Reactivation of dormant lumbar methicillin-resistant Staphylococcus aureus osteomyelitis after 12 years.

The adequate treatment of methicillin-resistant Staphylococcus aureus (MRSA) osteomyelitis has intrigued clinicians for some time. As the resistance of these pathogens, coupled with the increase in community-acquired cases, continues steadily to rise, clinicians are finding it useful to employ multi-modal approaches for efficacious treatment. The authors present a single case report of a patient with recurrent MRSA osteomyelitis, lumbar paraspinal and epidural abscess. He was found to have decreased muscle strength and was hyporeflexic in the involved extremity. Serum testing demonstrated MRSA bacteremia. Neuroimaging studies revealed evidence of paraspinal abscess and a presumed herniated nucleus pulposus at the L5/S1 interspace with significant nerve root compromise. Despite antimicrobials, his symptoms persisted, necessitating surgical exploration. At surgery, paraspinal and epidural abscesses were encountered and debrided; however, no herniated disc was visualized. This case demonstrates the diagnostic and therapeutic dilemmas with which these lesions present. We postulate that the MRSA osteomyelitis/discitis pathogens were walled off in the disc space and subsequently inoculated the soft tissues with ensuing bacteremia. We concur that antimicrobial treatment should be the first line of therapy for these patients; however, surgical debridements and cautious spinal instrumentation should be employed where appropriate.     

Pharmacokinetics of the 13C labeled anticancer agent temozolomide detected in vivo by selective cross-polarization transfer

The anticancer agent temozolomide labeled with ¹³C (8-Carbamoyl-3-13C-methylimidazo-[5,1-d]-1,2,3,5-tetrazin-4-(3H)-one), was noninvasively detected in subcutaneous RIF-1 tumors by a selective cross polarization ¹³C NMR method, at a field strength of 9.4T. Pharmacokinetics of the drug, at a dose of 150 mg/kg, were determined for intravenous and intraperitoneal modes of administration (three animals per mode). The half-life of the drug in the tumors was approximately 60 min. The uptake and clearance of the drug, however, varied significantly between individual hosts, for both modes of administration. These results demonstrate the feasibility of obtaining pharmacokinetics of anticancer agents for individual tumors without the need for a label that might modify drug activity (e.g., fluorine). The variability of the in vivo measurements, even within the same tumor model, demonstrates the necessity of directly monitoring the tumor to evaluate drug pharmacokinetics.     

Cylindrical spirals of myofilamentous origin associated with exertional cramps and rhabdomyolysis

We describe the presence of cylindrical spirals on muscle biopsy from a 31-year-old man who developed rhabodomyolysis following a long run. He had a prior history of exertional cramps and myoglobinuria. His maternal grandfather had similar symptoms. Transmission electron micrographs demonstrated continuity between the lamellae of the cylindrical spirals and native myofilaments. Whether these unusual structures confer a derangement in myofilament function is uncertain.     

Toxic shock syndrome after inguinal hernia repair. Report of a case with patient survival

A 40-year-old man developed fulminant multisystem failure several days after elective repair of an inguinal hernia. Toxic shock syndrome (TSS) was diagnosed. There was, however, no evidence of wound infection at the time of multisystem failure. Only later in his hospital course did the wound drain. Staphylococcus aureus was cultured from the wound and was the presumed etiologic agent in the patient's life-threatening illness. The patient recovered fully with supportive care, antibiotics, and surgical debridement of the inguinal hernia site. This case is discussed in the context of existing literature on the toxic shock syndrome. The site of infection is typically nonsuppurative, but the systemic manifestations are typically life threatening. The responsible organism is commonly believed to be a strain of S. aureus that expresses a toxin (TSS toxin-1) that effects multisystem failure, but which also diminishes the local inflammatory response and explains the benign appearance of the wound. Although this is a rare clinical entity, elective surgical procedures complicated by fatal TSS have been reported. Surgeons should understand this disease and the management necessary to avert mortality.     

Evidence for arsenic as the immunosuppressive component of gallium arsenide.

Gallium arsenide (GaAs) has been shown previously to suppress the in vivo antibody-forming cell (AFC) response to sheep erythrocytes (SRBC) when administered intratracheally at concentrations between 50 and 200 mg/kg. In the present studies, direct addition of GaAs to in vitro-generated antibody cultures resulted in dose-dependent suppression of the primary antibody response, and was only seen when GaAs was added within 36 hr following immunization. Using atomic absorption spectrophotometry on tissue samples from mice exposed to 200 mg/kg GaAs, arsenic concentrations were found to peak in the spleen at 24 hr and decline, whereas gallium concentrations continue to rise through 14 days. Concentrations of each metal in the spleen at 24 hr are comparable to the concentrations achieved for each metal when GaAs is added at 25 microM to the in vitro model system. The 24 hr time point was chosen for comparison because all in vivo-in vitro studies were conducted using spleens from mice 24 hr after GaAs exposure. NaAsO2 and Ga(NO3)3 suppressed the AFC response dose-dependently, and in a time-dependent manner similar to GaAs when added to the in vitro system. However, based on IC50 values for each salt, the role of the gallium component in the immunosuppression appears weak. Oxalic acid (OA) and meso-2,3-dimercaptosuccinic acid (DMSA), chelators of gallium and arsenic respectively, were added to cultures with GaAs to confirm that arsenic was the primary immunosuppressive component. DMSA dose-dependently blocked GaAs-induced immunosuppression in vitro, while OA had no effect. The metal-binding compounds were determined to be specific for the metals used in these studies and did not cross-react with one another. DMSA was evaluated for its ability to prevent suppression of the AFC response in splenocytes from GaAs-exposed mice and was able to block GaAs-induced suppression of the AFC response when given sc every 4 hr beginning 1 hr prior to GaAs exposure. These data indicate that the arsenic component of GaAs is the major contributor to the GaAs-induced immunosuppression and that this effect occurs within the first 36 hr of the 5-day culture period in a concentration-dependent manner.     

Exercise in claudicants is accompanied by excessive thrombin generation.

BACKGROUND: exercise in IC leads to ischaemia-reperfusion injury of leg muscles and a systemic inflammatory response, but the effect of on coagulation is unknown. OBJECTIVE: to compare the effect of exercise on thrombin formation and fibrin turnover in patients with IC (n = 10), and age and sex matched smokers ([S] n = 5) and non-smokers ([NS] n = 5) without peripheral vascular disease. METHODS: blood was taken from subjects 60 and 30 min before, and 1, 5, 20, 40, 60 and 120 min after, treadmill exercise. Markers of thrombin generation (thrombin-antithrombin complexes [TAT] and prothrombin fragments 1 + 2 [PF1 + 2]) and fibrin turnover (D-dimer and fibrin degradation products [FbDP]) were assayed at each time point. RESULTS: following exercise, thrombin generation was significantly greater in the claudicant group compared to the control groups (Area Under Curve [AUC] post exercise IC vs S vs NS; TAT 3960 vs 1623 vs 1476 vs = 0.007 Kruskal-Wallis [KW]; PF1 + 2 163 vs 107 vs 123 p = 0.024 KW). Pre and post-exercise, fibrin turnover in claudicants was similar to smoking controls, but higher than non-smoking controls. (AUC post exercise IC vs NS; D-dimer 6340 vs 2754 p = 0.055 Mann-Whitney U[MW]; FbDP 45113 vs 21511 p = 0.009 MW). CONCLUSION: when compared to non-claudicants, exercise in IC is associated with excessive production of thrombin. Despite this, claudicants have a similar level of fibrin turnover suggesting a possible defect in fibrinolysis. This prothrombotic state may contribute to the excess thrombotic morbidity and mortality suffered by claudicants.