Vaccine-derived polioviruses found in immunodeficient Iranian children

Vaccine-derived poliovirus type 2 was detected in five of six documented cases of immunodeficiency-associated vaccine-derived polioviruses in Iran from 1995 to 2008 — indicating a global need to change to an inactivated polio vaccine schedule.

Researchers from several institutions in Iran reviewed these cases to define the prevalence of vaccine-associated paralytic poliomyelitis. They also aimed to determine whether changing to an inactivated polio vaccine schedule and screening neonates for immunodeficiencies could reduce the risk for infection.

The first patient was a 17-month-old girl who acquired the infection in 1995. She was administered the inactivated polio vaccine due to a known antibody deficiency. She also had a healthy sibling who was administered the oral polio vaccine. Fecal samples indicated vaccine-derived poliovirus type 2. Recombination with the Sabin 1 strain was detected, with a crossover site at nt 5355, according to the results.

The second case occurred in a 7-month-old boy in 2005. He had been administered the oral polio vaccine at birth and at 2, 4 and 6 months. His fecal samples also indicated vaccine-derived poliovirus type 2 and recombination with the Sabin 1 strain with a crossover site at nt 5358. He did not have HIV, but the expression of human leukocyte antigen DR on his lymphocytes was low, indicating major histocompatibility complex class II deficiency.

The third patient was a boy who had a variety of health concerns in early 2006 at age 2 months. He was eventually admitted to a hospital with paralytic complications in October 2006. He was also administered the oral polio vaccine at birth and at 2, 4 and 6 months. A number of immunodeficiencies were observed, including decreased CD3+, CD4+ and CD8+ cell counts. Vaccine-derived poliovirus type 2 was detected and he was ultimately diagnosed with severe combined immunodeficiency caused by RAG2 mutation.

The fourth patient was a 15-month-old boy given the oral polio vaccine at birth and at 2, 4 and 6 months. Vaccine-derived poliovirus type 3 was isolated from his feces. Recombination with the Sabin 1 strain was detected at the 3Dpol region of the genome.

The fifth patient was a girl born in September 2006. She was given the oral polio vaccine at birth and at 2 months. In February 2007, she was admitted to a hospital with pneumonia and paraparesis, at which point fecal specimen results indicated the presence of vaccine-derived poliovirus types 1 and 2. She was diagnosed with B cell–negative T cell–negative severe combined immunodeficiency.

The final patient was a boy who developed paralysis at 7 months old. An initial fecal specimen indicated the presence of the Sabin 2 strain. After hospitalization for several complications, he was diagnosed with X-linked agammaglobulinemia. Subsequent fecal samples were positive for vaccine-derived poliovirus type 2. Treatment with IV immunoglobulin substitution at 600 mg/kg every four weeks was ongoing. Follow-up fecal samples became negative for polioviruses and his immunodeficiency was under control. Residual paralysis of the right leg remained. He was the only patient who survived.

The median interval between administration of the last oral vaccine dose and onset of vaccine-associated paralytic poliomyelitis was 3.1 months. Immune deficiency was diagnosed after onset of vaccine-associated paralytic poliomyelitis in five of the studied patients.

Along with switching to an inactivated polio vaccine schedule, the researchers also recommended screening children for immunodeficiencies.

“Introduction of neonatal screening programs for some immunodeficiencies such as severe combined immunodeficiency could help prevent inadvertent exposure of such patients to oral polio vaccine,” the researchers wrote.

Shahmahmoodi S. Emerg Infect Dis. 2010;16:DOI: 10.3201/eid1607.091606.