Epidemiology and clinical features of avian influenza in children

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Avian influenza viruses have caused a spectrum of disease in humans, including typical influenza-like illness, conjunctivitis and severe respiratory disease. More recent outbreaks, and the H5N1 virus in particular, have been more severe and more frequently associated with fatal illness. In general, avian influenza virus infections in children have been no less severe than in adults.

Mild respiratory disease was reported in 2 Dutch children due to reassortant human-avian influenza viruses in 1994 [6]. In 1997, a 3-year-old boy in Hong Kong died of acute respiratory failure and multiorgan system dysfunction due to an H5 influenza strain. Genomic sequencing and analysis of the virus showed that it was an H5N1 avian strain [36]. During that outbreak, 5 other children under the age of 18 were infected. A 13-year-old girl died of acute respiratory failure and multiorgan system dysfunction, a 2-year-old boy was hospitalized for 3 days with pneumonia and 3 other children experienced uneventful upper respiratory infection. The children who died were previously healthy. A total of 12 cases were reported, with more severe disease and higher fatality rate in the adults [37].

Outbreaks of avian influenza have continued since 1997, and have spread to broader geographic areas, particularly H5N1. There were 2 confirmed and 1 probable H5N1 cases in Hong Kong in February of 2003 [38]. A 33-year-old man developed fatal progressive respiratory failure and his 8-year-old son recovered from respiratory disease after a prolonged hospi-talization. Both had profound lymphopenia, hypoxia and consolidation of chest radiographs. The family also had a 7-year-old daughter who had died of a febrile pneumonia 1 week prior to the father and brother's illnesses, but she had not been tested for influenza.

Two cases of H9N2 avian influenza infection of humans occurred in Hong Kong, one a child, with typical influenza symptoms of fever, rhinor-rhea and cough [39]. Both patients fully recovered. There was also a large outbreak of H7N7 in the Netherlands in 2003 on poultry farms, with infection of both pigs and humans [40]. There were a total of 89 human cases, primarily among poultry workers. Most of the illnesses were conjunctivitis, with only a few typical influenza-like illnesses. There was one fatality, a veterinarian who visited one of the farms and developed acute respiratory distress syndrome (ARDS). Most of the cases were attributed to direct contact with infected poultry, although there were three possible instances of person-to-person transmission.

During 2003 and 2004, there were 34 cases of confirmed human H5N1 infection in Thailand and Vietnam [41-43]. Seven of the 12 laboratory-confirmed cases in Thailand were boys age 2-13, all of whom presented with fever, cough and tachypnea. Lymphopenia and elevated transaminases were noted in most. All 7 boys had abnormalities on chest radiograph consisting of focal or multifocal consolidation, and all required mechanical ventilation. Five of these 7 children died, and overall mortality in the Thailand outbreak was 8/12 (67%). In January 2004, 10 human H5N1 infections were reported in Vietnam. Seven patients were less than 18 years old, with a mean age of 12 and the youngest 5 years. All patients presented with fever, tachypnea, cough, and hypoxia. Five also had diarrhea, but none of the children had myalgia, rash or conjunctivitis. Similar to the Thailand cases, the most common laboratory abnormalities noted were lymphopenia, thrombocytopenia and elevated transaminases. All had extensive consolidations on chest radiographs, which progressed despite aggressive therapy. All developed respiratory failure requiring mechanical ventilation, and 7/8 children died, despite aggressive supportive care and treatment with oseltamivir, ribavirin and/or steroids for ARDS.

Two other children were identified with probable or confirmed H5N1 infection during the same outbreak [44]. A 9-year-old girl presented with fever, watery diarrhea, shock and lethargy. Initial laboratory tests including cerebrospinal fluid were normal. She had fulminant shock, became comatose and died within 24 hours. No influenza tests were performed. However, 8 days later, her 4-year-old brother presented with fever, headache, vomiting and profound watery diarrhea. His initial laboratory values were remarkable only for elevated transaminases. However, he developed pneumonia and lethargy, progressing to coma, and died of respiratory failure 5 days after admission. During his hospitalization, he developed lym-phopenia, thrombocytopenia, and bilateral infiltrates on chest radiograph. Cerebrospinal fluid was remarkable only for elevated protein. He was diagnosed with unexplained encephalitis, but postmortem testing detected H5N1 influenza by RT-PCR in cerebrospinal fluid, serum, throat and rectal swabs, and culture of cerebrospinal fluid grew H5N1 influenza virus. Thus, it is highly likely that his sister had been infected with H5N1. Notably, neither child initially presented with respiratory symptoms and the sister never had respiratory disease. Both had had frequent exposure to ducks and chickens at home and there were no other cases in the family.

As of April 30, 2006, a total of 205 cases of human H5N1 infection had been reported to the WHO [45]. One-half of these occurred in patients less than 20 years old, with a range from 3 months to 72 years. Twenty-one cases (10%) were in children < 5 years, 32 (16%) were in children from 5 to 9 years, and 49 (24%) were in 10-19-year olds. There was a male predominance in the younger cases, with a male:female ratio of 1.5 in the 53 cases < 10 years old. The sex ratio was equal in all other age groups. It is not known whether this finding reflects gender-specific epidemiological risk factors or biological differences.

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