Changes

==Description==

==Description==

Leucocyte adhesion deficiency (LAD) is caused by a defect in a surface molecule expressed by neutrophils which usually allows it to attach to vessel walls and move into tissues.  The disease was first reported in a dog in 1987<ref>Giger U, Boxer LA, Simpson PJ, Lucchesi BR, Todd RF 3rd. '''Deficiency of leukocyte surface glycoproteins Mo1, LFA-1, and Leu M5 in a dog with recurrent bacterial infections: an animal model.''' ''Blood. 1987 Jun;69(6):1622-30.''</ref> and it bears similarities to leucocyte adhesion deficiencies in mice and humans.  This molecule, the integrin subunit CD18, is affected by a mis-sense mutation of Cys-38-Ser and this results in a failure to express multiple integrin molecules as CD18 is a common subunit in many different heterodimeric complexes.  The disease is inherited in an autosomal recessive manner, with heterozygous carriers showing no signs of disease.

Leucocyte adhesion deficiency (LAD) is caused by a defect in a surface molecule expressed by neutrophils which usually allows this type of cell to attach to vessel walls and move into tissues.  The disease was first reported in a dog in 1987<ref>Giger U, Boxer LA, Simpson PJ, Lucchesi BR, Todd RF 3rd. '''Deficiency of leukocyte surface glycoproteins Mo1, LFA-1, and Leu M5 in a dog with recurrent bacterial infections: an animal model.''' ''Blood. 1987 Jun;69(6):1622-30.''</ref> and it bears similarities to leucocyte adhesion deficiencies in mice and humans.  The surface molecule, the integrin subunit CD18, is affected by a mis-sense mutation of Cys-38-Ser and this results in a failure to express multiple integrin molecules as CD18 is a common subunit in several heterodimeric complexes.  The disease is inherited in an autosomal recessive manner, with heterozygous carriers showing no signs of disease.

Since stimulatory cytokines are still released from inflamed tissues, neutrophils are produced in greater numbers and released into the circulation.  As these cells are unable to enter tissues however, affected animals develop a persistent [[Neutrophilia|neutrophilia]].  Neutrophils from affected animals also show defects in chemotaxis and phagocytosis.

Since stimulatory cytokines are still released from inflamed tissues, neutrophils are produced in greater numbers from the bone marrow and released into the circulation.  As these cells are unable to enter tissues, affected animals develop a persistent [[Neutrophilia|neutrophilia]].  Neutrophils from affected animals also show defects in chemotaxis and phagocytosis.

==Signalment==

==Signalment==

*'''Skin lesions''' including pyoderma, furunculosis and ulceration

*'''Skin lesions''' including pyoderma, furunculosis and ulceration

*'''Anorexia''' and failure to gain weight

*'''Anorexia''' and failure to gain weight

*'''Bone disorders''' including metaphyseal osteopathy, craniomandibular osteopathy and osteomyelitis

*'''Bone disorders''' including metaphyseal osteopathy, craniomandibular osteopathy and [[Osteomyelitis|osteomyelitis]]

*Generalised '''lymphadenopathy'''

*Generalised '''lymphadenopathy'''