In September 2002, the American Association of Colleges of Pharmacy (AACP) Council of Deans and Pharmacy Practice Section appointed this Task Force and charged it to develop a white paper addressing the role of colleges and schools in developing and administering residency programs. Specifically, the issues to be addressed included:1. What role should colleges and schools of pharmacy play in developing new residencies? Is there a national need at this time for new ones? If so, what should collegiate responsibility be? What are potential models of investment to help develop new residencies?Corollary: What role does residency training play in preparing future faculty? Are there educational experiences that should be incorporated into residency programs that prepare future faculty?2. Explore the postgraduate medical training model that involves schools holding the accreditation for a program and schools then approving the specific training sites. Such a model is already possible for community pharmacy residencies. Should it be applied to other types of pharmacy residency training? What are the advantages and disadvantages of such a model?3. What needs to be done to make available maximum resources for residency training?4. How can colleges partner with residency sites in residency research projects and encourage some residents to seek additional training in order to assume faculty positions? BACKGROUNDPharmacy residency programs are desirable for advanced patient care practice and future pharmacy leaders. Such programs are estimated to be equivalent to three to five years of work experience to prepare pharmacists for a variety of practice settings. Individuals with residency training can assist colleges and schools of pharmacy in several ways: (a) as full time faculty; (b) as preceptors for the experiential portion of the program; (c) as administrators at hospitals and clinics who can partner with colleges of pharmacy on a common educational mission; (d) as professional leaders on political advocacy issues that can enhance resources to support entry level and advanced pharmacy education; and (e) as pharmacist role models of patient care practice. For this reason, it is essential that colleges of pharmacy assume a significant role in residency training.Colleges and schools of pharmacy are also facing faculty shortages in departments/divisions of pharmacy practice.1 AACP contacted 84 member institutions to complete a survey in December 2002. Responses were received from 67 (79%) colleges/schools, which reported a total of 417 vacant teaching positions, or an average of 6 vacancies per college/school. Of the vacancies, 53.4% were in pharmacy practice and 45.6% were in pharmaceutical sciences. Of the vacancies, 94% were full time faculty positions. 2 The shortages are thought to be due to an inadequate supply of potential faculty, problems with faculty retention, and increased demand for faculty. Multiple etiologies have been proposed including lower salaries of faculty positions compared with industry, hospital, or c...

The cause and clinical manifestations of pneumonia were studied in 98 pediatric outpatients. A viral diagnosis was established in 38 (39%) of the 98 patients, and a bacterial diagnosis in 19 (19%). Ten (53%) of the 19 patients with bacterial pneumonia had a concurrent viral infection. No clinical, laboratory, or radiographic findings that would reliably differentiate viral from bacterial infection were identified. This study suggests that bacterial pneumonia is more common in pediatric outpatients than previously reported, and that the clinical, laboratory, and radiographic findings in patients with bacterial infection may be indistinguishable from findings in patients with viral infection.

To evaluate their role as a form of replacement therapy, frozen irradiated red blood cells were administered to a child with adenosine deaminase deficiency associated with severe combined immunodeficiency disease. In vitro lymphocyte responses to mitogens and allogeneic cells were restored. Subsequently, a "thymus shadow" appeared, and immunoglobulin synthesis was demonstrated. Frozen irradiated plasma, which alone had no effect on lymphocytes numbers or responses, promoted lymphocytosis when given with frozen irradiated red blood cells. The patient received the transfusions with or without irradiated plasma at four-week intervals and remained free of infection for 17 months. The patient's lymphocyte adenosine triphosphate levels were elevated before therapy, which consistently reduced them without altering the lymphocyte adenosine deaminase activity. Enzyme replacement therapy may provide a way to treat patients with adenosine deaminase deficiency associated with severe combined immunodeficiency disease who do not have histocompatible bone-marrow donors.

Human lymphocyte proliferation is inhibited in vitro in the presence of killed Pseudomonas aeruginosa or cell-free P. aeruginosa culture supernatants. A comparison of culture supernatants obtained under similar conditions from Staphylococcus aureus, Escherichia coli, P. aeruginosa, and Pseudomonas cepacia strains demonstrated that all P. aeruginosa supernatants were strongly inhibitory, whereas supernatants from other bacteria were mildly inhibitory or not inhibitory at all. These P. aeruginosa inhibitors prevent proliferative responses of resting cells upon mitogen activation and decrease [3H]thymidine uptake when added to human lymphocytes undergoing active proliferation in culture. The inhibitory effect is reversible and not due to cytotoxicity. Most of the inhibitory activity present in crude supernatants was detected in ultrafiltrates of molecular weights below 2,000. Purified P. aeruginosa pyocyanine, a low-molecular-weight phenazine pigment present in culture supernatant, was strongly inhibitory for lymphocyte proliferation. Extraction of pyocyanine and phenazine pigments from inhibitory P. aeruginosa supernatants eliminated their inhibitory activity. Inhibitors were recovered from reverse-phase chromatographic cartridges by both chloroform and methanol elution, indicating that pyocyanine and other phenazine pigments present in P. aeruginosa supernatants are responsible for the inhibition of lymphocyte proliferation. In addition to the identification of phenazine pigments as lymphocyte proliferation inhibitors, several criteria ruled out major contributions of P. aeruginosa polysaccharide, exotoxin A, and proteases to this phenomenon. P. aeruginosa strains selected for very low protease production or for very low exotoxin A production produced supernatants as inhibitory for lymphocyte proliferation as supernatants obtained from clinical P. aeruginosa isolates. Purified P. aeruginosa lipopolysaccharide and protease preparations failed to induce reversible lymphocyte proliferation inhibition. Finally, heat inactivation of P. aeruginosa supernatants at 100 degrees C for 60 min inactivates exotoxin A and proteases but produced only a moderate decrease of the inhibitory activity for lymphocyte proliferation.