Quality Parameters for Alpaca (Vicugna pacos) Semen are Affected by Semen Collection Procedure

Artificial insemination (AI) is poorly developed in camelids owing to the difficulty in collecting high quality semen and the highly viscous nature of the semen. Semen collected by artificial vagina (AV) is often of low quality and must be improved before any further development of AI technology can occur. The present study investigated the effects of adding a cervix‐like stricture to the AV, presence of females, collecting semen into Androhep^®, skim‐milk or Tris diluents, and catalase supplementation (0, 100, 200 or 600 units/ml) of Tris diluent on alpaca semen quality parameters. The addition of a cervix‐like stricture increased mating length (p < 0.05), whilst the presence of females during semen collection did not improve semen quality parameters (p > 0.05). Collection of semen into Tris diluent improved sperm motility (58.0 ± 11.9%) compared with the control (34.0 ± 10.8%; p < 0.05), Androhep^® (33.5 ± 10.7%) and skim‐milk diluents (28.2 ± 10.4%). Semen viscosity was reduced by collection into Androhep^® (4.6 ± 1.7 mm) and skim‐milk diluents (3.6 ± 1.3 mm) compared with Tris diluent (5.7 ± 2.1 mm) and no collection medium (9.3 ± 3.5 mm; p < 0.05). Tris diluent supplemented with 100, 200 or 600 units/ml catalase increased semen viscosity (5.0 ± 3.2 and 4.9 ± 3.2 mm). Collection of alpaca semen by AV into Tris diluent increased semen quality facilitating further development of AI technology in alpacas.     

The Effects of Blastomere Biopsy and Oxygen Tension on Bovine Embryo Development, Rate of Apoptosis and Interferon-τ Secretion

A series of experiments was performed to examine the effects of blastomere biopsies on subsequent development of IVF-derived bovine embryos. The first experiment was designed to assess the optimal time for blastomere removal. One blastomere was removed either 48 or 72 h after IVF. Biopsy at 48 h resulted in 17.2% of embryos proceeding to the blastocyst stage, which was lower than when biopsies were performed at 72 h (37.5%, p < 0.05). In the second experiment, embryos were cultured either under atmospheric or 5% O(2) following blastomere removal. Biopsies had no effect on rate of blastocyst formation with 36% of controls and 33.7% of biopsied embryos proceeding to that stage. However, culture under 5% O(2) significantly increased the number of blastocysts from 29.9% to 40.3% (p < 0.05). This effect was significant in both biopsied and control embryos. In the final experiment, biopsied embryos were again cultured under different oxygen tension. Blastocysts were collected and cultured individually for 48 h in medium droplets in their respective O(2) concentration after which time the medium was assayed for concentration of interferon-tau (IFN-tau). Reduced O(2) concentration again significantly increased blastocyst formation from 24.9% to 41.9% (p < 0.05). IFN-tau secretion was not affected by biopsies, but culture under atmospheric O(2) resulted in significantly increased IFN-tau concentration in medium droplets (12274.0 +/- 2825.9 pM vs 5046.5 +/- 2562.2 pM; p < 0.05).     

Spread bow leg syndrome in ostrich (Struthio camelus) chicks aged 2 to 12 weeks

1. The incidence of spread bow leg syndrome and associated pathology in 15 ostrich chicks aged 2, 4, 8 and 12 weeks is reported. Measurements were made of hind limbs: femur plus tibiotarsus; tarsometatarus; phalanx I, digit III; phalanx II, digit III plus phalanx III, digit III; and phalanx IV, digit III. 2. A run was constructed (6 m x 1.7 m) and subdivided into 2 m sections and the time taken to traverse it was recorded. Measurements (cm) were made of the left and right footprints; the number of footprints and average stride length in 0 to 2, 3 to 4 and 5 to 6 m. Speed was calculated using distance run (m) divided by time taken (s). 3. The number of steps was greater in bow leg chicks aged 4 and 8 weeks by comparison with healthy birds. Stride length, however, was smaller in all age groups with bow leg. All speeds in bow leg chicks were lower than those in healthy birds, except for that recorded at 2 m in chicks aged 2 weeks which did not differ markedly. 4. In affected birds, feathers were sparse. Icterus was present. The tarsometatarsus was twisted, with severely inflamed joints, eroded distal ends, thickening of the cartilage and the presence of fibrous material surrounding the ligaments. Muscles in the hind limb were emaciated. 5. The syndrome compromises the ability of chicks to keep up with adults in flocks, and may compromise their ability to escape predation.     

Prevalence of the AMHR2 mutation in Miniature Schnauzers and genetic investigation of a Belgian Malinois with persistent Müllerian duct syndrome

Persistent Müllerian duct syndrome (PMDS) is a sex‐limited disorder in which males develop portions of the female reproductive tract. Important consequences of PMDS are cryptorchidism and its sequelae of infertility and increased risk of testicular cancer. Anti‐Müllerian hormone (AMH) and its receptor (AMHR2) induce the regression of the Müllerian ducts in male embryos. In Miniature Schnauzer dogs, the genetic basis has been identified as an autosomal recessive nonsense mutation in AMHR2, but the allele frequency of the mutation is unknown. Thus, the primary objective of this study was to estimate the prevalence of the AMHR2 mutation in North American Miniature Schnauzers, in order to ascertain the value of genetic testing in this breed. An additional objective was to determine whether mutations in AMH or AMHR2 were responsible for PMDS in a Belgian Malinois; this would aid development of a genetic test for the Belgian Malinois breed. Genomic DNA from 216 Miniature Schnauzers (including one known PMDS case) was genotyped for the AMHR2 mutation, and DNA from a single PMDS‐affected Belgian Malinois was sequenced for all coding exons of AMH and AMHR2. The Miniature Schnauzer cohort had an AMHR2 mutation allele frequency of 0.16 and a carrier genotypic frequency of 0.27. The genetic basis for PMDS in the Belgian Malinois was not determined, as no coding or splicing mutations were identified in either AMH or AMHR2. These findings support a benefit to AMHR2 mutation testing Miniature Schnauzers used for breeding or with cryptorchidism.