Improved porcine model for Shiga toxin-producing Escherichia coli infection by deprivation of colostrum feeding in newborn piglets.

Porcine edema disease (ED) is a toxemia caused by enteric infection with Shiga toxin 2e (Stx2e)-producing Escherichia coli (STEC). ED occurs most frequently during the weaning period and is manifested as emaciation associated with high mortality. In our experimental infection with a specific STEC strain, we failed to cause the suppression of weight gain in piglets, which is a typical symptom of ED, in two consecutive experiments. Therefore, we examined the effects of deprivation of colostrum on the sensitivity of newborn piglets to STEC infection. Neonatal pigs were categorized into two groups: one fed artificial milk instead of colostrum in the first 24 h after birth and then returned to the care of their mother, the other breastfed by a surrogate mother until weaning. The oral challenge with 1011  colony-forming units of virulent STEC strain on days 25, 26 and 27 caused suppression of weight gain and other ED symptoms in both groups, suggesting that colostrum deprivation from piglets was effective in enhancing susceptibility to STEC. Two successive STEC infection experiments using colostrum-deprived piglets reproduced this result, leading us to conclude that this improved ED piglet model is more sensitive to STEC infection than the previously established models.

Relationship between the usage of carbapenem antibiotics and the incidence of imipenem-resistant Pseudomonas aeruginosa.

Metallo-beta-lactamase (MBL)-producing Pseudomonas aeruginosa isolates are resistant to almost all broad-spectrum beta-lactams and carbapenems. We investigated 389 P. aeruginosa isolates, collected from 29 hospitals in the Tohoku area of Japan, to determine their susceptibilities to ten antimicrobial drugs, and the rates of MBL-producing P. aeruginosa among them. Two hundred and one P. aeruginosa strains were isolated from small (group S)hospitals that had adopted imipenem as a carbapenem antibiotic, and 188 were isolated from general (group G) hospitals, which employed three or four carbapenems. MBL genes were analyzed by polymerase chain reaction (PCR) in all isolates for which the sodium mercaptoacetic acid (SMA) disk method gave positive results. The antimicrobial agents tested were imipenem, meropenem, biapenem, panipenem, piperacillin, ceftazidime, sulbactam/cefoperazone, amikacin, arbekacin, and ciprofloxacin. Sixteen (8.0%) of the 201 isolates from group S hospitals and three (1.6%) of the 188 isolates from group G hospitals were MBL-producing P. aeruginosa. In this study, the proportion of MBL-producing P. aeruginosa in group S was significantly higher than that found in group G (P < 0.01). The use of only one agent as a carbapenem antibiotic may have been one of the factors contributing to the high detection rate of MBL-producing P. aeruginosa observed in group S hospitals.

Auditory-conditioned-fear-dependent c-Fos expression is altered in the emotion-related brain structures of Fyn-deficient mice.

Fyn-tyrosine-kinase-deficient mice exhibit increased fearfulness. To elucidate the neural mechanisms of their emotional defects, we compared fyn(-/-) and fyn(+/-) mice by behavioral analysis of conditioned fear and by functional neuroanatomical analysis of the distribution of highly responsive neurons associated with conditioned fear. The mice were exposed to the auditory conditioned stimulus paired with electric shock as the unconditioned stimulus. After the fear conditioning, auditory stimulus-induced freezing behavior was enhanced in fyn(-/-) mice. When the occurrence of c-Fos-immunoreactive neurons in the brain of fear-conditioned mice was examined following exposure to the auditory stimulus, a significant increase in immunoreactive neurons was found in the amygdala, hypothalamus, and midbrain of both genotypes. The occurrence of conditioned-fear-dependent c-Fos-immunoreactive neurons was enhanced in the central, medial, cortical, and basomedial amygdaloid subdivisions, the hypothalamic nuclei, and the midbrain periaqueductal gray of the fyn(-/-) mice in comparison with the fyn(+/-) mice. However, remarkably, the occurrence of conditioned-fear-dependent c-Fos-immunoreactive neurons was very low in the basolateral and lateral amygdaloid subdivisions of the fyn(-/-) mice, in striking contrast to a significant increase in c-Fos-immunoreactive neurons in these subdivisions in the fyn(+/-) mice. These findings suggest that the increased excitability of the specific amygdaloid subdivisions including the central nucleus, and of the projection targets such as the hypothalamus and midbrain in fyn(-/-) mice, is directly related to the enhanced fear response, and that the decreased excitability in the basolateral and lateral amygdaloid subdivisions is involved in the defective control of the neural circuit for emotional expression in this mutant.