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PubMedDate not supplied

Clinical outcome of invasive infections in children caused by highly penicillin-resistant Streptococcus pneumoniae compared with infections caused by penicillin-susceptible strains.

BACKGROUND: In this report based on data from the Institutional Surveillance System during 1994-1998, we document the continuing emergence of drug-resistant Streptococcus pneumoniae strains at the Hospital Infantil de Mexico Federico Gómez in Mexico City. METHODS: We evaluate the clinical course of 49 invasive pneumococcal infection outside the central nervous system (CNS) by a number of factors including the site, severity, and place where the infection was acquired, the underlying health of the patient, and the adequacy of antimicrobial therapy. RESULTS: An underlying illness was present in 21 of 49 (43%) patients, 37 (75%) patients had taken previous antimicrobial therapy, and 25% of the infections were nosocomially acquired. Overall, 25 of 49 (51%) of the pneumococcal strains tested were pencillin-resistant; strains with the highest resistance to penicillin were also resistant to cephalosporins. Twenty-two percent of all strains were considered to be multidrug-resistant. Eleven of 25 penicillin-resistant strains were identified as multidrug-resistant, i.e., to erythromycin, TMP/SMX, and chloramphenicol. Ten serotypes accounted for 88% of the isolates, the most frequent serotypes being 23F, 14, 19V, 6A, and 6B. The overall case-fatality rate was 37% (18 of 49), with most deaths occurring within 3-5 days after antibiotic therapy was initiated. There was no difference in the case fatality rate between children with penicillin-nonsusceptible and penicillin-susceptible pneumococcal infections; instead; case-fatality rate correlated with severity of illness on admission and presence of underlying disease. CONCLUSIONS: Characterizing groups at risk for invasive pneumococcal disease could aid in the development of preventive programs and increase the benefits from wide use of future conjugated vaccines.

AIDS-Related Opportunistic Infections↗
PubMed2001

[Anterior compartment syndrome of the forearm caused by exercise: unusual cause of recurrent episodes of acute effort rhabdomyolysis].

INTRODUCTION: An effort-related compartmental syndrome is well known in the leg, but may be present infrequently, acutely or chronically in the anterior compartment of the forearm. EXEGESIS: We report a case of a 32-year-old man who presented four times after climbing exercises a bilateral compartment of the forearm, unusual because of the observation of rhabdomyolysis, but without irreversible damage. Clinical information and follow-up on two acute and 14 chronic cases were reexamined, showing a homogenous presentation. He refused fasciotomy because he stopped athletic activities. Measurement of intramuscular pressure after exertion was useful for diagnosis. CONCLUSION: A local effort-related pain must call to mind a chronic compartment syndrome of the forearm, which may risk incurring the acute form, with irreversible lesions of muscle and nerve, and possibly renal failure because of rhabdomyolysis.

Acute Disease↗
PubMed1990

[Hepatic veno-occlusive disease caused by Deticene: a cause of acute hypovolemic shock].

A case is reported of severe hypovolaemic shock occurring in a 53-year-old female patient undergoing a second course of chemotherapy with intravenous DTIC for a malignant melanoma. A few hours after the injection of DTIC, she became shocked, with loss of peripheral pulses, polypnoea and cutaneous vasoconstriction. She also had pain and guarding of the right hypocondrium. She was given 4 litres of colloids within 2 hours, together with 10 micrograms.kg-1.min-1 dopamine. Abdominal echography showed hepatomegaly, with a permeable portal vein. However biological investigations revealed lactic acidosis with hepatic cytolysis and hepatic failure. Nuclear magnetic resonance imaging displayed a reduced portal venous flow, with abnormally small hepatic veins. Fluid replacement was continued, together with administration of small doses of heparin (1 mg.kg-1.day-1) and hydrocortisone hemisuccinate 5 mg.kg-1.day-1. The status of patient worsened over the next few hours, because of the development of a very large volume of exudative ascites and bilateral pleural effusions. Despite continuing fluid replacement (91), she became anuric at the 24th hour, requiring haemodialysis. However, her condition became stable, and then slowly improved. Fluid replacement was stopped after 72 h, steroids after a fortnight. Liver function tests returned to normal after the third week, together with diuresis. The patient was able to leave the ICU after 24 days. Physicians should be aware of this rare, often fatal side-effect, probably of immuno-allergic origin.

Abdominal Pain↗
PubMed2005

Candidacidal effects of two antimicrobial peptides: histatin 5 causes small membrane defects, but LL-37 causes massive disruption of the cell membrane.

The effects of antimicrobial peptides on artificial membranes have been well-documented; however, reports on the ultrastructural effects on the membranes of micro-organisms are relatively scarce. We compared the effects of histatin 5 and LL-37, two antimicrobial peptides present in human saliva, on the functional and morphological properties of the Candida albicans cell membrane. Fluorescence microscopy and immunogold transmission electron microscopy revealed that LL-37 remained associated with the cell wall and cell membrane, whereas histatin 5 transmigrated over the membrane and accumulated intracellularly. Freeze-fracture electron microscopy revealed that LL-37 severely affected the membrane morphology, resulting in the disintegration of the membrane bilayer into discrete vesicles, and an instantaneous efflux of small molecules such as ATP as well as larger molecules such as proteins with molecular masses up to 40 kDa. The effects of histatin 5 on the membrane morphology were less pronounced, but still resulted in the efflux of nucleotides. As the morphological defects induced by histatin 5 are much smaller than those induced by LL-37, but the efflux of nucleotides is similar at comparable candidacidal concentrations, we suggest that the loss of nucleotides plays an important role in the killing process.

Antifungal Agents↗
PubMed1993

Magnesium sulphate reverses the carotid vasoconstriction caused by endothelin-I, angiotensin II and neuropeptide-Y, but not that caused by NG-nitro-L-arginine methyl ester, in conscious rats.

1. Magnesium sulphate (MgSO4) has been used for many years in the prevention of eclamptic seizures, but its mechanism of action has never been elucidated. Recent studies suggest that cerebral vasospasm is an important feature of eclampsia and we have developed and tested the hypothesis that MgSO4 can reverse cerebral vasoconstriction. 2. Studies were performed in conscious, male Long Evans rats with pulsed Doppler probes sutured around both common carotid arteries after the external carotid artery had been ligated on the left, thus allowing simultaneous measurement of changes in common and internal carotid blood flow. Intravascular catheters were placed in the abdominal aorta for measurement of systemic blood pressure and in the right jugular vein for administration of drugs. Mean arterial blood pressure and mean Doppler shift signals were used to calculate percentage changes in common and internal carotid vascular conductance. 3. After a period of recovery the animals were infused with endothelin-1, angiotensin II, neuropeptide-Y or NG-nitro-L-arginine methyl ester alone or in combination, and MgSO4 in low or high dose was infused when the effects of the vasoconstrictors had become established. 4. MgSO4 itself, at the low dose, had no effect on carotid vascular conductance. Endothelin-1, angiotensin II and neuropeptide-Y all reduced common and internal carotid vascular conductance and this effect was significantly attenuated by low dose MgSO4. The carotid vasoconstrictor action of endothelin-1 was completely abolished by high dose MgSO4.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed2001

New mutations in keratin 1 that cause bullous congenital ichthyosiform erythroderma and keratin 2e that cause ichthyosis bullosa of Siemens.

The intermediate filaments of epithelial cells are formed by keratins, a family of structurally related proteins, which are expressed in pairs of acidic (type I) and basic (type II) polypeptides in a tissue- and differentiation-specific manner. Mutations in the genes encoding several keratins have been implicated in the pathogenesis of diseases of keratinization. We report molecular analysis of two patients with the rare autosomal dominant disorders bullous congenital ichthyosiform erythroderma (BCIE) and ichthyosis bullosa of Siemens (IBS). Previous studies have shown that these genodermatoses are due to mutations in the KRT1 and KRT2E genes, respectively. We report a new amino acid substitution mutation in codon 155 of KRT1 (valine to aspartic acid) in the conserved H1 domain of the protein in the patient with BCIE. We also report a novel amino acid substitution mutation in codon 192 of KRT2E (asparagine to lysine) in the conserved 1A helix initiation peptide of the protein in the patient with IBS. Our results demonstrate that these mutations are deleterious to keratin filament network stability and lead to specific clinical inherited disorders of keratinization.

Adult↗
PubMed1998

Farmers' occupational health: cause for concern, cause for action.

This study examines occupational health and safety provision from farmers' perspectives, to address the question 'Are farmers' health and safety needs being met?' Given that farmers encounter a variety of health and safety risks in the course of their daily work, and that available statistics clearly indicate they are a high risk group, a review of the literature suggests that this area has attracted little research attention. No study has critically examined the system of occupational health and safety provision for farmers and no attempts have been made to elicit farmers' perspectives on the subject. A telephone survey using a questionnaire divided into four sections, involving a random sample of 150 farmers from the counties of Cumbria, Cheshire and Cambridgeshire in England, found that farmers considered the system of occupational health and safety provision to be inadequate and that their occupational health and safety needs were not being met. Recommendations for improvements are made based on the results of the survey.

Adolescent↗
PubMed1997

Spontaneous duplication of a 661 bp element within a two-component sensor regulator gene causes phenotypic switching in colonies of Pseudomonas tolaasii, cause of brown blotch disease of mushrooms.

Spontaneous sectoring of Pseudomonas tolaasii colonies results in a phenotypic switch from the smooth, pathogenic form (designated 1116S) to the rough non-pathogenic form (designated 1116R). This phenotypic switch can also be induced by mutation of the pheN master regulatory locus, which encodes a 99 kDa protein with homology to the conserved family of sensor regulator proteins. Southern blot analysis of genomic DNA from 1116S and 1116R probed with a 3.4 kb Xhol-BamHI fragment containing the pheN gene has revealed restriction fragment length polymorphisms in the pheN locus of 1116R. In order to characterize the genetic basis of this variation, the pheN locus (designated pheN') was cloned from 1116R and its nucleotide sequence determined. A 661 bp duplication was identified within pheN' introducing a frameshift mutation in the predicted pheN open reading frame (ORF). A resulting predicted ORF of pheN' designated ORF2 encodes a polypeptide of 706 amino acid residues, with a predicted molecular weight of 77 kDa, and which lacks part of the PheN sensor domain. Southern blot analysis of genomic DNA using a probe within the duplicated sequence revealed the presence of two bands in 1116R but only one band in the 1116S form. Polymerase chain reaction (PCR) analysis of 25 independently isolated 1116R sectors using primers flanking the duplication site in pheN confirmed the presence of the duplicated 661 bp sequence within this region in all of the sectors and the absence of the duplicated sequence in spontaneous revertants from 1116R to 1116S. Northern blot analysis of RNA from 1116S and 1116R using a pheN probe showed that ORF2 was transcribed in the 1116R form. The presence of a truncated PheN protein in 1116R was verified by Western blot analysis of total cell protein using a LemA antiserum, which revealed the presence of 99kDa and 77kDa cross-reactive bands in 1116S and 1116R respectively. It is concluded that the spontaneous colony-sectoring event that results in the 1116R phenotypic variant form of P. tolaasii arises owing to a 661 bp DNA duplication within the 5' end of the pheN gene, which results in loss of the periplasmic sensor domain of PheN and elimination of normal PheN function.

Fungi↗