Pathomechanics of Gowers' sign: a video analysis of a spectrum of Gowers' maneuvers.

BACKGROUND: Gowers' sign is a screening test for muscle weakness, typically seen in Duchenne muscular dystrophy but also seen in numerous other conditions. The mildest presentations and the variations of Gowers' sign are poorly described in the literature but are important to recognize to help with early diagnosis of a neuromuscular problem. QUESTIONS/PURPOSES: We therefore (1) defined the characteristics of the mildest forms and the compensatory mechanism used, (2) categorized the spectrum of this sign as seen in various neuromuscular diseases, and (3) provide educational videos for clinicians. METHODS: We videotaped 33 patients with Gowers' sign and three healthy children. Weakness was categorized as: mild = prolonged or rise using single-hand action; moderate = forming prone crawl position and using one or two hands on thigh; severe = more than two thigh maneuvers, rising with additional aid, or unable to rise. RESULTS: The earliest changes were exaggerated torso flexion, wide base, and equinus posturing, which reduce hip extension moment, keep forces anterior to the knee, and improve balance. Patients with moderate weakness have wide hip abduction, shifts in pelvic tilt, and lordosis, which reduce knee extension moment, improve hamstrings moment arm, and aide truncal extension. The classic Gowers' sign (severe) exaggerates all mechanisms. CONCLUSIONS: The classically described Gowers' sign is usually a late finding. However more subtle forms of Gowers' sign including mild hand pressure against the thigh and prone crawl position should be recognized by clinicians to initiate additional diagnostic tests.

Roles of 34 virulence genes in the evolution of hospital- and community-associated strains of methicillin-resistant Staphylococcus aureus.

BACKGROUND: The extent to which the horizontal transfer of virulence genes has contributed to the emergence of contemporary virulent strains of methicillin-resistant Staphylococcus aureus (MRSA) in hospital and community settings is poorly understood. METHODS: Epidemiologically well-characterized MRSA isolates collected over 8.5 years were genotyped and tested for the presence of 34 virulence genes. RESULTS: Six strain types accounted for 88.2% of all MRSA infections. The evolution of contemporary hospital and community phenotypes within the CC8 and CC30 lineages--2 background genomes that produced historical pandemic MRSA clones--were associated with multiple horizontal acquisitions of virulence genes. The epidemic community phenotype of a CC8 strain, designated ST8:USA300, was linked to the acquisition of staphylococcal cassette chromosome (SCC)mec type IV, the genes for Panton-Valentine leukocidin (PVL), and the enterotoxin Q and K genes. Similarly, the epidemic community phenotype of a CC30 strain, ST30:USA1100, was linked to the acquisition of SCCmec type IV and the pvl genes. In contrast, the epidemic hospital phenotype of another CC30 strain, ST36:USA200, was associated with the acquisition of SCCmec type II, the enterotoxin A gene, and the toxic shock syndrome toxin 1 gene. The pvl genes appear not to be essential for the evolution OF other community-associated strains of mrsa, including ST8:USA500 and ST59:USA1000. CONCLUSIONS: The horizontal transfer of virulence genes, although infrequent, is epidemiologically associated with the emergence of new virulent strains of MRSA.

Complete genome sequence of USA300, an epidemic clone of community-acquired meticillin-resistant Staphylococcus aureus.

BACKGROUND: USA300, a clone of meticillin-resistant Staphylococcus aureus, is a major source of community-acquired infections in the USA, Canada, and Europe. Our aim was to sequence its genome and compare it with those of other strains of S aureus to try to identify genes responsible for its distinctive epidemiological and virulence properties. METHODS: We ascertained the genome sequence of FPR3757, a multidrug resistant USA300 strain, by random shotgun sequencing, then compared it with the sequences of ten other staphylococcal strains. FINDINGS: Compared with closely related S aureus, we noted that almost all of the unique genes in USA300 clustered in novel allotypes of mobile genetic elements. Some of the unique genes are involved in pathogenesis, including Panton-Valentine leucocidin and molecular variants of enterotoxin Q and K. The most striking feature of the USA300 genome is the horizontal acquisition of a novel mobile genetic element that encodes an arginine deiminase pathway and an oligopeptide permease system that could contribute to growth and survival of USA300. We did not detect this element, termed arginine catabolic mobile element (ACME), in other S aureus strains. We noted a high prevalence of ACME in S epidermidis, suggesting not only that ACME transfers into USA300 from S epidermidis, but also that this element confers a selective advantage to this ubiquitous commensal of the human skin. INTERPRETATION: USA300 has acquired mobile genetic elements that encode resistance and virulence determinants that could enhance fitness and pathogenicity.