Clinical presentation and outcome

The reported symptoms of avian influenza in children have ranged from typical influenza-like symptoms (e.g., fever, cough, sore throat, and muscle aches) to eye infections (conjunctivitis), pneumonia, acute respiratory distress, viral pneumonia, and other severe and life-threatening complications (Tab. 2). The majority of children have presented with fever and respiratory symptoms, although in the Vietnam cases, diarrhea was prominent. Notably,

Table 2. Clinical features of H5N1 avian influenza in children

Reference

[36]

[42]

[41, 43]

Number of patients

7

7

9

Male (%)

57

43

56

Previously healthy (%)

71

100

87

Fever (%)

100

100

100

Cough (%)

43

100

90

Rhinorrhea (%)

71

35

Dyspnea (%)

100

69

GI symptoms (%)

29

57

25

Pneumonia (%)

29

100

100

Ventilated (%)

29

86

100

Mortality (%)

29

86

*Not reported.

a number of pediatric cases have presented without any respiratory symptoms but with severe gastrointestinal (GI) or neurological symptoms. A key historical element of virtually all cases is a recent exposure to domestic or wild birds. A high index of suspicion is necessary to consider the diagnosis. In most cases, the onset of symptoms occurs within 1 week of the bird exposure. The median duration of symptoms prior to hospitalization was 4 days (range 0-18 days).

Prominent laboratory findings include leukopenia (especially lymphopenia), thrombocytopenia and elevated liver transaminases (Tab. 3). Most pediatric patients do not manifest hemoconcentration; this finding and the prominent respiratory symptoms help distinguish the illness from dengue virus infection in dengue-endemic areas. Renal failure, hyperglycemia and hemophagocytosis have been noted in some patients. Most have abnormal chest radiographs at presentation. Many patients develop complications such as respiratory failure requiring assisted ventilation, ARDS, shock and multiorgan system dysfunction. Severe infections have typically progressed rapidly, with a median duration of symptoms prior to death of 9 days (range 2-31 days). The proximate cause of death is usually respiratory failure.

The overall mortality in the cumulative human H5N1 cases reported to date is 59% (Tab. 1). However, the highest mortality rates occurred in patients age 10-19 (73%, n = 49), 20-29 (65%, n = 45), 30-39 (61%, n = 33) and 40-49 years (45%, n = 11). Very high mortality rates were also observed in children < 5 years (43%, n = 21) and 5-9 years (41%, n = 32). The lowest rates were in the patients older than 50 (18%, n = 11) [45]. This distribution

Table 3. Laboratory and radiological findings of H5N1 avian influenza in children

Reference

[36]

[42]

[41, 43]

Leukopenia (%)

29

100

100

Thrombocytopenia (%)

29

86

44

Elevated transaminases (%)

43

80*

71

Radiographic infiltrates (%)

29

100

100

transaminases not reported for two patients.

transaminases not reported for two patients.

is reminiscent of the mortality associated with the highly virulent 1918 pandemic virus and, again, is quite unlike the mortality curve associated with seasonal influenza. Pediatric mortality in cases reported outside of Thailand and Vietnam vary widely (Tab. 4).

Autopsy examination reveals severe lung pathology, including necrotiz-ing diffuse alveolar damage with patchy and interstitial paucicellular fibro-sis [46, 47]. H5N1 has been detected in lung tissue by RT-PCR up to day 17 of illness. H5N1 has been isolated in respiratory specimens, blood, GI tract, and cerebrospinal fluid. However, it is not clear whether viral replication and direct cytopathology occurs in tissues outside of the respiratory tract, or whether the major systemic effects are due to cytokine responses. Virus replication was not detected outside of the lungs and tonsils during experimental infection of macaques [48]. However, the same investigators recently reported that experimental H5N1 infection of cats led to virus replication in multiple extra-respiratory tissues, including brain, liver, kidney, heart and GI tract [28]. Further studies in humans are needed to further elucidate the mechanisms of H5N1 pathogenesis.

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