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Outbreak of aplastic crises in sickle cell anaemia associated with parvovirus-like agent
Insights
A parvovirus-like agent is likely the primary cause of aplastic crisis in children with sickle cell anaemia (SCA). This study found strong evidence of this virus in Jamaican children experiencing this severe complication.
Area of Science:
- Virology
- Hematology
- Pediatrics
Background:
- Sickle cell anaemia (SCA) is a genetic blood disorder associated with serious complications.
- Aplastic crisis, a sudden drop in blood cell production, is a known complication in SCA patients, particularly children.
- Previous outbreaks of aplastic crisis in Jamaican children with SCA have been documented since 1952.
Purpose of the Study:
- To investigate the potential viral etiology of aplastic crisis in children with sickle cell anaemia (SCA).
- To identify specific viral agents associated with aplastic crisis outbreaks in Jamaica.
Main Methods:
- Serum specimens from 28 children experiencing aplastic crisis during a 1979-80 outbreak were analyzed.
- Tests for viral antigen and antibody were performed to detect evidence of infection.
- Control groups with SCA (SS genotype) and normal hemoglobin (AA genotype) were included for comparison.
Main Results:
- Evidence of parvovirus-like agent infection was found in 24 out of 28 patients with aplastic crisis.
- Viral antigen was detected in 2 patients, with seroconversion observed.
- Significantly higher antibody prevalence was noted in patients with aplastic crisis compared to controls.
Conclusions:
- The findings strongly support the hypothesis that a parvovirus-like agent is the principal cause of aplastic crisis in sickle cell anaemia.
- This viral infection represents a significant trigger for aplastic crisis in this vulnerable pediatric population.
Abstract:
Since 1952, 112 children with sickle cell anaemia (SCA) in Jamaica have had an aplastic crisis. Outbreaks occurred in 1956, 1960, 1065-67, 1971-73, and 1979-80. Most cases occurred in children under 10 years of age, and an aplastic crisis in a patient over the age of 15 years is rare. There were 38 cases in 1979-80 and stored serum specimens from 28 of these were available for virus studies. Evidence for infection with a parvovirus-like agent was found in 24 of these 28 cases. Viral antigen was detected in 2 patients, both of whom demonstrated seroconversion. Seroconversion during 1980 was detected in a further 7, increasing amounts of antibody during the convalescent period were found in 5, antibody was found in 2 of 4 patients from whom only an acute phase specimen was available and the remaining 10 were antibody positive in the only convalescent phase sample available for testing. Antibody was found in 4 of 94 controls with the SS genotype (in retrospect 2 of these may have had an aplastic crisis) and in 17% of 48 controls with a normal haemoglobin (AA) genotype. The results accord with the possibility that the parvovirus-like agent is the principal cause of aplastic crisis in SCA.