Comparison of mortality risk associated with bacteremia due to methicillin-resistant and methicillin-susceptible Staphylococcus aureus.

OBJECTIVE: To quantify the clinical impact of methicillin-resistance in Staphylococcus aureus causing infection complicated by bacteremia in adult patients, while controlling for the severity of patients' underlying illnesses. DESIGN: Retrospective cohort study from October 1, 1995, through December 31, 2003. PATIENTS AND SETTING: A total of 438 patients with S. aureus infection complicated by bacteremia from a single Veterans Affairs healthcare system. RESULTS: We found that 193 (44%) of the 438 patients had methicillin-resistant S. aureus (MRSA) infection and 114 (26%) died of causes attributable to S. aureus infection within 90 days after the infection was identified. Patients with MRSA infection had a higher mortality risk, compared with patients with methicillin-susceptible S. aureus (MSSA) infections (relative risk, 1.7 [95% confidence interval, 1.3-2.4]; P<.01), except for patients with pneumonia (relative risk, 0.7 [95% confidence interval, 0.4-1.3]). Patients with MRSA infections were significantly older (P<.01), had more underlying diseases (P=.02), and were more likely to have severe sepsis in response to their infection (P<.01) compared with patients with MSSA bacteremia. Patients who died within 90 days after S. aureus infection was identified were significantly older (P<.01) and more likely to have severe sepsis (P<.01) and pneumonia (P=.01), compared with patients who survived. After adjusting for age as a confounder, comorbidities, and pneumonia as an effect modifier, S. aureus infection-related mortality remained significantly higher in patients with MRSA infection than in those with MSSA infection, among those without pneumonia (hazard ratio, 1.8 [95% confidence interval, 1.2-3.0]); P<.01. CONCLUSIONS: The results of this study suggest that patients with MRSA infections other than pneumonia have a higher mortality risk than patients with MSSA infections other than pneumonia, independent of the severity of patients' underlying illnesses.     

Effect of dietary zinc deficiency on the endogenous phosphorylation and dephosphorylation of rat erythrocyte membrane

The effect of dietary zinc deficiency on patterns of phosphorylation and dephosphorylation of rat erythrocyte membrane proteins and erythrocyte filterability was examined. Weanling male Wistar rats were fed an egg white-based diet containing less than 1.1 mg zinc/kg diet ad libitum for 3 wk. Control rats were either pair-fed or ad libitum-fed the basal diet supplemented with 100 mg zinc/kg diet. Net phosphorylation and dephosphorylation of erythrocyte membrane proteins were carried out by an in vitro assay utilizing [gamma-32P]ATP. The membrane proteins were subsequently separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the 32P content of gel slices was counted by Cerenkov counting. Erythrocyte filterability was measured as the filtration time of suspensions of erythrocytes, both untreated and preincubated with diamide, under constant pressure. Erythrocyte ghosts from zinc-deficient rats demonstrated greater dephosphorylation of protein bands R1 plus R2 and R7 than pair-fed rats and greater net phosphorylation of band R2.2 than pair-fed or ad libitum-fed control rats (P less than 0.05). Erythrocytes from ad libitum-fed control rats showed significantly longer filtration times than those from zinc-deficient or pair-fed control rats. In conclusion, dietary zinc deficiency alters in vitro patterns of erythrocyte membrane protein phosphorylation and dephosphorylation, whereas the depression in food intake associated with the zinc deficiency increases erythrocyte filterability.     

Reperfusion pulmonary edema

Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B4 and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. We conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and, third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.     

Revisiting the Relationship between Managed Care and Hospital Consolidation

Objective. This paper analyzes whether the rise in managed care during the 1990s caused the increase in hospital concentration.
Data Sources. We assemble data from the American Hospital Association, InterStudy and government censuses from 1990 to 2000.
Study Design. We employ linear regression analyses on long differenced data to estimate the impact of managed care penetration on hospital consolidation. Instrumental variable analogs of these regressions are also analyzed to control for potential endogeneity.
Data Collection. All data are from secondary sources merged at the level of the Health Care Services Area.
Principle Findings. In 1990, the mean population-weighted hospital Herfindahl–Hirschman index (HHI) in a Health Services Area was .19. By 2000, the HHI had risen to .26. Most of this increase in hospital concentration is due to hospital consolidation. Over the same time frame HMO penetration increased three fold. However, our regression analysis strongly implies that the rise of managed care did not cause the hospital consolidation wave. This finding is robust to a number of different specifications.     

A rat model of otitis media with effusion caused by eustachian tube obstruction with and without Streptococcus pneumoniae infection: methods and disease course.

OBJECTIVE: To describe the clinical and histopathologic progression of a rat model of otitis media with effusion caused by eustachian tube obstruction (ETO) with and without Streptococcus pneumoniae infection. METHODS: In 164 rats, the left, bony eustachian tube was approached via a ventral incision and obstructed with dental material. Then 108 rats were infected via an intrabullar injection with S pneumoniae. At 48 hours, the infected rats were treated for 5 days with ampicillin. All ears were evaluated by weekly otomicroscopy. On each of days 1, 2, 7, 21, 35, 56, and 112, four rats were killed for histologic study. All effusions were cultured for bacteria. RESULTS: Fourteen rats died of surgical complications; effusion resolved by 2 weeks in 9 rats. During the first few days, infected ears with ETO had bulging tympanic membranes, followed by tympanic membrane retraction, purulent effusion, and otorrhea (50%) over the next few weeks, whereas uninfected ears with ETO developed retraction and serous effusion during the same time frame. At later times, all ears with ETO presented with retraction and serous or serous-mucoid effusion. S pneumoniae was recovered only from the infected ears with ETO (days 1 and 2), with some colonization by nonpathogenic microorganisms observed equally in both groups of ears. Histology showed a typical acute inflammatory reaction in the challenged ears with ETO through day 14 and then a chronic inflammation for all ears with ETO. CONCLUSION: The experimental methods provoked reproducible pathologic signs similar to those for otitis media with effusion. Given the availability of rat-specific reagents, this model is well suited for studies of cytokine elaboration during disease pathogenesis.     

Optic chiasm glioma associated with inappropriate secretion of antidiuretic hormone,cerebral ischemia,nonobstructive hydrocephalus and chronic ascites following ventriculoperitoneal shunting

An optic chiasm glioma may cause loss of vision, endocrine disturbances, hydrocephalus and cerebral ischemia due to its proximity to the pituitary, hypothalamus, III ventricle and internal carotids. A 3-month-old infant with optic chiasm glioma developed hypopituitarism and inappropriate secretion of antidiuretic hormone with plasma hypo-osmolality. The cerebrospinal fluid (CSF) protein concentration was markedly elevated. The impairment of fluid absorption via arachnoid villi and peritoneum by the high protein content, and reversed osmotic gradient between protein-rich CSF and hypo-osmolar plasma may have contributed to both nonobstructive hydrocephalus and recurrent ascites following ventriculoperitoneal shunting. Cerebral ischemia from carotid compression may have led to cerebral atrophy.     

Radical cystectomy after coronary artery bypass graft

Nine patients have undergone single-stage radical cystectomy and ileal conduit urinary diversion two to fifty-one months after coronary artery bypass procedures. Two patients presenting with intractable angina at the time their malignant disease was being evaluated required bypass surgery before cystectomy could be undertaken. No significant cardiac morbidity occurred postoperatively, and all remain alive without evidence of malignant disease.