Welcome to the all-new Vetlearn

  • What’s new on Vetlearn?
  • The latest issues of Compendium and
    Veterinary Technician
  • New CE articles for veterinarians and technicians
  • Expert advice on practice management
  • Care guides on more than 400 subjects
    to give to your clients
  • And more!

To access Vetlearn, you must first sign in or register.


Become a Member

Compendium March 2012 (Vol 34, No 3)

Methicillin-Resistant Staphylococcus Infections

by Reid K. Nakamura, DVM, DACVECC, Emily Tompkins, DVM

    CETEST This course is approved for 3.0 CE credits

    Start Test


    Methicillin-resistant Staphylococcus aureus infection is currently the most common skin infection identified in human emergency rooms, and the development of methicillin resistance is increasing in veterinary medicine. This article reviews the current knowledge about methicillin-resistant Staphylococcus infections in human medicine as well as the limited information available in veterinary medicine, including options for diagnosis, treatment, and prevention.

    Staphylococci are gram-positive organisms that are morphologically characterized by a cell wall, a single cytoplasmic membrane, and cytosol.1,2 Staphylococci are normal flora of domestic animals; they are generally not invasive and colonize intact epithelium without causing disease.1,2 (A person or animal that carries an infectious agent on his or her body but does not exhibit signs of disease is said to be colonized.) Infection occurs when the bacteria are found in abnormal locations and precipitate tissue inflammation and pathogenic changes.1,2 Before the development of penicillin, Staphylococcus infections were associated with high morbidity and mortality.3

    Penicillin was first used widely as the initial therapy for Staphylococcus aureus infections during World War II. It is a β-lactam antibiotic that acts by binding to transpeptidase, which is involved in cell wall peptidoglycan synthesis, thereby disrupting the formation of bacterial cell walls and causing cell death.4 However, within 10 years of its introduction, penicillin began to wane in effectiveness against Staphylococcus infections because of bacterial acquisition of plasmid-encoded β-lactamase, an enzyme that inactivates the lactam ring of β-lactam antibiotics.4 Methicillin was hailed as a means to counteract β-lactamase resistance; however, methicillin-resistant S. aureus (MRSA) was first identified in 1961 just 2 years after methicillin was introduced.5

    Methicillin-resistant Staphylococcus (MRS) infections are caused by Staphylococcus spp that are resistant to all currently available β-lactam antimicrobials and carbepenems.6 MRS species have acquired a mobile genetic element known as the staphylococcal cassette chromosome (SCC).6 The SCC carries a gene (the mecA gene) that encodes for the production of an altered penicillin-binding protein (PBP2a).7 This protein is able to perform all of the required cellular functions but does not allow binding of β-lactam antimicrobials.7 The SCC also contains insertion sequences that allow incorporation of additional antimicrobial resistance markers.8–10 These insertion sequences are why many MRS are resistant to non-β-lactam antimicrobials that act through mechanisms other than interference with bacterial cell wall synthesis.

    Both methicillin-susceptible Staphylococcus spp (MSS) and MRS can cause serious infection and may possess virulence factors such as superantigenic toxins, leukocidin, and fibronectins.11,12 However, there is greater concern about infection with MRS compared with infection with MSS due to the difficulty in identifying effective antibiotics to eradicate infection. As such, several studies in humans have reported a worse clinical outcome for patients infected with MRS than for those infected with MSS.5,13–15


    When MRSA was first reported, it was commonly identified in people who were immunocompromised or critically ill, such as those who frequented health care facilities, were in contact with a person who had an MRSA infection, or had a history of illicit drug use.16 This type of MRSA, termed health care–associated MRSA (HA-MRSA), is typically associated with resistance to multiple antibiotics in addition to β-lactams and is reported to increase morbidity and mortality in people.5,17 Bacteremia is most commonly reported in association with HA-MRSA infections; pneumonia, cellulitis, osteomyelitis, endocarditis, and septic shock are reported less frequently.18 Mortality rates of 20% to 50% from HA-MRSA bloodstream infections, 55% from septic shock, and 33% from pneumonia have been reported.18,19

    Key Points

    • Methicillin-resistant Staphylococcus isolates are resistant to all β-lactam antimicrobials and are frequently resistant to many other antimicrobial classes.
    • CA-MRSA is the most common pathogen cultured from human patients with skin and soft tissue infections in emergency departments.
    • No clinical features distinguish with certainty skin and soft tissue infections caused by MRSA from those caused by methicillin-susceptibleS. aureus.
    In the mid 1990s, MRSA infections began to be identified in people who did not have contact with the health care system.20 The strains causing these infections are termed community-acquired MRSA (CA-MRSA). These isolates are often susceptible to non-β-lactam antimicrobials.21 Numerous reports have suggested the transmission of CA-MRSA in settings where people are in close contact, such as households,22 jails,23 and athletic facilities.24 In addition, CA-MRSA has been shown to persist on environmental surfaces in homes of colonized or infected individuals and pets.25 There is also some concern that CA-MRSA may travel through the air and play a role in nasal colonization or in respiratory tract infections.26 The emergence of CA-MRSA strains is of great concern due to the apparent increased virulence of the bacteria, as apparently healthy humans with no risk factors are being infected.22–26

    In most US cities, CA-MRSA is the most common pathogen cultured from patients with skin and soft tissue infections in emergency departments.27 Necrotic skin lesions are a common presentation and are often incorrectly attributed to bites by brown recluse spiders or insects.28

    Identification of MRSA Strains

    MRSA strains can be described using molecular and phenotypic methods, although human medicine lacks a universal nomenclature to describe the different strains. Molecular typing methods include pulsed field electrophoresis, multilocus sequence typing, SCCmec allele identification, and staphylococcal protein A (spa) typing.29 Phenotypic typing methods include the use of biochemical reactions, antibiotic susceptibility patterns, susceptibility to various phages, and toxin production.29 Molecular pulsed-field electrophoresis, SCCmec allele identification, antibiotic susceptibility patterns, and toxin production appear to be the most common methods used for description of MRSA strains in the human literature. To date, the veterinary data are very sparse and do not distinguish between CA-MRSA and HA-MRSA.

    Molecular Methods

    Molecular typing studies in the United States and Australia demonstrated that most CA-MRSA infections are caused by one of several clones or pulsed-field types.30,31 In the United States, two clones, designated USA300 and USA400, have been identified as the primary types that cause CA-MRSA infections.30,31 Other strains of CA-MRSA include USA1000 and USA1100.19,21,30 Strains most frequently associated with HA-MRSA infections were USA100 and USA200; USA500 was less common.19,21,30,31 The CA-MRSA clones most commonly display the presence of the SCCmec type IV allele; the type V allele is also reported.21,32–34 In contrast, HA-MRSA strains usually are associated with SCCmec alleles I, II, and III, with type II being most common.19

    Phenotypic Methods

    Phenotypically, CA-MRSA isolates are typically resistant to only β-lactam antibiotics, whereas HA-MRSA strains are typically resistant to other antibiotics as well.17,27 CA-MRSA isolates also have a high prevalence of genes encoding the two-component Panton-Valentine leukocidin exotoxin.35 This exotoxin causes cytolysis and pore formation in phagocytic host cells and is associated with skin necrosis and abscess formation, although its role in the pathogenesis of CA-MRSA infections remains controversial.35 A summary of the molecular and phenotypic characteristics of HA-MRSA and CA-MRSA is provided in TABLE 1. However, distinguishing between HA-MRSA and CA-MRSA is becoming increasingly difficult due to overlapping molecular and phenotypic characteristics between the two strains.36

    Table 1. Comparison Between HA-MRSA and CA-MRSA Strains in Humans in the United States18,21,30,31,60




    Clinical presentation

    • Surgical site infections
    • Invasive (pneumonia, bloodstream infections)
    • Skin infections
    • Rarely invasive
    • Recurrent


    • Elderly
    • Contact with health care facilities
    • Young
    • Athletes
    • Correctional facility inmates
    • Military recruits

    Antibiotic resistance



    Molecular markers

    PVL –

    PVL +

    Clone type

    USA100, USA500, USA800

    USA300, USA400, USA1000, USA1100

    SCCmec type

    I, II, III

    IV, V

    CA-MRSA = community-acquired MRSA, HA-MRSA = hospital-acquired MRSA, PVL = Panton-Valentine leukocidin, SCCmec = staphylococcal chromosome cassette mec allele

    MRS Species in Veterinary Medicine

    MRSA infections were identified in horses and cows as early as the 1970s,37,38 but they were not reported in dogs until the 1990s.39 Most reported MRS infections in small animals have been associated with pyoderma or postoperative wound infections.40–46 Otitis, urinary tract infections, and arthropathies have also been reported.39,47,48 Although the human literature regarding MRSA is extensive, S. aureus is infrequently isolated from dogs and cats, and Staphylococcus pseudintermedius (formerly misclassified as Staphylococcus intermedius) is the Staphylococcus sp most commonly isolated from dogs and cats.49–51 It has been speculated that the true prevalence of S. pseudintermedius infection in veterinary medicine may be higher than that documented in the literature because these isolates are easily missed by routine disk diffusion and broth microdilution methods.52

    A rise in the frequency of oxacillin resistance and multidrug resistance in S. pseudintermedius isolates from dogs has been reported.43 Even more concerning is the finding thatStaphylococcus schleiferi had a higher incidence of oxacillin43 and methicillin resistance40 than S. pseudintermedius andS. aureus, despite S. schleiferi being identified less commonly in veterinary patients.53

    A comparative study found isolation rates of MRSA to be similar between dogs and cats, with approximately one-third of S. aureus isolates identified as being methicillin resistant.54 However, methicillin-resistantS. pseudintermedius (MRSP) and methicillin-resistantS. schleiferi (MRSS) isolation rates were significantly greater in dogs than in cats. MRSS was more commonly associated with superficial (skin and ear canal) infections, whereas MRSA was more commonly associated with deep tissue infections. Although rates of methicillin resistance were highest in theS. schleiferi group, MRSS was sensitive to more classes of non-β-lactam antimicrobials than MRSA.54 These findings are summarized in TABLE 2.

    Table 2. Summary of Most Common Methicillin-Resistant Staphylococcus Species in Veterinary Medicine39–54


    Staphylococcus aureus

    Staphylococcus pseudintermedius

    Staphylococcus schleiferi

    Natural reservoir



    Dogs, humans

    Incidence of methicillin resistance




    Incidence of resistance to non-β-lactam antibiotics




    Incidence in dogs versus cats


    More commonly identified in dogs than in cats

    More commonly identified in dogs than in cats

    Location of isolation

    Deep infection

    Equal incidence of superficial and deep infection

    Superficial infection (pyoderma, otitis)

    Diagnosis of Methicillin Resistance

    Diagnosis of methicillin resistance involves bacterial culture and susceptibility testing of appropriate specimens. Special transport media are not required, and refrigerated samples survive well during routine transport. Oxacillin is used for in vitro testing because the disks have greater stability and the test results correlate better with the methicillin resistance ofS. aureus isolates from people.40

    Other tests that can be used include polymerase chain reaction (PCR) assay for the detection of the mecA gene and a latex particle agglutination test that detects the PBP2a antigen.40 Molecular detection of the mecA gene using PCR is considered the gold standard for making a definitive diagnosis of methicillin resistance in people.55–58 However, veterinary studies have shown a poor correlation between the presence of the mecA gene and PBP2a antigen and methicillin resistance in Staphylococcus spp.40 In human medicine, suspicion for MRSA is heightened by a history of previous MRSA infection or contact with a colonized individual. However, many human patients have no apparent risk factors. In addition, there are no clinical features that distinguish with certainty skin and soft tissue infections caused by MRSA from those caused by methicillin-susceptibleS. aureus in people.59 Comparison studies of lesion appearance between MRSA and methicillin-susceptible S. aureus infections in veterinary species have not been reported.

    Treatment of MRSA Infections

    Treatment of CA-MRSA infections in humans depends on the severity of the clinical presentation and the type of skin and soft tissue infection. Purulent skin and soft tissue infections without associated systemic signs, such as fever, tachycardia, or hemodynamic instability, are generally managed with incision and drainage with or without oral antimicrobial therapy.60 However, the optimal treatment strategy is still intensely debated in human medicine.60

    Clindamycin is active in vitro against at least 80% of CA-MRSA strains and has been used with success in the treatment of CA-MRSA infections, mainly in skin and soft tissue.61,62 The disadvantages of this medication include its association with diarrhea caused by Clostridium difficile and increasing rates of clindamycin resistance in some regions of the world.63,64 In addition, the results of testing for clindamycin susceptibility may be misleading, as treatment failures have been documented despite test results showing that an MRSA isolate was susceptible to clindamycin.61 Many HA-MRSA strains have inducible resistance to clindamycin; therefore, clindamycin should not be used to treat these infections.65

    Tetracyclines and trimethoprim-sulfamethoxazole (TMS) are not recommended as sole empirical therapy for nonpurulent cellulitis because of concerns regarding resistance of group A streptococci to these agents.66 However, these antimicrobials are reasonable choices in cases of confirmed CA-MRSA.60 Doxycycline and minocycline appear effective in the treatment of skin and soft tissue infections caused by CA-MRSA and have greater antistaphylococcal activity than tetracycline.67–69 A retrospective review of skin and soft tissue infections caused by CA-MRSA in people reported a cure rate of 83% for treatment with doxycycline.69

    Sulfa drugs are reportedly active against 90% to 100% of CA-MRSA isolates in people.70–72 However, efficacy data to evaluate this drug therapy for CA-MRSA are inconsistent.70,71,73 In a study at a human outpatient clinic in Boston, the percentage of patients with clinical resolution of MRSA infections increased in parallel with TMS use.63 However, in another study, treatment failure occurred in 50% of patients who received double-strength TMS.73

    Resistant strains are observed rapidly when rifampin is used as a single agent for treatment of CA-MRSA.72 Rifampin has been used in combination with other antimicrobial agents that are active against S. aureus to treat MRSA infections.74 Rifampin achieves high concentrations in mucosal surfaces75 and thus has a theoretical benefit in that it may help eradicate MRSA carriage.76 However, little information is available on the benefit of adding rifampin for the treatment of staphylococcal infections, and drug-drug interactions are common.60

    Linezolid is one of the standard treatments for complicated skin infections and hospital-acquired pneumonia due to MRSA in human adults.60 However, failures of linezolid to treat endocarditis in human patients with intravascular MRSA have been reported.77,78 Linezolid use has been associated with reversible myelosuppression, peripheral and optic neuropathy, and lactic acidosis.79,80 To limit the potential for widespread resistance, clinicians should reserve linezolid for use in more severe infections in consultation with an infectious disease specialist.60

    In human medicine, other treatment options for CA-MRSA are chloramphenicol and aminoglycosides.81 Chloramphenicol can be used as a single-agent therapy and is typically recommended for central nervous system MRSA infection, although caution must be exercised because precipitation of bone marrow aplasia is a rare adverse effect. Aminoglycosides are not recommended as monotherapy and are associated with adverse effects such as ototoxicity and renal toxicity.81 Fluoroquinolones should not be used to treat skin and soft tissue infections caused by CA-MRSA because resistance to them develops readily and is widely prevalent.27

    Vancomycin is still considered the optimal treatment for hospitalized human patients with suspected HA-MRSA.60 However, to limit the risk for the development of vancomycin resistance, a different drug should be used if susceptibility testing indicates that a more rapidly bacteriocidal β-lactam agent such as oxacillin would be appropriate.60,82 Vancomycin is poorly absorbed after oral administration83; oral therapy with vancomycin is useful only against enteric organisms such as C. difficile.82 Consequently, parenteral administration is the only effective route. Because the confirmation of bacteremia by culture and susceptibility testing typically requires >48 hours, empiric antimicrobial therapy must be initiated before results are obtained. Several studies have suggested that poorly chosen or delayed empiric treatment of bacteremia is associated with a significantly higher risk of adverse outcomes.84–86 For a summary of treatment options for MRSA infections in people, see TABLE 3.

    Despite the potential severity of MRSA infections, successful treatment is possible in veterinary medicine. Tomlin et al39 reported improvement or resolution of MRSA infection with oral antimicrobial therapy in nine of 11 dogs. Drugs reported in this case series included clindamycin (four dogs), fluoroquinolones (four dogs), amoxicillin-clavulanic acid (three dogs), trimethoprim-sulfamethoxazole (two dogs), and metronidazole (one dog). Multiple antibiotics were used in four dogs.39 However, larger outcome studies for evaluation of treatment of MRS infections in veterinary medicine are lacking. As MRSA infections become more common, it will become increasingly important to emphasize submission of diagnostic samples before initiation of empirical antimicrobial therapy.60 Often, empirical therapy for wound and incisional infections involves use of β-lactam antimicrobials, which would be ineffective against MRSA.

    Table 3. Treatment Options for Methicillin-Resistant Staphylococcus aureus Infections in Humans 60–86,a–e


    Use as Monotherapy?


    Adverse Effects





    Ototoxicity, particularly in patients with renal impairment; nephrotoxicity, especially when combined with vancomycin



    Central nervous system infections

    Marrow aplasia (rare)



    Skin and soft tissue infections, bone and joint effect

    Clostridium difficilecolitis and antibiotic-associated diarrhea

    Rising incidence of resistance

    Sulfa drugs


    Skin and soft tissue infections

    Bone marrow effects,

    immune-mediated effects

    Outcome studies lacking



    Pneumonia, serious soft tissue infections, bacteremia

    Bone marrow suppression, peripheral neuropathy,

    lactic acidosis

    Consult with infectious disease specialist before using



    (nasal carriage)

    For eradication of colonization


    High-level resistance



    Bone and joint infections, skin and soft tissue infections

    Hepatic enzyme elevations,

    multiple drug interactions

    Emergence of resistance



    Skin, soft tissue, and urinary tract infections;

    eradication of carriage

    Gastrointestinal upset

    Emergence of resistance




    (usually reserved for HA-MRSA)

    Renal toxicity associated with concurrent aminoglycoside use

    Dose adjustment required in patients with renal impairment

    aLiu C, Graber CJ, Karr M, et al. A population-based study of the incidence and molecular epidemiology of methicillin-resistant Staphylococcus aureus disease in San Francisco, 2004-2005. Clin Infect Dis 2008;46(11):1637-1646.

    bCenizal MJ, Skiest D, Luber S, et al. Prospective randomized trial of empiric therapy with trimethoprim-sulfamethoxazole or doxycycline for outpatient skin and soft tissue infection in an area of high prevalence of methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother 2007;51(7):2628-2630.

    cGerson SL, Kaplan SL, Bruss JB, et al. Hematologic effects of linezolid: summary of clinical experience. Antimicrob Agents Chemother 2002;46(8):2723-2726.

    dApodaca AA, Rakita RM. Linezolid-induced lactic acidosis. N Engl J Med 2003;348(1):86-87.

    eBressler AM, Zimmer SM, Gilmore JL, Somani J. Peripheral neuropathy associated with prolonged use of linezolid. Lancet Infect Dis 2004;4(8):528-531.

    Public Health Significance

    Reports in human medicine suggest that animals may serve as reservoirs for MRSA that, in turn, can infect humans.87,88 The resistance patterns and genetic makeup of MRSA isolates from dogs and cats are generally indistinguishable from those of the most prevalent HA-MRSA strains in the human population.89–91 This suggests interspecies transmission but does not indicate the direction of transmission, although it is assumed that animals become colonized through contact with colonized or infected humans and serve as a source of reinfection or recolonization.89,90 This is important when examining pets owned by health care workers, as it is unknown whether ownership by a health care worker increases a pet’s risk of MRSA colonization.92,93

    Although MRSP is predominantly associated with infections of companion animals, humans can also become infected. Human MRSP infection, which likely results from exposure to colonized or infected pets, results in difficult-to-treat infections and increased risk of mortality.94–97 Even when people are not directly infected by exposure to pets with MRSP, concern exists that MRSP may provide the genetic source material to convert methicillin-susceptibleS. aureus colonizing humans into MRSA through transfer of its mobile SCCmec.98

    Surveillance and Decolonization Strategies

    Asymptomatic human colonization with MRSA is more common than infection, and while colonization does not necessarily lead to infection, it increases the relative risk of MRSA infection up to 10-fold.99–101 Colonization may be transient or persistent.102 Routine screening of healthy pets for MRSA colonization is not indicated except when a person or a pet has recurrent infection with MRSA despite consistent use of suggested hygiene practices.8 The ideal site for collection of samples for culture from animals has not been determined; culture of nasal or perineal swabs is usually recommended.103,104 However, even when a colonized human or animal is identified, there is no clear course of action.60

    MRSA decolonization involves using antimicrobials or antiseptics to eliminate or reduce the burden of MRSA.105 A study quantified the effect of chlorhexidine bathing and intranasal mupirocin therapy for decolonization of MRSA-colonized human patients in a 16-bed medical coronary intensive care unit.106 Compared with a baseline period during which all MRSA cases were identified through active surveillance, the intervention was associated with a 48% decrease in MRSA colonization and infection. Active screening and strict implementation of infection control protocols in two equine facilities resulted in a rapid reduction in the number of colonized horses and eradication of MRSA colonization on one farm.107 More recently, a study reported that high rates of nasal colonization among veterinary personnel were associated with increased numbers of MRSA infections in small animal patients. Consequently, surveillance protocols were recommended for nosocomial infection control.108

    Prevention of MRSA Transmission

    Studies in human medicine have found that institution of MRSA prevention practices among health care workers can decrease the rate of MRSA transmission in individual facilities as well as across a large population of people.109–111 The most critical step for reduction in MRSA transmission is hand hygiene. In veterinary practice, this means that caretakers should wash their hands thoroughly after handling any animal and between handling different animals. Pittet et al112 identified hand hygiene as a simple but key infection control measure to reduce nosocomial and MRSA infections. In their study, a hospital-wide hand hygiene program that increased hand hygiene compliance from 48% to 66% was associated with halving the MRSA transmission rate and decreasing the nosocomial infection rate. These findings have been confirmed by other studies.113,114 Specific means of hand hygiene have been described elsewhere, although the use of alcohol-based hand rubs has been shown to reduce MRSA rates and is the standard of care recommended by the Centers for Disease Control and Prevention.60,115

    The hospital environment acts as a major reservoir for MRSA, which can survive up to months on inanimate surfaces, depending on environmental conditions.107,116,117 MRSA is readily removed from surfaces by disinfectants commonly used in hospitals; lack of adherence to cleaning protocols and ongoing recontamination of surfaces seem to be responsible for the persistence of environmental reservoirs.118,119 An observational study of intensive care units in 16 hospitals found that only 57.1% of standardized environmental sites in patient rooms were cleaned after patient discharge, and many of the areas missed were at high risk of microbial contamination, such as toilet handles, doorknobs, and light switches.120 Guidelines proposed by Leonard and Markey29 for control measures for MRSA infection in animals are summarized in TABLE 4.

    Table 4. Summary of Control Measures for MRSA Infection and Colonization in Animals29

    Control Measure


    Prevent introduction of infection

    Screen all incoming cases for infection via nasal swab at admission and isolate until negative status established

    Prevent zoonosis and reverse zoonosis

    • Use hand hygiene (alcohol-based hand rubs)
    • Cover wounds and skin lesions
    • Use gloves, masks, eye protection, disposable aprons for contact with wounds, body fluids, or contaminated areas
    • Use strict aseptic technique during surgery
    • Screen staff for MRSA colonization

    Prevent transmission from animal to animal

    Isolate all suspected cases of MRSA infection

    Prevent indirect transmission

    • Disinfect environment, particularly high contact areas (light switches, cage doors, etc.)
    • Use dedicated thermometers, leads, and other handling equipment for known positive or suspected cases


    MRSA is currently the most common skin infection in human medicine, even in patients with no exposure to health care facilities.60 Methicillin resistance is increasing in veterinary medicine, although the most commonly identified MRS species is S. pseudintermedius.43,49–51 The optimal management strategy remains unclear, but increased awareness and submission of appropriate samples for culture and susceptibility testing are critical to instituting appropriate antimicrobial therapy and obtaining a successful outcome.60 Hand hygiene is a simple and effective means of reducing MRSA transmission rates.60,115

    Downloadable PDF


    1. DeLeo FR, Diep BA, Otto M. Host defense and pathogenesis in Staphylococcus aureus infections. Infect Dis Clin North Am 2009;23(1):17-34.

    2. Biberstein EL, Jang SS, Hirsh DC. Species distribution of coagulase-positive staphylococci in animals. J Clin Microbiol 1984;19(5):610-615.

    3. Chambers HF. Community-associated MRSA—resistance and virulence converge. N Engl J Med 2005;352(14):1485-1487.

    4. Kirby WM. Extraction of a highly potent penicillin inactivation from penicillin resistant staphylococci. Science 1944;99(2579):452-453.

    5. Cosgrove SE, Sakoulas G, Perencevich EN, et al. Comparison of mortality associated with methicillin-resistant and methicillin-susceptible Staphylococcus aureus bacteremia: a meta-analysis. Clin Infect Dis 2003;36(1):592-598.

    6. Crawford S, Boyle-Vavra S, Daum RS. Community associated methicillin-resistant Staphylococcus aureus. In Scheld M, Hooper D, Hughes JM, eds. Emerging Infections 7. Herndon, VA: ASM Press; 2006:153-170.

    7. Utsui Y, Yokota T. Role of an altered penicillin-binding protein in methicillin- and cephem-resistant Staphylococcus aureus. Antimicrob Agents Chemother 1985;28(3):397-403.

    8. Barton M, Hawkes M, Moore D, et al. Guidelines for the prevention and management of community-associated methicillin resistant Staphylococcus aureus: a perspective for Canadian health care practitioners. Can J Infect Dis Med Microbiol 2006;17(suppl C):4C-24C.

    9. Descloux S, Rossano A, Perreten V. Characterization of new staphylococcal cassette chromosome mec (SCCmec) and topoisomerase genes in fluoroquinolone- and methicillin-resistant Staphylococcus pseudintermedius. J Clin Microbiol 2008;46(5):1818-1823.

    10. Holden MT, Feil EN, Lindsay JA, et al. Complete genomes of two clinical Staphylococcus aureus strains: evidence for the rapid evolution of virulence and drug resistance. Proc Natl Acad Sci USA 2004;101(26):9786-9791.

    11. Durand G, Bes M, Meugnier H, et al. Detection of new methicillin-resistant Staphylococcus aureus clones containing the toxic shock syndrome toxin 1 gene responsible for hospital- and community-acquired infections in France. J Clin Microbiol 2006;44(3):847-853.

    12. Diep BA, Carleton HA, Chang RF, et al. Roles of 34 virulence genes in the evolution of hospital- and community-associated strains of methicillin-resistant Staphylococcus aureus. J Infect Dis 2006;193(11):1495-1503.

    13. Cosgrove SE, Qi Y, Kaye KS, et al. The impact of methicillin resistance in Staphylococcus aureus bacteremia on patient outcomes: mortality, length of stay, and hospital charges. Infect Control Hosp Epidemiol 2005;26(2):166-174.

    14. Shurland S, Zhan M, Bradham DD, Roghmann MC. Comparison of mortality risk associated with bacteremia due to methicillin-resistant and methicillin-susceptible Staphylococcus aureus. Infect Control Hosp Epidemiol 2007;28(3):273-279.

    15. Reed SD, Friedman JY, Engemann JJ, et al. Costs and outcomes among hemodialysis-dependent patients with methicillin-resistant or methicillin-susceptible Staphylococcus aureus bacteremia. Infect Control Hosp Epidemiol 2005;26(2):175-183.

    16. Chambers HF. The changing epidemiology of Staphylococcus aureus? Emerg Infect Dis 2001;7(2):178-182.

    17. Melzer M, Eykyn SJ, Graunsden WR, Chinn S. Is methicillin-resistant Staphylococcus aureus more virulent than methicillin-susceptibleS. aureus? A comparative cohort study of British patients with nosocomial infections and bacteremia. Clin Infect Dis 2003;37(11):1453-1460.

    18. Klevens RM, Morrison MA, Nadle J, et al. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA 2007;298(15):1763-1771.

    19. McHugh CG, Riley LW. Risk factors and costs associated with methicillin-resistant Staphylococcus aureus bloodstream infections. Infect Control Hosp Epidemiol 2004;25(5):425-430.

    20. Herold BC, Immergluck LC, Maranan MC, et al. Community-acquired methicillin-resistant Staphylococcus aureus in children with no predisposing risk. JAMA 1998;279(8):593-598.

    21. Naimi TS, LeDell KH, Como-Sabetti K, et al. Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection. JAMA 2003;290(22):2976-2984.

    22. Dietrich DW, Auld DB, Mermel LA. Community-acquired methicillin-resistant Staphylococcus aureus in southern New England children. Pediatrics 2004;113(4):e347-e352.

    23. Aiello AE, Lowy FD, Wright LN, Larson EL. Meticillin-resistant Staphylococcus aureus among US prisoners and military personnel: review and recommendations for future studies. Lancet Infect Dis 2006;6(6):335-341.

    24. Kazakova SV, Hageman JC, Matava M, et al. A clone of methicillin-resistant Staphylococcus aureus among professional football players. N Engl J Med 2005;352(5):468-475.

    25. Scott E, Duty S, Callahan M. A pilot study to isolate Staphylococcus aureus and methicillin-resistant S. aureus from environmental surfaces in the home. Am J Infect Control 2008;36(6):458-460.

    26. Shiomori T, Miyamoto H, Makishima K. Significance of airborne transmission of methicillin-resistant Staphylococcus aureus in an otolaryngology–head and neck surgery unit. Arch Otolaryngol Head Neck Surg 2001;127(6):644-648.

    27. Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillin-resistant Staphylococcus aureus infections among patients in the emergency department. N Engl J Med 2006;355(7):666-674.

    28. Kaplan SL, Hulten KG, Gonzalez BE, et al. Three-year surveillance of community acquired Staphylococcus aureus infections in children. Clin Infect Dis 2005;40(12):1785-1791.

    29. Leonard FC, Markey BK. Meticillin-resistant Staphylococcus aureus in animals: a review. Vet J 2008;175(1):27-36.

    30. McDougal LK, Steward CD, Killgore GE, et al. Pulsed-field gel electrophoresis typing of oxacillin-resistant Staphylococcus aureus isolates from the United States: establishing a national database. J Clin Micrbiol 2003;41(11):5113-5120.

    31. Okuma K, Iwakawa K, Turnidge JD, et al. Dissemination of new methicillin-resistant Staphylococcus aureus clones in the community. J Clin Microbiol 2002;40(11):4289-4294.

    32. Ma XX, Ito T, Tiensasitorn C, et al. Novel type of staphylococcal cassette chromosome mec identified in community-acquired methicillin-resistant Staphylococcus aureus strains. Antimicrob Agents Chemother 2002;46(4):1147-1152.

    33. Diep BA, Sensabaugh GF, Somboonna NS, et al. Widespread skin and soft-tissue infections due to two methicillin-resistant Staphylococcus aureus strains harboring the genes for Panton-Valentine leukocidin. J Clin Microbiol 2004;42(5):2080-2084.

    34. Baggett HC, Hennessy TW, Rudolph K, et al. Community-onset methicillin-resistant Staphylococcus aureus associated with antibiotic use and the cytoxin Panton-Valentine leukocidin during furunculosis outbreak in rural Alaska. J Infect Dis 2004;189(9):1565-1573.

    35. Vandenesch F, Naimi T, Enright MC, et al. Community-acquired methicillin-resistant Staphylococcus aureus carrying Panton-Valentine leukocidin genes: worldwide emergence. Emerg Infect Dis 2003;9(8):978-984.

    36. Popovich KJ, Weinstein RA. Commentary: The graying of methicillin-resistant Staphylococcus aureus. Infect Control Hosp Epidemiol 2009;30(1):9-12.

    37. Shimizu A, Kawano J, Yamamoto C, et al. Genetic analysis of equine methicillin-resistant Staphylococcus aureus by pulsed-field gel electrophoresis. J Vet Med Sci 1997;59(10):935-937.

    38. Devriese LA, Van Damme LR, Fameree L. Methicillin (cloxacillin)-resistant Staphylococcus aureus strains isolated from bovine mastitis cases. Zentralbl Veterinarmed B 1972;19(7):598-605.

    39. Tomlin J, Pead MJ, Lloyd DH, et al. Methicillin-resistant Staphylococcus aureus infections in 11 dogs. Vet Rec 1999;144(3):60-64.

    40. Kania SA, Williamson NL, Frank LA, et al. Methicillin resistance of staphylococci isolated from the skin of dogs with pyoderma. Am J Vet Res 2004;65(9):1265-1268.

    41. Kruse H, Hofshagen M, Thoresen SI, et al. The antimicrobial susceptibility of Staphylococcus species isolated from canine dermatitis. Vet Res Commun 1996;20(3):205-214.

    42. Guardabassi L, Leober ME, Jacobson A. Transmission of multiple antimicrobial-resistant Staphylococcus intermedius between dogs affected by deep pyoderma and their owners. Vet Microbiol 2004;98(1):23-27.

    43. Jones RD, Kania SA, Rohrbach BW, et al. Prevalence of oxacillin and multi-drug resistant staphylococci in clinical samples from dogs: 1,772 samples (2001-2005). J Am Vet Med Assoc 2007;230(2):221-227.

    44. Leonard FC, Abbott Y, Rossney A, et al. Methicillin-resistant Staphylococcus aureus isolated from a veterinary surgeon and five dogs in one practice. Vet Rec 2006;158(5):155-159.

    45. Ruscher C, Lubke-Becker A, Wleklinski CG, et al. Prevalence of methicillin-resistant Staphylococcus pseudintermedius isolated from clinical samples of companion animals and equidaes. Vet Microbiol 2009;136(1-2):197-201.

    46. Weese JS, Faires M, Rousseau J, et al. Cluster of methicillin-resistant Staphylococcus aureus colonization in a small animal intensive care unit. J Am Vet Med Assoc 2007;231(9):1361-1364.

    47. Wettstein K, Descloux S, Rossano A, Perreten V. Emergence of methicillin-resistant Staphylococcus pseudintermedius in Switzerland: three cases of urinary tract infections in cats. Schweiz Arch Tierheilkd 2008;150(7):339-343.

    48. Grinberg A, Kingsbury DD, Gibson IR, et al. Clinically overt infections with methicillin-resistant Staphylococcus aureus in animals in New Zealand: a pilot study. NZ Vet J 2008;56(5):237-242.

    49. Sasaki T, Kikuchi K, Tanaka Y, et al. Reclassification of phenotypically identified Staphylococcus intermedius strains. J Clin Microbiol 2007;45(9):2770-2778.

    50. Bannoehr J, Franco A, Iurescia M, et al. Molecular diagnostic identification of Staphylococcus pseudintermedius. J Clin Microbiol 2009;47(2):469-471.

    51. Cox HU, Hoskins JD, Newman SS, et al. Distribution of staphylococcal species on clinically healthy cats. Am J Vet Res 1985;46(9):1824-1828.

    52. Gortel K, Campbell KL, Kakoma I, et al. Methicillin resistance among staphylococci isolated from dogs. Am J Vet Res 1999;60(12):1526-1530.

    53. Holm BR, Petersson U, Mörner A, et al. Antimicrobial resistance in staphylococci from canine pyoderma: a prospective study of first time and recurrent cases in Sweden. Vet Rec 2002;151(20):600-605.

    54. Morris DO, Rook KA, Shofer FS, Ranking SC. Screening of Staphylococcus aureus, Staphylococcus intermedius, and Staphylococcus schleiferi isolates obtained from small companion animals for antimicrobial resistance: a retrospective review of 749 isolates (2003-04). Vet Dermatol 2006;17(5):332-337.

    55. Counts JM, Astles JR, Tenover FC, Hindler J. Systems approach to improving antimicrobial susceptibility testing in clinical laboratories in the United States. J Clin Microbiol 2007;45(7):2230-2234.

    56. Fluit AC, Visser MR, Schmitz FJ. Molecular detection of antimicrobial resistance. Clin Microbiol Rev 2001;14(4):836-871.

    57. Ribeiro J, Vieira FD, King T, et al. Misclassification of susceptible strains of Staphylococcus aureus as methicillin-resistant S aureus by a rapid automated susceptibility testing system. J Clin Microbiol 1999;37(5):1619-1620.

    58. Francois P, Hochmann A, Huyghe A, et al. Rapid and high-throughput genotyping of Staphylococcus epidermidis isolates by automated multilocus variable-number of tandem repeats: a tool for real-time epidemiology. J Microbiol Methods 2008;72(3):296-305.

    59. Miller LG, Perdreau-Remington F, Bayer AS, et al. Clinical and epidemiologic characteristics cannot distinguish community-associated methicillin-resistant Staphylococcus aureus infection from methicillin-susceptible Staphylococcus aureus infection: a prospective investigation. Clin Infect Dis 2007;44(4):471-482.

    60. Gorwitz RJ, Jernigan DB, Powers JH, et al. Strategies for clinical management of MRSA in the community: summary of an experts’ meeting convened by the Centers for Disease Control and Prevention. http://www.cdc.gov/mrsa/pdf/MRSA-Strategies-ExpMtgSummary-2006.pdf. Published March 2006. Accessed October 19, 2011.

    61. Frank AL, Marcinak JF, Mangat PD, et al. Clindamycin treatment of methicillin-resistant Staphylococcus aureus infections in children. Pediatr Infect Dis J 2002;21(6):530-534.

    62. Martinez-Aguilar G, Hammerman WA, Mason EO Jr, Kaplan SL. Clindamycin treatment of invasive infections caused by community-acquired methicillin-resistant and methicillin-susceptible Staphylococcus aureus in children. Pediatr Infect Dis J 2003;22(7):593-598.

    63. Szumowski JD, Cohen DE, Kanaya F, Mayer KH. Treatment and outcomes of infections by methicillin-resistant Staphylococcus aureus at an ambulatory clinic. Antimicrob Agents Chemother 2007;51(2):423-428.

    64. Braun L, Craft D, Williams R, et al. Increasing clindamycin resistance among methicillin-resistant Staphylococcus aureus in 57 northeast United States military treatment facilities. Pediatr Infect Dis J 2005;24(7):622-626.

    65. Rich M, Deighton L, Roberts L. Clindamycin-resistance in methicillin-resistant Staphylococcus aureus isolated from animals. Vet Microbiol 2005;111(3-4):237-240.

    66. Swartz MN. Cellulitis. N Engl J Med 2004;350(9):904-912.

    67. Minuth JN, Holmes TM, Musher DM. Activity of tetracycline, doxycycline, and minocycline against methicillin-susceptible and resistant staphylococci. Antimicrob Agents Chemother 1974;6(4):411-414.

    68. Ruhe JJ, Menon A. Tetracyclines as an oral treatment option for patients with community onset skin and soft tissue infections caused by methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother 2007;51(9):3298-3303.

    69. Ruhe JJ, Monson T, Bradsher RW, Menon A. Use of long-acting tetracyclines for methicillin-resistant Staphylococcus aureus infections: case series and review of the literature. Clin Infect Dis 2005;40(10):1429-1434.

    70. Proctor RA. Role of folate antagonists in the treatment of methicillin-resistant Staphylococcus aureus infections. Clin Infect Dis 2008;46(4):584-593.

    71. DeLeo FR, Chambers AF. Reemergence of antibiotic resistant Staphylococcus aureus in the genomics era. J Clin Invest 2009;119(9):2464-2474.

    72. Strausbaugh LJ, Jacobson C, Sewell DL, et al. Antimicrobial therapy for methicillin-resistant Staphylococcus aureus colonization in residents and staff on a Veterans Affairs nursing home care unit Infect Control Hosp Epidemiol. 1992;13(3):151-159.

    73. Markowitz N, Quinn EL, Saravolatz LD. Trimethoprim-sulfamethoxazole compared with vancomycin for the treatment of Staphylococcus aureus infection. Ann Intern Med 1992;117(5):390-398.

    74. Iyer S, Jones DH. Community-acquired methicillin-resistant Staphylococcus aureus skin infection: a retrospective analysis of clinical presentation and treatment of a local outbreak. J Am Acad Dermatol 2004;50(6):854-858.

    75. Kauffman C, BradleyS. Epidemiology of community-acquired infection. In: Crossley KB, Archer GL, eds. The Staphylococci in Human Disease. New York: Churchill Livingstone; 1997:287-308.

    76. Yu VL, Goetz A, Wagener M, et al. Staphylococcus aureus nasal carriage and infection in patients with hemodialysis. Efficacy of antibiotic prophylaxis. N Engl J Med 1986;315(2):91-96.

    77. Corne P, Marchandin H, Macia JC, Jonquet O. Treatment failure of methicillin-resistant Staphylococcus aureus endocarditis with linezolid. Scand J Infect Dis 2005;37(11-12):946-949.

    78. Ruiz ME, Guerrero IC, Tuazon CU. Endocarditis caused by methicillin-resistant Staphylococcus aureus: treatment failure with linezolid. Clin Infect Dis 2002;35(8):1018-1020.

    79. French G. Safety and tolerability of linezolid. J Antimicrob Chemother 2003;51(suppl 2):ii45-ii53.

    80. Lee E, Burger S, Shah J, et al. Linezolid-associated toxic optic neuropathy: report of 2 cases. Clin Infect Dis 2003;37(10):1389-1391.

    81. Gould FK, Brindle R, Chadwick PR, et al. Guidelines (2008) for the prophylaxis and treatment of methicillin-resistant Staphylococcus aureus (MRSA) infections in the United Kingdom. J Antimicrob Chemother 2009;63(5):849-861.

    82. Weese JS. Issues regarding the use of vancomycin in companion animals. J Am Vet Med Assoc 2008;233(4):565-567.

    83. Moehering RC, Krogstad DJ, Greenblatt DJ. Pharmacokinetics of vancomycin in normal subjects and in patients with reduced renal function. Rev Infect Dis 1981;3(suppl 3):S230-S235.

    84. Ibrahim EH, Sherman G, Ward S, et al. The influence of inadequate antimicrobial treatment of bloodstream infections on patient outcomes in the ICU setting. Chest 2000;118(1):146-155.

    85. Lodise TP, McKinnon PS, Swiderski L, Rybak MJ. Outcome analysis of delayed antibiotic treatment for hospital-acquired Staphylococcus aureus bacteremia. Clin Infect Dis 2003;36(11):1418-1423.

    86. Schramm GE, Johnson JA, Doherty JA, et al. Methicillin-resistant Staphylococcus aureus sterile-site infection: the importance of appropriate initial antimicrobial treatment. Crit Care Med 2006;34(8):2069-2074.

    87. Cefai C, Ashurst S, Owens C. Human carriage of methicillin-resistant Staphylococcus aureus linked with pet dog. Lancet 1994;344(8921):539-540.

    88. Scott GM, Thomson R, Malone-Lee J, Ridgway, GL. Cross-infection between animals and man: possible feline transmission of Staphylococcus aureus infection in humans? J Hosp Infect 1988;12(1):29-34.

    89. O’Mahony R, Abbott Y, Leonard FC, et al. Methicillin-resistant Staphylococcus aureus (MRSA) isolated from animals and veterinary personnel in Ireland. Vet Microbiol 2005;109(3-4):285-296.

    90. Baptiste KE, Williams K, Williams NJ, et al. Methicillin-resistant staphylococci in companion animals. Emerg Infect Dis 2005;11(12):1942-1944.

    91. Strommenger B, Kehrenberg C, Kettilitz C, et al. Molecular characterization of methicillin-resistant Staphylococcus aureus strains from pet animals and their relationship to human isolates. J Antimicrob Chemother 2006;57(3):461-465.

    92. Boost MV, O’Donoghue MM, James A. Prevalence of Staphylococcus aureus carriage among dogs and their owners. Epidemiol Infect 2008;136(7):953-964.

    93. Kottler S, Middleton JR, Perry J, et al. Prevalence of Staphylococcus aureus and MRSA carriage in three populations. J Vet Intern Med 2010;24(1):132-139.

    94. van Duijkeren E, Houwers DJ, Schoormans A, et al. Transmission of methicillin-resistant Staphylococcus intermedius between humans and animals. Vet Microbiol 2008;128(1-2):213-215.

    95. Van Hoovels L, Vankeerberghen A, Boel A, et al. First case of Staphylococcus pseudintermedius infection in a human. J Clin Microbiol 2006;44(12):4609-4612.

    96. Tanner MA, Everett Cl, Youvan DC. Molecular phylogenetic evidence for noninvasive zoonotic transmission of Staphylococcus intermedius from a canine pet to a human. J Clin Microbiol 2000;38(4):1628-1631.

    97. Campanile F, Bongiorno D, Borborne S, et al. Characterization of a variant of the SCCmec element in a bloodstream isolate of Staphylococcus intermedius. Microb Drug Resist 2007;13(1):7-10.

    98. Epstein CR, Yam WC, Peiris JS, Epstein RJ. Methicillin-resistant commensal staphylococci in healthy dogs as a potential zoonotic reservoir for community-acquired antibiotic resistance. Infect Genet Evol 2009;9(2):283-285.

    99. Ellis MW, Hospenthal DR, Dooley DP, et al. Natural history of community-acquired methicillin-resistant Staphylococcus aureus colonization and infection in soldiers. Clin Infect Dis 2004;39(7):971-979.

    100. Johnson LB, Jose J, Yousif F, et al. Prevalence of colonization with community-associated methicillin-resistant Staphylococcus aureus among end-stage renal disease patients and health workers. Infect Control Hosp Epidemiol 2009;30(1):4-8.

    101. Safdar N, Bradley EA. The risk of infection after nasal colonization with Staphylococcus aureus. Am J Med 2008;121(4):310-315.

    102. Kluytmans JA, Wertheim HF. Nasal carriage of Staphylococcus aureus and prevention of nosocomial infections. Infection 2005;33(1):3-8.

    103. Epsterin CR, Yam WC, Peiris JS, et al. Methicillin-resistant commensal staphylococci in healthy dogs as a potential zoonotic reservoir for community-acquired antibiotic resistance. Infect Genet Evol 2009;9(2):283-285.

    104. van Duijkeren E, Wolfhagen MJ, Box AT, et al. Human-to-dog transmission of methicillin-resistant Staphylococcus aureus. Emerg Infect Dis 2004;10(12):2235-2237.

    105. Calfee DP, Salgado CD, Classen D, et al. Strategies to prevent transmission of methicillin-resistant Staphylococcus aureus in acute care hospitals. Infect Control Hosp Epidemiol 2008;29(suppl 1):S62-S80.

    106. Ridenour G, Lampen R, Federspiel J, et al. Selective use of intranasal mupirocin and chlorhexidine bathing and the incidence of methicillin-resistant Staphylococcus aureus colonization and infection among intensive care unit patients. Infect Control Hosp Epidemiol 2007;28(10):1155-1161.

    107. Kramer A, Schwebke I, Kampf G. How long do nosocomial pathogens persist on inanimate surfaces? A systematic review. BMC Infect Dis 2006;6:130-138.

    108. Walther B, Wieler LH, Friedrich AW, et al. Staphylococcus aureus and MRSA colonization rates among personnel and dogs in a small animal hospital: association with nosocomial infections. Berl Munch Tierarztl Wochenschr 2009;122(5-6):178-185.

    109. Huang SS, Yokoe DS, Hinrichsen VL, et al. Impact of routine intensive unit surveillance cultures and resultant barrier precautions on hospital-wide methicillin-resistant Staphylococcus aureus bacteremia. Clin Infect Dis 2006;43(8):971-978.

    110. Harbarth S, Fanhauser C, Schrenzel J, et al. Universal screening for methicillin-resistant Staphylococcus aureus at hospital admission and nosocomial infection in surgical patients. JAMA 2008;299(10):1149-1157.

    111. Kallen AJ, Mu Y, Bulens S, et al. Health care-associated invasive MRSA infections, 2005-2008. JAMA 2010;304(6):641-648.

    112. Pittet D, Hugonnet S, Harbarth S, et al. Effectiveness of a hospital-wide programme to improve compliance with hand hygiene. Lancet 2000;356(9238):1307-1312.

    113. Gopal Rao G, jeans A, Osman M, et al. Marketing hand hygiene in hospitals—a case study. J Hosp Infect 2002;50(1):42-47.

    114. Johnson PD, Martin R, Burrell LJ, et al. Efficacy of an alcohol/chlorhexidine hand hygiene program in hospital with high rates of nosocomial methicillin-resistant Staphylococcus aureus (MRSA) infection. Med J Aust 2005;183(10):509-514.

    115. Sroka S, Gastmeier P, Meyer E. Impact of alchol hand-rub use on meticillin resistant Staphylococcus aureus: an analysis of the literature. J Hosp Inf 2010;74(3):204-211.

    116. Beard-Pegler MA, Stubbs E, Vickery AM. Observations on the resistance to drying of staphylococcal strains. J Med Microbiol 1988;26(4):251-255.

    117. Boyce JM, Havill NL, Otter JA, Adams NM. Widespread environmental contamination associated with patients with diarrhea and methicillin-resistant Staphylococcus aureus colonization of the gastrointestinal tract. Infect Control Hosp Epidemiol 2007;28(10):1142-1147.

    118. Boyce JM. Environmental contamination makes an important contribution to hospital infection. J Hosp Infect 2007;65(suppl 2):50-54.

    119. Dancer SJ. Importance of the environment in methicillin-resistant Staphylococcus aureus acquisition: the case for hospital cleaning. Lancet Infect Dis 2008;8(2):101-113.

    120. Carling PC, Parry MM, Rupp ME, et al. Improving cleaning of the environment surrounding patients in 36 acute care hospitals. Infect Control Hosp Epidemiol 2008;29(11):1035-1041.

    References »

    NEXT: Applied Dermatology: Postcard Presentation: A Dog With Claw Atrophy part 1

    CETEST This course is approved for 3.0 CE credits

    Start Test


    Did you know... Tick survival in nature depends on (1) energy resources, (2) environmental factors such as temperature and relative humidity, and (3) host availability.Read More

    These Care Guides are written to help your clients understand common conditions. They are formatted to print and give to your clients for their information.

    Stay on top of all our latest content — sign up for the Vetlearn newsletters.
    • More