Attitudes towards dog ownership on St. Kitts, West Indies.

A structured face-to- face interview was held with 64 arbitrarily selected local people attending a vegetable market in the capital of St. Kitts on a Saturday morning. Most (67%) respondents liked dogs and many (57%) owned one (41%) or two (29%) for protection (67%) and as a pet (65%). The main reason people disliked dogs were because they feared them (56%) and because they created a mess (50%). Generally people had purebred (40%) male (56%) dogs which were always outside (50%), in fenced yards (43%), on chains (34%) or running free (22%). All owners fed their dogs, mainly on table scraps (44%) or commercial dog food (39%). Only 16% of animals were neutered and many had puppies (range 3-11) and there was a high mortality rate (>2 puppies in 73% of litters). Only 24% of the dogs were over 4 years. Relatively few owners (55%) took their dogs to the veterinarian, principally for vaccination and checkups (85%) but when their animal was ill (24%). Most people (54%) used insecticides for external parasites on their dogs and some (44%) dewormed their animals. Many people (24%) had been bitten by a dog but 64% did not believe people could acquire diseases from dogs. Only 6% of respondents thought there were too many dogs on the island.

Attitudes towards dog ownership on St. Kitts, West Indies.

A structured face-to- face interview was held with 64 arbitrarily selected local people attending a vegetable market in the capital of St. Kitts on a Saturday morning. Most (67%) respondents liked dogs and many (57%) owned one (41%) or two (29%) for protection (67%) and as a pet (65%). The main reason people disliked dogs were because they feared them (56%) and because they created a mess (50%). Generally people had purebred (40%) male (56%) dogs which were always outside (50%), in fenced yards (43%), on chains (34%) or running free (22%). All owners fed their dogs, mainly on table scraps (44%) or commercial dog food (39%). Only 16% of animals were neutered and many had puppies (range 3-11) and there was a high mortality rate (>2 puppies in 73% of litters). Only 24% of the dogs were over 4 years. Relatively few owners (55%) took their dogs to the veterinarian, principally for vaccination and checkups (85%) but when their animal was ill (24%). Most people (54%) used insecticides for external parasites on their dogs and some (44%) dewormed their animals. Many people (24%) had been bitten by a dog but 64% did not believe people could acquire diseases from dogs. Only 6% of respondents thought there were too many dogs on the island.

Stickler syndrome. A mutation in the nonhelical 3' end of type II procollagen gene.

BACKGROUND: All of the mutations in the type II procollagen (COL2A1) gene that have been identified in families affected with Stickler syndrome have been located primarily in the triple helical region of the gene. We report what we believe is the first premature stop codon in the globular C-propeptide region encoded by the COL2A1 gene, in a family affected with Stickler syndrome. DESIGN: Genomic DNA from affected and unaffected family members of this three-generation family was amplified using the polymerase chain reaction. The polymerase chain reaction products were directly sequenced for DNA analysis. RESULTS: Direct sequencing showed a single base deletion in exon 50, resulting in a premature stop codon in exon 51 in the globular C-propeptide of COL2A1 gene in all affected members. CONCLUSIONS: These results implicate premature stop codons as a common cause of Stickler syndrome. The location of this premature stop codon in the far end of the nonhelical 3' end of the gene indicates that a truncated C-propeptide of at least 84 amino acid residues is inadequate for the functional gene product.

A second mutation in the type II procollagen gene (COL2AI) causing stickler syndrome (arthro-ophthalmopathy) is also a premature termination codon.

Genetic linkage analyses suggest that mutations in type II collagen may be responsible for Stickler syndrome, or arthro-ophthalmopathy (AO), in many families. In the present study oligonucleotide primers were developed to amplify and directly sequence eight of the first nine exons of the gene for type II procollagen (COL2A1). Analysis of the eight exons in 10 unrelated probands with AO revealed that one had a single-base mutation in one allele that changed the codon of -CGA- for arginine at amino acid position alpha 1-9 in exon 7 to a premature termination signal for translation. The second mutation found to cause AO was, therefore, similar to the first in that both created premature termination signals in the COL2A1 gene. Since mutations producing premature termination signals have not previously been detected in genes for fibrillar collagens, the results raise the possibility that such mutations in the COL2A1 gene are a common cause of AO.

Detection of sequence variants in the gene for human type II procollagen (COL2A1) by direct sequencing of polymerase chain reaction-amplified genomic DNA.

The direct sequencing of the human type II procollagen (COL2A1) gene from polymerase chain reaction (PCR)-amplified genomic DNA is described. Thirty-two regions of the COL2A1 gene were asymmetrically amplified with intron primers which were specifically chosen to amplify a region spanning 500 to 800 bp of sequence encoding one or more exons and their accompanying intervening sequences. Primers for dideoxynucleotide sequencing of the PCR products were then designed to provide complete exon sequence information and to insure that intron:exon splice junction sequence data would be obtained. Amplification and sequencing reactions were performed on an automated workstation to facilitate the handling of multiple DNA templates. The procedure allowed efficient sequencing of over 25,000 bp of each allele of the COL2A1 gene per diploid genome. We used this method for the comparative analyses of COL2A1 sequences in DNA isolated from the blood of 42 unrelated individuals and we identified 21 neutral sequence variants in the gene. The sequence variations were confirmed by independent assays, including restriction enzyme digestion. The sequence variants described here will be important for identifying haplotypes of the type II procollagen gene that will be useful in defining a genetic etiology for diseases of cartilaginous tissues.