Linked Life Data

2982527

Source:http://linkedlifedata.com/resource/pubmed/id/2982527

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1985-3-27
pubmed:abstractText
The clinical manifestations of a genetically determined deficiency of C3 were examined in a closed colony of dogs. One hundred and twelve dogs, including twenty C3-deficient dogs, were studied over a period of 6 years. Five of the C3-deficient dogs developed significant bacterial infections, such as pneumonia, sepsis, and pyometra, which were caused by Clostridium spp., Escherichia coli, and Klebsiella spp. Two of the C3-deficient dogs who had had significant infections also subsequently developed renal disease. Secondary amyloidosis was the predominant renal lesion in one dog. The predominant renal lesion in the second dog was membranoproliferative glomerulonephritis, although some amyloid was also present. The two dogs with renal disease also had positive rheumatoid factors. No other clinical or serological evidence of autoimmune disease or immune complex disease has been found. None of the dogs heterozygous for C3 deficiency, and none of the homozygous normal dogs in the colony has developed significant bacterial infections or renal disease. Thus, dogs deficient in C3, like C3-deficient humans, demonstrate both an increased susceptibility to infection and renal disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0090-1229
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
304-15
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
The clinical manifestations of a genetically determined deficiency of the third component of complement in the dog.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't