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Transient hypogammaglobulinaemia of infancy (THI) is characterised by prolongation of the physiological decline in serum immunoglobulin concentrations seen in the first six months of life.1 The incidence reported from an Australian paediatric centre was estimated as 23 per 106 live births.2 It has been reported that THI does not usually predispose to significant infection.1,2
A male infant born at term to non-consanguinous parents presented at 3.5 months with cough, tachypnoea (70 breaths/minute), wheeze, crepitations, and hypoxia. A chest radiograph showed hyperinflation and patchy opacification in the hilar regions and upper lobes. Pneumocystis carinii was identified in brochoalveolar lavage by toluidine blue staining. The immunological findings of this child were consistent with those of THI with an IgG level less than the fifth centile2 and absent serum IgA1,2 which resolved with age (IgG at presentation 3.9 g/l (normal: 1.39–8.04); at 5 months 2.23 (1.39–8.04); at 10 months 1.77 (2.02–11.76); at 17 months 7.51 (2.71–13.78); IgA at 5 months <0.07 g/l (normal: 0.14–0.69); at 13 months 0.14 (0.17–1.34)) and evidence of specific antibody production to tetanus, diphtheria, and Haemophilus influenza type b following immunisation.1 T cell numbers (total lymphocytes 6.2 × 109/l, CD3 68%, CD4 56%, CD8 15%) and phytohaemagglutinin induced proliferation were normal. At 3 years the child was well with normal IgG, IgA, and IgM levels.
Pneumocystis carinii pneumonia presenting in the first three months of life is an infection typically seen in patients with significant T cell immunodeficiencies and X linked hyper IgM. These were excluded by normal T cell numbers and function and by normal CD40 ligand expression and mutation analysis. There are reports of Pneumocystis carinii pneumonia in immunocompetent infants3 and agammaglobulinaemia.4 This is the first description of Pneumocystis carinii pneumonia in a patient with THI.
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