPV campaigns are done well, so that we see complete success in the year 2000 itself.
T. Jacob John,
1. Singh J, Khare S, Bhatia R, Jain DC, Sokhey J. Epidemiological characteristics of poliomyelitis in Delhi, 1997. Indian Pediatr 1999; 36: 1211-1219.
2. John TJ. India's polio eradication efforts at cross roads. Indian Pediatr. 1998; 35: 307-310.
3. John TJ. Poliomyelitis in Taiwan: Lessons for developing countries. Lancet 1985; 1: 872.
4. John TJ, Joseph A, Vijayaratnam P. A better system for polio vaccination in developing coutnries. Brit Med J 1980; 281: 542-543.