Consumers lived experiences and satisfaction with sub-acute mental health residential services.

PURPOSE: Sub-acute recovery-oriented facilities offer short-term residential support for people living with mental illness. They are generally highly regarded by consumers, with emerging evidence indicating that these services may support recovery. The aim of the current study was to explore the relationship between personal recovery and consumers' satisfaction with sub-acute residential services, and consumers' views about service features that aid recovery. METHODS: Consumers at 19 adult Prevention and Recovery Care Services in Victoria, Australia, were invited to complete measures containing sociodemographic information and measures on personal recovery and wellbeing. After going home, participants were invited to complete measures on service satisfaction and experience. RESULTS: Total and intrapersonal scores on the personal recovery measure increased significantly between Time 1 and Time 2, indicating marked improvement. Personal recovery and satisfaction measures were moderately to strongly correlated. Thematically analysed open-ended responses revealed themes of feeling connected, finding meaning and purpose, and self-empowerment as important aspects of these services, with some recommendations for improvements. CONCLUSION: Sub-acute residential mental health care may support individuals' personal recovery; consumer satisfaction indicates these services also offer an acceptable and supportive environment for the provision of recovery-oriented care. Further exploring consumers' experiences of sub-acute residential services is essential to understand their effectiveness, opportunities for improvement and intended impacts on personal recovery.

Secretion of cell wall polymers into the growth medium of lysis-defective pneumococci during treatment with penicillin and other inhibitors of cell wall synthesis.

Autolysin-defective pneumococci secrete into the growth medium choline-containing macromolecules during treatment with any one of a large number of inhibitors of cell wall biosynthesis, including beta-lactams, beta-halogeno-d-alanines, cephalosporins, and d-cycloserine. Secretion is closely related to the dose response of the bacteria to the various drugs: (i) secretion can already be detected at the minimum inhibitory concentration; (ii) the rate and extent of secretion is dependent upon the drug concentration; and (iii) secretion commences within minutes after the addition of the antibiotics to the cultures. Reversal of the growth-inhibitory effect of benzylpenicillin (by penicillinase addition) is accompanied by a halt in secretion just at the time when the bacteria resume normal growth. Secretion of the choline-containing macromolecules seems to be a specific consequence of the inhibition of peptidoglycan biosynthesis, since inhibition of growth by drugs affecting protein, ribonucleic acid, or deoxyribonucleic acid synthesis does not cause secretion. The choline-containing macromolecules include both the pneumococcal lipid-containing teichoic acid (Forssman antigen) and wall teichoic acids made after the addition of antibiotics. The appearance of these macromolecules in the growth medium is not due to the hydrolytic activity of an autolysin, since penicillin-induced secretion could be demonstrated in autolysin-defective mutants, in pneumococci grown on ethanolamine-containing medium (such cells are known to have defective autolytic systems), and in wildtype pneumococci grown under conditions nonpermissive for lysis.

Characterization of cell wall polymers secreted into the growth medium of lysis-defective pneumococci during treatment with penicillin and other inhibitors of cell wall synthesis.

Autolysin-defective pneumococci secrete large quantities of choline-containing cell wall polymers into the growth medium during treatment with inhibitors of peptidoglycan synthesis. The secreted polymers were separated into three fractions by a combination of gel filtration on agarose and sodium dodecyl sulfate-gel electrophoresis. Fraction I had a high apparent molecular size and contained the Forssman antigen in complex with material exhibiting properties of cell wall teichoic acid. Choline-containing polymers of as yet uncharacterized structure were present in both fractions IIA and IIB, and fraction IIA also contained peptidoglycan components.

Suppression of the lytic and bactericidal effects of cell wallinhibitory antibiotics.

The bacteriolytic effect of beta-lactam antibiotics on Bacillus subtilis and on Streptococcus pneumoniae was found to be a function of the pH; lysis was suppressed if the pH of the pneumococcal culture was below 6.0 during penicillin treatment. In the case of B. subtilis, growth at pH 6.6 prevented penicillin-induced lysis. In pneumococci, the addition of trypsin to the growth medium also protected against lysis. The pH-dependent protection phenomenon resembled in several respects the antibiotic "tolerance" of pneumococci with a defective autolytic system. (i) At the pH nonpermissive for lysis, the bacteria retained their normal sensitivity to beta-lactam and to other cell wall inhibitors; however, instead of lysis, the drug-treated bacteria simply stopped growing. Loss of viability of the cells was also greatly reduced. (ii) Protection against lysis was independent of the dose and chemical nature of the cell wall inhibitors. (iii) The protection effect was reversible; lysis and loss of viability could be triggered by a postincubation of the drug-treated bacteria at the pH permissive for lysis.

Mechanism of action of penicillin: triggering of the pneumococcal autolytic enzyme by inhibitors of cell wall synthesis.

During penicillin treatment of an autolysin defective mutant pneumococcus we have observed three novel phenomena: (i) Growth of the mutant cultures is inhibited by the same concentrations of penicillin that induce lysis in the wild type. (ii) Mutant bacteria treated with the minimum growth inhibitory concentration of penicillin will lyse upon the addition of wild-type autolysin to the growth medium. Chloramphenicol and other inhibitors of protein synthesis protect the cells against lysis by exogenous enzyme. Sensitivity of the cells to exogenous autolysin requires treatment with penicillin or other inhibitors of cell wall synthesis (e.g., D-cycloserine or fosfonomycin) since exogenous autolysin alone has no effect on bacterial growth. (iii) Treatment with penicillin (or other inhibitors of cell wall synthesis) causes the escape into the medium of a choline-containing macromolecule that has properties suggesting that it contains pneumococcal lipoteichoic acid (Forssman antigen). Each one of these three phenomena (growth inhibition, sensitization to exogenous autolysin, and leakage of lipoteichoic acid) shows the same dose response as that of the penicillin-induced lysis of wild-type pneumococci. On the basis of these findings we propose a new hypothesis for the mechanism of penicillin-induced lysis of bacteria. It is suggested that inhibition of cell wall synthesis by any means triggers bacterial autolytic enzymes by destabilizing the endogenous complex of an autolysin inhibitor (lipoteichoic acid) and autolytic enzyme. Escape of lipoteichoic acid-like material to the growth medium is a consequence of this labilization. Chloramphenicol protects bacteria against penicillin-induced lysis by interfering with the activity of the autolytic enzyme, rather than by depleting the concentration of the enzyme at the cell surface.