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Indian Journal of Community Medicine

Some Exaggerated or Non-existing Properties of OPV

Author(s): Yash Paul

Vol. 30, No. 4 (2005-10 - 2005-12)

I seek comments from Dr. (Mrs.) Park, the learned author of Park's Textbook of Preventive and Social Medicine, regarding some of the properties or advantages of oral polio vaccine (OPV) as mentioned in the text book.

On page 164 of the eighteenth edition of the textbook it is stated: "The vaccine progeny is excreted in the faeces and secondary spread occurs to household contacts and susceptiable contacts in the community. Non-immunized persons may therefore, be immunized. Thus widespread 'herd immunity' results, even if only approximately 66 percent of the community is immunized."

Different studies from 1959 onwards had demonstrated that this herd effect was very low to be of any clinical value1. These include studies by Sabin2 and WHO3. The WHO study3 had stated: "These observations cast doubt on the importance of indirect spread of vaccine virus in raising overall levels of humoral immunity to poliovirus types 1 and 3, at least during the first 6 months of life,..........."

The herd immunity caused by OPV is not widespread but is negligible because of two reasons: (i) Attenuated polioviruses contained in OPV have markedly reduced infectivity, resulting in infrequent transmission from vaccinated children to contacts4, and low load of vaccine viruses spread through faces. There are about 10 lakh type 1 polioviruses, about 1 lakh type 2 polioviruses and about 6 lakh type 3 polioviruses i.e. about 17 lakh vaccine polioviruses in each does of two drops of OPV. On the other hand one gram of fecal matter contains about 100 polioviruses5, i.e. 17 Kg of fecal matter will provide same quantity of vaccine polioviruses as are contained in one does of OPV. It has been observed that in India many children have developed paralytic poliomyelitis even after taking ten or more doses of OPV. How much antibodies would be generted by few thousand vaccine polioviruses spread through faces when many doses of OPV, each does containing about 17 lakh vaccine polioviruses have failed to generate protective immunity?

Further it is stated in the textbook: "This property (herd immunity) of OPV has been exploited in controlling epidemics of polio by administering the vaccine simultaneously in a short period to all susceptibles in a community".

The study by Nightingale6 quoted in the textbook had stated: "The OPV was favoured because of its ease of administration (oral instead of injected), expected long lasting immunity, and the production of bowel immunity, which in turn would lead to interruption in the chain of transmission of wild viruses from population". The issue had been elaborated further by Melnick7, again quoted in the textbook: "Because the live vaccine viruses become established quickly in the alimentary tract of the vaccine recipient, they are capable of blocking infection with epidemic virus strain within a matter of days even before the vaccine-induced antibody becomes fully effective." This property of quick establishment in alimentary tract makes OPV superior to IPV during epidemics, and not the herd immunity caused by OPV.

It is further stated in the textbook: "This procedure virtually eliminates the wild polio strains in the community and replaces them by attenuated strains." The author (YP) failed to find any study or reference which supported the argument that vaccine polioviruses replace wild polioviruses. He raised the issue with the virologists, who opined : "It is primarily a question of which virus gets access to the host first. If the child is first exposed to the vaccine strains then the vaccine strain would cause gut immunity and systemic immunity against poliovirus, causing large proportion of the previolusly susceptiable population to be thus immune. It will break the natural cycle of transmission of wild poliovirus at a community level. In a given individual the vaccine virus, if given after the exposure to the wild virus, will not replace the former".8

Thus, repeated doses of OPV are given not to replace wild polioviruses, but to replace susceptible non-immune population with immune population, so that wild polioviruses may not find suitable host to replicate and this will eventually abolish the wild poliovirus circulation.9

References:

  1. Paul Y, Priya. Current Controversies in Immunization. In: Gupta S, (ed). Recent Advances in Pediatrics, Special Vol. 11, Community Pediatrics, New Delhi, Jaypee Brothers, 2002: 65-86.
  2. Sabin AB, Michales RH, Spigland I et al. Community wide use of oral poliovirus vaccine. Am J Dis Child 1961; 101: 546-567.
  3. World Health Organization Collaborative Study Group on real poliovirus vaccine. Factors affecting the immunogenicity of oral poliovirus vaccine. A Prospective Evaluation in Brazil and the Gambia. J Infect Dis 1995; 171: 1097-1106.
  4. John TJ. Immunization against polioviruses in developing countries. Rev Med Virol 1993; 3: 149-160.
  5. Onorato IM, Modlin JF, McBean AM, Thomas ML, Lossosky GA, Bewnier R. Mucosal Immnuity induced by enhanced potency IPV and OPV. J Infect Dis 1991; 163:1-6.
  6. Nightingale EO. Recommendations for a national policy on poliomyelitis vaccination. N Engl J Med 1977; 297: 249- 253.
  7. Melnick JL. Advantages and disadvantages of killed and live poliomyelitis vaccine. Bull WHO 1978; 56: 21-38.
  8. Paul Y, Sridharan G, Abraham P. How do the vaccine polio viruses replace the wild polio viruses? Indian J Med Microbiology 2002; 20 : 56.
  9. Paul Y. Are We Teaching Some Wrong Facts Pertaining to Oral Polio Vaccine? Indian J Pediatr 2002;69 : 1101-1102.

Yash Paul
A-D-7, Devi Marg, Bani Park. Jaipur-302016, India
[email protected]


COMMEMNTS OF THE REVIEWER

Author of this letter raised two important issues:

  1. Does the vaccine virus spread in the community to vaccinate the immediate contacts?
  2. Does the vaccine virus displace the wild virus strain in the human intestine?

OPV induces the intestinal immunity against the wild poliovirus infection, which explains its effectiveness in controlling wild virus circulation.

In addition OPV persists on the pharynx for 1-2 weeks and is excreted for several weeks or longer after administration. Consequently virus can be transmitted to contacts and results in their immunization1. That is why close contacts of the vaccinated child develop vaccine virus associated paralysis (rarely).

Is this spread in the community sufficient enough to immunize the close contacts?

There are two references supporting this view;

Oral polio vaccine is shed from the gut of an immunized individual, providing constant boosting to the community, whilst also preventing carriage of wild virus2.

Secondary spread of vaccine virus plays a modest role in increasing the polio immunity in inner city populations, especially against types 1 and 33.

However the exact quantification of OPV coverage (e.g. 64%) is not verifiable from any source. Out of three references quoted by the Dr. Park, only two could be obtained. This information was not available in those references.

In an individual the vaccine virus, after the exposure to the wild virus, will not replace the former. So pre-emptive intervention with the vaccine regularly in the community reducing the build up of susceptible indivudual (children) will eventually abolish the wild virus circulation as it appears that humans are only natural reservoirs of infection4.

Hence according to the available evidence OPV cannot displace the wild poliovirus from the gut.

References:

  1. Committee on Infectious diseases: Poliomyelitis prevention: Recommendations for the use of IPV and live OPV - American Academy of Pediatrics, American Pediatrics, 1997; 99: 300-305.
  2. Bedford H, Ellison D: Misconceptions about the new combination vaccine. Editorial BMJ; 329:411-412.
  3. Chen R T, Hausinger H, Dajani A S et al. Seroprevalence of antibody against polio virus in inner city preschool children. Implications for vaccination policy in the United States. National Immuzation programme, Centre for Disease Control and Prevention, Atlanta, GA 30333, USA.
  4. Sridharan G., Abraham P. In reply. Indian J Med Microbial 2002;20: 56.
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