Peri- and postpubertal boars accumulate substances (e.g., androstenone and skatole) in their fatty tissue that are responsible for boar taint in pork. The objective of this study was to assess the efficacy of a GnRH vaccine, Improvac, in eliminating boar taint. Three hundred male (200 intact boars, 100 barrows) crossbred (Large White x Landrace) pigs were used in a 2 x 3 factorially arranged experiment. The respective factors were sex group (barrows, boars treated with placebo, or boars treated with Improvac) and slaughter age (23 or 26 wk). Vaccines were administered 8 and 4 wk before slaughter. All Improvac-treated pigs exhibited anti-GnRH titers. Testes and bulbo-urethral gland weights in treated pigs were reduced by approximately 50% (P < 0.001) and serum testosterone levels were below 2 ng/mL in the majority of treated boars (94 and 92% across both age groups at 2 and 4 wk, respectively). Boar taint, as assessed by the concentration of androstenone and skatole in s.c. fat, was suppressed to low or undetectable levels in 100% of Improvac-treated boars. No Improvac-treated pigs had significant concentrations of either androstenone (> 1.0 microg/g) or skatole (> 0.20 microg/g). In contrast, 49.5% of placebo-treated controls had significant androstenone and 10.8% had significant skatole levels, resulting in 10% of the control boars with high concentrations of both compounds. The mean concentrations of taint compounds in the Improvac-treated pigs were not significantly different from those in barrows. Improvac-treated boars grew more rapidly (P = 0.051 and < 0.001 for pigs slaughtered at 23 and 26 wk of age, respectively) than control boars over the 4 wk after the secondary vaccination, possibly because of reduced sexual and aggressive activities. Compared with barrows, Improvac-treated boars were leaner and had superior feed conversion efficiency. The vaccine was well tolerated by the pigs, and no observable site reactions could be detected at the time of slaughter. Vaccination of boars with Improvac allows production of heavy boars with improved meat quality through prevention and control of boar taint.

No abstract

Feral carp, Cyprinus carpio L., were collected at bimonthly intervals for 12 months from Lake Wellington, where there was no evidence of significant growth of Microcystis aeruginosa. Various blood parameters of these carp were measured to ascertain the normal range values for feral carp in this region. A similar study was conducted at Lake Mokoan, where M. aeruginosa formed a visible scum that contained detectable levels of microcystins for 4 consecutive months. Carp were taken from Lake Mokoan each month, and the histology and blood biochemistry of the fish were examined for indications of microcystin toxicity. During February, March and April, 66% of the carp from Lake Mokoan had livers with widespread hepatocyte atrophy, and 37% of the fish had gills with pinpoint necrosis, epithelial ballooning, folded lamellar tips and exfoliation of the lamellar epithelium. Compared to carp from Lake Wellington, the serum aspartate aminotransferase activity and the serum bilirubin concentrations of carp from Lake Mokoan were elevated during January, February, March and April. The data were consistent with impaired hepatocyte function in some carp from Lake Mokoan. Serum sodium and chloride concentrations in carp from Lake Mokoan were lower than those for carp at Lake Wellington from December to April, indicating that most carp from Lake Mokoan had difficulty maintaining cation‐anion homeostasis during this period. Nevertheless, carp at Lake Mokoan always appeared healthy, and no mortalities were reported.

Carp liver, gills, intestine, kidneys, heart and spleen were studied by histology after the fish were exposed to microcystins by gavage, immersion and intraperitoneal administration, Intraperitoneal inoculation with microcystins caused necrosis or dosedependent degeneration in the liver, gills and kidneys. Gavaging v^^ith microcystins caused changes in the histopathology of the liver and gills. Cellular degeneration and necrosis occurred in the liver, gills and kidneys when carp were introduced to a tank containing 1-7 fJ% ml"' of microcystins. Lesions were not observed in the heart, spleen or intestines from atiy of the treated catp. Microcystins adtninistered by intraperitoneal injection at a concentration of 50 (^ kg"' were lethal to all fish within 8 h, while gavaging with 250 /^ kg"' of microcystins caused minimal damage in the tissues studied.

Two hundred and twenty-four pigs (112 boars, 112 gilts) housed in pens of seven pigs per pen were used in a 2 x 2 x 2 factorial design, with the factors of vaccination with a gonadotropin-releasing factor (GnRF) vaccine (Improvac; 0 or 2 mL at 13 and 17 wk of age), porcine somatotropin (pST; 0 or 5 mg/d from 17 wk of age), and gender. Pigs were weighed and feed intake was measured from 17 wk of age until slaughter at 21 wk of age. Body composition was estimated by dual-energy X-ray absorptiometry in two focus pigs per pen at 17 and 21 wk of age. Testes and ovary weights at slaughter were decreased by Improvac treatment (P < 0.001), but were not altered by pST treatment (P > 0.44). Daily gain was lower for gilts than boars (1,128 vs. 1,299 g/d, P < 0.001) and was increased by pST (1,172 vs. 1,255 g/d, P = 0.003) and Improvac (1,150 vs. 1,276 g/d, P < 0.001) treatments. Feed intake (as-fed basis) was lower in gilts than in boars (2,774 vs. 3,033 g/d, P = 0.002), was decreased by pST (3,037 vs. 2,770 g/ d, P = 0.002), and was increased by Improvac treatment (2,702 vs. 3,105 g/d, P < 0.001). As a result of the differences in feed intake and daily gain, feed conversion efficiency (gain:feed) was lower for gilts than for boars (0.403 vs. 0.427 P = 0.025), was improved by pST (0.385 vs. 0.452, P < 0.001), but was unchanged by Improvac treatment (0.423 vs. 0.410, P = 0.22). Carcass weight was lower in gilts than in boars (75.3 vs. 77.0 kg, P = 0.012), was unchanged by pST treatment (75.9 vs. 76.4 kg, P = 0.40), and was increased by Improvac treatment (75.1 vs. 77.2 kg, P = 0.003). Lean tissue deposition rate was lower in gilts than in boars (579 vs. 725 g/d, P < 0.001), was increased by pST (609 vs. 696 g/d, P < 0.001) and by Improvac treatment (623 vs. 682 g/d, P = 0.014). Fat deposition rate tended to be lower in gilts than in boars (214 vs. 247 g/d, P = 0.063), decreased by pST treatment (263 vs. 198 g/d, P < 0.001), and increased by Improvac treatment (197 vs. 264 g/d, P < 0.001). For pigs treated with both pST and Improvac, daily gain and lean tissue deposition rate was greater than for pigs that received either treatment alone, whereas fat deposition rate and feed intake did not differ from untreated control pigs. In conclusion, Improvac increased growth rate through increased lean and fat deposition, but concomitant use of Improvac and pST increased lean gain above either alone, while negating the increase in fat deposition in pigs treated with Improvac.