Pelvic Outlet Obstruction Secondary to Salmonella enterica serovar Bovismorbificans Abscess.

We present a case of a 30-year-old Hispanic male with pelvic outlet obstruction syndrome secondary to a large pelvic abscess caused by Salmonella enterica Bovismorbificans. This case demonstrates a potentially serious complication of a rare foodborne illness in the United States, in which an urgent surgical intervention was warranted. A computed tomography (CT) scan of the abdomen and pelvis demonstrated a large pelvic cystic mass causing near-total pelvic outlet obstruction of both gastrointestinal and genitourinary systems. A total of 1,250 mg of IV vancomycin and 3.375 mg of IV piperacillin-tazobactam were administered every eight hours, and an urgent decompressive transverse loop colostomy, Foley catheter placement, and percutaneous drainage were performed. Culture of the abscess fluid identified Salmonella enterica serotype Bovismorbificans, and the antibiotic regimen was changed to 1,000 mg IV ceftriaxone every 24 hours. Subsequent CT imaging displayed a reduction in abscess size. The patient was then discharged with a 14-day course of 500 mg of oral ciprofloxacin every 12 hours and 500 mg of oral metronidazole every eight hours. Imaging at three weeks post-discharge displayed resolution of the abscess, and the drain was removed. The patient had complete recovery and did well several months following treatment. While rare, Salmonella enterica serotype Bovismorbificans could potentially lead to serious complications such as giant pelvic abscess, in which a multidisciplinary team approach (i.e., medical, surgical, and interventional) is critical for a good outcome.

Transmural heterogeneity of cellular level power output is reduced in human heart failure.

Heart failure is associated with pump dysfunction and remodeling but it is not yet known if the condition affects different transmural regions of the heart in the same way. We tested the hypotheses that the left ventricles of non-failing human hearts exhibit transmural heterogeneity of cellular level contractile properties, and that heart failure produces transmural region-specific changes in contractile function. Permeabilized samples were prepared from the sub-epicardial, mid-myocardial, and sub-endocardial regions of the left ventricular free wall of non-failing (n=6) and failing (n=10) human hearts. Power, an in vitro index of systolic function, was higher in non-failing mid-myocardial samples (0.59±0.06µWmg(-1)) than in samples from the sub-epicardium (p=0.021) and the sub-endocardium (p=0.015). Non-failing mid-myocardial samples also produced more isometric force (14.3±1.33kNm(-2)) than samples from the sub-epicardium (p=0.008) and the sub-endocardium (p=0.026). Heart failure reduced power (p=0.009) and force (p=0.042) but affected the mid-myocardium more than the other transmural regions. Fibrosis increased with heart failure (p=0.021) and mid-myocardial tissue from failing hearts contained more collagen than matched sub-epicardial (p<0.001) and sub-endocardial (p=0.043) samples. Power output was correlated with the relative content of actin and troponin I, and was also statistically linked to the relative content and phosphorylation of desmin and myosin light chain-1. Non-failing human hearts exhibit transmural heterogeneity of contractile properties. In failing organs, region-specific fibrosis produces the greatest contractile deficits in the mid-myocardium. Targeting fibrosis and sarcomeric proteins in the mid-myocardium may be particularly effective therapies for heart failure.

Altered ventricular torsion and transmural patterns of myocyte relaxation precede heart failure in aging F344 rats.

The purpose of this study was to identify and explain changes in ventricular and cellular function that contribute to aging-associated cardiovascular disease in aging F344 rats. Three groups of female F344 rats, aged 6, 18, and 22 mo, were studied. Echocardiographic measurements in isoflurane-anesthetized animals showed an increase in peak left ventricular torsion between the 6- and the 18-mo-old groups that was partially reversed in the 22-mo-old animals (P < 0.05). Epicardial, midmyocardial, and endocardial myocytes were subsequently isolated from the left ventricles of each group of rats. Unloaded sarcomere shortening and Ca(2+) transients were then measured in these cells (n = >75 cells for each of the nine age-region groups). The decay time of the Ca(2+) transient and the time required for 50% length relaxation both increased with age but not uniformly across the three regions (P < 0.02). Further analysis revealed a significant shift in the transmural distribution of these properties between 18 and 22 mo of age, with the largest changes occurring in epicardial myocytes. Computational modeling suggested that these changes were due in part to slower Ca(2+) dissociation from troponin in aging epicardial myocytes. Subsequent biochemical assays revealed a >50% reduction in troponin I phosphoprotein content in 22-mo-old epicardium relative to the other regions. These data suggest that between 18 and 22 mo of age (before the onset of heart failure), F344 rats display epicardial-specific myofilament-level modifications that 1) break from the progression observed between 6 and 18 mo and 2) coincide with aberrant patterns of cardiac torsion.