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Immune-deficiency diseases have serious consequences and often lower the body's defenses against infection. Some are inherited, and others are caused by viral infections or cancer.
Deficiencies in Phagocytosis
Phagocytosis is an essential mechanism of the immune system. Phagocytes are cells that engulf (phagocytize), digest, and kill foreign invaders. They can also serve as part of the adaptive immune system by presenting antigens to other cells in the adaptive system, thereby alerting them to the presence of the foreign invaders. Phagocytes are produced in the bone marrow, spread throughout the body via the bloodstream, and then gather in either tissue or the blood. They are found in the skin, spleen, lymph nodes, the coverings of the brain and spinal cord, bone marrow, and blood vessels throughout the body.
A deficiency in phagocytosis can be caused by a low number of phagocytes in the blood or by a viral infection or congenital defect (birth defect). The deficiency causes an increased susceptibility to bacterial infection of the skin, respiratory system, and gastrointestinal tract. These infections respond poorly to antibiotics.
Immunoglobulin Deficiency
This condition is due to a failure of the body to produce antibodies (immunoglobulins). This deficiency can be acquired (caused by other diseases) or congenital (present at birth). Congenital deficiencies of one type of immunoglobulin (immunoglobulin A, or IgA) have occurred in Beagles, German Shepherds, and Chinese Shar-Peis, leading to respiratory infections, digestive system disorders, skin disease, or allergies.
Acquired deficiencies occur in puppies that do not receive adequate maternal antibodies when nursing during the first several days of life. For older animals the cause is often a decrease in antibody production.
Immunoglobulin deficiency can occur as part of any disease that disrupts the production of antibodies in the body. For example, certain tumors (such as lymphosarcoma and plasma cell myeloma) cause the production of abnormal antibodies, which decreases production of normal antibodies. Some viral infections, including canine distemper and parvovirus, can damage the tissues that produce antibody-forming cells.
Combined Immunodeficiency Disease
Combined immunodeficiency disease involves a defect in both cell-mediated immunity and antibody production. Affected animals lack both T and B cells, which makes it impossible for the body to fight foreign invaders. Cases have been seen in Bassett Hounds, Toy Poodles, Rottweilers, and mixed-breed puppies. Affected dogs are healthy during the first several months of life but become progressively more susceptible to bacterial infections as the antibodies they received during nursing disappear. No treatment is available and the longterm outlook is poor.
Selective Immunodeficiencies
Rottweiler puppies have a predisposition for severe and often fatal canine parvovirus infections. Their resistance to other diseases is essentially normal, and the basis of this selective immunodeficiency is unknown.
Localized and whole-body fungal infections affect certain types of dogs. Long-nosed breeds, in particular German Shepherds and shepherd mixes, are more likely to develop fungal infections in their nasal passages. Whole-body aspergillosis (a type of fungal infection) is seen almost exclusively in German Shepherds and occurs more commonly in western Australia than in other areas. Signs of this disease include infection of the kidneys, bones, and the discs between the vertebrae of the spinal cord.
Immunodeficiencies Caused by Viruses
These types of diseases can be caused by a number of viruses in animals. In dogs, distemper virus causes a profound immunodeficiency in infected puppies. The infection is associated with a progressive decline in levels of antibodies and an increased susceptibility to bacterial infections that are normally controlled by the immune system. Parvovirus infection in dogs causes a huge decrease in the number of white blood cells and a weakened immune response to bacterial and fungal infections.
Last full review/revision July 2011 by Christine Andreoni; Kevin T. Schultz, DVM, PhD
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