Cooccurrence of Multiple AmpC β-Lactamases in Escherichia coli,Klebsiella pneumoniae,and Proteus mirabilis in Tunisia

Over a period of 40 months, plasmid-mediated AmpC β-lactamases were detected in Tunis, Tunisia, in 78 isolates (0.59%) of Escherichia coli, Klebsiella pneumoniae, and Proteus mirabilis. In 67 isolates, only one ampC gene was detected, i.e., bla_CMY-2-type (n = 33), bla_ACC (n = 23), bla_DHA (n = 6) or bla_EBC (n = 5). Multiple ampC genes were detected in 11 isolates, with the following distribution: bla_MOX-2, bla_FOX-3, and bla_CMY-4/16 (n = 6), bla_FOX-3 and bla_MOX-2 (n = 3), and bla_CMY-4 and bla_MOX-2 (n = 2). A great variety of plasmids carrying these genes was found, independently of the species and the bla gene. If the genetic context of bla_CMY-2-type is variable, that of bla_MOX-2, reported in part previously, is unique and that of bla_FOX-3 is unique and new.     

Protein kinase Czeta (PKCzeta) regulates ocular inflammation and apoptosis in endotoxin-induced uveitis (EIU): signaling molecules involved in EIU resolution by PKCzeta inhibitor and interleukin-13

We show that inhibitory effect of interleukin-13 on endotoxin-induced uveitis in the Lewis rat is dependent on signaling activity of protein kinase Czeta (PKCzeta). To understand the effect of interleukin-13 or PKCzeta inhibitor treatment, the activation status of rat bone marrow-derived macrophages was studied in vitro. At 6 hours, lipopolysaccharide-stimulated macrophages produced tumor necrosis factor-alpha (TNF-alpha) with nuclear factor kappaB (NF-kappaB)/p65 expression. Treatment led to absence of NF-kappaB/p65 expression and low levels of TNF-alpha, suggesting accelerated inactivation of macrophages. At 24 hours after lipopolysaccharide stimulation, nuclear NF-kappaB/p65 decreased and nuclear NF-kappaB/p50 increased, associated with nuclear BCL-3 and a low level of TNF-alpha, indicating onset of spontaneous resolution. Treatment limited PKCzeta cleavage, with expression of nuclear NF-kappaB/p50 and BCL-3 and low nuclear NF-kappaB/p65 promoting macrophage survival, as evidenced by Bcl-2 expression. At 24 hours, intraocular treatment decreased membranous expression of PKCzeta by ocular cells, reduced vascular leakage with low nitric-oxide synthase-2 expression in vascular endothelial cells, and limited inflammatory cell infiltration with decreased intraocular TNF-alpha, interleukin-6, and nitric-oxide synthase-2 mRNA. Importantly, treatment decreased nuclear NF-kappaB/p65, increased transforming growth factor-beta2, and reduced caspase 3 expression in infiltrating macrophages, implying a change of their phenotype within ocular microenvironment. Treatment accelerated endotoxin-induced uveitis resolution through premature apoptosis of neutrophils related to high expression of toll-like receptor 4 and caspase 3.     

Familial cases of glomerulonephritis complicating Crohn's disease

A part from nephrolithiasis, renal involvement is rare in the course of Crohn's disease, particularly glomerulonephritis. On the other hand, while onset of Crohn's disease is strongly influenced by environmental and genetic factors, little is known regarding influence of these factors on extra intestinal manifestations. We report a familial case of glomerulonephritis that occurred in a 38-year old woman and her mother, 59 years old with a 7-year and a 37 year history of stenosing ileocolonic disease, respectively. Both of them developed peripheral oedema with nephrotic syndrome during the course of their Crohn's disease while they had no intestinal symptoms and were not receiving any maintenance therapy. Renal function was conserved in the former while the latter developed renal failure and had already small size kidneys on abdominal sonography. Thus, renal biopsy had been performed only in the former patient and had showed membranous glomerulonephritis. Investigations showed no other underlying disease than Crohn's disease. Through this report we emphasis possible genetic influence on extra intestinal manifestations, particularly glomerulonephritis, in Crohn's disease patients.     

Idiopathic avascular necrosis of the femoral heads in five members of a Moroccan family

Avascular necrosis (AVN) is idiopathic in about 40% of cases. The pathophysiology of avascular necrosis remains incompletely elucidated. Here, we report a case that underlines the role for inherited factors in AVN of the femoral heads. Idiopathic AVN of the femoral heads occurred in five members of the same family (a woman, her two paternal aunts, her male paternal cousin and her female paternal cousin) at a mean age of 42.4 years (range, 33–58 years). Standard pelvic radiographs showed Arlet and Ficat stage 4 AVN in three patients and stage 3 in two patients. None of the patients had a history of glucocorticoid therapy, alcohol abuse, or trauma. All five patients underwent investigations for a cause, including blood cell counts, a lipid profile, coagulation tests, testing for antinuclear antibodies, hemoglobin electrophoresis, ultrasonography of the abdomen, and standard radiographs of the long limb bones. The results were normal or negative, ruling out known hereditary causes of AVN such as sickle cell anemia and Gaucher disease. Many cases of familial AVN of the femoral head have been described in patients with sickle cell anemia or Gaucher disease. However, only five families with idiopathic familial AVN of the femoral heads have been reported (three in the US and two in Taiwan). All the patients in these families had isolated bilateral AVN of the femoral heads without AVN at other sites.