Healthy Aging Requires a Healthy Home Care Workforce: the Occupational Safety and Health of Home Care Aides.

PURPOSE OF REVIEW: To identify important home care (HC) aide occupational safety and health (OSH) hazards and examine how addressing these can improve aide health and the delivery of HC services overall. Specifically, this review seeks to answer: Why is HC aide OSH important? What are the most significant OSH challenges? How can improving HC aide OSH also improve the safety and health of their clients? What implications do the findings have for future research? RECENT FINDINGS: HC is one of the fastest growing US industries. Aides comprise its largest workforce and are increasingly needed to care for the rapidly aging population. There is an aide shortage due in part to instabilities in HC work organization and to serious job-specific hazards, resulting in aides losing work time. Recent social, economic, and technological factors are rapidly changing the nature of HC work, creating OSH hazards similar to those found in nursing homes. At the same time, aides are experiencing social and economic inequities that increase their vulnerability to OSH hazards. These hazards are also a burden on employers who are challenged to recruit, retain, and train aides. OSH injuries and illness interrupt the continuity of care delivery to clients. Many OSH hazards also put HC clients and families at risk. A new framework and methodologies are needed to assess aide and client safety together in order to guide future HC research, policies, and practices. Government, industry, and labor commitment is needed to fund and coordinate a comprehensive, multidisciplinary research program.

Construction of delta aroA his delta pur strains of Salmonella typhi.

Salmonella typhi strains with two deletion mutations, each causing an attenuating auxotrophy, have been constructed from strains Ty2 and CDC 10-80 for possible use as oral-route live vaccines. An aroA(serC)::Tn10 transposon insertion was first transduced from a Salmonella typhimurium donor into each wild-type S. typhi strain. Transductants of the Aro- SerC- phenotype were treated with transducing phage grown on an S. typhimurium strain with an extensive deletion at aroA; selection for SerC+ yielded transductants, some of which were delta aroA. A his mutation was next inserted into a delta aroA strain in each line by two steps of transduction. Two deletions affecting de novo purine biosynthesis were used as second attenuating mutations: delta purHD343, causing a requirement for hypoxanthine (or any other purine) and thiamine, and delta purA155, causing an adenine requirement. The purHD343 deletion was introduced into the delta aroA his derivatives of each strain by cotransduction with purH::Tn10, and the purA155 deletion was introduced into the CDC 10-80 delta aroA his derivative by cotransduction with an adjacent silent Tn10 insertion by selection for tetracycline resistance. Tetracycline-sensitive mutants of each of the three delta aroA his delta pur strains were isolated by selection for resistance to fusaric acid. The tetracycline-sensitive derivative of the CDC 10-80 delta aroA his delta purA155 strain, designated 541Ty, and its Vi-negative mutant, 543Ty, constitute the candidate oral-route live-vaccine strains used in a recent volunteer trail (M. M. Levine, D. Herrington, J. R. Murphy, J. G. Morris, G. Losonsky, B. Tall, A. A. Lindberg, S. Stevenson, S. Baqar, M. F. Edwards, and B. A. D. Stocker, J. Clin. Invest. 79:885-902, 1987). Tetracycline-sensitive mutants of the delta aroA his delta purHD derivative of strains Ty2 and CDC 10-80 may also be appropriate as live vaccines but have not been tested as such.

Plasmid-associated virulence of Salmonella enteritidis.

Plasmid-associated virulence of Salmonella enteritidis was studied using plasmid-cured and plasmid-reintroduced strains. The plasmidless strain was unable to grow in the liver of mice after intravenous inoculation. Reintroduction of the plasmid pEX106 from the original S. enteritidis fully restored its capacity to grow in the mice. The plasmid pEX102 of Salmonella typhimurium introduced into the plasmid-cured S. enteritidis had a similar effect. The smooth lipopolysaccharide character of the S. enteritidis strains was not affected by the presence or absence of the plasmid, and the same was true of their high resistance to complement in guinea-pig serum as such or with added antibody.

Safety, infectivity, immunogenicity, and in vivo stability of two attenuated auxotrophic mutant strains of Salmonella typhi, 541Ty and 543Ty, as live oral vaccines in humans.

Two Salmonella typhi mutants, 541Ty (Vi+) and 543Ty (Vi-), auxotrophic for p-aminobenzoate and adenine, were evaluated as live oral vaccines. 33 volunteers ingested single doses of 10(8), 10(9), or 10(10) vaccine organisms, while four others received two 2 X 10(9) organism doses 4 d apart. No adverse reactions were observed. Vaccine was recovered from coprocultures of 29 of 37 vaccinees (78%) and from duodenal string cultures of two; repeated blood cultures were negative. The humoral antibody response to S. typhi O, H, Vi, and lysate antigens in serum and intestinal fluid was meager. In contrast, all vaccinees manifested cell-mediated immune responses. After vaccination, 69% of vaccinees overall and 89% of recipients of doses greater than or equal to 10(9) responded to S. typhi particulate or purified O polysaccharide antigens in lymphocyte replication studies but not to antigens of other Salmonella or Escherichia coli. All individuals, postvaccination, demonstrated a significant plasma-dependent mononuclear cell inhibition of wild S. typhi.

The traT protein is able to normalize the phenotype of a plasmid-carried permeability mutation of Salmonella typhimurium.

The isolation of different classes of antibiotic-supersensitive outer membrane permeability mutants of Salmonella typhimurium has been described previously (Sukupolvi et al., 1984, Journal of Bacteriology 159, 704-712). One of these, the SS-A mutation, sensitizes the bacteria to gentian violet and to hydrophobic antibiotics. The phenotype of the SS-A mutant was restored to normal when a cloned fragment of the F plasmid, or the R plasmid R6-5, carrying the genes traS, T and D was introduced on a multicopy plasmid. The introduction of a plasmid carrying only the traT gene showed that this gene was sufficient to restore the phenotype. Only clones with functioning traT (irrespective of copy number) restored the normal antibiotic-resistant phenotype in the SS-A mutant. An incompatibility test using a donor strain which carried transposon Tn10 in the 60 MDa plasmid of S. typhimurium and a recipient in which Tn5 was placed close to the SS-A mutation indicated that the SS-A mutation was located in the 60 MDa virulence plasmid (previously called the cryptic plasmid) of S. typhimurium. The introduction of the large virulence plasmid carrying the SS-A mutant allele into wild-type S. typhimurium or Escherichia coli resulted in strains with a phenotype identical to that of the original SS-A mutant.

Mucormycosis in patients with multiple-organ failure.

Mucormycosis in two patients with multiple-organ failure appeared as a cutaneous lesion and spread rapidly. In the first case, wet mounts and potassium hydroxide preparations were unhelpful, but a punch biopsy specimen established the diagnosis. Prompt and extensive debridement and amphotericin B administration arrested the infection. In the second case, virulent progression of the lesion occurred despite limited amputation, debridement, transfer factor, and amphotericin B, but finally responded to further amputation. Diagnosis was made by histologic examination of infected tissue. Both patients shared the following predisposing factors: sepsis, low blood flow, acidosis, multiple-organ failure, and multiple-antibiotic therapy. Although the mucormycosis was controlled, as confirmed in the first case at autopsy and in the second case by clear margins following reamputation, the outcome was fatal in both cases due to other features of multiple-organ failure.

Antiarrhythmic action of labetalol and its effect on adenine metabolism in the isolated rat heart.

Labetalol, a combined alpha- and beta-adrenergic antagonist, was assessed for antiarrhythmic activity in the isolated perfused rat heart. Inclusion of 5.0 and 7.5 mumol/liter labetalol in the perfusate reduced the fall in ventricular fibrillation threshold and eliminated ventricular arrhythmias during the coronary occlusion period of 15 minutes. In treated hearts, levels of high energy phosphates were significantly higher and lactate, adenosine and hypoxanthine levels were lower in ischemic myocardium. Cyclic adenosine monophosphate levels were reduced in uninvolved myocardium (0.31 +/- 0.01 and 0.24 +/- 0.02 versus 0.43 +/- 0.02 nmol/g fresh weight) and in the ischemic myocardium (0.38 +/- 0.02 and 0.34 +/- 0.04 versus 0.65 +/- 0.05 nmol/g) in hearts treated respectively with 5.0 and 7.5 mumol/liter labetalol versus control hearts. When untreated hearts were perfused with 3.0 mmol/liter potassium in perfusate, all had ventricular tachycardia or fibrillation during coronary ligation and developed ventricular fibrillation after reperfusion. Labetalol, 5.0 mumol/liter, reduced ventricular tachyarrhythmias during coronary occlusion and after reperfusion, whereas labetalol, 7.5 mumol/liter, eliminated tachyarrhythmias during occlusion and reperfusion. Labetalol had potent antiarrhythmic activity in the hearts rendered uniformly prone to arrhythmias by perfusion with a low potassium solution.