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Lethal toxic encephalopathy due to childhood shigellosis in a developed country
A Goren1, S Freier, J H Passwell
1Department of Pediatrics, Sheba Medical Center, Tel-Aviv, Israel.
Insights
Pediatric deaths from shigellosis in developed countries are rare but can occur. Toxic encephalopathy is the primary cause of death, often presenting with severe headache.
Area of Science:
- Pediatric Infectious Diseases
- Neurology
- Public Health
Background:
- Shigellosis causes significant illness globally, but mortality is uncommon in developed nations.
- This study investigates pediatric fatalities attributed to shigellosis in Israel over a decade.
Purpose of the Study:
- To analyze the clinical characteristics and causes of death in children who died from shigellosis in Israel.
- To identify risk factors and distinguishing features of fatal shigellosis cases.
Main Methods:
- Retrospective review of all pediatric deaths (n=15) linked to shigellosis in Israel over 10 years.
- Case-control study comparing deceased patients with surviving hospitalized shigellosis patients.
- Analysis of clinical signs, symptoms, laboratory data, and Shigella species.
Main Results:
- Toxic encephalopathy was the cause of death in 12 of 15 pediatric cases.
- Headache was significantly more prevalent in patients who died compared to controls (P < .01).
- Hyponatremia was more frequent in the fatal cases, with no other significant hematological or biochemical differences noted.
Conclusions:
- Mortality from shigellosis in developed countries is primarily due to toxic encephalopathy.
- Severe headache and hyponatremia may indicate a higher risk of fatal outcome in pediatric shigellosis.
- Prompt recognition and management of toxic encephalopathy are crucial in severe shigellosis cases.
Abstract:
Shigellosis results in considerable morbidity in endemic areas, but mortality is rare in developed countries. All pediatric deaths (n = 15) in Israel following shigellosis in the past 10 years were reviewed. The patients' ages ranged from 5 months to 11 years; there were eight boys and seven girls. Three were institutionalized mentally retarded patients, 11 were healthy children. Twelve had definite clinical signs of brain death within 48 hours of onset of disease. Cause of death in all patients was consistent with toxic encephalopathy. No other systemic complication was implicated as the cause of death except for one case consistent with a "Reye-like" syndrome. Shigella species were as follows: 8 flexneri, 4 sonnei, 1 dysenteriae, and 2 were not identified. Case-control study of these patients vs surviving, hospitalized patients with shigellosis showed similar severity of fever, diarrhea, vomiting, and dehydration and similar incidence of convulsions. Headache was a prominent feature of patients who died; 5 of 7 verbal patients complained of this symptom as opposed to 2 of 20 in the control group (P less than .01). There were no significant differences in the hematological and biochemical profile (except for an increased incidence of hyponatremia in the study group), pattern of shigella species, or antibiotic sensitivity. These findings indicate that mortality from shigellosis in a developed country is due primarily to the toxic encephalopathy syndrome.