Page 1302 - Veterinary Immunology, 10th Edition
P. 1302

their own antibodies and eventually become agammaglobulinemic.
  VetBooks.ir  Affected foals are therefore born healthy but begin to sicken by 2

               months of age. The precise time of onset depends on the quantity of
               colostral antibodies absorbed. All die by 4 to 6 months as a result of

               overwhelming infection. Severe bronchopneumonia is the
               predominant presenting sign. Organisms that have been implicated
               in this bronchopneumonia include equine adenovirus, Rhodococcus
               equi, and Pneumocystis (an opportunistic fungal pathogen). The

               disease is manifested by a nasal discharge, coughing, dyspnea,
               weight loss, and fevers. Affected foals may also develop enteritis,
               omphalophlebitis, and many other infections. Cryptosporidium
               parvum and many different bacteria have been implicated in the

               enteritis.
                  On necropsy, the spleens of these foals lack germinal centers and
               periarteriolar lymphoid sheaths. Their lymph nodes lack lymphoid
               follicles and germinal centers, and there are few cells in the

               paracortex. Their thymus may be difficult to find. Neutrophil,
               monocyte, and NK functions are normal.
                  SCID is an autosomal recessive disease, and its occurrence
               therefore indicates that both parents carry the mutation. Accurate

               diagnosis is of great importance since the presence of the mutation
               significantly reduces the value of the parent animals. Thus all
               suspected cases must be confirmed by postmortem examination.
               The clinical diagnosis of SCID requires that at least two of the

               following three criteria be established: (1) very low (consistently
                                     3
               below 1000/mm ) circulating lymphocytes; (2) histology typical of
               SCID; that is, gross hypoplasia of the primary and secondary
               lymphoid organs; and (3) an absence of IgM from presuckle serum.

               (The normal equine fetus synthesizes small amounts of IgM. As a
               result, IgM in normal newborn foals is about 160 µg/mL. If the foal
               successfully suckles, it will obtain immunoglobulins of all isotypes
               from the mare's colostrum. However, the half-life of IgM is only

               about 6 days, so maternal IgM will disappear within a few days of
               birth. Thus a normal foal will always have some IgM in its serum,
               but a SCID foal will have none.)


               Pathogenesis


               When B and T cell antigen receptors are produced, large segments




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