Research Paper on:
An Examination of Selective Immunoglobulin Isotype Deficiencies and Agammaglobulinaemia

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to the viruses and bacteria of the toddlers expanding world, and when are they indicative of conditions that could be life threatening? By far, most are of the immunity-building  variety, but there are those that can be symptomatic of a far more serious condition. Agammaglobulinaemia is an X-linked immunodeficiency in which mature  B lymphocyte cells fail to develop and Ig heavy chain rearrangement fails to progress as it should (Anonymous, 2000). This immunodeficiency was the first to be specifically identified as  having a genetic origin. Bruton first described the immunodeficiency in 1952 (McKusick and Smith, 2000), and the origin of the defect is named for him. It resides in  Bruton tyrosine kinase (BTK), which Rawlings and Witte found in 1994 to be a key regulator in B-cell development (McKusick and Smith, 2000).  Clinical Features McKusick and Smith (2000) report that those with X-linked agammaglobulinaemia (XLA) are highly susceptible to bacterial infections, but that they  develop viral infections at the same rate as other segments of the population. Many will develop symptoms like those of rheumatoid arthritis. In the days before effective antibiotics  were widely available, many children affected with XLA did not live through their first decade. The less common alymphocytotic type XLA is more "virulent than the Bruton form, leading  to death in the first 18 months after birth from severe thrush, chronic diarrhea, and recurrent pulmonary infections" (McKusick and Smith, 2000; p. 300300).  Diseases other than those caused by bacteria have been attributed to XLA in the past decade. Van der Meer, Weening, Schellekens, van Munster and Nagengast (1993) found XLA