Page 1305 - Veterinary Immunology, 10th Edition

showing normal responses to T cell mitogens and an absence of B
VetBooks.ir cells.

Selective IgM deficiencies have been described in foals. Serum
IgM levels in these animals are at least two standard deviations

below normal, but IgG and IgA levels and B cell numbers are
normal. In most cases, foals develop septicemia or recurrent
respiratory tract infections, often involving Klebsiella pneumoniae or
R. equi, and die by 10 months. Some affected foals live longer and

respond to therapy but fail to grow, have recurrent respiratory
infections, and usually die by 24 months. Most affected foals have
been Arabians or Quarter Horses, suggesting that the disease has a
genetic basis. IgM deficiency has also been described in adult

horses over 2 years of age. In many cases, such horses also have a
lymphoreticular neoplasm.
A single case of IgG deficiency has been described in a 3-month-
old foal with salmonellosis. The animal had normal IgA and IgM

but no germinal centers, lymphoid follicles, splenic follicles, or
periarteriolar lymphoid sheaths. Serum IgG was extremely low.
Between 2 and 3 months of age, some foals experience a transient
hypogammaglobulinemia as a result of a delayed onset of

immunoglobulin synthesis. These animals may have recurrent
infections during the period when their immunoglobulin levels are
low. Lymphocyte numbers and responsiveness remain normal at
this time.

Common Variable Immunodeficiency

Common variable immunodeficiency is the second most common
primary immunodeficiency syndrome in humans (after selective
IgA deficiency). It is a heterogeneous group of sporadic diseases all

characterized by a late-onset B cell lymphopenia as a result of
impaired B cell production in the bone marrow. It occurs in horses
where four genes, E2A, PAX5, CD19, and IGD, have significantly

reduced expression. Immunohistochemistry has confirmed the
absence of PAX5 in the bone marrow of these horses. PAX5 and the
other molecules are known to be transcription factors that regulate
the early differentiation of B cells. Their B cell development seems
to be blocked at the transition to pro-B cells. Mutations in genes

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