The muscle changes related to pelvic floor disorders are poorly understood. We conducted an anatomical and histological study of the perineum of the normal mouse and of a transgenic mouse strain deficient in urokinase-type plasminogen activator (uPA−/−) that was previously reported to develop a high incidence of rectal prolapse. We could clearly identify the iliococcygeus (ILC) and pubococcygeus (PC) muscles and anal (SPA) and urethral (SPU) sphincters in male and female mice. The bulbocavernosus (BC), ischiocavernosus (ISC) and levator ani (LA) muscles could be found only in male mice. Histochemical analysis of the pelvic floor muscles revealed a majority of type IIA fibres. Rectal prolapses were observed only in male uPA−/− mice. The most obvious finding was an irreducible evagination of the rectal mucosa and a swelling of the entire perineal region corresponding to an irreducible hernia of the seminal vesicles through the pelvic outlet. The hernia caused stretching and thinning of the ISC, BC and LA. Myopathic damage, with degenerated and centronucleated myofibres, were observed in these muscles. The PC, ILC, SPA and SPU were not affected. This study provides an original description of a model of pelvic floor disorder and illustrates the differences existing between the perineum of humans and that of a quadruped species. In spite of these differences, the histopathologic changes observed in the pelvic floor muscles of uPA−/− mice with rectal prolapse suggest that prolonged muscular stretching causes a primary myopathic injury. This should be taken into account in the evaluation of pelvic floor disorders.

To date there have been few reports on the impact of dietary intervention on the clinical course of acute shigellosis. Current management of acute shigellosis is primarily focused on antibiotic therapy with less emphasis on nutritional management. In a randomised clinical trial, we examined the role of an energy-dense diet on the clinical outcome in malnourished children with acute dysentery due to shigellosis. Seventy-five children aged 12–48 months with acute dysentery randomly received either a milk–cereal formula with an energy density of 4960 kJ/l (test group) or a milk–cereal formula with energy of 2480 kJ/l (control group) for 10 d in hospital. In both milk–cereal formulas, protein provided 11 % energy. In addition, the standard hospital diet was offered to all children and all children received an appropriate antibiotic for 5 d. The mean food intakes (g/kg per d) in the test and control groups were: 112 (SE 2·28) AND 116 (se 3·48) (P=0·16) on day 1; 118 (se 2·72) and 107 (se 3·13) (P=0·04) on day 5; 120 (se 2·25) and 100 (se 3·83) (P=0·04) on day 10. The mean energy intakes (kJ/kg per d) in the test and control groups respectively were: 622 (se 13·2) and 315 (se 11·3) (P<0·05) on day 1; 655 (se 15·1) and 311 (se 7·98) (P<0·05) on day 5; 672 (se 14·7) and 294 (se 11·1) (P<0·05) on day 10. The food and energy intakes were mostly from the milk–cereal diet. There was no difference between two groups in resolution of fever, dysenteric (bloody and or mucoid) stools, stool frequency and tenesmus. However, vomiting was more frequently observed among the test-group children during the first 5 d of intervention (67 % v. 41 %, P=0·04). There was an increase in the mean weight-for-age (%) in the test group compared with the control group after the 10 d of dietary intervention (6·2 (se 0·6) v. 2·7 (se 0·4), P<0·01). In addition, resolution of rectal prolapse was better (26 % v. 8 %, P=0·04) in the test group v. control group after 5 d, and 13 % v. 6 %, (P=0·08) after 10 d of dietary intervention. Supplementation with a high-energy diet does not have any adverse effect on clinical course of acute shigellosis and reduces the incidence of rectal prolapse in malnourished children.