Immunodeficiencies

Transient hypogammaglobulinaemia of the young in a Thoroughbred yearling

“…Documented humoral immunodeficiencies in horses, independent of the breed, include failure of passive transfer in neonates, agammaglobulinaemia, common variable immunodeficiency (CVID) and potentially selective IgM deficiency (Felippe, 2016; Riggs, 1987). In these disorders, inadequate serum IgG concentrations, with or without concurrent inadequate IgM concentrations, result in impaired host immune defence mechanisms, including antigen neutralisation and opsonisation, and complement activation, with resultant increased susceptibility to infections and potential septicaemia (Crisman & Scarratt, 2008; Felippe, 2016; Gardner et al., 2007). Transient peripheral blood CD4 T cell lymphopenia may accompany the hypogammaglobulinaemia in some cases, which may also affect cellular immune function (Felippe, 2019).…”

“…Transient hypogammaglobulinaemia of the young is a primary humoral immunodeficiency described in developing humans and animals (Felippe, 2018). Humoral immunodeficiencies are the most frequently diagnosed immunodeficiencies in mammals, and result from impaired antibody production due to intrinsic B cell failure to develop or differentiate into antibody‐secreting plasma cells, or impaired T cell help for B cell activation and differentiation in lymphoid tissues; in any of these conditions, the ultimate result is hypo‐ or agammaglobulinaemia, and increased susceptibility to infections with opportunistic pathogens, particularly encapsulated bacteria (Felippe, 2016). Documented humoral immunodeficiencies in horses, independent of the breed, include failure of passive transfer in neonates, agammaglobulinaemia, common variable immunodeficiency (CVID) and potentially selective IgM deficiency (Felippe, 2016; Riggs, 1987).…”

“…Humoral immunodeficiencies are the most frequently diagnosed immunodeficiencies in mammals, and result from impaired antibody production due to intrinsic B cell failure to develop or differentiate into antibody‐secreting plasma cells, or impaired T cell help for B cell activation and differentiation in lymphoid tissues; in any of these conditions, the ultimate result is hypo‐ or agammaglobulinaemia, and increased susceptibility to infections with opportunistic pathogens, particularly encapsulated bacteria (Felippe, 2016). Documented humoral immunodeficiencies in horses, independent of the breed, include failure of passive transfer in neonates, agammaglobulinaemia, common variable immunodeficiency (CVID) and potentially selective IgM deficiency (Felippe, 2016; Riggs, 1987). In these disorders, inadequate serum IgG concentrations, with or without concurrent inadequate IgM concentrations, result in impaired host immune defence mechanisms, including antigen neutralisation and opsonisation, and complement activation, with resultant increased susceptibility to infections and potential septicaemia (Crisman & Scarratt, 2008; Felippe, 2016; Gardner et al., 2007).…”

Effectiveness of immunization with multi-component bacterial immunomodulator in foals at 35th day of life

“…However, the nature, the dose of the antigen, and the type of adjuvant, if any, can all have a profound effect on the intensity of the response and the class of immunoglobulin produced. The speci c functions for IgG2 are still poorly understood [39]. Few authors describe IgG2 in horses.…”

Effectiveness of immunization with multi-component bacterial immunomodulator in foals at 35th day of life

“…However, the nature, the dose of the antigen, and the type of adjuvant, if any, can all have a profound effect on the intensity of the response and the class of immunoglobulin produced. The specific functions for IgG2 are still poorly understood 37 . Few authors describe IgG2 in horses.…”