Interrupting the courtroom organism: screaming bodies, material affects and the theatre of cruelty

This article offers a method of reading the courtroom which produces an alternative mapping of the space. My method combines a reading of Antonin Artaud’s Theatre of Cruelty with a Deleuzian theoretical analysis. I suggest that this is a useful method since it allows examination of the spatial praxes of the courtroom which pulsate with a power to organize, terrorize and to judge. This method is also able to conceptualize the presence of ‘‘screaming’’ bodies and living matter which are appropriated to build, as well as feed the presence and functioning of the courtroom space, or organism. By using a method that articulates the cry of these bodies in the shadow of the organism, it becomes clear that this cry is both unwelcome and suppressed by the courtroom. The howl of anxious bodies enduring the process and space of the law can be materialized through interruptions to the courtroom, such as when bodies stand when they should not and when they speak when they should be silent. These vociferous actualizations of the scream serve only to feed the organism they seek to disturb, yet if the scream is listened to before it disrupts, the interruption becomes-imperceptible to the courtroom. Through my Artaudian/Deleuzian reading, I give a voice to the corporeal gasp that lingers before the cry, which is embedded within the embodied multiplicity from which it is possible to draw a creative line of flight. The creative momentum of this line of flight produces a sustainable interruption to the courtroom process, which instead of being consumed by the system, has the potential to produce new courtroom alignments. My text therefore offers an alternative reading of the courtroom, and in doing so also offers a refined understanding of how to productively ‘‘interrupt’’ the courtroom process.

Identification of Streptococcus gallolyticus subsp. macedonicus as the etiological agent in a case of culture-negative multivalve infective endocarditis by 16S rDNA PCR analysis of resected valvular tissue

Today, PCR using broad-range primers is being used increasingly to detect pathogens from resected heart valves. Herein is described the first case of multivalve infective endocarditis where 16S rDNA PCR was used to detect a single pathogen from two affected valves in a 61-year-old man. Triple heart valve replacement was required despite six weeks of appropriate antimicrobial therapy. The organism was confirmed as Streptococcus gallolyticus subsp. macedonicus, a member of the 'S. equinus/S. bovis' complex. To date, only one report has been made of human infection due to this organism. This may be due to the limited resolution of the routine diagnostic methods used and/or as a consequence of the complex nomenclature associated with this group of organisms.

Presence and characterisation of ecotin in F. necrophorum

Fusobacterium necrophorum is a causative agent of Lemierre’s syndrome (LS) in humans. LS is characterised by thrombophlebitis of the jugular vein and bacteraemia. Disseminated intravascular coagulation is also a documented symptom. F. necrophorum is a Gram-negative, anaerobic bacterium known to possess virulence genes such as a haemolysin, filamentous haemagglutinin and leukotoxin, which target host blood components. Ecotin is a serine protease inhibitor that has not previously been characterised in F. necrophorum, but in E.coli has been shown to have a potent anticoagulant effect. Next generation and Sanger sequencing were used to confirm the presence of the ecotin gene in the genomes of a collection of F. necrophorum clinical and reference strains. When translated, it was found to be a highly conserved protein made up of159 amino acids. Enzyme/substrate inhibition assays demonstrated that F. necrophorum ecotin inhibits human plasma kallikrein and human neutrophil elastase in a dose-dependent manner. Data will also be presented on the anticoagulant effects of ecotin during activated partial thromboplastin time, thrombin time and prothrombin time tests on human donor blood. The mechanisms for how this organism reaches the bloodstream and the significance of this serine protease inhibitor during F. necrophorum infections remain to be elucidated