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(2001).","npl_type":"a","external_id":["10.1146/annurev.micro.55.1.561","11544367"],"record_lens_id":"065-082-795-550-209","lens_id":["123-499-760-753-917","065-082-795-550-209","089-516-651-294-433"],"sequence":13,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":11,"text":"Feil et al., \"How Clonal is Staphylococcus aureus?\" J Bacteriol 185:3307-3316 (2003).","npl_type":"a","external_id":["10.1128/jb.185.11.3307-3316.2003","12754228","pmc155367"],"record_lens_id":"006-503-504-253-689","lens_id":["124-950-157-284-773","006-503-504-253-689","197-234-899-174-240"],"sequence":14,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":12,"text":"Firsov et al., \"Testing the mutant selection window hypothesis with Staphylococcus aureus exposed to daptomycin and vancomycin in an in vitro dynamic model,\" J Antimicrob Chemother 58:1185-92 (2006).","npl_type":"a","external_id":["17028094","10.1093/jac/dkl387"],"record_lens_id":"121-387-777-728-356","lens_id":["157-713-032-896-010","121-387-777-728-356","195-894-494-252-539"],"sequence":15,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":13,"text":"Fowler et al., \"Potential Association between Hematogenous Complications and Bacterial Genotype in Staphylococcus aureus Infection,\" J. Infect. 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Agents Chemother. 39:1505-1511 (1995).","npl_type":"a","external_id":["7492094","pmc162771","10.1128/aac.39.7.1505"],"record_lens_id":"023-408-230-477-159","lens_id":["144-399-001-528-069","023-408-230-477-159","194-752-880-995-824"],"sequence":23,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":21,"text":"Karlsson et al., \"Protection of Rhesus macaques against Lethal Plasmodium knowlesi Malaria by a Heterologous DNA Priming and Poxvirus Boosting Immunization Regimen,\" Infect Immun. 70:4239-46 (2002).","npl_type":"a","external_id":["10.1128/iai.70.8.4329-4335.2002","pmc128201","12117942"],"record_lens_id":"035-746-490-912-513","lens_id":["135-526-023-135-12X","035-746-490-912-513","197-945-827-785-510"],"sequence":24,"category":[],"us_category":[],"cited_phase":"APP","rel_claims":[]}},{"npl":{"num":22,"text":"Koreen et al., \"spa Typing Method for Discriminating among Staphylococcus aureus Isolates: Implications for Use of a Single Marker to Detect 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The extracellular microorganism can be of the bacterial genus Staphylococcus , for example, Staphylococcus aureus . The extracellular microorganism can be a strain that is resistant to at least one antibiotic. The strain can be selected from the group consisting of methycillin-resistant Staphylococcus aureus (MRSA), vancomycin-intermediate Staphylococcus aureus (VISA) and vancomycin-resistant Staphylococcus aureus (VRSA). The invention also provides a method for preventing or treating an infectious disease caused by of methycillin-resistant Staphylococcus aureus (MRSA), vancomycin-intermediate Staphylococcus aureus (VISA) or vancomycin-resistant Staphylococcus aureus (VRSA), comprising systemically coadministering in a synergistic combination to a subject in need thereof prophylactically or therapeutically effective amounts, individually or collectively, of a salicylic acid (SAL) or a SAL analogue and at least one additional antimicrobial agent, for example, vancomycin and/or linezolid.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"}]},"abstract_lang":["en"],"has_abstract":true,"claim":{"en":[{"text":"1. A method for preventing or treating an infection caused by a microorganism, said method comprising systemically administering to a subject in need thereof a therapeutically effective amount of a salicylic acid (SAL) analogue comprising one or more halogenated phenyl moieties, wherein said subject has an infection caused by a microorganism.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"2. The method of claim 1 , wherein the microorganism is a species of the bacterial genus Staphylococcus.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"3. The method of claim 2 , wherein said species is Staphylococcus aureus.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"4. The method of claim 1 , wherein said microorganism is a strain that is resistant to at least one antibiotic.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"5. The method of claim 4 , wherein said strain is methicillin-resistant Staphylococcus aureus (MRSA).","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"6. The method of claim 1 , wherein said SAL analogue is Diflunisal.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"7. A method for preventing or treating an infection caused by methicillin-resistant Staphylococcus aureus (MRSA), comprising systemically co-administering to a subject in need thereof therapeutically effective amounts of a salicylic acid (SAL) analogue comprising one or more halogenated phenyl moieties and at least one additional antimicrobial agent, where said SAL analogue and said at least one additional antimicrobial agent are co-administered individually or collectively, and wherein said subject has an infection caused by MRSA.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"8. The method of claim 7 , wherein said additional antimicrobial agent is vancomycin, daptomycin or linezolid.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"9. The method of claim 7 , wherein said SAL analogue is Diflunisal.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"10. A method for preventing or treating an infection caused by vancomycin-resistant enterococci (VRE), comprising systemically co-administering to a subject in need thereof therapeutically effective amounts of a salicylic acid (SAL) analogue comprising one or more halogenated phenyl moieties and at least one additional antimicrobial agent, where said SAL analogue and said at least one additional antimicrobial agent are co-administered individually or collectively, and wherein said subject has an infection caused by VRE.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"11. The method of claim 10 , wherein said additional antimicrobial agent is linezolid.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"12. The method of claim 10 , wherein said SAL analogue is Diflunisal.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"13. The method of claim 5 , wherein said MRSA stain is vancomycin susceptible (VSSA), vancomycin-intermediate susceptible (VISA) or vancomycin-resistant (VRSA).","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"14. The method of claim 1 , wherein said infection is an acute infection.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"15. The method of claim 7 , wherein said infection is an acute infection.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"16. The method of claim 10 , wherein said infection is an acute infection.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"}]},"claim_lang":["en"],"has_claim":true,"description":{"en":{"text":"CROSS-REFERENCE TO RELATED APPLICATIONS This application is a U.S. National Stage Application under U.S.C. §371 of International Patent Application No. PCT/US2009/062123, filed Oct. 26, 2009, which claims the benefit of priority to U.S. Provisional Application Ser. No. 61/108,408, filed Oct. 24, 2008. BACKGROUND OF THE INVENTION Invasive infections by Staphylococcus aureus are now common and life-threatening. As methicillin-resistant (MRSA) or vancomycin-refractory (VISA, VRSA) strains are leading community-acquired and nosocomial pathogens, invasive S. aureus infections now have attributable mortalities approaching 40%-50%, even with modern therapeutics. Costs associated with such infections now exceed $2 billion per year in the US alone. Such a clear and present threat to public health emphasizes the urgency to address this unmet medical need. Yet, remarkably little is known of pharmacologic approaches to minimize resistance or enhance antibiotic efficacy vs. MRSA. As an alternative to the time and cost of developing new anti-staphylococcal antibiotics, there is a need to discover adjunctive combinations that mitigate resistance and optimize therapeutic outcomes to serious or life threatening bacterial infections, including methicillin-resistant SA (MRSA), that are increasingly refractory to most if not all forms of conventional antimicrobial therapy (pan-resistant). The present invention meets this need and provides related advantages. SUMMARY OF INVENTION The invention provides a method for preventing or treating a disease caused by an extracellular microorganism, said method comprising systemically administering to a subject in need thereof a prophylactically or therapeutically effective amount of a salicylic acid (SAL) or a SAL analogue. The extracellular microorganism can be of the bacterial genus Staphylococcus , for example, Staphylococcus aureus . The extracellular microorganism can be a strain that is resistant to at least one antibiotic. The strain can be selected from the group consisting of methycillin-resistant Staphylococcus aureus (MRSA), vancomycin-intermediate Staphylococcus aureus (VISA) and vancomycin-resistant Staphylococcus aureus (VRSA). The invention also provides a method for preventing or treating an infectious disease caused by of methycillin-resistant Staphylococcus aureus (MRSA), vancomycin-intermediate Staphylococcus aureus (VISA) or vancomycin-resistant Staphylococcus aureus (VRSA), comprising systemically co-administering in a synergistic combination to a subject in need thereof prophylactically or therapeutically effective amounts, individually or collectively, of a salicylic acid (SAL) or a SAL analogue and at least one additional antimicrobial agent, for example, vancomycin and/or linezolid. BRIEF DESCRIPTION OF THE DRAWINGS FIG. 1 shows that SAL mitigates the binding of S. aureus to human platelets ( 1 B), as compared to organisms prior to SAL exposure ( 1 A). FIG. 2 shows that SAL treatment modulates expression of sar regulon components sarA, sarB, and sarC within S. aureus . GFP outcomes ( 2 A) are in very close agreement with transcriptional expression results from Northern analyses ( 2 B). FIG. 3 shows that SAL induces sigB expression (as measured by increases in asp23 expression) in S. aureus. FIG. 4 shows a hypothesized model of SAL-mitigation of antibiotic resistance and virulence factor expression in MRSA in vitro, ex vivo, and in vivo. SAL exerts its anti-MRSA effects by modulating expression of adaptive genes and/or regulators thereof, such as sigB, agr, and sar. FIG. 5 shows that aspirin therapy mitigates MRSA Treatment (Log CFU/g±SD) FIG. 6 shows that Aspirin suppresses sarA P1 expression in vivo. FIG. 7 shows a quantitative model for SAL mitigation of MRSA vancomycin and daptomycin resistance in vitro. FIG. 8 shows kinetic in vitro modeling of SAL-mitigated MRSA resistance to vancomycin and daptomycin. FIG. 9 shows xx vivo PD model of MRSA invasive infection used in the Examples. FIG. 10 depicts how SAL treatment mitigates ligand adhesion and α-toxin production among laboratory and clinical S. aureus strains. FIG. 11 depicts how aspirin (ASA) benefits outcomes in a rabbit model of S. aureus IE. FIG. 12 depicts the beneficial impact of aspirin on vancomycin therapy of MRSA in the rabbit model of IE. Key: *p<0.05 vs. controls; **p<0.05 vs. controls and p<0.05 vs. vancomycin and ASA alone. FIG. 13 depicts strategic MRSA strain panel to be prioritized in the methods of the invention. FIG. 14 shows lists strategic target genes to be assessed for SAL-antibiotic impact. FIG. 15 shows candidate compounds for practicing the methods of the invention. FIG. 16 shows examples of S. aureus strains suitable for practicing in the methods of the invention. FIG. 17 shows genotypic and phenotypic markers utilized in the invention. FIG. 18 shows the experimental design for Example 12. FIG. 19 shows that the impact of SAL and DIF on gene expression in S. aureus strains SH1000 and USA300 2 hours into the log phase. FIG. 20 shows that the impact of SAL and DIF on gene expression in S. aureus strains SH1000 and USA300 4 hours into the log phase. FIG. 21 shows that the impact of SAL and DIF on gene expression in S. aureus strains SH1000 and USA300 6 hours into the log phase. FIG. 22 shows the impact of ASA, SAL, GTA, SUA and DIF on hemolysis in S. aureus. FIG. 23 shows net hemolytic expression in S. aureus strains SH1000 and USA300 as a result of addition of ASA, SAL, GTA, SUA and DIF as percent of control. FIG. 24 shows the impact of ASA, SAL, GTA, SUA and DIF on proteolysis in S. aureus. FIG. 25 shows net protease expression in S. aureus strains SH1000 and USA300 as a result of addition of ASA, SAL, GTA, SUA and DIF as percent of control. FIG. 26 shows the impact of ASA, SAL and DIF on antibiotic minimum inhibitory concentrations (MICs). DETAILED DESCRIPTION OF THE INVENTION The present invention is based, in part, on the discovery that salicylic acid (SAL), a major biometabolite of aspirin, modulates S. aureus phenotypic and genotypic determinants to mitigate resistance and enhance efficacy of anti-staphylococcal antibiotics. The invention provides methods of mitigating resistance and enhancing efficacy of anti-staphylococcal antibiotics. The invention also provides methods for predicting antimicrobial activities of agents not presently recognized to have such antimicrobial activities, based upon structure-activity correlates. The invention is based, in part, on the surprising discovery that salicylate analogues of the chemical structure containing one or more halogenated fluorophenyl moieties have unexpected capacities with regard to mitigating resistance and enhancing efficacy of anti-staphylococcal antibiotics. For example, the chemical 5-(2,4-difluorophenyl)-2-hydroxy-benzoic acid, generic clinical drug name, Diflunisal [DIF] or Dolobid, unexpectedly and surprisingly has markedly greater anti-SA activities than SAL. Traditionally, DIF is considered to be of clinical use as a non-steroidal anti-inflammatory drug (NSAID), having analgesic and anti-inflammatory effects. Originally, DIF was marketed by Merck, but has not been widely used in the United States. It is believed to be of greatest clinical use as an NSAID in Australia. As disclosed herein, the physicochemical moieties in DIF and analogous compounds perturb virulence factor regulation and expression in SA. The perturbation occurs due to the relatively specific inhibition of agr, RNAIII, or sigB and related regulatory systems in SA. As disclosed herein, the virulence factors controlled by these regulators is suppressed, and such suppression translates to improved outcomes. The present invention is based, in part, on the discovery that salicylic acid (SAL; a major biometabolite of aspirin) modulates S. aureus phenotypic and genotypic determinants to mitigate resistance and enhance efficacy of anti-staphylococcal antibiotics. The invention ptovides PK-PD systems to model and therapeutically translate the beneficial impact of salicylates on vancom ycin or daptomycin efficacy. Strategic, genetically-defined S. aureus strains can be used to elucidate the quantitative relationships between SAL exposure and phenotypic or genotypic resistance to vancomycin or daptomycin in vitro. The methods described herein include an integrated approach to quantify the impact of SAL on the MRSA mutation prevention concentration (MPC) and mutation selection window (MSW), and assessment of SAL str uctural analogues for enhanced down-modulation of S. aureus resistance to peptide antibiotics. This invention provides methods of adjunctive SAL-peptide antibiotic therapy to mitigate resistance and improve outcomes of life-threatening invasive MRSA infections in humans. The invention further provides an ex vivo model of S. aureus infection simulating fluid and tissue phases of human cardiovascular infection will be used to define kinetic relationships between SAL, vancomycin, or daptomycin that mitigate phenotypic and genotypic resistance profiles in MRSA. This controlled system simulates targeted and dynamic peak and trough antibiotic concentrations, and affords pharmacokinetic (PK) optimization. SAL mitigation of antibiotic resistance will be assessed in MRSA residing in distinct contexts: circulating bacteria versus bacteria embedded within infected vegetations. The purpose of the invention addresses existing or novel molecules for developed as novel antiinfective (principally anti-SA or anti-MRSA) agents to act alone or in combination with other antiinfective therapies or strategies. A main focus of the utility of the invention would be treatment or prevention of life-threatening infections caused by pathogens resistant to existing therapies, or to enhance the efficacy of existing antimicrobial agents against SA or other organisms. The method of claim 1 , wherein the extracellular microorganism is a species of a genus selected from the group consisting of bacterial genera Staphylococcus, Enterococcus, Escherichia, Streptococcus, Campylobacter, Salmonella, Helicobacter, Bacillus, Clostridium, Corynebacterium, Chlamydia, Coxilla, Ehrlichia, Francisella, Pasteurella, Brucella, Proteus, Klebsiella, Enterobacter, Tropheryma, Acinetobacter, Aeromonas, Alcaligenes, Capnocytophaga, Erysipelothrix, Listeria , and Yersinia. The method of claim 2 , wherein said species is selected from the group consisting of Staphylococcus aureus, Staphylococcus epidermidis, Enterococcus faecalis, Enterococcus faecium, Salmonella typhi, Salmonella typhimurium, Salmonella enterica, Escherichia coli, Streptococcus pneumoniae, Streptococcus pyogenes, Streptococcus agalactiae, Helicobacter pylori , and Campylobacter jejuni. Based on structure-activity correlates, the invention provides method for the discovery of novel compounds with significant anti-SA or other antimicrobial activities alone or in combination with antibiotics, due to similar or greater effects on suppression of virulence factors in MRSA or other human pathogenic microbes. DIF and other structural analogues of SAL achieve anti-SA efficacy in vitro and in vivo by suppression of regulons and the virulence factors they control. In particular, the regulatory genes agr, RNAIII, and sigB, the well-characterized virulence factors hla (α-hemolysin) and sspA (V8 protease), and certain antibiotic resistance sensor or effector genes such as vraA, dltA, mprF, or yycG/F are abnormally regulated or expressed in the presence of DIF or analogues thereof (see attached materials). DIF and related compounds can be used as an anti-infective strategy alone or in combination with conventional antibiotics to suppress virulence and/or enhance efficacy of antimicrobial regimens, particularly against resistant organisms. The invention is further based on the discovery of a relatively narrow concentration range that effects the desirable anti-SA activities, without untoward effects on the host or the pathogen. SAL, DIF, and certain structural analogues thereof structurally or functionally mimic auto-inducing peptides generated by SA to govern regulation of genes in adaptation of the organism that allow it to survive and cause infection in the host. This process, termed quorum-sensing, is integral to the ability of the organism to sense excess organism density, depletion of nutrients, or injurious immune context, and counter-regulate gene expression. The result of this process is the tight regulation of virulence factor expression for optimal survival of the organism in vivo. Thus, inhibition of the capability by DIF or related analogues prevents a normal adaptive capability of the organism, making it susceptible to immune mechanisms as well as antimicrobial therapy. Prior art antibiotics employ mechanisms that inhibit essential functions of microbes, resulting in static growth or killing. In contrast, SAL, DIF or analogues thereof have only modest effects on organism growth, and do not cause organism death. Rather, they suppress regulatory and effector genes that encode adaptive and virulence proteins needed to cause infection. SALs, DIF, or derivatives thereof can be to be developed as novel antiinfective agents to act against human pathogens that are refractory to existing anti-infectives. Invasive infections caused by Staphylococcus aureus are life-threatening conditions now reported at an alarming frequency. Presently, S. aureus is the most common cause of skin 3-6 and endovascular infections, including infective endocarditis (IE) and device-related infections, and the second most common agent of bacteremia. The incidence of invasive S. aureus continues to increase rapidly. For example, IE due to S. aureus occurs in up to 10,000 new patients per year in the United States, and 1-year mortality remains near 40% despite advances in anti-staphylococcal therapy and surgical methods. Even more troubling has been the global explosion in S. aureus antibiotic resistance. In just the past decade alone, MRSA infections have become epidemic in communities among the US and worldwide. Reports of multiple pan-antibiotic resistant S. aureus , including resistance to vancomycin, daptomycin, and linezolid, illustrate the daunting scope of this problem. Unacceptably, the mortality due to invasive S. aureus infections such as IE has remained unchanged in the last two decades. Finally, invasive MRSA infections affect many risk populations, including those in: i) jails; ii) public health facilities; iii) long term care facilities; iv) dialysis centers; and v) pediatric practices. Although most of these infections have been of skin and soft tissue origin, an increasing proportion (up to 10%) involves complicated blood stream infections. Methicillin-resistance in nosocomial and community-acquired isolates of S. aureus has been steadily increasing, and now approaches national rates between 30-60% among patients in intensive care units. In recent reports, the median length of hospital stay for nosocomial infections was 12 days for MRSA, versus 4 days for methicillin-susceptible S. aureus (MSSA), and 23 days for MRSA versus 14 days for MSSA in patients with surgical site infections. The rise in hospital cost is significantly higher for treatment of MRSA than for MSSA infections, and has a greater mortality due to nosocomial MRSA infections than MSSA. Further complicating these issues is the limited availability of effective antimicrobial therapy against MRSA. Vancomycin has been a mainstay of therapy for decades; yet its role in therapy has raised questions. Vancomycin failure against S. aureus having minimum inhibition concentrations (MICs) of 2 μg/ml has occurred, despite proactive and aggressive dosing. This problem is compounded by increased prevalence of S. aureus strains with MICs of 2 μg/ml. Moreover, most strains exhibiting vancomycin MICs of ≧2 μg/ml also display heteroresistance to vancomycin (hVISA). Even in the currently susceptible range established by the CLSI, infections caused by hVISA have been linked to vancomycin failure. Several centers have now reported the vancomycin MIC upward shift (“MIC creep”). For example, a leading center in North Carolina evaluated MRSA isolates from 2001 and 2005 and demonstrated that the proportion of strains with vancomycin MIC >1 μg/ml increased from 0% in 2001 to 7% in 2005. Rates as high as 54% of strains with vancomycin MICs of ≧2 μg/ml among nosocomial MRSA isolates have been reported, raising new concerns for vancomycin efficacy. In addition, there are several recent case reports of daptomycin-resistance emerging during therapy associated with clinical failures. A link exists between vancomycin failure and S. aureus accessory gene regulator (agr) function. In S. aureus , the agr regulon controls exoprotein, exotoxin, and adhesin expression; many of these proteins are established virulence factors. Four predominant agr types predominate, and specific agr genotype strains appear to be associated with particular infectious syndromes in certain locales. In the US, VISA strains in agr group II, and mutations or defects in this operon, are correlated with decreased vancomycin efficacy. Loss of agr function appears to offer a survival advantage for the organism. The prevalence of the agr group types can vary in different hospitals, and agr group II is not an absolute requirement for the development of vancomycin resistance. However, a majority of MRSA isolates in U.S. hospitals are agr type II. Suboptimal vancomycin dosing drives development of VISA strains. A correlation exists between vancomycin dosing and resistance in the setting of agr locus dysfunction; roughly 48% of hospital-acquired MRSA are defective in agr function. Agr dysfunction may result in hypo- or hyper-expression of one or more virulence factors. In S. aureus , vancomycin resistance manifests as two principal types: VISA and VRSA. In VISA strains, no individual genetic defect has been identified, but rather appears to involve complex metabolic perturbations which result in excess D-alanine residues in the pentapeptide bridge; abnormal muropeptide species; and thick cell walls. These abnormalities appear to be responsible for reduced access of vancomycin via the cell wall to reach its target. In contrast, VRSA strains contain a vancomycin-resistance determinant (commonly vanA) that is apparently acquired from vancomycin-resistant enterococci, and encodes an aberrant pentapeptide target for vancomycin (D-alanine-D-lactate or D-alanine-D-serine) instead of a native D-alanine-D-alanine. This putative pseudo-target prevents binding of vancomycin to its mechanistic target. “Hetero-VISA” isolates are defined as those with vancomycin MICs within the CLSI-defined susceptible range (≦2 ug/ml), but which possess resistant clones upon population analyses. Such strains are associated with clinical treatment failures. Specific genes are potential candidate effectors in daptomycin resistance. For example, genes correlating with daptomycin resistance phenotypes include mprF and yycF/G; variations ranging from point to frameshift mutations have been seen and reported in these gene loci. Paradoxically, mutations in mprF yield a “gain in function”, affording excess translocation of positively charged phospholipids (lysyl-phosphotidyl glycerol [LPG]) from the inner to the outer cell membrane bilayer. These events yield an increased net positive charge of the bacterial cell surface, postulated to enable charge repulsion of the calciumdecorated active form of daptomycin. Also, mutations in these genes proceed in a coordinated, sequential manner, with mprF being an initial mutation, followed in-turn by mutations in yycF/G. Aspirin and its major human biometabolite, SAL, can influence responsivity of MRSA to antibiotic therapy in experimental model systems. This effect appears to be due at least in-part to SAL modulation of genes integral to the MRSA “resistome” adaptations active in antibiotic resistance, and the “virulon” for endovascular pathogenesis. The invention provides methods of treating a microbial infection by administering to an individual in need thereof an agent such as, for example, a SAL analogue, such as DIF or a structure function analogue of SAL. The invention also provides methods to enhance efficacy or suppress emergence of antibiotic resistance in MRSA by administering to an individual in need thereof an agent such as, for example, SAL, a SAL analogue, such as DIF or a structure function analogue of SAL. State-of-the art pharmacologic modeling in relevant in vitro, ex vivo, and in vivo systems was performed to define the essential relationships for therapeutic optimization of antimicrobial efficacy and dampening of antibiotic resistance versus MRSA or other pathogens. As disclosed herein, SAL, DIF, or analogues thereof enhance efficacies of standard antimicrobial therapy. In the rabbit model of S. aureus IE, two intravenous (iv) aspirin dose regimens designed to encompass those used in a previous aspirin-alone efficacy study (4 or 8 mg/kg/d) were employed. Animals received aspirin alone, vancomycin alone at a low dose regimen (7.5 mg/kg bid iv), or the two agents combined. Treatment was only for 2d, based on the rationale that as the in vivo effects of vancomycin are traditionally slow in onset, maximal disclosure of any synergistic effect of the two compounds may emerge at this early time point. Aspirin dosed at 8 mg/kg/d (but not 4 mg/kg/d) or vancomycin significantly reduced bacterial counts in vegetations and kidneys. Importantly, aspirin (8 mg/kg/d) combined with vancomycin further decreased target tissue counts by at least 1 log 10 cfu/g. DIF+vancomycin or other analogue+antibiotic combination regimens have not been evaluated in discriminatory animal models of SA or MRSA infection. The results obtained underscore the potential for combined SAL-, DIF-, or like analogue-plus antibiotic synergy in vivo to optimize efficacy and suppress emergence of antimicrobial resistance. In vitro studies showed that DIF is approximately 10-fold more effective than SAL in suppressing virulence factor regulation or expression in MRSA, including the highly publicized epidemic MRSA strain, USA300. Examples of infectious diseases treatable by the present invention are those as to which the subject to be treated can benefit from a systemic administration of SAL analogues and include, but are not limited to, those caused by extracellular bacteria of the species of Staphylococcus , such as Staphylococcus aureus, Staphylococcus epidermidis , and the like; of Enterococcus , such as Enterococcus faecalis, Enterococcus faecium , and the like; of Salmonella , such as Salmonella typhi, Salmonella typhimurium, Salmonella enterica , and the like; of Escherichia , such as Escherichia coli , and the like; of Streptococcus , such as Streptococcus pneumoniae, Streptococcus pyogenes, Streptococcus agalactiae , and the like; of Helicobacter , such as Helicobacter pylori , and the like; of Campylobacter , such as Campylobacter jejuni , and the like; as well as the species of genera, Yersinia, Chlamydia, Coxilla, Ehrlichia, Francisella, Legionella, Pasteurella, Brucella, Proteus, Klebsiella, Enterobacter, Tropheryma, Acinetobacter, Aeromonas, Alcaligenes, Capnocytophaga, Bacillus, Clostridium, Corynebacterium, Erysipelothrix, Listeria and the like. Examples of infectious diseases treatable by the present invention also include infections caused by fungi, such as Candida albicans, Microsporum canis, Sporothrix schenckii, Trichophyton rubrum, Trichophyton mentagrophytes, Malassezia furfur, Pityriasis versicolor, Exophiala werneckii, Trichosporon beigelii, Coccidioides immitis, Blastomyces dermatitidis, Aspergillus fumigatus, Epidermophyton spp., Fusarium spp., Zygomyces spp., Rhizopus spp. Mucor spp., and so forth. SAL analogues can be administered by any methods that result in systemic distribution or delivery of the SAL analogues and include oral administration and parenteral administration, such as intravenous administration, intramuscular administration, subcutaneous administration, intraperitoneal administration, and the like. In certain infections, oral administration of SAL analogues provides not only systemic distribution/delivery of the SAL analogues to the affected area but also a direct contact of the compounds with the causative microorganisms in the affected area, such as within the digestive tracts. Thus, oral administration of the SAL analogues is especially useful in preventing or treating digestive tract infections caused by various microorganisms, including, but not limited to, Staphylococcus aureus, Enterococcus faecalis, Enterococcus faecium, Salmonella typhi, Salmonella typhimurium, Salmonella enterica, Escherichia coli, Campylobacter jejuni, Clostridium difficile, Clostridium perfringens , and the like. Helicobacter pylori that causes gastric and duodenal ulcers, gastritis, duodenitis, and gastric cancer, is also a good target for the methods of the present invention. Furthermore, the methods of the present invention can be applied to preventing or treating infectious diseases caused by microorganisms that are resistant to at least one antimicrobial agent other than SAL analogues. The term “antimicrobial agent” used herein refers to any naturally or synthetically derived agent that kills microorganisms or inhibits the growth thereof, directly or indirectly, and includes conventional antibiotics as well as synthetic chemotherapeutic agents, such as sulfonamides, isoniazid, ethambutol, AZT, synthetic peptide antibiotics, and the like. Thus, in a specific embodiment, the infectious diseases preventable or treatable by the present invention are caused by antimicrobial-resistant strains of microorganisms mentioned above, in particular, of Staphylococcus aureus, Enterococcus faecium, Enterococcus faecalis, E. coli, Salmonella typhi, Campylobacter jejuni, Klebsiella pneumoniae, Neisseria gonorrhoeae, Candida albicans , and the like. More specifically, such antimicrobial-resistant organisms include methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE), ampicillin-resistant E. coli (e.g., E. coli O157:H7), fluoroquinolone-resistant Salmonella thyphi, ceftazidime-resistant Klebsiella pneumoniae , fluoroquinolone-resistant Neisseria gonorrhoeae , and the like. The methods of the present invention can be applied to any other pathogenic microorganisms which have become resistant to antimicrobial agents other than gallium, as far as they are dependent on iron for their growth and survival. SAL analogues to be used in the present invention can be formulated in conventional manner using one or more pharmaceutically acceptable carriers or excipients. As used herein the phrase “pharmaceutically acceptable carriers or excipients” is intended to include any and all solvents, dispersion media, coatings, isotonic and absorption delaying agents, and the like, which are compatible with pharmaceutical administration. The use of various pharmaceutically acceptable carriers or excipients for pharmaceutically active substances is well known in the art. The therapeutically effective amount (i.e., dosage) of a SAL analogue can vary based on the nature and severity of the infection to be treated, the types of etiologic microorganism, the location of the affected area, the method of administration, the age and immunological background of a subject, the types of SAL analogues used, as well as other factors apparent to those skilled in the art. Typically, a therapeutically effective amount of a SAL analogue can be that amount which gives a concentration at the affected area of the body or in blood plasma, of at least about 1 μM, at least about 50 μM, at least about 100 μM, at least about 500 μM, at least about 1 mM, at least about 10 mM, at least about 50 mM, at least about 100 mM, at least about 200 mM, up to about 500 mM. Due to gallium's low toxicity, the amount may be liberally increased to more than 500 mM but less than that amount which causes any toxicity. For the methods of the present invention, what is contemplated is administration of the SAL analogues at dosages of, at least about 10 mg/m2/day, at least about 50 mg/m 2 /day, at least about 100 mg/m 2 /day, at least about 200 mg/m 2 /day, at least about 300 mg/m 2 /day, at least about 500 mg/m 2 /day, at least about 600 mg m 2 /day, at least about 700 mg/m 2 /day, or at least about 800 mg/m 2 /day, but less than that dosage which causes any toxicity. The prophylactically effective amount of a SAL analogue may be that amount sufficient to prevent a disease or disorder associated with pathogenic microorganisms and may vary based on the location of the affected area, the types and the number of the pathogenic organisms in the area, the types of SAL analogue to be used, as well as on the methods of application and other factors apparent to those skilled in the art. Typically, the prophylactically effective amount of a SAL analogue may be that amount which gives a concentration at the affected area of the body or in blood plasma, of at least about 0.1 .mu.M, at least about 50 μM, at least about 100 μM, at least about 500 μM, at least about 1 mM, at least about 10 mM, at least about 50 mM, at least about 100 mM, up to about 200 mM. Again, the amount of a SAL analogue for prophylactic purposes may be liberally increased to more than 200 mM but less than the amount that causes any toxicity. In another aspect, the present invention provides a method for preventing and/or treating infectious diseases caused by extracellular microorganisms, said method comprising co-administering to a subject in need thereof prophylactically or therapeutically effective amounts, individually or collectively, of a SAL analogue and at least one additional antimicrobial agent. The term “co-administration” or “co-administering” used herein refers to the administration of SAL analogue and at least one additional antimicrobial agent either sequentially in any order or simultaneously, by the same administration method or a combination of different administration methods, for example, by an intravenous administration of the SAL analogue and an oral administration of the additional antimicrobial agent, or vice versa. Such co-administration of one or more additional antimicrobial agents together with the SAL analogue is especially beneficial because the drugs attack the causative organisms by non-overlapping, completely different mechanisms, and/or because the development of antimicrobial resistance in the organisms may involve different mechanisms for the different antimicrobial agents, thereby causing nearly complete eradication of the organisms, by the drugs themselves or in combination with the actions by the host's own immune system and reducing or eliminating the chance for the causative organisms to develop resistance to the drugs. Furthermore, thanks to the low toxicity of gallium, by increasing the dosage of gallium, a combination therapy can reduce the dosage of an additional antimicrobial agent to an amount less than that required when the latter is used alone, thereby reducing adverse effects of the latter. Moreover, co-administration of a SAL analogue and an additional antimicrobial agent may result in a synergistic effect and, thus, require less dosages than those required when each is used alone. Examples of antibacterial agents include, but not by way of limitation, those in the classes of penicillins, including amipicillin, flucloxacillin, dicloxacillin, methicillin, ticarcillin, piperacillin, carbapenems, mecillinams, and the like; cephems, including cephalosporin and cephamycins; sulfonamides; aminoglycosides, including amikacin, gentamicin, kanamycin, neomycin, netilmicin, paromomycin, streptomycin, tobramycin, apramycin, and the like; chloramphenicol; tetracyclines, including chlortetracycline, oxytetracycline, demeclocycline, doxycycline, lymecycline, meclocycline, methacycline, minocycline, rolitetracycline, and the like; macrolides, including erythromycin, azithromycin, clarithromycin, dirithromycin, roxithromycin, carbomycin A, josamycin, iktasamycin, oleandomycin, spiramycin, troleandomycin, tylosin/tylocine, telithromycin, cethromycin, ansamycin, and the like; lincosamides, including lincomycin, clindamycin, and the like; streptogramins, including mikamycins, pristinamycins, oestreomycins, virginiamycins, and the like; glycopeptides, including acanthomycin, actaplanin, avoparcin, balhimycin, bleomycin B (copper bleomycin), chloroorienticin, chloropolysporin, demethylvancomycin, enduracidin, galacardin, guanidylfungin, hachimycin, demethylvancomycin, N-nonanoyl-teicoplanin, phleomycin, platomycin, ristocetin, staphylocidin, talisomycin, teicoplanin, vancomycin, victomycin, xylocandin, zorbamycin, and the like; rifamycins, including rifampicin, rifabutin, rifapentine, and the like; nitroimidazoles, including metronidazole, nitrothiazoles, and the like; quinolones, including nalidixic acid, cinoxacin, flumequine, oxolinic acid, piromidic acid, pipemidic acid, ciprofloxacin, enoxacin, fleroxacin, lomefloxacin, nadifloxacin, norfloxacin, ofloxacin, pefloxacin rufloxacin, balofloxacin, grepafloxacin, levofloxacin, pazufloxacin mesilate, sparfloxacin, temafloxacin, tosufloxacin, clinafloxacin, gemifloxacin, moxifloxacin, gatifloxacin, sitafloxacin, trovafloxacin, and the like; dihydrofolate reductase inhibitors, including trimethoprim; oxazolidinones, including linezolid, eperezolid, and the like; lipopeptides, including gramicidins, polymyxins, surfactin, and the like; and analogs, salts and derivatives thereof. Examples of antifungal agents include, but are not limited to, polyenes, such as amphotericin, nystatin, pimaricin, and the like; azole drugs, such as fluconazole, itraconazole, ketoco, and the like; allylamine and morpholine drugs, such as naftifine, terbinafine, amorolfine, and the like; antimetabolite antifungal drugs, such as 5-fluorocytosine, and the like; and analogs, salts and derivatives thereof. Which antimicrobial agent should be used in combination with the SAL, DIF, or analogues thereof in any given infection can be determined by various simple and routine methods known to one skilled in the art. For example, an infectious microorganism isolated from a patient can be tested for its sensitivity to various antimicrobial agents using a standardized disk-diffusion method (e.g., Kirby-Bauer disk-diffusion method). Briefly, in this method, an appropriate agar plate is uniformly inoculated with the test organism and paper disks impregnated with predetermined concentrations of different antibiotics are placed on the agar surface. After incubation, the diameter of a circular zone, around the disks, in which the growth of the organism is inhibited is measured. The diameter of the inhibition zone is a function of the amount of the antibiotic in the disk as well as the susceptibility of the organism to the antibiotic. The antibiotics to which the organism shows susceptibility can be used for a combination treatment with the SAL analogues. Other examples of antibiotic susceptibility tests include, but are not limited to, a broth tube dilution method for determining Minimum Inhibitory Concentration (MIC) and Minimum Bactericidal Concentration (MBC) of a given antimicrobial agent against a given organism. Thus, in a specific embodiment, an infection caused by MRSA can be treated by co-administration of SAL or a SAL analogue and vancomycin or linezolid (e.g., ZyVox™ by Pfizer, N.Y.) to a subject in need thereof. Vancomycin and Zyvox™, respectively, are currently used as the antibiotics of choice to treat MRSA infections. Likewise, in another specific embodiment, an infection caused by VRE can be treated by co-administration of a SAL, DIF, or analogues thereof and linezolid. In yet another specific embodiment, an infection or a disease/disorder (e.g., peptic ulcers, gastritis, duodenitis, gastric cancer, and the like) caused by Helicobacter pylori can be treated by co-administration of SAL, DIF or analogues thereof and clarithromycin, amoxicillin and/or metronidazole. Other agents that directly or indirectly inhibit or suppress the growth of Helicobacter pylori can be also co-administered with the SAL, DIF or analogues thereof. Such agents include, but are not limited to, proton pump inhibitors, such as omeprazole that is currently used together with clarithromycin and amoxicillin in triple therapy for peptic ulcers; and urease inhibitors, such as fluorofamide, acetohydroxamic acid, certain divalent metal ions, including Zn, Cu, Co, and Mn, and the like; as well as other agents, such as bismuth compounds (e.g., bismuth subsalicylate) that not only protect the stomach lining by coating the latter, but also suppress H. pylori growth (S. Wagner et al., 1992, “Bismuth subsalicylate in the treatment of H2 blocker resistant duodenal ulcers: role of Helicobacter pylori ”, Gut 33:179-183). In another aspect, the present invention provides a kit comprising one or more vials containing a SAL analogue and one or more additional antimicrobial agents. As used herein, “SAL analogue” refers to an structural or functional analogue of salicylic acid. SAL analogues include, for example, Diflunisal and other hydroxyl-phenyl-benzoates. Salicylate analogues of the chemical structure containing one or more halogenated fluorophenyl moieties, for example, 5-(2,4-difluorophenyl)-2-hydroxy-benzoic acid are particularly useful for practicing the claimed methods. SAL analogues structurally or functionally mimic auto-inducing peptides generated by Staphylococcus aureus to govern regulation of genes in adaptation of the organism that allow it to survive and cause infection in the host. As used herein, “salicylate” encompasses any salt or ester of salicylic acid. The salicylates used as drugs for their analgesic, antipyretic and anti-inflammatory effects include aspirin (acetylsalicylic acid, ASA), methyl salicylate and sodium salicylate. Extracellular microorganisms that have developed resistance to antimicrobial drugs. Common examples of these organisms include, for example, MRSA, VRE (vancomycin-resistant enterococci), ESBLs (extended-spectrum beta-lactamases) (which are resistant to cephalosporins and monobactams) and PRSP (penicillin-resistant Streptococcus pneumoniae ). Of these, MRSA and VRE are the most commonly encountered multidrug-resistant organisms in patients residing in non-hospital healthcare facilities, such as nursing homes and other long-term care facilities. PRSP are more common in patients seeking care in outpatient settings such as physicians' offices and clinics, especially in pediatric settings. Staphylococcus aureus , often simply referred to simply as “staph”, are bacteria commonly found on the skin and in the noses of healthy people. Occasionally, staph can cause infection; staph bacteria are one of the most common causes of skin infections in the United States. Most of these infections are minor (such as pimples, boils, and other skin conditions) and most can be treated without antimicrobial agents (also known as antibiotics or antibacterial agents). However, staph bacteria can also cause serious and sometimes fatal infections (such as bloodstream infections, surgical wound infections, and pneumonia). In the past, most serious staph bacterial infections were treated with a type of antimicrobial agent related to penicillin. Over the past 50 years, treatment of these infections has become more difficult because staph bacteria have become resistant to various antimicrobial agents, including the commonly used penicillin-related antibiotics. VISA and VRSA are specific types of antimicrobial-resistant staph bacteria. While most staph bacteria are susceptible to the antimicrobial agent vancomycin some have developed resistance. VISA and VRSA cannot be successfully treated with vancomycin because these organisms are no longer susceptibile to vancomycin. However, to date, all VISA and VRSA isolates have been susceptible to other Food and Drug Administration (FDA) approved drugs. Staph bacteria are classified as VISA or VRSA based on laboratory tests. Laboratories perform tests to determine if staph bacteria are resistant to antimicrobial agents that might be used for treatment of infections. For vancomycin and other antimicrobial agents, laboratories determine how much of the agent it requires to inhibit the growth of the organism in a test tube. The result of the test is usually expressed as a minimum inhibitory concentration (MIC) or the minimum amount of antimicrobial agent that inhibits bacterial growth in the test tube. Therefore, staph bacteria are classified as VISA if the MIC for vancomycin is 4-8 μg/ml, and classified as VRSA if the vancomycin MIC is >16 μg/ml. Individuals targeted by the methods of the invention are those individuals with several underlying health conditions (such as diabetes and kidney disease), previous infections with methicillin-resistant Staphylococcus aureus (MRSA), tubes going into their bodies (such as intravenous [IV] catheters), recent hospitalizations, and recent exposure to vancomycin and other antimicrobial agents. The invention provides a method for preventing or treating a disease caused by an extracellular microorganism, said method comprising systemically administering to a subject in need thereof a prophylactically or therapeutically effective amount of a salicylic acid (SAL) or a SAL analogue. The extracellular microorganism can be of the bacterial genus Staphylococcus , for example, Staphylococcus aureus . The extracellular microorganism can be a strain that is resistant to at least one antibiotic. The strain can be selected from the group consisting of methycillin-resistant Staphylococcus aureus (MRSA), vancomycin-intermediate Staphylococcus aureus (VISA) and vancomycin-resistant Staphylococcus aureus (VRSA). The invention provides a method for preventing or treating an infectious disease caused by MRSA, comprising systemically co-administering in a synergistic combination to a subject in need thereof prophylactically or therapeutically effective amounts, individually or collectively, of a salicylic acid (SAL) or a SAL analogue and at least one additional antimicrobial agent, for example, vancomycin and/or linezolid. The invention provides a method for preventing or treating an infectious disease caused by VRE, comprising systemically co-administering to a subject in need thereof prophylactically or therapeutically effective amounts, individually or collectively, of a salicylic acid (SAL) or a SAL analogue and at least one additional antimicrobial agent. Disease caused by an extracellular organism can be selected from the groups consisting of skin infection, soft tissue infection, blood stream infection, bacteremia, pneumonia, osteomyelitis, acute endocarditis, myocarditis, pericarditis, cerebritis, meningitis, antibiotic-associated diarrhea, scalded skin syndrome, abscesses formation and combinations thereof. The disease targeted by the methods of the invention can further be selected from the group consisting of skin infection, soft tissue infection, blood stream infection, and combinations thereof, and the mixture is topically administered to the patient. A therapeutic mixture can be administered from one to twelve or twenty-four times daily as well as continuously. Admisitration can be intravenous, topical or by any other method known to those skilled in the art Throughout this application various publications are referenced. The disclosures of these publications in their entireties are hereby incorporated by reference in this application in order to more fully describe the state of the art to which this invention pertains. Although the invention has been described with reference to the examples provided above, it should be understood that various modifications can be made without departing from the spirit of the invention. It is understood that modifications which do not substantially affect the activity of the various embodiments of this invention are also provided within the definition of the invention provided herein. Accordingly, the following examples are intended to illustrate but not limit the present invention. EXAMPLE I DIF and SAL Modulate agr and Subordinate Gene Expression in Early Log Phase Growth and at Sublethal Concentrations In vitro This example demonstrates that DIF and SAL modulated agr and subordinate gene expression in early log phase growth and at sublethal concentrations in vitro. Such suppression arrests virulence determinant expression and benefits efficacy of anti-SA therapy in vivo. Coordinated virulence gene expression is critical to S. aureus (SA) pathogenesis. A narrow salicylate (SAL) concentration range reduces SA virulence in animal models of infection. This example demonstrates the ability of SAL or analogues to modulate SA gene expression as a basis for anti-SA efficacy in vivo. SAL or its parent compound acetylsalicylic acid (ASA), its biometabolites gentisic acid (GTA) and salicyluric acid (SCU), or its structural analogue diflunisal (DIF) were tested for efficacy (25 μg/ml) in modulating expression of SA regulon (sigB, sarA, agr RNAIII), exoprotein (hla, sspA), or putative antibiotic resistance (mprF, vraR) genes in vitro. Gene expression was quantified by realtime PCR in distinct growth phases; two SA strains were studied to test potential strain specificities: SH1000 (MSSA), USA300 (MRSA). Hemolysin or antibiotic resistance phenotypes were compared to gene expression. In early log phase (2-4 hr) in SH1000, DIF caused a >20-fold suppression of agr RNAIII, hla, and vraR. Likewise in USA300, DIF suppressed agr RNAIII, hla, mprF, and sspA. Hemolysis phenotypes were suppressed in parallel to hla. SAL and ASA exhibited limited modulation of gene expression or hemolysis, but GTA or SCU did not alter gene expression. DIF prevented increases in ciprofloxacin MIC vs. both strains. No compound attenuated sigB or sarA expression in log phase, or any gene in stationary phase, nor was lethal to either strain. EXAMPLE II Salicylates Enhance In vivo Efficacy of Vancomycin in Established S. aureus IE This example demonstrates that aspirin treatment improves antibiotic therapeutic outcomes within a rigorous efficacy challenge model, rabbit IE. A rabbit model of S. aureus IE was previously employed involving two intravenous (iv) aspirin dose-regimens designed to encompass those used in a prior aspirin-alone efficacy study (4 or 8 mg/kg/d). Kupferwasser et al. J Clin Invest. 2003 112:222-33; Kupferwasser et al. Circulation. 1999 99:2791-7. In this follow-up study, animals received aspirin alone, vancomycin alone at a lowdose regimen (7.5 mg/kg bid iv), or the two agents combined. Treatment was only for 2d, based upon the rationale that as the in vivo effects of vancomycin are traditionally slow in onset, maximal disclosure of any synergistic effect of the two compounds emerge at this early time point. Aspirin dosed at 8 mg/kg/d (but not 4 mg/kg/d) or vancomycin significantly reduces bacterial counts in vegetations and kidneys. Importantly, aspirin (8 mg/kg/d) combined with vancomycin further decreased target tissue counts by at least 1 log 10 cfu/g. Neither of the regimens fully prevented relapse of infection (4d post-therapy) after this short-course treatment. These results confirm the potential for combined SAL-antibiotic synergy in vivo. EXAMPLE III Aspirin and SAL Modify Phenotypic or Genotypic Profiles in S. aureus to Benefit Antibiotic Therapy Through Increased Efficacy and/or Reduced Resistance Emergence This example demonstrates that SAL benefits antibiotic therapy through increased efficacy and/or reduced resistance emergence and causes these effects by modulating genetic responses required for antibiotic resistance and virulence. SAL does not Directly Inhibit S. aureus Growth at Clinically-Relevant Concentrations. The in vitro MICs of aspirin and SAL against three well-known laboratory strains of S. aureus : ISP479C, Newman and COL were tested. A range of drug concentrations was tested, from human-equivalent therapeutic range for the anti-platelet aggregation effects of aspirin (10-50 ug/ml), up to supra-physiologic concentrations (8 mg/ml). Over this large concentration range, no substantial growth inhibition was observed. Moreover, there was no measurable change in baseline media pH over this concentration range. These data affirmed a relative lack of in vitro growth inhibitory impact, and predicted that selection of aspirin-SAL resistance would be unlikely at human-equivalent PK-PDs. SAL Mitigates S. aureus Adhesion to Human Ligands Involved in Endovascular Pathogenesis Induction of endovascular infections is linked to the microbial binding to relevant vascular damage sites. The in vitro capacity of S. aureus strains to bind to ligands for surface adhesins (i.e. MSCRAMMs), platelets, platelet-fibrin matrices, and endothelial cells in vitro, in the presence of absence of overnight culture in SAL (50 μg/ml) was tested as follows: A. MSCRAMMs. Fibrinogen and fibronectin play key roles as ligands for S. aureus binding to cellular docking sites (e.g., platelets and endothelial cells), as well as bridging molecules that facilitate these same interactions in which additional factors are operative (e.g., gC1qR-platelet or endothelial cell binding). Peerschke and Ghebrehiwet, Immunobiology. 2007 212:333-42 The capacity of SAL at two clinically-relevant serum levels (30 and 50 μg/ml) to influence S. aureus -tofibrinogen or -fibronectin binding in solid-phase assays was investigated using 9 individual strains, including well-known MSSA laboratory strains, ISP479C, ISP479R, RN6390 and Newman, MRSA lab strains 67-0 and COL, and three bacteremic isolates from patients with MSSA IE. Importantly, significant anti-adhesive effects of SAL were observed to an equivalent extent in all nine strains; thus, data are presented as a composite of the 9-strain data set ( FIG. 10 ). Of note, there were similar and significant reductions in fibrinogen and fibronectin binding among both laboratory and clinical strains pre-exposed to SAL, in a SAL dose-dependent manner. FIG. 10 shows that SAL treatment mitigates ligand adhesion and α-toxin production among laboratory and clinical S. aureus strains. Mean reduction (±SD) vs. control (100%). Data are composite results of laboratory S. aureus RN6390, COL, Newman, and ISP479C, and clinical MRSA 67-0, 6850, Duke 28, Duke 153, and Duke 237. Data and methods are found in Wann et al. J Biol. Chem. 2000 275:13863-71. Key: A P<0.005; B
Staphylococcus. "],"number":2,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 2, wherein said species is Staphylococcus aureus. "],"number":3,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 1, wherein said microorganism is a strain that is resistant to at least one antibiotic."],"number":4,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 4, wherein said strain is methicillin-resistant Staphylococcus aureus (MRSA)."],"number":5,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 1, wherein said SAL analogue is Diflunisal."],"number":6,"annotation":false,"title":false,"claim":true},{"lines":["A method for preventing or treating an infection caused by methicillin-resistant Staphylococcus aureus (MRSA), comprising systemically co-administering to a subject in need thereof therapeutically effective amounts of a salicylic acid (SAL) analogue comprising one or more halogenated phenyl moieties and at least one additional antimicrobial agent, where said SAL analogue and said at least one additional antimicrobial agent are co-administered individually or collectively, and wherein said subject has an infection caused by MRSA."],"number":7,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 7, wherein said additional antimicrobial agent is vancomycin, daptomycin or linezolid."],"number":8,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 7, wherein said SAL analogue is Diflunisal."],"number":9,"annotation":false,"title":false,"claim":true},{"lines":["A method for preventing or treating an infection caused by vancomycin-resistant enterococci (VRE), comprising systemically co-administering to a subject in need thereof therapeutically effective amounts of a salicylic acid (SAL) analogue comprising one or more halogenated phenyl moieties and at least one additional antimicrobial agent, where said SAL analogue and said at least one additional antimicrobial agent are co-administered individually or collectively, and wherein said subject has an infection caused by VRE."],"number":10,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 10, wherein said additional antimicrobial agent is linezolid."],"number":11,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 10, wherein said SAL analogue is Diflunisal."],"number":12,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 5, wherein said MRSA stain is vancomycin susceptible (VSSA), vancomycin-intermediate susceptible (VISA) or vancomycin-resistant (VRSA)."],"number":13,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 1, wherein said infection is an acute infection."],"number":14,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 7, wherein said infection is an acute infection."],"number":15,"annotation":false,"title":false,"claim":true},{"lines":["The method of claim 10, wherein said infection is an acute infection."],"number":16,"annotation":false,"title":false,"claim":true}]}},"filters":{"npl":[],"notNpl":[],"applicant":[],"notApplicant":[],"inventor":[],"notInventor":[],"owner":[],"notOwner":[],"tags":[],"dates":[],"types":[],"notTypes":[],"j":[],"notJ":[],"fj":[],"notFj":[],"classIpcr":[],"notClassIpcr":[],"classNat":[],"notClassNat":[],"classCpc":[],"notClassCpc":[],"so":[],"notSo":[],"sat":[]},"sequenceFilters":{"s":"SEQIDNO","d":"ASCENDING","p":0,"n":10,"sp":[],"si":[],"len":[],"t":[],"loc":[]}}