The report on rabies developing in a child even after immunoprophylaxis has some lessons to teach us(1). Post-exposure prophylaxis consists of wound treatment and immunoprophylaxis. In this child the wound should have been flushed with soap and water immediately after the bite. By taking the child to the dispensary first aid was delayed, but even then soap and water flushing should have preceded providone iodine application. Soap disrupts rabies virus particles instantaneously by dissolving the lipid coat, rendering them non-infectious. Water disperses soap into the wound and also mechanically removes un-adsorbed virus particles. Since soap and water are available in every household, there should be no delay in washing after animal bite. There is actually no need of chemical treatment (which require longer contact time to kill virus) after flushing with water and soap.

Viruses deposited in the wound get adsorbed on to local fibroblastic cells within a short period. Soap prevents virus adsorption or kills even adsorbed virus before cell entry. If first aid was delayed or unsuccessful, then virus enters and multiplies in the cells, and huge numbers are released into the surrounding tissue. Eventually viruses meet with nerve endings and enter nerve cells.

Each cell cycle of multiplication takes several hours. Passive immunization provides immediate antibody-block to virus entry in fibroblasts, either in the first cycle itself or in subsequent cycles. Thus, virus entry into nerve endings is prevented, especially by the locally injected immunoglobulin. Antibodies in body fluids (from intramuscular injection) keep up this block. Active immunization ensures sustained high antibody levels.

When the bite is at a site with sparse nerve endings (e.g., the leg), there is a window period (of up to a few days) between the bite and virus entry into nerve endings. Only in such cases may active immunization alone suffice. In the recommended vaccination schedule, antibody production would commence after the second dose, and will be detectable by laboratory testing by day 7 (always before day 10). However, if the biting animal was rabid, passive immunization must be given irrespective of the site of bite.

The window period is too short in case of bite on sites with high density of nerve endings (e.g., face, hand, genitalia), as in the reported child. Here, viruses may come directly into contact with nerve endings. Any delay, even of minutes, could make the difference between life and death. In general, immune protection will not help once rabies virus has entered the nerve cell. In the reported case there was deficiency in first aid and delay in passive immunization (of 6 hours). The fact that rabies developed after a short incubation period (of 17 days) shows not only that virus travel to the brain was quick, but also that virus entered nerve endings early. Thus the case was not one of ‘therapeutic failure’ of ‘appropriate’ post-exposure prophylaxis, but one of delay in starting the prophylaxis. The delay was not on the part of the investigators, but of the parents. Rabid animal bite must be treated as medical emergency in which every minute of delay increases the risk to life.

T. Jacob John,
439 Civil Supplies Godown Lane,
Kamalakshipuram,
Vellore, TN, 632 002,
India.

1. John BM, Patnaik SK. Fatal rabies despite appropriate post-exposure prophylaxis. Indian Pediatr 2005; 42: 839-840.