Investigating risk factors and possible infectious aetiologies of mummified fetuses on a large piggery in Australia.

OBJECTIVE: To investigate risk factors and potential infectious aetiologies of an increased mummification rate (>2%) identified over time on a 1200-sow farrow-to-finish farm in Australia. METHODS: Association of potential non-infectious risk factors and the mummification rate was investigated using 15 years of breeding herd data (40,940 litters) and logistic regression analysis. Samples from a limited number of mummified fetuses were taken to identify potential infectious aetiologies (porcine parvovirus, Leptospira pomona, porcine circovirus type 2, Bungowannah virus and enterovirus). RESULTS: Logistic regression analysis suggested that the mummification rate was significantly associated with sow breed and parity, year and total born and stillborn piglets per litter. The mummification rate was lower (P < 0.001) in Landrace (3.4%) and Large White (2.6%) sows than in Duroc sows (4.9%). Gilts (2.9%) had a lower (P < 0.001) mummification rate than older sows. The mummification rate increased with total born litter size and decreased with the number of stillborn piglets (P < 0.001). A clustering effect within individual sows was identified, indicating that some sows with mummified fetuses in a litter were more likely to have repeated mummifications in subsequent litters. No infectious agents were identified in the samples taken. CONCLUSION: Results from this study suggest that the increased mummification rate identified over time on this farm is likely to be a non-infectious multifactorial problem predisposing the occurrence of mummification. Further research is required to better understand the pathophysiology of mummification and the role that different non-infectious factors play in the occurrence of mummified fetuses.

Assessment of cardiovascular risk factors in menopausal Argentinian women.

The cardiovascular risk factor profile was assessed in a population sample consisting of 60 nonmenopausal (control) and 100 menopausal women from different cities in Buenos Aires Province, Argentina. Each subject was individually interviewed and asked to complete a specially designed questionnaire aimed at identifying cardiovascular risk factors. A clinical general and gynecological examination including blood pressure and anthropometric measurements as well as a Papanicolaou smear were performed. The most prevalent risk factor in the menopausal group was low physical activity (87% of the subjects), followed by nervous complaints (67%), obesity (64%), familial antecedents of cardiovascular disease (CVD; 38%) and hypertension (33%). Other risk factors assessed showed a level of prevalence below 10%. In the control group, a tobacco smoking habit was the CVD risk factor with the highest prevalence (47%). Nervous complaints also showed a high prevalence (48%). Most menopausal patients (77%) had a cardiovascular risk index (RI) level between 1.5 and 4.0, whereas 17% of these subjects had an RI greater than 4.0 (high-risk patients). The present study reveals that, in the studied community, the menopause is associated with increased levels of both estrogen-dependent and psychosocial risk factors for CVD.

Sleep-dependent hyperprolactinemia and Corpus luteum pathogenesis.

The results obtained in wake and sleep conditions by PRL determinations performed in 6 normoprolactinemic infertile women with luteal phase deficiency (LPD) are reported. Infertility was apparently due to LPD. PRL levels were determined by RIA in blood samples collected at 20-min intervals from 18(00) to 08(00). LPD has been previously demonstrated by endometrial biopsy, basal temperature and circulating progesterone determinations. PRL levels were also determined in 5 normal women used as control subjects under the same experimental conditions. The results obtained, expressed as means +/- SD of LPD vs. control group, were 15.9 +/- 4.6 vs. 11.6 +/- 3.3 ng/ml (p greater than 0.1) in wake conditions and 31.9 +/- 5.9 vs. 21.4 +/- 5.7 ng/ml (p less than 0.01) in sleep conditions. PRL values during the highest pulse (HP) in sleep and wake conditions were 20.9 +/- 5.2 vs. 17.0 +/- 3.3 ng/ml (p less than 0.1) and 51.1 +/- 17.1 vs. 34.3 +/- 2.4 ng/ml (p less than 0.01), respectively. In 2 out of the 6 patients mean PRL values were 22.0 and 26.5 ng/ml during sleep, and 26.0 and 33.0 ng/ml during HP. These values were not statistically significant when compared with those obtained in the control group. The results obtained show that 4 out of the 6 patients with LPD and normal PRL levels in wake conditions had sleep-dependent hyperprolactinemia due to the pulses with a more significant amplitude. These findings suggest that in some cases sleep-induced hyperprolactinemia might be involved in LPD pathogenesis.