Spider Lamb Syndrome Research Articles

Poisonous Spiders: Bites, Symptoms, and Treatment; an Educational Review.

More than 40,000 species of spiders have been identified in the world. Spider bites is a common problem among people, however few of them are harmful but delay in treatment can cause death. Since the spider bites are risk full to human, they should be taken seriously, especially in endemic areas. Our objective in this review was to study about poisonous spiders and find out treatments of them. Therefore, we collected related articles from PubMed database and Google Scholar. Three important syndromes caused by spider bites are loxoscelism, latrodectism and funnel web spider syndrome. Many treatments are used but much more studies should have done to decrease the mortality. In this review, we describes different venomous spiders according to their appearance, symptoms after their bites and available treatments.

Allele frequency of the spider lamb syndrome in Brazilian Hampshire Down and Suffolk flocks

The spider lamb syndrome (SLS) is an autosomal recessive condition of sheep, characterized by severe bone lesions. The disease is caused by a mutation at codon 700 of the gene fibroblast growth factor receptor 3 (FGFR3), resulting in a valine (V) to glutamate (E) substitution, and leading to an abnormal bone growth. Congenital diseases as SLS may have an important impact on animal production. The objective of this work was to detect the frequency of E allele on Suffolk and H. Down breeds in three flocks from the southern region of Brazil. A total of 256 samples, 146 from two Suffolk flocks and 110 from one H. Down flocks were evaluated. The genomic DNA extracted from peripheral blood was PCR amplified and cleaved with XhoI restriction enzyme. Allele E frequency varied among the different herds: Suffolk, 6% in one flock and 3% in the other, and H. Down 6%, corresponding to 6–12% of heterozygotes for the condition. These results emphasize the need for preventive measures to minimize the birth of affected lambs. Also, the culling of animals, mainly rams, carrying the E allele will bring more efficiency to the sheep industry. These data are important also for sheep breeders, as the genotyping of the breed stock will afford more security to breeding programs and stop the spread of this undesirable allele, reducing economic losses. It is important to note that, in Brazil, the DNA test for SLS is not a routine procedure.

Non-Carrier Identification of Spider Lamb Syndrome in Iranian Baluchi and Karakul Sheep by PCR-RFLP

Non-Carrier Identification of Spider Lamb Syndrome in Iranian Baluchi and Karakul Sheep by PCR-RFLP

Enhanced skeletal growth of sheep heterozygous for an inactivated fibroblast growth factor receptor 31

Normal fibroblast growth factor receptor 3 (FGFR3) acts as a negative bone growth regulator by restricting chondrocyte proliferation and endochondral bone elongation. In sheep, a heritable mutation that inactivates FGFR3 produces skeletal overgrowth when homozygous, this condition is commonly referred to as spider lamb syndrome (SLS). We hypothesized that sheep heterozygous for the inactivated FGFR3 mutation (FGFR3(SLS/+)) would exhibit enhanced long bone growth and greater frame size; additionally, the isolated effects of increased bone growth would translate into greater BW and larger LM area relative to normal lambs at harvest. The current study investigated bone length and LM area of FGFR3(SLS/+) sheep at maturity and during growth. At maturity, FGFR3(SLS/+) ewes exhibited a larger frame size and longer bones than normal FGFR3(+/+) ewes (P < 0.05). Similarly, FGFR3(SLS/+) lambs had greater frame sizes than normal FGFR3(+/+) lambs, as indicated by increased metacarpal III length and height at withers (P < 0.05). The FGFR3(SLS/+) lambs took longer than the normal FGFR3(+/+) lambs to reach the 60-kg common BW harvest end point (P < 0.05). The FGFR3(SLS/+) lambs showed no difference in BW, ADG, or LM area at any age compared with normal FGFR3(+/+) lambs (P > 0.2). A similar LM area produced in the context of a greater frame size and skeletal length produces a greater muscle volume, thereby potentially increasing meat yield. The results of this study suggest that FGFR3(SLS/+) animals exhibit a relaxation of the normal inhibition of chondrocyte proliferation, resulting in an increase in the overall frame size. The sheep industry could utilize the naturally occurring genetic mutation in FGFR3 to potentially increase meat yields with enhanced skeletal growth as an alternative to exogenous growth promotants.

A single‐base change in the tyrosine kinase II domain of ovine FGFR3 causes hereditary chondrodysplasia in sheep

Ovine hereditary chondrodysplasia, or spider lamb syndrome (SLS), is a genetic disorder that is characterized by severe skeletal abnormalities and has resulted in substantial economic losses for sheep producers. Here we demonstrate that a non-synonymous T>A transversion in the highly conserved tyrosine kinase II domain of a positional candidate gene, fibroblast growth factor receptor 3 (FGFR3), is responsible for SLS. We also demonstrate that the mutant FGFR3 allele has an additive effect on long-bone length, calling into question the long-standing belief that SLS is inherited as a strict monogenic, Mendelian recessive trait. Instead, we suggest that SLS manifestation is determined primarily by the presence of the mutant FGFR3 allele, but it is also influenced by an animal's genetic background. In contrast to FGFR3 mutations causing dwarfism in humans, this single-base change is the only known natural mutation of FGFR3 that results in a skeletal overgrowth phenotype in any species.

Spider Lamb Syndrome (SLS) mutation frequency in German Suffolk sheep

Spider Lamb Syndrome (SLS) mutation frequency in German Suffolk sheep

Localization of the locus causing Spider Lamb Syndrome to the distal end of ovine Chromosome 6.

Spider Lamb Syndrome (SLS) is a semi-lethal congenital disorder, causing severe skeletal abnormalities in sheep. The syndrome has now been disseminated into several sheep breeds in the United States, Canada, and Australia. The mode of inheritance for SLS is autosomal recessive, making the identification and culling of carrier animals difficult due to their normal phenotype. Two large pedigrees segregating for the SLS mutation were established, and a genome scan with genetic markers from previously published genome maps of cattle and sheep was used to map the locus causing SLS. Genetic linkage between SLS and several microsatellite markers, OarJMP8, McM214, OarJMP12, and BL1038, was detected, thereby mapping the SLS locus to the telomeric end of ovine Chromosome (Chr) 6. Alignment of ovine Chr 6 with its evolutionary ortholog, human Chr 4, revealed a positional candidate gene, fibroblast growth factor receptor 3 (FGFR3).

Developmental progression of the Spider Lamb Syndrome

The progression of ovine hereditary chondrodysplasia, referred to as the Spider Lamb Syndrome (SLS), was characterized by collecting fetuses at the end of the second trimester, the middle of the third trimester, and the end of gestation. The SLS fetuses were produced by artificially inseminating three affected SLS ewes with frozen semen collected from an affected SLS ram, and surgically transferring the resulting embryos to unaffected recipient ewes. All resultant offspring possessed morphologic abnormalities consistent with a clinical diagnosis of SLS, although the degree of symptoms of the syndrome varied from animal to animal. The variable SLS clinical involvement was not correlated with the degree of symptoms expressed by the parents. We have confirmed an autosomal recessive mode of inheritance with complete penetrance and variable expressivity of the SLS phenotype with developmental expression of gross pathological changes apparent by the completion of the second gestational trimester.

Hereditary chondrodysplasia (“spider syndrome”) in a New Zealand Suffolk lamb of American origin

The first case of hereditary chondrodysplasia ("spider syndrome") in a New Zealand Suffolk lamb of American origin is described. An imported Suffolk ram of American origin was test mated to 27 of his daughters. In one of the resulting progeny, found dead at birth, a diagnosis of hereditary chondrodysplasia was made based on the typical radiographical abnormalities of multiple centres of ossification in the anconeal process of the ulna, vertebrae, sternebrae and pelvic bones. These changes were confirmed histopathologically.

Analysis of tissues from normal lambs and those with spider syndrome

This study was undertaken to examine tissue abnormalities in sheep with spider lamb syndrome (SLS). The major skeletal abnormalities found in SLS animals were cartilage erosion and bone abnormalities with large amounts of cartilaginous tissues present in the spongy bone (chondrodysplasia). Eroded cartilage contained lower (P &lt; 0.05) than normal concentrations of both collagen and proteoglycan. Key words: Spider lamb syndrome, cartilage, bone, sheep

Ovine hereditary chondrodysplasia (spider syndrome) in Suffolk lambs

Ovine hereditary chondrodysplasia (spider syndrome) in Suffolk lambs

Insulin-like growth factor-I levels and gene expression in ovine hereditary chondrodysplasia (Spider Lamb Syndrome)

Hereditary Chondrodysplasia or Spider Lamb Syndrome (SLS) is an inherited, semi-lethal, musculo-skeletal disease affecting lambs primarily of Suffolk or Hampshire breeding. Deformities of the limbs and spinal column along with multiple sites of ossification at the anconeal process are diagnostic for the disease. Muscle atrophy is also predominant. We have investigated the relationship between SLS and circulating levels of IGF-I and the IGF-BPs in older (50–80 d of age) animals. Serum IGF-I levels were lower (P<0.01) in SLS affected lambs (117 ng/ml) than in phenotypically normal lambs (188 ng/ml) while serum levels of the 32 kDa BP increased (P<0.01) 77% in SLS affected lambs as compared to contemporary controls. All other IGF-BPs appeared to be unaffected in this group. Gene expression of IGF-I and -II in the liver and muscle of younger (16–22 d of age) lambs was also measured. There were no differences in IGF-II expression in either muscle or liver between SLS affected and phenotypically normal control lambs. Muscle IGF-I expression also did not differ. However, liver IGF-I expression in SLS affected lambs was nearly double that of control lambs (P<0.01). These data suggest that the regulation of IGF-I and the IGF-BPs may be involved in the physical manifestations of this disorder.

Unsolved Problems Confronting the Sheep Industry

To support a sheep production system, veterinary practitioners must integrate diagnosis, treatment, and prevention with management, nutrition, and economics. Scrapie, spider syndrome, prolapses, and parasitism are a few of the less dramatic but constant problems in sheep practice. Problems with drug availability and residues may be as difficult to solve as predation and economic problems.

A morphologic and biochemical evaluation of the spider syndrome in Suffolk sheep.

SummaryThe distal radial growth plates of six pairs of spider‐affected and non‐affected lambs were compared after light and electron microscopic evaluation. Light microscopy revealed regions within the spider‐affected physes that lacked the distinctly columnized appearance of the normal ones. However, provisional calculation as revealed by von Kossa staining did not differ between the two groups; nor were there marked ultrastructural differences between control and spider lamb growth plate chondrocytes or matrices. The spider growth plates were also studied after concanavalin A and wheat germ agglutinin lectin histochemistry. Intracellular and extracellular staining patterns did not differ from previously reported normal patterns. Finally, SDS‐PAGE analysis of collagen extracted in the native state from spider‐affected cortical bone revealed that it is comprised of type I collagen that is normal in its primary structure; furthermore, there is no type III collagen present.