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Summaryobjective To examine the long-term effects of neonatal hypothermia (HT) on survival. methods Using the longitudinal community and hospital surveillance system of the Bandim Health Project, we followed children born between 1997 and 2002 at the only maternity ward in the city. All children's axillary temperature was measured within 12 h of birth. They were followed from birth to 6 months of life through regular home visits.results We identified 2926 live births in the study area and 177 deaths before 6 months of age. Based on mortality risk, we defined a temperature below 34.5°C as the cut-off point for HT. Two hundred and thirty-eight (8%) children had HT. Controlled for birth weight, HT was associated with a nearly fivefold increase in mortality during the first 7 days of life [mortality ratio (MR) = 4.81 (2.90-8.00)] and with increased mortality from 8 to 56 days of life [MR = 2.55 (1.29-5.04)].conclusion HT is associated with excess mortality beyond the perinatal period up to at least 2 months of age, especially among low-birth-weight children. Hence, failure to comply with the WHO guidelines for care of newborns in low-income countries may have long-term consequences for child survival which have not previously been assessed. The WHO definition of HT should be based on mortality data.

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Partial defects in interferon (IFN)-γ signaling lead to susceptibility to infections with nontuberculous mycobacteria. The receptors for IFN-α and IFN-γ activate components of the Janus kinase-signal transducer and activator of transcription (STAT) signaling pathway. Some defects in STAT1 mainly affect IFN-γ signaling, thus resulting in mendelian susceptibility to mycobacterial disease (MSMD). MSMD is a severe disease but patients show a favorable response to anti-mycobacterial chemotherapy. Other defects in STAT1 affect both IFN-α and IFN-γ signaling resulting in mycobacterial and lethal viral disease. We report here a patient with two novel STAT1 alleles, which in combination results in a recessive trait with partial STAT1 deficiency and mycobacterial disease. Cells from the patient did respond to mycobacterial antigen, but both the expression of STAT1 and phosphorylation of STAT1 in response to IFN-γ treatment were reduced. This is the first report of a mutation in the N-terminal part of STAT1 involved in causing mycobacterial disease.