Diagnostic strategies and outcomes on three New Zealand deer farms with severe outbreaks of bovine tuberculosis

SETTING: Three commercial deer herds, each containing more than 500 deer, experienced outbreaks of tuberculosis (TB) ranging from a 6% prevalence to disease levels >50%. Intensive diagnostic testing was carried out over short time intervals after the initial diagnosis of TB. OBJECTIVE: To eradicate M. bovis infection from herds of farmed red deer (Cervus elaphus) in New Zealand, which had significant outbreaks of tuberculosis (>5%), using complementary diagnostic tests and elective slaughter of all test positive animals. DESIGN: Whole herd mid cervical skin tests (MCT) were used as the primary test and a comparative cervical test (CCT) as an ancillary test. In an attempt to enhance TB eradication, ancillary blood tests comprising; lymphocyte transformation tests (LT) and enzyme-linked immunosorbent assays (ELISA) were used in parallel with MCT, or as serial tests, to complement skin testing. RESULTS: One deer herd (N), which had an acute outbreak (6%) of TB in adult stock, responded quickly to testing and the disease was eradicated within 12 months. A second more chronically infected herd (B), with low prevalence (2%) of TB initially in pregnant hinds which were retained over the breeding cycle, developed widespread uncontrollable spread of infection, that could not be contained by exhaustive testing. The final herd (S), which had an acute outbreak of TB at a prevalence >90% in young fawns, responded well to testing and became TB-free within 1 year. CONCLUSIONS: TB can be eradicated from infected farmed deer herds, using currently available TB tests, irrespective of disease prevalence. The caveat is that disease must be diagnosed early in the acute phase of infection. Undiagnosed infection over winter in breeding hinds in one herd produced a refractory infection in adult males and females and uncontrollable spread to newborn fawns. Disease could not be eradicated using comprehensive diagnostic schedules. A widespread but controllable outbreak of acute TB in another herd, appeared to have caused sufficient selective pressure on adult stock that genetically resistant adults were selected within a very short time frame (<1 year).     

Sparing effect of hemoglobin F and hemoglobin A2 on the polymerization of hemoglobin S at physiologic ligand saturations.

Recent interest in therapies for sickle cell anemia based on elevating fetal Hb has made accurate estimates of the sparing effect of fetal Hb (Hb F) and other non-sickle Hbs on sickle Hb (Hb S) polymerization essential. We have developed a technique, using HbCO as surrogate for HbO2, that enables us to assess the solubility of Hb S as a function of ligand saturation under conditions that mimic those of the sickling disorders. Equimolar mixtures of unliganded Hb S with Hb F or normal Hb A2 were isosoluble. Solubilities for equimolar mixtures with normal (Hb A) or abnormal (Hb C) Hbs were also identical but were lower than in the prior case. Thus, the sparing effect of both Hb F and Hb A2 should be considered in therapeutic strategies designed to modify Hb S polymerization. Hemolysates, stripped of 2,3-bisphosphoglycerate, from sickle cell disease patients with Hb (F + A2) levels varying from 6 to 25%, as well as from a sickle trait individual, were used to evaluate equilibrium solubility as a function of ligand saturation over the range of pathophysiologic interest (25-70%). Our results show that the sparing effect of Hb (F + A2) increases relative to that of Hb A as ligand saturation increases, and that in the absence of ligand, approximately 30% Hb (F + A2) is essentially isosoluble with the 60% Hb A of sickle trait. Although detailed knowledge of expected therapeutic benefits is confounded by the heterogeneity of Hb F distribution and other variables, these data should provide a framework for estimating likely clinical benefit from pharmacologic efforts to modulate globin gene expression.     

Systematic review of pressure injury prevalence in Australian and New Zealand hospitals

BackgroundPressure injuries have a major impact on patients and healthcare organisations. The complications of pressure injuries increase morbidity and mortality rates and are costly to individuals and healthcare systems. The total prevalence rate of pressure injuries within acute care hospitals in Australia and New Zealand is unknown, and despite a focus on prevention, pressure injuries still occur within these hospital settings.AimTo report the prevalence of pressure injuries within acute care settings in Australian and New Zealand hospitals and to identify the stage and location of pressure injuries and analyse the methods used to conduct pressure injury point prevalence studies.MethodsA systematic review of studies published in CINAHL, MEDLINE and Cochrane databases and a two-part grey literature search, including a customised Google search and a targeted website search, was undertaken up to July 2019. The systematic review was prospectively registered with PROSPERO (CRD42018105566).FindingsThe overall prevalence of pressure injuries in acute-care hospitals in Australia and New Zealand is 12.9% (95% CI, 9.5%–16.8%) and the hospital-acquired pressure injury prevalence is 7.9% (95% CI, 5.7%–10.3%). Stage I and stage II are the most common pressure injuries. The most frequent locations for pressure injuries are the sacrum/buttock/coccyx area (41%) and the heels (31%). The reporting of details about methodology varies considerably between studies.DiscussionPressure injuries remain a significant problem within acute-care hospital settings. Total prevalence rates are decreasing over time with the numbers of stage I and II pressure injuries decreasing faster than other pressure injuries.ConclusionThe findings from this study can be used to set performance benchmarks within acute-care hospitals in Australia and New Zealand. Pressure injuries are preventable and pressure injury prevalence studies can be used to monitor the effectiveness of nursing care processes to improve patient outcomes.     

Method to map antigenic determinants recognized by monoclonal antibodies: localization of a determinant of virus neutralization on the feline leukemia virus envelope protein gp70.

A method is presented whereby antigenic determinants recognized by specific monoclonal antibodies can be mapped to specific sites on a protein sequence with high resolution. Short DNase I-generated DNA fragments encoding portions of the protein of interest are molecularly cloned into the EcoRI site of the beta-galactosidase gene of phage lambda Charon 16 so as to obtain expression of random protein fragments as fusion proteins. The monoclonal antibody is used to screen the phage library to isolate phage expressing the specific antigenic determinant. DNA of immunoreactive phage can be analyzed rapidly and subcloned to allow DNA sequence determination. The method is generally applicable and permits antigenic determinants of functionally interesting monoclonal antibodies to be mapped and related to specific protein sequences. We have used this procedure to determine the region of the feline leukemia virus envelope protein gp70 recognized by a virus-neutralizing monoclonal antibody, cl.25. Antibody binding was mapped to a 14-amino acid region in the amino-terminal half of gp70. This region may be directly involved in an essential function of the gp70 protein, perhaps in gp70-mediated host recognition functions. Synthetic peptides derived from this region may provide useful vaccine antigens for the prevention of feline leukemia virus-associated disease in cats.     

Inhibition of pentagastrin-stimulated gastric secretion by duodenal acidification or administration of fat in normal subjects and in patients with duodenal ulcer

The inhibitory effect of duodenal acidification and intraduodenal fat infusion on pentagastrin-stimulated gastric secretion in normal subjects and in patients with duodenal ulcer was studied. Intraduodenal infusion of acid resulted in inhibition of HCl secretion found to be significant only in ulcer patients. Pepsin output, although lower during the first 15 minutes of duodenal acidification, later increased. Intraduodenal infusion of olive oil resulted in significant inhibition of HCl and pepsin output in both groups of patients, which was maximal 45–60 minutes after the beginning of fat infusion. Gastric secretion was more readily inhibited in ulcer patients than in normal subjects; this difference was particularly evident in inhibition of pepsin secretion. In addition, decrease in concentration of HCl and pepsin was observed to be significant only in ulcer patients. Mechanisms by which duodenal acidification and fat inhibit gastric secretion are discussed. The results obtained suggest that secretin, which is probably responsible for inhibition after duodenal acidification, is not the inhibitor during inhibition by fat. The ulcer patients were found to have unimpaired mechanisms of inhibition by acid and fat.