Hypogammaglobulinemia and Thymic Hypoplasia in Horses: a Primary Combined Immunodeficiency Disorder

McGuire, Travis C.; Poppie, Marinel J.

doi:10.1128/iai.8.2.272-277.1973

Cited by 90 publications

(19 citation statements)

References 22 publications

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“…EIAV offers unique opportunity to compare lentivirus infection in immunologically normal and immunodeficient hosts. Horses with combined immunodeficiency (CID) lack functional B and T lymphocytes and cannot manifest antigen-specific immune responses (12,17,18,27). Infection of foals with CID with cloned pathogenic variants of EIAV allows evaluation of the role of specific immune responses in control of viral replication, selection of antigenic variants, and contribution to tissue injury.…”

mentioning

confidence: 99%

Immune responses are required to terminate viremia in equine infectious anemia lentivirus infection

Perryman

O’Rourke

McGuire

1988

J Virol

112

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Six normal and four immunodeficient horses were injected with a cloned variant of equine infectious anemia virus (EIAV). The six normal horses had detectable EIAV in their plasma by 7 days postinjection. During their primary viremic episode, which was accompanied by fever and anemia, maximum titers of EIAV in plasma ranged from 103.8 to 10-48 50% tissue culture infective doses per ml. All six normal horses cleared detectable virus from their plasma by 21 to 35 days after injection. Horses with combined immunodeficiency became viremic by 9 days postinjection and also developed anemia. In contrast to normal horses, foals with combined immunodeficiency did not eliminate the virus from their plasma.

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mentioning

confidence: 99%

Immune responses are required to terminate viremia in equine infectious anemia lentivirus infection

Perryman

O’Rourke

McGuire

1988

J Virol

112

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“…Previously, McGuire et al (7)(8)(9) described the combined immunodeficiency in foals characterized by an absence of T and B lymphocytes with a resultant lack of cell-mediated immunity and antibody production. The data of this study may suggest a complexity of immunological deficiencies in horses with chronic diarrhea characterized by hypoagammaglobulinemia A, decrease in cell-mediated immunity, and reduction in inflammatory responsiveness.…”

Section: Discussionmentioning

confidence: 99%

Serum immunoglobulin, dermal response, and lymphocyte transformation studies in horses with chronic diarrhea

Targowski¹

1975

Infect Immun

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Serum specimens from 12 sick and 20 normal horses were examined for levels of different classes of immunoglobulin (Ig) by a single radial immunodiffusion. The level of IgA in the sera of sick horses was about 50% lower than in the sera of normal horses. By contrast, the level of serum IgG was higher in sick than in normal horses. Phytohemagglutinin (PHA) responsiveness of blood lymphocytes showed transient suppression during the stage of severe diarrhea. The regaining of PHA responsiveness of lymphocytes was observed simultaneously with the recovery process. However, the responsiveness of lymphocytes in recovered horses was still markedly lower than in normal horses. Allergic reactions in sick and normal horses were studied by observing dermal response to the injections of saline extracts from some of the horse feeds. A delayed hypersensitivity reaction to streptokinase-streptodornase and PHA was also studied. The allergic reactions to these extracts were not induced in either sick or normal horses; however, inflammatory response to the extracts was about 50% greater in normal than sick horses. Response to the intradermal injection, either streptokinase-streptodornase or PHA, was significantly greater in normal horses than sick horses. These findings are discussed with respect to the pathogenesis of chronic diarrhea and the complexity of immunodeficiency demonstrated in this disease. The possibility that transient defects of cell-mediated immunity may predispose to chronic diarrhea is proposed.

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“…CID in young horses is similar to severe CID of children (9)(10)(11). Affected foals have lymphopenia, absence of serum immunoglobulin M, decrease of B lymphocytes, absence of specific antibody response to challenge, decreased lymphocyte proliferation to phytolectins, absence of organized lymphoid structures in the spleen and lymph nodes, and thymic hypoplasia.…”

mentioning

confidence: 80%

Evaluation of adenosine deaminase and other purine salvage pathway enzymes in horses with combined immunodeficiency

McGuire¹,

Pollara²,

Moore³

et al. 1976

Infect Immun

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Foals with combined immunodeficiency had normal levels of purine salvage pathway enzymes, including adenosine deaminase, nucleoside phosphorylase, and xanthine oxidase.Functional studies of primary immunodeficiency disorders have increased our understanding of these conditions, but have not provided a molecular basis for the disorders. In one syndrome, severe combined immunodeficiency (CID), approximately half of the children examined lacked adenosine deaminase (ADA), which converts adenosine to inosine in a purine salvage pathway (reviewed in references 12 and 14). Most CID children with ADA deficiency had an autosomal recessive mode of inheritance, whereas normal ADA levels were associated with sex-linked CID (3,5,6,(12)(13)(14)(15).CID in young horses is similar to severe CID of children (9-11). Affected foals have lymphopenia, absence of serum immunoglobulin M, decrease of B lymphocytes, absence of specific antibody response to challenge, decreased lymphocyte proliferation to phytolectins, absence of organized lymphoid structures in the spleen and lymph nodes, and thymic hypoplasia. Af-fected foals die before 4 to 5 months of age from a variety of infectious diseases, notably, though not exclusively, adenoviral and Pneumocystis carinii pneumonias. The defect occurs in Arabian and part-Arabian foals and appears to be inherited as an autosomal recessive trait. We felt it was important to determine whether ADA deficiency or deficiency of other enzymes (nucleoside phosphorylase [NPI or xanthine oxidase [XO]) of the same purine salvage pathway was associated with CID in foals.Tissue (4), erythrocyte, lymphocyte (2), and platelet preparations were prepared from five CID foals (four males and one female) and five normal foals. Lymphocyte counts in the five CID foals ranged from 76 to 580/m3, whereas the normal range was 1,150 to 8,570/mm'. ADA was measured by adenosine conversion to inosine by recording the decrease in optical density at 265 nm (8). Another ADA assay was a coupled reaction requiring the addition of 70 ,ug of TABLE 1. Amounts of ADA in tissues from normal and CID foals CID Normal Tissue No. exam-M No. examined Mean Range ined Mean Range Lymph node 5 93" 43-153

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Hypogammaglobulinemia and Thymic Hypoplasia in Horses: a Primary Combined Immunodeficiency Disorder

Cited by 90 publications

References 22 publications

Immune responses are required to terminate viremia in equine infectious anemia lentivirus infection

Immune responses are required to terminate viremia in equine infectious anemia lentivirus infection

Serum immunoglobulin, dermal response, and lymphocyte transformation studies in horses with chronic diarrhea

Evaluation of adenosine deaminase and other purine salvage pathway enzymes in horses with combined immunodeficiency

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