Search PubMed⌕ Search

Biomedical subjects

D L Stevens

Publications and source records attributed to D L Stevens.

171 records · Page 10Linked to original sources

Spontaneous, nontraumatic gangrene due to Clostridium septicum.

Clostridium septicum is a major cause of spontaneous, nontraumatic gas gangrene. Unlike Clostridium perfringens, C. septicum is relatively aerotolerant and thus appears to be more capable of initiating infection in the absence of obvious damage to tissues. Six cases illustrate the clinical setting and fulminant nature of spontaneous gangrene caused by C. septicum. A lesion in the colon such as carcinoma is often present and is presumed to serve as a portal of entry to the bloodstream. Diabetes and leukopenia are also common predisposing conditions; compromise of vital host responses may facilitate proliferation of those organisms that settle out in the tissues. Acute lymphoma or leukemia during a course of chemotherapy is accompanied by damage to bowel mucosa and granulocytopenia, thus predisposing to spontaneous clostridial gangrene. Infection progresses in a fulminating manner; the majority of patients die within 24 hours of onset. Characteristic symptoms and signs include excruciating pain (although a sense of heaviness may be the only early symptom), swelling of tissues, crepitance, and bulla formation. A hallmark of C. septicum infection is the absence of acute inflammatory cells in involved tissues or in bulla fluid. A series of laboratory investigations demonstrated that fluid obtained from a bulla adversely affected the viability, morphology, and function of polymorphonuclear leukocytes (PMNs), which may explain the paucity of PMNs in involved tissues and may in part contribute to the fulminant progression observed in infection due to this organism.

Adenocarcinoma↗

The toxins of group A streptococcus, the flesh eating bacteria.

Streptococcus pyogenes causes a wide variety of infections in individuals of all ages in most countries of the world. Because of the frequency with which these infections occur, physicians are quite familiar with the diversity of clinical presentations associated with the Group A streptococcus. Yet in the late 1980's, a severe form of streptococcal infection, the Streptococcal Toxic Shock Syndrome, emerged and has persisted for the last 10 years. This syndrome is associated with invasive soft tissue infections and the early onset of shock and organ failure. The purpose of this paper is to briefly describe the epidemiologic and clinical features of the Streptococcal Toxic Shock Syndromes and to emphasize the role that toxins produced by S. pyogenes play in the pathogenesis of this disease.

Exotoxins↗

Superantigens: their role in infectious diseases.

In the last 10 years many of the superantigens of the microbial world have been defined and the mechanisms of cellular interaction between lymphocytes and antigen presenting cells has been elucidated in great detail. The consequences of superantigen stimulation of the immune system, though less well defined, can be considered in three separate stages: T-cell proliferation, apoptosis, and recovery. Understanding these stages may explain why diverse superantigens may cause markedly different clinical processes ranging from acute shock to chronic arthritis and may form the basis for novel treatments of these diverse diseases.

Bacterial Infections↗

Streptococcal toxic-shock syndrome: spectrum of disease, pathogenesis, and new concepts in treatment.

Since the 1980s there has been a marked increase in the recognition and reporting of highly invasive group A streptococcal infections with or without necrotizing fasciitis associated with shock and organ failure. Such dramatic cases have been defined as streptococcal toxic-shock syndrome. Strains of group A streptococci isolated from patients with invasive disease have been predominantly M types 1 and 3 that produce pyrogenic exotoxin A or B or both. In this paper, the clinical and demographic features of streptococcal bacteremia, myositis, and necrotizing fasciitis are presented and compared to those of streptococcal toxic-shock syndrome. Current concepts in the pathogenesis of invasive streptococcal infection are also presented, with emphasis on the interaction between group A Streptococcus virulence factors and host defense mechanisms. Finally, new concepts in the treatment of streptococcal toxic-shock syndrome are discussed.

Animals↗

Toxicity of aerosols of sodium reaction products.

Sodium is used as the heat transfer medium in several new energy technologies such as liquid-metal fast-breeder reactors and solar-thermal collection systems. Because sodium burns in air and reacts violently with water, the potential exists for an airborne release of sodium combustion products and subsequent human exposure. To help evaluate the potential short-term hazard from an accidental sodium fire, male juvenile or adult Wistar rats were exposed to sodium aerosols for 2 hours to determine the dose at which 50 percent of the animals were affected (ED50) for each age group. The estimated ED50 of 510 microgram/l for adults was not significantly different from the estimated ED50 of 489 microgram/l for juveniles. The incidence of acute laryngitis, attributed to exposure, was three times higher for juvenile rats than for adults, and the degree of severity of this lesion was significantly (P less than 0.05) higher for juveniles.

Aerosols↗

Epilepsy in the accident and emergency department.

Patients with epilepsy commonly present to the accident and emergency department. This review offers guidelines on a standardised approach to their assessment and management and a framework for potential audit.

Algorithms↗

Progressive myoclonus epilepsy with focal brainstem degeneration and paternal inheritance. An autopsy report of 4 cases from 2 pedigrees.

Four autopsied cases of myoclonus, ataxia, and epilepsy from 2 separate pedigrees are described. An identical pattern of focal brainstem lesions was found in all the cases with selective and symmetrical degeneration of the dentate and second order somatosensory nuclei. The combined clinical and pathological features did not appear to match any familial disorder previously described as causing progressive myoclonus epilepsy. Myoclonus epilepsy with ragged red fibres was excluded on the grounds of paternal inheritance and negative muscle biopsy findings, but the more acute lesions seen in 1 case are reminiscent of those found in Leigh's syndrome, and suggest that some other form of inherited defect of oxidative metabolism may be involved.

Brain Stem↗