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Ann Saudi Med 31(2) March-April 2011 www.saudiannals.net 203 tially restored immune function to explore the extent of immune dysfunction rather than to confirm the diagnosis.1,2 • Although the immunological phenotype is obscure because of the maternal engraftment, the best could be described is T + (? maternal origin, B+, and NK low, which was clearly mentioned in the paper. Unlike the international data, the far most common phenotype is T-, BNK+;3 probably due to the high prevalence of consanguinity in our population with predominance of AR-SCID.4 The possible involved genes in this phenotype have been tested which were negative. • The patient reported here was being investigated further to delineate the underlying genetic defect. Although the patient did not manifest any manifestation of radiosensitivity, the suggested tests will be considered; along with the exploration of other genes that might be involved including common gamma chain (gc) defect. • The hyper IgM studies were performed on the basis of clinical presentation (recurrent chest infection, and confirmation of Pneumocystis jiroveci pneumonia (PJP) infection), normal IgM (0.54) and low IgG (2.34), which was suspected at the initial presentation. However, with a high IgE level indicating intact immunoglobulin class-isotype switch, highlighting the better terminology of this disease as (B-cell intrinsic immunoglobulin class switch recombination)5 will rule out the possibility of hyper IgM syndrome as clearly stated in the paper. In addition, the documentation of maternal T cells indicates a genuine T cell defect as SCID. Saleh Z. AL-Muhsen Department of Pediatrics, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia almuhsen@ksu.edu.sa

Re-infection of typhoid fever and typhoid vaccine (comment on “An imported enteric fever caused by a quinolone-resistantSalmonella typhi”)