What Is Staphylococcus Aureus?

Staphylococcus (in Greek staphyle means bunch of grapes and coccos means granule) is a genus of gram-positive bacteria. Under the microscope they appear round (cocci), and form in grape-like clusters .

There are many species of staphylococci, most are completely harmless, and reside normally on the skin and mucous membranes of humans and other organisms. They are a small component of soil microbial flora. This genus is found world wide.

Staphylococci can cause a wide variety of diseases in humans either through toxin production or invasion. For example the most common cause of food poisoning is staphylococci toxins. The bacteria grow in improperly stored food, the cooking process kills them but the toxins they produce are heat resistant. Staphylococci can grow in foods with relatively low water activity (such as cheese and salami).

One harmful species is Staphylococcus aureus, which can infect wounds. Of this type, Methicillin-resistant Staphylococcus aureus (MRSA) has recently become a major cause of hospital-acquired infections. These bacteria can survive on dry surfaces increasing the chance of transmission. Staphylococcus aureus is also implicated in Toxic Shock Syndrome, during the 1980s some tampons allowed the rapid growth of S. aureus releasing toxins that were absorbed into the bloodstream.

S. epidermidis, a coagulase-negative staphylococcus species, is a commensal of the skin, but can cause severe infections in immune suppressed patients and those with central venous catheters.

Staphylococcus aureus (also known as golden staph) is a bacterium, frequently living on the skin or in the nose of a healthy person, that can cause illnesses ranging from minor skin infections (such as pimples, boils, and cellulitis) and abscesses, to life-threatening diseases such as pneumonia, meningitis, endocarditis and septicemia.

Each year some 500,000 patients in American hospitals contract a staphylococcal infection. By changing its chemical makeup slightly to evade attack, S. aureus has become resistant to many commonly used antibiotics (see discussion about MRSA). In 1997, physicians were alarmed to encounter staph strains that resist even vancomycin, which used to work when all else failed. Problems with S. aureus in hospitals are not a recent occurance, as penicillin resistant forms have existed since the 1950's.

Staphylococcus aureus appears as a gram-positive coccus, in grape-like clusters when viewed through a microscope. More characteristic is its appearance when grown out on agar plates. It appears as large, round golden-yellow (which is where the name aureus comes from) colonies, with beta-haemolysis of blood agar.

Staph infections can be spread through contact with pus from an infected wound, skin to skin contact with an infected person, and contact with objects such as towels, sheets, clothing, or athletic equipment used by an infected person.

In the hospital laboratory, Staphylococcus aureus is differentiated from most other staphylococci by the coagulase test. Staphylococcus aureus is coagulase-positive.

MRSA, or methicillin-resistant Staphylococcus aureus, is a bacterium that has developed antibiotic resistance, first to penicillin in 1947, and later to methicillin. Popularly termed a "superbug", it was first discovered in Britain in 1961 and is now widespread. While an MRSA colonisation in an otherwise healthy individual is not usually a serious matter, infection with the organism can be life-threatening to patients with deep wounds, intravenous catheters or other foreign-body instrumentation; or as a secondary infection in patients with compromised immune systems.

Because cystic fibrosis patients are often treated with multiple antibiotics in hospital settings, they are often colonized with MRSA, potentially increasing the rate of life-threatening MRSA pneumonias among them. The risk of cross-colonization has led to increased use of isolation protocols among these patients.

In the USA there are increasing reports of outbreaks of MRSA colonisation through skin contact in locker rooms and gymnasiums, even among healthy populations, and MRSA causes as many as 20% of Staph aureus infections in populations that use intravenous drugs.

A last-resort antibiotic, Vancomycin, is used to kill MRSA but several new strains of the bacterium (since the first report in 1997) has been found showing resistance to Vancomycin; those new evolutions of the MRSA bateria are dubbed Vancomycin Intermediate-resistant Staphylococcus aureus (VISA).

From the US CDC's MRSA Fact Sheet:

"How are staph and MRSA spread? - Staph bacteria and MRSA can spread among people having close contact with infected people. MRSA is almost always spread by direct physical contact, and not through the air. Spread may also occur through indirect contact by touching objects (i.e., towels, sheets, wound dressings, clothes, workout areas, sports equipment) contaminated by the infected skin of a person with MRSA or staph bacteria." and

"Are staph and MRSA infections treatable? - Yes. Most staph bacteria and MRSA are susceptible to several antibiotics. Furthermore, most staph skin infections can be treated without antibiotics by draining the sore. However, if antibiotics are prescribed, patients should complete the full course and call their doctors if the infection does not get better. Patients who are only colonized with staph bacteria or MRSA usually do not need treatment."

Vancomycin-resistant Staphylococcus aureus (VRSA) is a strain of Staphylococcus aureus that has become resistant to the glycopeptide antibiotic vancomycin. With the increase of staphylococcal resistance to methicillin, vancomycin (or teicoplanin) is often a treatment of choice in infections with methicillin-resistant Staphylococcus aureus (MRSA).

Vancomycin resistance is still a rare occurrence. Unfortunately, VRSA may also be resistant to meropenem and imipenem, two other antibiotics that can be used in sensitive staphylococcus strains.

VISA (vancomycin intermediate Staphylococcus aureus) was first identified in Japan in 1997 and has since been found in hospitals in England, France, the US, Asia and Brazil. It is also termed GISA (glycopeptide intermediate Staphylococcus aureus) or VISA (vancomycin intermediate Staphylococcus aureus), indicating resistance to all glycopeptide antibiotics. These bacterial strains present a thickening of the cell wall which is believed to deplete the vancomycin available to kill the bacterium. This mechanism of resistance to vancomycin is different to that which happens in enterococcus where there is a change in the target site of the antibiotic, leading to a lower affinity for vancomycin which gives vancomycin resistant enterococci high levels of resistance.

Many enterococcus strains display resistance against vancomycin, and it has been suggested that vancomycin resistance has been transmitted between enterococci and staphylococci on a plasmid in at least on two occasions in the United States. This is rather worrying because it leads to high level resistance to vancomycin in Staphylococcus aureus, and has the potential of spreading rapidly throughout large populations of Staphylococcus aureus in hospitals, as opposed to the traditional VISA mode of intermediate resistance to vancomycin, which has to be acquired by the bacterium during treatment with this drug.

Throughout recorded history, humans have been prey to infections caused by virulent strains of staphylococci and streptococci. The advent of the antibiotic era -50 years ago- brought with it great optimism about the control of Staphylococcus aureus and Streptococcus pyogenes. Fortunately, despite five decades of penicillin use, all strains of Streptococcus pyogenes remain very susceptible to penicillin.

The story of S. aureus is more complex. By the late 1950s, almost 50% of all strains were resistant to penicillin. The organism had developed the ability to break the beta-lactam ring by producing a beta-lactamase referred to as penicillinase. In 1960, however, methicillin-a penicillinase-resistant beta-lactam effective for treating penicillin-resistant S. aureus-was discovered. The subsequent availability of oral cephalosporins added greatly to outpatient management of infections caused by this organism.

Methicillin-resistant strains cf staphylococci emerged by the late 1970s and have become increasingly more prevalent as nosocomial pathogens. The medical community was comforted by the fact that vancomycin-available since 1958-provided effective therapy for aIl strains of methicillin-resistant S. aureus.

Nevertheless, the emergence of vancomycin-resistant strains of coagulase-negative staphylococci (I, 2) caused concern that such observations might presage similar developments in S aureus. Adding to these concerns were observations that

1) vancomycin-resistant enterococci caused isolated infections or epidemics in some U.S. hospitals and were becoming increasingly prevalent in critical care units (3, 4);

and 2) high-level vancomycin resistance was experimentally transferred from Enterococcus faecalis to S. aureus in both in vitro and in vivo models (5).

It seems likely that vancomycin-resistant S. aureus will emerge as a nosocomial pathogen with disastrous consequences if widespread nosocomial transmission occurs. Thus, we believe that hospitals should adopt a proactive approach. To that end, we provide perspectives on isolation guidelines for care of the patient with vancomycin-resistant S aureus colonization or infection and for the handling of the organism in the clinical microbiology laboratory. Developers of formal guidelines should take into account the background issues and control measures described below. It is important to note that our comments are based on the limited data available on the transmission and control of S aureus. Transmission and control of Staphylococcus aureus

The reservoir for S. aureus is the anterior nares (6). The prevalence of nasal colonization is approximately 40% among healthy adults (7). Three patterns of nasal colonization have been observed: Some persons are never colonized, some are persistently colonized, and others are intermittently colonized. Half of those with nasal colonization also carry the organism on their hands (8); transmission by the hands is probably the major mode of transmission (9-12).

Certain patient populations (patients with diabetes (13), patients receiving hemodialysis (14), patients receiving continuous ambulatory peritoneal dialysis (15), injecting drug users (16), and patients with human immunodeficiency virus infection (17,18), for example) have higher rates of staphylococcal colonization and infection.

Once nasal colonization has been established, inections occur through contamination of the hands and subsequent inoculation of any traumatized area of skin. Studies show that staphylococcal infections in colonized persons are often due to the staphylococcal strain responsible for colonization (19-22); thus, the infections have an endogenous origin.

Calcium mupirocin ointment has been shown to be effective in eliminating staphylococcal nasal coloniration (8, 23), and it significantly decreases hand carriage as well (8). In patients receiving hemodialysis, it has been shown that elimination of nasal colonization is associated with a decrease in S.aureus infection (19, 24).

Staphylococci can survive desiccation for days to weeks and can travel considerable distances through the air (25). Studies done in the 1950s and later established that nasal carriers of S.aureus can shed the organism into the air (25-28) and that aerial dissemination is greatest in those with the heaviest burdens of organisms on their nasal mucosa (28). It is unclear whether aerial dissemination from nasal carriers is associated with transmission of the organism to others. Patients with large burns have been shown to shed large numbers of staphylococci into the air (29, 30).

Washing with medicated soaps has been shown to remove S. aureus from the hands (31-35). For vancomycin.-resistant enterococci, 60% isopropyl aIcohol has a direct effect, but chlorhexidine has been shown to eliminate the organism from the hands both directly and residually (36, 37). Although alcohol-based hand.washing agents are used extensively in Europe, limited data suggest that health care workers in the United States wash more frequently with chlorhexidine than with alcohol (38).

Anecdotal data from the University of Iowa Hospitals and Clinics suggest that concentrating on infection control activities decreases nosocomial transmission. Asking the primary nurse of the infected or colonized patient to monitor visitors' compliance with barrier precautions has proved useful. Using intensive microbiologic and epidemiologic surveillance (admission and weekly stool surveillance cultures and concurrent unit-based surveillance for nosocomial infections, for example), we discovered only three infections; furthermore, using molecular typing, we documented only one case of nosocomial transmission, in which the patient became colonized only (unpublished data).

Haley and colleagues (39), in an effort to eradicate endemic methicillin-resistant S.aureus infections from a neonatal intensive care unit, had an infection controI nurse dedicated to the unit. One of her duties was to observe compliance with infection controI practices. Although the authors could not determine the independent effect of the nurse due to the concomitant implementation of several other control measures. they deemed that her presence had led to successful eradication of the pathogen and increased compliance with aseptic practices (39).

The duration of colonization with methicillin-resistant S. aureus is long; the estimated half-life of nasal colonization is 40 months (40). However, twice-daily intranasal application of mupirocin ointment for 5 days has been shown to have a long-term effect with a downward trend in the rate of nasal colonization and a statistically significant decrease in the rate of hand carriage at 6 months (41). Although resistance to mupirocin among S. aureus isolates has been reported, it remains uncommon (42-48). High-level resistance bas been observed primarily when mupirocin therapy has been prolonged (44) or extensive (as in dermatology wards)(42, 43, 45,48). Identification of Vancomycin-Reslstant Staphylococcus aureus

The Centers for Disease Control and Prevention (CDC) recommend that all clinical isolates of S. aureus be tested for susceptibility to vancomycin (49). Laboratoiy personnel should notify the laboratory director if vancomycin-resistant S. aureus is discovered.

Many isolates of S. aureus presumed to have been vancomycin-resistant have been found to be mixed with other organisms in cultures; therefore, vancomycin resistance should be confirmed by re-streaking the colony to certify that the culture is pure (49). The hospital epidemiology program should be notified so that it can institute appropriate isolation procedures. The public health department, other hospitals in the vicinity and the CDC should also be notified. Precautions for Vancomycin-Resistant Staphylococcus aureus

The proposals we outline below are designed to help standardize the approach to infected or colonized patients, and are based on the limited data cited above. Indîvidual institutions may adopt some or aIl of our proposals, depending on local circumstances and resources. Isolation of Infected or Colonized Patients

A patient who is infected or colonîzed with vancomycin-resistant S. aureus should be placed in a private room, and all persons entering the room should wear clean, nonsterîle gloves and a disposable gown. Gloves and gowns should be removed before leaving the room. After the gloves are removed, hand washing with 4 % chlorhexidine or 60 % isopropyl alcohol is required (37). A monitor could be placed at the door to prevent unauthorized access and to enforce hand washing and barrier precautions (39). The names of all persons entering the room should be recorded for future use should obtaining nasal surveillance cultures become necessary

A standard surgical mask and safety glasses must be worn by persons doing procedures that might generate an aerosol (suction, bronchoscopy, sputum induction, or aerosol treatment, for example). Patients with vancomycin-resistant S.aureus pneumonia requiring mechanical ventilation should have a filter or condensate trap placed on the expiratory phase tubing of the mechanical ventilator circuit. If oxygen therapy by nasal cannula is required, a standard surgical mask should be worn by all persons entering the room. Although few data support the idea that airborne transmission of staphylococci is possible (25>, we prefer a conservative approach until the epidemiology of vancomycin-resistant S. aureus is delineated.

If the patient is colonized in the nares, decolonization with mupirocin should be attempted (8, 50-52). However, because clinical isolates have not been available for the performance of susceptibility testing, the activity of mupirocin against vancomycin-resistant S. aureus is unknown. We do not recommend adding other drugs, such as rifampin or trimethoprim-sulfamethoxazole, because these drugs have not been necessary with mupirocin and -unlike mupirocin- may cause serious adverse effects.

Sharing of noncritical equipment (such as electronic thermometers, blood pressure cuffs, stethoscopes, intravenous poles, bedside commodes, and wheelchairs) is not permitted.

-Infectious disease consultants should review the patient's antimicrobial therapy, making every effort to reduce the selection of vancomycin-resistant S. aureus by eliminating or substituting antibiotics. Prudent use of antimicrobial agents should be stressed in both inpatint and outpatient settings, even before the emergence of vancomycin-resistant S.aureus. Vancomycin use should be reduced throughout the hospital. Oral metronidazole rather than oral vancomycin should he used to treat antibiotic-associated colitis when possible (49).

The number of health care workers who have contact with the patient infected or colonized with vancomycin-resistant S. aureus should be limited. Care of the patient should be done by no more than one nurse and one physician per shift when possible. Phebotomy and other ancillary services should be done by the primaiy nurse or primary physician. Until more is learned about the epidemiology of vancomycin-resistant S. aureus aIl health care workers caring for the patient should have nasal surveillance cultures done every 2 weeks. Health care workers known to be at higher risk for staphylococcal colonization (those with exfoliative dermatitides or diabetes mellitus requiring treatment with insulin) should not care for patients with vancomycin-resistant S aureus colonization or infection. The recommended hand-washing agents (alcohol and chlorhexidine) may themselves cause dermatitis; health care workers who develop dermatitis should be reassigned.

Housekeeping personnel should be instructed to clean all horizontal surfaces in the patient's immediate vicinity daily with a quaternary ammonium compound. Cleaning cloths used in the room should not be used to clean other patients' rooms and equipment, but should be carefully discarded.

Isolation must continue for the duration of the hospital stay. After the infected or colonized patient is discharged and housekeeping personnel have completed terminal disinfection of the room, environmental cultures should be obtained. The room should remain closed to new admissions until negative cultures have been reported. All equipment used in the room must be disinfected.

Before discharge, an epidemiology alert sticker should be affixed to the cover of the patient's chart and a notation should be made in the hospital's information system. Any patient with previons vancornycin-resistant S. aureus infection or colonization who is readmitted should be placed in isolation immediately. Isolation should continue until surveillance cultures at the nares and of any previously infected, open sites have been obtained and are negative.

If a nosocomial transmission is documented on a hospitai unit, the unit should be closed to new admissions. Any previousiy uninfected patient from this unit who requires transfer to another hospital unit should be placed in isolation in the receiving unit until, two nasal cultures- 48 hours apart- are negative.

Diagnostic and therapeutic procedures that require the patient to leave the isolation room should be postponed. When testing is done at the bedside (portable radiography, electrocardiography), equipment should be wiped down with a disinfectant when the test is complete. Collection of microbiologic and other specimens for clinical testing should be done in the patient's room with health care workers wearing protective attire as described above.

Specimens should be kept in a leakproot container and placed in a sealable, leakproof plastic bag for transport (53). Laboratory forms should not be placed in the bag with the specimen. Care must be taken to prevent contamination of the outside of the bag. The specimen should be taken to the laboratory immediately; it should not be sent through a pneumatic tube system. MicrobioIogy Laboratory Precautions

To minimize the possibility for colonization or infection of hospital staff, as few staff members as possible should handle specimens from a patient with vancomycin-resistant S aureus infection. All specimens from an infected or colonized patient should be delivered directly to the laboratory without routing through a centralized specimen receiving area.

When a specimen for culture from a patient with vancomycin-resistant S. aureus infection is delivered, it should be immediately placed in a biological safety cabinet until it can be processed. The laboratory director should review aIl culture requests before plates are inoculated, eliminating the unnecessary processing of cultures that contain vancomycin-resistant S aureus

Specimen processing requires two persons, one working only within the biological safety cabinet (technologist 1) and the other (technologist 2) assisting technologist 1. The biological safety cabinet should contain a squirt bottie filled with a disinfectant, a beaker containing a disinfectant for the disposaI of loops, a heavy, clear biohazard bag for the disposaI of specimens and other material, and clear specimen bags for holding inoculated plates.

Specimens should be inoculated onto as few plates as possible. Each plate should be placed directly into a clear specimen bag as soon as it is inoculated. When all plates have been inoculated, the specimen bag should be closed with a twist closure, sprayed on the outside with a disinfectant, and wiped off with a paper towel. The used paper towel should be placed in the biohazard bag for disposaI, along with the remainder of the specimen and any rejected specimens.

The bag containing the inoculated plates should be placed in a large anaerobic jar with no catalyst and no gas-generating envelope. For this step, technologist 2 should hold the jar outside the biological safety cabinet while technologist 1 gently transfers the bag containing the plates to the jar. Once the plates are inside, technologist 2 should close the jar and place it in the incubator.

All remains of the specimen and transport material should be placed in the biohazard bag and closed with a twist tie. While still in the biological safety cabinet, the biohazard bag should be placed into a second biohazard bag and closed with another twist tie. Technologist 1 should spray the work surface, sides, and windshield of the biologîcal safety cabinet with a disinfectant. After a 10-minute exposure time, the disinfectant residue should be wiped from aIl surfaces with 70 % ethanol. Technologist I should hand the closed bag to technologist 2, who should immediately take the bag to the autoclave. It should be autoclaved for 30 minutes.

All cultures should be worked up in the biological safety cabinet using the same two-technologist system . Technologist 1 should stay in the biological safety cabinet at all times while technologist 2 obtains supplies and monitors the technique of technologist 1. All subcultures, susceptibility tests, and biochemical tests will be placed in either zip-lock specimen bags or anaerobic jars before being placed in the incubator.

All reagents used during the examination of any culture from a patient colonized or infected with vancomycin-resistant S. aureus should be placed in a biohazard bag contained in the hood and discarded. No nondisposable reagents or equipment should be used to work on cultures from a patient colonized or infected with vancomycin-resistant S. aureus Plates that need to be held until test results are finalized should be placed in zip-lock specimen bags and left in the safety cabinet until discarded. All discarded plates, slides, and biochemicals should be placed in bags and autoclaved as described above.

A stock culture of the organism may be made for future studies (molecular typing, study of resistance mechanisms, testing of new antimicrobial agents). A suitable stock can be made by placing 5 to 10 colonies in 1 mL of nutrient broth containing 15% (v/v,) glycerol. The stock culture should be frozen at -70 °C in a freezer located in an area of the laboratory to which there is limited access.

Glycopeptide Intermediate-Resistant Staphylococcus Aureus TRENDS Staphylococcus aureus is one of the most common causes of community- and hospital-acquired infection. In the 1980s, methicillin-resistant S. aureus (MRSA) emerged and became endemic in many U.S. hospitals. Vancomycin was the only antimicrobial agent with uniform effectiveness against MRSA. In the 1990s, vancomycin-resistant enterococci (VRE) emerged and also became endemic in many U.S. hospitals. In 1996, the first S. aureus strain with decreased susceptibility to vancomycin (glycopeptide intermediate-resistant S. aureus [GISA]) was reported in Japan. In 1997, the first GISA strains were reported in the United States.

SCOPE OF PROBLEM The spread of antimicrobial-resistant nosocomial pathogens such as MRSA, VRE and GISA is secondary to both over- and misuse of antimicrobials and incomplete compliance with recommended infection control precautions. Some studies have documented that as much as 63 percent of vancomycin use is inappropriate. Other studies show that health care workers often fail to wash their hands as recommended or to fully implement recommended infection control precautions.

SEQUELAE GISA (and other antibiotic-resistant pathogens) cause serious morbidity and mortality. Treatment requires removal of colonized invasive devices, therapy with agents to which the organism is susceptible and monitoring of drug levels to ensure that adequate levels are maintained. If the prevalence of GISA strains increases, they may lead to increased health care costs, since the infected patients will require combined antimicrobial therapy.

CHALLENGES AND GOALS In 1997, the Hospital Infections Program, Centers for Disease Control and Prevention, issued interim recommendations for the prevention and control of S. aureus with reduced susceptibility to vancomycin. These recommendations highlight the importance of improving the appropriate use of antimicrobials, provide guidance for when vancomycin should and should not be used and describe the enhanced isolation precautions that patients colonized or infected with GISA strains should be placed in. In addition, these recommendations describe the microbiologic methods needed to identify these strains. Educational programs for physicians and other health care workers are needed to ensure that these recommendations are understood and fully implemented.

RISK GROUPS Patients at greatest risk are those who are severely ill, those receiving prolonged courses of vancomycin, those with prior colonization with MRSA or VRE and particularly those with peritoneal catheters.

Staphylococcus aureus has long been recognized to be a cause of contagious mastitis. This organism can spread from cow to cow during the milking process and remain in a herd indefinitely due to a chronic carrier state. Economic losses due to elevated somatic cell counts (SCC), decreased milk production, higher treatment costs, and excessive discarded milk are commonplace in herds infected with S. aureus. Implementation of post-milking teat dipping and complete dry cow therapy has controlled this disease in most herds. Yet, losses due to S. aureus still occur, even in herds which faithfully practice these two key management procedures.

Dairy producers considering expansion may inadvertently introduce S. aureus into their herds. Initially, the organism may not generate significant losses. Eventually, as more cows develop intramammary infections (IMI), the somatic cell count starts to climb, clinical cases emerge, and the losses begin to pile up. This paper will offer some insights into diagnosing, eliminating, preventing, and living with S. aureus in your herd. DIAGNOSING STAPHYLOCOCCUS AUREUS IMI

Detection at the bulk tank The first signs of a herd problem with S. aureus may appear in the bulk tank. Bulk tank somatic cell counts (BTSCC) in excess of 400,000 could indicate a problem with contagious mastitis pathogens. Elevations in BTSCC are generally dependent on the number of cows and quarters infected with S. aureus. Very well managed herds can maintain relatively low BTSCC even though many cows are affected. Bulk tank bacteria counts do not tend to increase as more cows become infected with S. aureus. Graphing BTSCC and bacteria counts can indicate changing conditions and offer a warning sign to management.

Monthly bulk tank culturing has proven useful in monitoring udder health, particularly with regard to contagious pathogens (Staphylococcus aureus, Streptococcus agalactia and Mycoplasma bovis). The sensitivity of a single bulk tank culture for contagious organisms is fairly low, especially when the herd prevalence of contagious mastitis is low as well. In other words, often one bulk tank sample will be culture negative for S. aureus even though a herd may have cows infected with this organism. Bulk tank cultures for contagious organisms is highly specific (94%). So, it is rare that a bulk tank culture will be positive when in reality no cows in the herd have contagious mastitis.

Multiple sampling will improve the sensitivity of bulk tank culturing, particularly with intermittently shedding organisms like S. aureus. Serial testing can be performed by aseptically collecting an agitated bulk tank sample in a sterile container. This procedure can be repeated every other day when the bulk tank contains four milkings. The samples can be frozen immediately after they are obtained and delivered to the testing facility once each month.

Detection of individual cows Although S. aureus can cause a severe, gangrenous mastitis which can lead to death in cows, greater than 80% of all S. aureus IMI are subclinical. Usually there will be no elevation in body temperature and the only visible sign will be the presence of garget in the fore-milk. Many producers are inclined to treat these quarters, leading to discarded milk and potential antibiotic residues. After treatment, these cases usually recur in two to three weeks and the treatment/discarded milk cycle is repeated. As much as 88% of the losses incurred when treating cases of mastitis are due to dumped milk and decreased milk production.

Cows with one or more quarters infected with S. aureus tend to have elevated SCC. Keep in mind that one high score may not be indicative of a chronic infection. Cows with multiple SCC above 300,000 or multiple somatic cell scores (SCS) above 4.0 are most likely to be infected. The monthly Dairy Herd Improvement Association (DHIA) somatic cell data is generated from a composite milk sample. Average SCC when one quarter is infected is 500,000/ml. When two or three quarters are infected, the average SCC can reach 700,000 or 1,500,000/ml, respectively. Generally these cows can be detected with the California Mastitis Test (CMT), but monthly (DHIA) data can be more revealing, and requires less time to obtain.

Milk cultures are the best method to determine if clinical and subclinical mastitis is due to S. aureus. Selecting cows to culture can be a involved process. With the use of individual cow SCC, the procedure can be streamlined. All cows with several counts above 300,000 should be sampled. Once cows are selected, the CMT paddle can be used to determine which quarter(s) to culture. Combining positive CMT quarters into one composite vial may be acceptable, but individual quarter samples are preferred over pooled milk samples. Even under the best conditions, many composite samples become contaminated. Contaminated milk samples are impossible to interpret and a waste of resources.

A small (3-5 ml), sterile quarter sample is preferable to a voluminous contaminated composite. Teat ends should be thoroughly scrubbed with an alcohol pad. The fore-milk should be discarded and a mid-stream milk sample obtained in a sterile container. Milk cultures should be immediately chilled to prevent overgrowth of environmental bacteria. If microbiologic procedures are to be delayed, the samples should be frozen. A veterinarian's assistance in obtaining high quality samples may be warranted.

Eliminating existing IMI Antibiotic therapy of clinical mastitis caused by S. aureus during lactation has been unrewarding. It is often difficult to get the antibiotic to the invading organisms, and many times the selected antibiotic is ineffective. Staphylococcus aureus produces an enzyme that breaks down the lining of the milk ducts and allows the bacteria to invade deep within the udder. The cow attempts to wall off the infection into small abscesses. Approved antibiotics are unable to penetrate these micro-abscesses. These cows become chronic carriers and potential reservoirs for infection of herd mates. Early detection and treatment has the greatest success rate for lactational therapy. Treating cows within the first 30 days of infection may offer an 80-90% cure rate. Every month treatment is delayed, the chance of a cure drops by 20%. Someone once declared, "Once a Staph cow, always a Staph cow!" It is best to respect this statement. Dry cow therapy is not always effective at curing existing infections, particularly those caused by S. aureus. Although, the overall cure rate for S. aureus by infusion with a dry-cow, antibiotic preparation may approach 50%. All quarters of all cows should be medicated with an approved product at dry-off. There is some evidence that repeat infusions after three weeks may improve the success rate. This is an extra label use of a dry cow preparation and should only be used within the context of a valid veterinarian/client/patient relationship. Currently, there are no systemic antibiotics that are effective against S. aureus approved for use in dry, dairy cows.

One sure method to eliminate S. aureus IMI is to remove the cow from the herd, ie. cull her. Several studies have been performed evaluating the economics of culling cows chronically infected with S. aureus. The prevalence of IMI within a herd will play a major role in the decision process. In herds with very few cows infected, culling chronic cows should receive high priority. This practice will help the prevention strategies to be discussed next. When several cows in a herd are infected (greater than 5%), the value of the milk may be more important to cash flow and control measures should be considered a higher priority.

Preventing new IMI Milking-time procedures can greatly influence the spread of S. aureus to uninfected cows. Contamination -- milkers' hands, common wash rags, and milking clusters -- with milk from infected cows is the primary means of transmission. Care should be exercised when fore-stripping cows so that milk from infected quarters does not contaminate the milkers' hands or environment. Wearing latex gloves during milking can reduce the potential for spread. When soiled, gloves are much easier to sanitize than the skin on your hands.

Common wash rags or sponges used to prepare udders for milking are often laden with microorganisms. Staphylococcus aureus can easily be spread from cow to cow with a common rag even when sanitizer is used in the udder wash. Single service cloth towels or disposable paper towels will eliminate this method of transmission. During the milking process, milk within the inflation covers the teat skin. If the milk contains S. aureus organisms, all contact surfaces are potentially contaminated. Post-milking teat dipping with an approved, germicidal product will help reduce the number of viable organisms remaining on the teat skin after the milking unit is removed.

Worn out inflations will contain microscopic cracks in the rubber and S. aureus bacteria can remain in those recesses. Stepping up the replacement schedule for inflations will help. Back-flushing of the milking cluster can reduce the number of S. aureus organisms within the inflations. Automatic back-flushing units can be installed in most parlors, but are expensive. Manual systems have proven ineffective. Improper milking machine function, to a lesser extent, contributes to new IMI with S. aureus. Excessive trauma to the teat ends and reverse impacts of contaminated milk droplets are the primary means of transmission by the milking units.

Staphylococci are spherical, gram positive bacteria of the micrococcaceae family. They are found primarily on the skin and in the mucous membranes of humans and other warm-blooded animals, and aggregate into small, grape-like clumps. Staphylococci-related infections are one of the most common causes of nosocomial (hospital-acquired) infections, yet they are increasingly difficult to treat due to the rate at which the bacteria acquire antibiotic resistance. Ninety percent of Staphylococci strains are penicillin resistant --- leaving only methicillin and vancomycin to treat the majority of infections. However, with increasing numbers of reports of methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococci (VRE) chemists are faced with the daunting task of generating new antibiotics with novel modes of action, and doctors with the task of curing seemingly incurable infections. The Staphylococcus genus is divided into two groups: the aureus and non-aureus Staphylococci. The two types are distnguished from each other, traditionally, by their coagulase activity. S. aureus staphylococci are the only variety that test positive in the coagulase test (they maintain the ability to clot blood plasma). Staphylococcus can cause skin, heart valve, blood, and bone infections, which can lead to septic shock and death. These infections are primarily caused by the toxins which Staphylococci produce. For example, the enterotoxins produced by S. aureus are a significant cause of food poisoning and the superantigens can cause toxic shock syndrome if present in the blood stream. In their more potent forms, the toxins are responsible for damaging host tissues, inhibiting phagocytosis (whereby the host neutralizes the Staphylococci toxins and eliminates the bacteria), and causing disease symptoms. i, h. Ninety percent of Staphylococcus strains are resistant to penicillin and penicillin-derived antibiotiocs. The next line of attack, methicillin, is increasingly becoming less effective: between 1975 and 1991, the prevalence of methicillin-resistant strains of S. aureus increased ~26%. While non-hospital acquired Staphylococcus infections can be treated with penicillin-derived antibiotics, hospital-acquired infections are entirely resistant to penicillin and require more aggressive antibiotic treatments.

Good teat skin condition is vital to controlling S. aureus. This bacteria grows very well under scabs and on irritated teat skin. Higher incidence of S. aureus mastitis can be expected in winter months when teat skin becomes chapped. Irritating teat dips, excessive contamination by urine and feces, as well as improperly functioning milking machines can all cause teat end and teat skin damage. Staphylococcus aureus only needs a tiny break in the teat skin to invade and begin multiplication. Selecting a teat dip with five to ten percent glycerine or some other skin conditioner will help tremendously. When the wind chill is below freezing and cows are kept in cold housing, post-milking teat dipping should be postponed. Some producers blot the teat ends with a clean paper towel prior to turning the cows out into a cold environment.

Segregation of infected cows or using separate milking clusters on infected cows is a viable option for herds not choosing to cull. Smaller herds can designate one or two milking clusters as "Staph" units. These claws should be clearly marked and only used on infected cows. Another option is to milk the uninfected cows first and the "Staph" cows last. This method relies on the post milking sanitation procedures to effectively remove potential contamina- tion. Larger herds can create a "Staph" milking string. Even though these cows are housed in the same free stall barn, they can be separated at milking time and milked last. Dry treated cows which were infected in the previous lactation can be milked in between the two groups. Once the new infection status is determined, the cow can become a member of the proper group.

Heifers and new herd additions can be potential sources for introduction of S. aureus into uninfected herds. When heifers are fed dump milk contaminated with S. aureus, they become seeded with the organism. At first calving, these mastitic milk-fed heifers are more prone to acquiring IMI with S. aureus. Some will eliminate the infection on their own, while others will become chronically infected. Early treatment may save some of these animals. Heifers, as a reservoir of S. aureus are more of a problem in herds with a high prevalence of chronically infected cows. All new herd additions including heifers should be cultured within 30 days of entering the lactating herd. Animals testing positive should be immediately segregated. Milk culturing should be repeated to determine if the infections have become chronic. Somatic cell count data can help determine the chronicity of the infections.

Staphylococci are gram positive bacteria of which there are over 400 strains with some virulent and others not. In terms of high frequency and a broad spectrum of hosts, three strains, S. Xylosus, S. Sciuri and S. Aureus are the most common. S. Aureus is a virulent strain found mainly in air and dust. It is resistant to common disinfectants and can survive outside the host for extended periods. Healthy birds carry the organism on the skin and in the mucosa of the respiratory and digestive tract.

Staphylococcus infections can be classified as endogenous (internal) or exogenous (external). While endogenous infections can be primary, they are most frequently a secondary infection. Exogenous infections have a number of triggering factors necessary for establishment because birds are extremely resistant to wound infections. Damage of the skin, other primary infections, immuno-suppression, prolonged antibiotic use, and environmental stressors all play a role in the establishment of exogenous infections.

Coagulase-negative staphylococcus (CNS) species are the organisms most frequently isolated from bovine milk samples. Mastitis researchers do not classify CNS as contagious or environmental pathogens. They designate them as "skin flora opportunists" since CNS are a part of the normal teat skin flora. CNS can colonize the teat canal. Some species are also found free-living in the environment.

In the mastitis literature, researchers report CNS intramammary infections to occur in 10 to 20% of quarters. The infection rate is generally higher in primiparous cows. Most CNS infections are transient. Cows and heifers will have a higher prevalence of CNS infection after calving, with a rapid decline over the first week or two of lactation. Researchers believe cow to cow spread is rare.

S. aureus is one of the major causes of hospital-acquired infection. One study ranked it fourth in a listing of the “Pathogens Most Frequently Isolated From Hospitalized Patients When All Anatomic Sites Are Considered”. Approximately 40% of the general population and 50 – 90% of health care practitioners harbor an S. aureus colony in their anterior nasal passage. Infection becomes a problem when bacteria migrate from their normal habitat, especially in individuals already suffering from a compromised immunologic response. S. aureus most commonly causes a localized skin infection, although it can also infect the eye, nose, throat, urethra, vagina, and gastrointestinal tract. In addition, S. aureus can cause more serious ailments when it enters the bloodstream, such as pneumonia, osteomyelitis, arthritism endocarditis, myocarditis, brain abscesses and meningitis. (See inset on S. aureus virulence factors and toxins). The toxins most relevant to disease causing symptoms in humans are the superantigens and a-toxins. The a-toxins oligomerize to form pores in the host cellular membrane, allowing cellular contents to leak into the extracellular matrix. The superantigens, consisting of enterotoxins and the toxic shock syndrome toxin, are responsible for S. aureus-related food poisoning and toxic shock syndrome, respectively. (See insets on “How do Superantigens work?" and "How do Alpha Toxins Work?") Individuals with damaged or severely compromised immune systems, such as recent surgical recoveries or burn victims, IV drug users, insulin-dependent diabetics and hemodialysis patients are more susceptible to Staphylococcus infection than healthy individuals. Individuals identified with Staphylococcus infections are most commonly found in hospital intensive care units, burn units, and dermatology and surgical units, reflecting the increased susceptibility of these individuals to Staphylococcus infections due to compromised immune function. b, b, i.  Treatment of S. aureus infections showing no signs of broad-antibiotic resistance is achieved with a cocktail of antibiotics, including some of the following: flucloxacillin, gentamycin, rifamicin, fusidic acid, erythromycin, vancomyin, and cefotaxime. However, 90% of S. aureus strains are penicillin resistant. In these scenarios, methicillin and vancomycin are the only available treatment options.

CNS are of low pathogenicity. Infections are usually subclinical and result in quarter somatic cell counts (SCC) only about two- to three-fold above that of uninfected glands. The impact on composite sample SCCs (such as those on the DHI report) will therefore be minor. Despite their low pathogenicity, CNS infections can occasionally contribute to clinical cases of mastitis in dairy herds, but CNS are rarely a major cause.

A positive culture may show recovery of an organism but this does not mean inflammation of the mammary gland has occurred. Because CNS are commonly found on teat skin and in the streak canal, they are a common cause of contamination of milk samples. Repeated isolation from a particular quarter sampled multiple times builds the case for a persistent and important infection.

Isolation in association with elevated SCC also supports the diagnosis of mastitis versus non-significant infection. The most likely mastitis-causing bacteria should be ruled out before CNS are considered significant in suspected mastitis cases.

To improve the interpretation of culture results, prevent the contamination of milk with CNS from skin sites when collecting milk samples. Prepare teat ends carefully using cotton swabs moistened with alcohol. Scrub the teats on the far side of the udder first, then those on the near side. Begin aseptic sample collection from the closest teat and move to teats on the far side of the udder (the reverse order from cleaning). Do not allow the tube to touch teat end. Do not allow milk entering tube to touch fingers or hands. Frequent isolation of CNS from milk samples suggests either poor sampling technique and/or poor teat end hygiene.

The staphylococci, often in association with streptococci, produce abscesses, boil, carbuncles, osteomyelitis (infections of the bone) and fatal septicemia's (blood infections). The staphylococci are G+, catalase +, non-spore-forming, facultative anaerobic, large cocci, that tend to grow in grape-like clusters. They are normal inhabitants of the SKIN and the NASAL MEMBRANES of healthy people. Human staphylococci strains tend to be salt tolerant and are able to grow in the presence of NaCl concentrations that inhibit most other bacteria. Important pathogenic strains include Staphylococcus aureus which produces a variety of diseases including food poisoning, impetigo, boils, carbuncles, osteomyelitis (infections of the bone), toxic shock syndrome and fatal septicemia's (blood infections). Approximately 10% of the general public carry this organism. Further, 90% of hospital personnel have been reported to harbor staphylococci and thus are the reservoir for the frequent #nosocomial staph infections. S. aureus, along with Pseudomonas strains, are especially dangerous to burn patients. Staph hospital infections are one of the most dangerous infections you can contract; it is sometimes called the "GOLDEN PLAGUE" because of the yellow color of its colonies. S. aureus is considered one of the most dangerous microbes on earth and thousands of Americans die every year from staph infections they contacted while in the hospital. A major concern is that most hospital staph strains are resistant to most of the antibiotics available. It is perhaps ironic that the first infection treated with an antibiotic (penicillin) was a fatal staph infection and now we have come almost full circle to where staph will soon be resistant to all the antibiotics we have in our arsenal.

When we get an infectious disease we all wonder "How did I catch that bug and from whom?" This is the first question a professional epidemiologist also asks, only they couch it in terms of the general population: "How did anyone catch that bug and from whom or what?" Knowing how a disease is spread is one of three crucial pieces of information public health officials need to know in order to control the spread of disease. The other two are: "What is the etiological agent responsible for the disease?" and "How can the disease best be treated so as to stop/minimize its further spread or occurrence?" With these three pieces of information almost all diseases, including those caused by infectious agents, can be limited, if not prevented. If, as is sometimes the case, answers to all three can not be determined, then the first question assumes predominance, for if the "source" of an infection is known immediate steps can usually be taken to limit the further spread of a pathogen. For example, although #John Snow did not know the answer to the last two questions, he was able to stop the London Cholera infection by removing the handle of the Broad Street Pump, from which people were obtaining Cholera-contaminated drinking water.

Treatment of S. aureus infections showing no signs of broad-antibiotic resistance is achieved with a cocktail of antibiotics, including some of the following: flucloxacillin, gentamycin, rifamicin, fusidic acid, erythromycin, vancomyin, and cefotaxime. However, 90% of S. aureus strains are penicillin resistant. In these scenarios, methicillin and vancomycin are the only available treatment options.(See inset on antibiotic strategies for treating S. aureus-related infections). S. epidermis is a coagulase-negative bacteria. Like S. aureus, S. epidermis is a common cause of nosocomial infections, particularly blood infections which can lead to complications of the central nervous system. S. epidermis resides primarily in the skin, leaving those who have frequent contact with needles and other invasive health care appliances particularly susceptible to illness. S. epidermis is very likely to contaminate patient-care equipment and environmental surfaces, possibly explaining the high incidence of S. epidermis in hospital settings. While there is extensive information concerning S. aureus virulence factors, there is relatively little known about S. epidermis mode of action. Infection is treated primarily with vancomycin or rifampin. S. saprophyticus is a common cause of urinary tract infections in men and women. Risk factors and treatment guidelines are the same as those described for S. aureus. In 1929, Alexander Flemming first discovered penicillin, but it was not until 1940 that it was fully integrated into infectious disease treatment strategies. In the intervening decade, the medical world saw the discovery of a variety of antibiotic agents. Among the most successful were the sulfonamides, prodrugs that arrested infection by inhibiting nucleic acid biosynthesis. Sulfonamides are“prodrugs.” These compounds are made active once ingested. j, l, f, i, k. The sulfonamides inhibit nucleic acid synthesis by prevening the synthesis of purine bases. With the successful use of penicillin and sulfonamides, the 1940s were dubbed the antibiotic age. Suddenly, there were a wealth of ways (comparatively) to combat infectious disease. Penicillin was seen as the “cure-all.”  By 1944, however, there were dark clouds moving into an otherwise sunny picture. Strains of Staphylococcus, S. aureus particularly, were becoming resistant to penicillin. These penicillin-resistant strains produced penicillinase, a b-lactamase, that deactivated the drug by cleaving a bond in the b-lactam ring. By 1947, Staphylococcus and gonorrhea were completely resistant to penicillin. It was not until 1960 that researchers had developed new drugs that were resistant to b-lactamase activities and capable of fighting Staphylococcus infections. These new drugs, such as methicillin and oxacillin, were semi-synthetic penicillin derivatives, with functional groups placed in novel locations.

Typically, when epidemiologists investigate the origin and nature of an epidemic they initially collect detailed information on the victims, and their close associates including, if possible, those currently ill with the disease. This information includes asking questions like: "Where have you been/visited the past few weeks?", "What foods have you eaten lately?", "What animals have you had contact with recently?", "Have you had any insect bites recently?", "Who have you associated with and in what way?" etc. Obtaining useful information requires considerable thought, since the wrong data will delay solving the problem. Large areas (cities, even entire countries) may have to be covered and 1,000s of people questioned using everything from personal interviews to questionnaires. The data then has to be compiled and analyzed to extract the useful information, which is often obscured by the mass of unrelated data or "noise". Often the location of each case is placed on a map to determine if a physical source of the disease can be found. Frequently, no logical pattern emerges and the process must be repeated with a new set of questions or a different approach.

Methicillin resistant Staphylococcus aureus (MRSA) is an organism that is frequently transmitted in hospitals and perinatal units. The MRSA is considered a public health problem in neonatology because of its strong potential for dissemination in the wards associated with high rates of morbidity and mortality. In this study we describe the bacteriological, epidemiological and molecular characteristics of MRSA isolated from anterior nares and blood cultures of newborns hospitalized in a public maternity hospital in the city of Rio de Janeiro, Brazil. The frequency of MRSA isolated from nasal swabs of newborns was 47.8% (43/90). The genetic analysis of MRSA strains from anterior nares, showed 8 different pulsed field gel electrophoresis patterns (PFGE). Upon analysis of PFGE patterns of the 12 MRSA strains isolated from blood cultures, 8 different patterns were observed, 9 (75%) strains were genetic related to nasal secretion isolates patterns. In conclusion, our data demonstrate the importance of screening of newborns for the presence of MRSA in Brazilian hospitals and the usefulness of genetic typing of these pathogen during epidemiologic studies. This should lead to a better knowledge on the significancy and spreading of MRSA in the hospitals.

The newborns in intensive and/or intermediate care units are considerably susceptible to acquire hospital infections of several microrganisms (Pujol et al. 1994, Haley et al. 1995). Methicillin resistant Staphylococcus aureus (MRSA) has emerged over the past 30 years as an important cause of hospital infections and is actually an organism that is frequently transmitted in hospitals and perinatal units (Haley et al. 1982, Boyce et al. 1994, Na'Was et al. 1998). Outbreaks causing several pathological problems to the newborns and mothers have been reported (Pujol et al. 1996, Corbella et al. 1997). The MRSA is considered a public health problem in neonatology because of its strong potential for dissemination in the wards, high levels of antibiotic resistance, associated with high rates of morbidity and mortality (Soares et al. 1997, Tambic et al. 1997, Conterno et al. 1998).

The prevalence of MRSA in Brazil is considered elevated, specially in large hospitals (Branchini et al. 1993, Sader et al. 1994a), and in despite of the wide distribution, there are some hospitals that never had MRSA outbreak (Teixeira et al. 1996).

Risk factors associated with aquisition of MRSA include premature birth, low weight, respiratory problems, immunodeficiency, prophilatic antimicrobial use, long time of hospitalization, infections of the respiratory tract, and invasives diagnostic and cirurgical procedures (Haley et al. 1995, Pujol et al. 1996, Corbella et al. 1997, Villari et al. 1998). Transmission of strains occurs generally through contact of health care workers with colonized or infected patient before their isolation and proper management (Corbella et al. 1997).

Epidemiological transmission studies of MRSA have been traditionally performed by phenotypic characterization (Bannerman et al. 1995, Na'Was et al.1998), therefore, the increasing of the molecular epidemiology studies revolutioned our understanding of diseases transmission and allowed to recognize and investigate outbreaks in ways never before possible (Ostroff 1999). The identification of several new clones and distribution of endemics and epidemics strains became feasable through the use of molecular tools as pulsed field gel electrophoresis (PFGE) and restriction fragment length polymorphism (RFLP) of chromossomal DNA associated with hybridization techniques (Kreiswirth et al. 1993, Teixeira et al. 1995,Tambic et al. 1997).

Purified protein A from Staphylococcus aureus Cowan I was injected intraperitoneally or was incorporated in filters ex vivo through which plasma from cats with feline leukemia virus (FeLV)-associated leukemia-lymphoma was passed. Before treatment, 65% of the FeLV-infected cats were anemic, and 70% were thrombocytopenic. Concomitant infections, or immune-mediated disease, was common. During treatment 50% of the cats with FeLV-associated disease improved objectively with normal posttreatment hematocrits, thrombocyte and leukocyte counts, disappearance of dysplastic hematologic elements, and correction of marrow dyscrasias. A 33% response to treatment occurred in cats with unequivocal manifestations of malignant disease and was characterized by reductions in tumor size and marrow and peripheral blood neoplastic cell populations. Clearance of FeLV viremia was documented in 28% of the treated cats. The several possible mechanisms by which treatment with staphylococcal protein A causes reduction in the extent of malignant disease are considered.

Staphyloccus aureus is a pathogen that colonizes or infects both normal or inmunologically altered patients, either as a hospital or community acquired infecbon. The incidence of bacteremias due to S. aureus has shown a considerable increase in the lastyears, causing a strong impact on pabents morbimortality. Between January 1989 and December 1992, 102 episodes of bacteremia due to S. aureus in pediatric patients were analyzed. Underlying conditions were found in 76,5% of patients, with predominance of neoplasias. Nosocomial source of the infection wasidentified in 62% of thecases. Secondaryfocciwereidenhfied in 29% of the children, with prevalence of bone and joint localization. Casefatalityrates was21,6%. Arterialhypotension wasseen as one risk factor for mortality (RR 4,65 Cl 95% 2,38 to 9,08). Neither the place of origin of the infecbon, the presence of a clinical focus of infection, the presence of leukopenia nor the underlying condibon in these pahents were seen as factors influencing their mortality. A higher mortality rate is observed in pabents with bacteremia due to methicillin-resistant S. aureus and in patients less than 1 year of age.

Why are MRSA important?

Pathogenicity.

MRSA are pathogenic and are common causes of hospital-acquired infections.

Limited treatment options.

Vancomycin often is the only drug of choice for treatment of severe MRSA infections, although some strains remain susceptible to fluoroquinolones, trimethoprim/sulfamethoxazole, gentamicin, or rifampin. Because of the rapid emergence of rifampin resistance, this drug should never be used as a single agent to treat MRSA infections.

MRSA are transmissible.

A MRSA outbreak can occur when one strain is transmitted to other patients. Often this occurs when a patient or health care worker is colonized with an MRSA strain (i.e., carries the organism but shows no clinical signs or symptoms of infection) and, through contact with others, spreads the strain. Handwashing and screening patients for MRSA should be performed to decrease transmission and reduce the number of patients infected with MRSA.

How should clinical laboratories screen for MRSA?

The National Committee for Clinical Laboratory Standards (NCCLS)-recommended "Screening Test for Oxacillin-resistant S. aureus" uses an agar plate containing 6 µg/ml of oxacillin and Mueller-Hinton agar supplemented with NaCl (4% w/v; 0.68 mol/L). For methods of inoculation, see NCCLS Approved Standard M100-S10.

Is it difficult to detect oxacillin/methicillin resistance?

Accurate detection of oxacillin/methicillin resistance can be difficult due to the presence of two subpopulations (one susceptible and the other resistant) that may coexist within a culture. All cells in a culture may carry the genetic information for resistance but only a small number can express the resistance in vitro. This phenomenon is termed heteroresistance and occurs in staphylococci resistant to penicillinase-stable penicillins, such as oxacillin. Heteroresistance is a problem for clinical laboratory personnel because cells expressing resistance may grow more slowly than the susceptible population. This is why NCCLS recommends incubating isolates being tested against oxacillin, methicillin, or nafcillin at 35? C for a full 24 hours before reading .

Can all susceptibility tests detect MRSA?

When used correctly, broth-based and agar-based tests usually can detect MRSA. Oxacillin screen plates can be used in addition to routine susceptibility test methods or as a back-up method.

How is the mecA gene involved in the mechanism of resistance?

Staphylococcal resistance to oxacillin/methicillin occurs when an isolate carries an altered penicillin-binding protein, PBP2a, which is encoded by the mecA gene. The alteration of the penicillin-binding protein does not allow the drug to bind well to the bacterial cell, causing resistance to ß-lactam antimicrobial agents.

Why is oxacillin tested instead of methicillin? Oxacillin is more resistant to degradation in storage and is more likely to detect most heteroresistant strains. In addition, methicillin is no longer commercially available in the United States. Antimicrobials like oxacillin and nafcillin now are used for treatment of S. aureus infections. Since methicillin was first used to test and treat infections by S. aureus, the acronym MRSA is still used by many to describe these isolates because of its historic role.

What is Staphylococcus aureus? Staphylococcus aureus is the most common cause of foodborne illness. Commonly called "staph," this bacterium produces a poison/toxin that causes the illness.

What are the symptoms of "staph?" Symptoms of staphylococcal food poisoning are usually rapid and in many cases serious, depending on individual response to the toxin, the amount of contaminated food eaten, the amount of toxin in the food ingested, and the general health of the victim. The most common symptoms are nausea, vomiting, abdominal cramping, and prostration. Some individuals may not always demonstrate all the symptoms associated with the illness. In more severe cases, headache, muscle cramping, and changes in blood pressure and pulse rate may occur. Recovery generally takes two days. It is not unusual for complete recovery to take three days and sometimes longer.

What foods could make me sick? Foods that are frequently a problem with staphylococcal food poisoning include meat and meat products; poultry and egg products; salads such as egg, tuna, chicken, potato, and macaroni; bakery products such as cream-filled pastries, cream pies, and chocolate eclairs; sandwich fillings; and milk and dairy products. Foods that require considerable handling during preparation and that are kept at slightly elevated temperatures after preparation are frequently involved in staphylococcal food poisoning.

In 1975, the methicillin bubble burst with reports of methicillin-resistant S. aureus (MRSA). At this time, approximately 2.4% of all S. aureus strains were methicillin resistant. MRSA has been reported primarily in patients with severely compromised immune systems. Three cases reported in the late nineties existed in a man suffering from metastatic lung cancer and end-stage renal disease, a patient known already to be contaminated with vancomycin-resistant Enterococci, and an elderly patient requiring haemodialysis (10). Health care practitioners have been cited as the primary means of MRSA transmissioin. In 1988, the first cases of vancomycin-resistant Enterococci were reported in the United States. In 1989, it was estimated that .3% of Enterococci infections were vancomycin-resistant; in 1993, the numbers had risen to 7.9%. In 1991, 29% of S. aureus strains were methicillin-resistant, and in 1996, there was a report of an S. aureus strain with intermediate vancomycin resistance (VISA or GISA). S. aureus strains acquired in the hospital are often resistant to many types of antibiotics. A significant portion of S. aureus strains are now methicillin-resistant, in addition to being resistant to other penicillin-derived drugs. For these methicillin-resistant strains, vancomycin is the only available, effective drug for treatment. However, in 1996, there were reports of strains of S. aureus with decreased susceptibility to vancomycin, labelled glycopeptide intermediate-resistant S. aureus, or vancomycin-intermediate S. aureus (GISA and VISA, respectively). b, e, k, a, d. In the early 1990s, vancomycin-resistant enterococci (VRE) emerged. Laboratory tests have shown that resistance, coded in the VanA, VanB and VanC genes, can be transferred from Enterococci to Staphylococcus and other gram positive bacteria. Were such transfer to occur in a non-laboratory controlled environment, there would be no FDA-approved, effective means of combating multi-drug resistant staph infections.

Staph may also be present in raw milk and raw milk products. Staph can cause mastitis in dairy cows, and other infections in meat animals. In this way, such meat sources may cause staph outbreaks in people.

Where do staphylococci come from? Staphylococci exist in air, dust, sewage, water, milk, and food or on food equipment, environmental surfaces, humans, and animals. Humans and animals are the primary methods of transport. Staphylococci are present in the nasal passages and throats and on the hair and skin of 50 percent or more of healthy individuals. This incidence is even higher for those who associate with or who come in contact with sick individuals and hospital environments. Although food handlers are usually the main source of food contamination in food poisoning outbreaks, equipment and environmental surfaces can also be sources of contamination with staph. People can contract the illness by eating food that is contaminated with any one of many strains of staph, usually because the food has not been kept hot enough or cold enough. Staph bacteria grow and reproduce at temperatures from 50 degrees F to 120 degrees F, with the most rapid growth occurring near body temperature (about 98 degrees F).

The toxin produced by staph bacteria is very heat-stable - it is not easily destroyed by heat at normal cooking temperatures. The bacteria themselves may be killed, but the toxin remains. Careful handling of food that is prepared ahead is important. This is especially important of foods left over after one meal and planned to be used again at a later meal. Quick cooling and refrigeration, or holding at or above 140 degrees F, can help ensure that toxin has no chance to be formed.

How frequently do people get sick? It is hard to determine how often staph food poisoning has occurred because many persons do not report it or it is confused with flu symptoms. Death from staphylococcal food poisoning is rare, although such cases have occurred among the elderly, in infants, and ill persons.

What is the treatment for staph? The objective of treatment is to replace fluids, salt, and minerals that are lost by vomiting or diarrhea.

How can I prevent spreading staph? Wash hands thoroughly before and after all food preparation. Any food service worker who has skin infections should not be handling food. Food preparation equipment must be thoroughly washed before it is used. Refrigerate meats and leftovers promptly. Keep hot foods hot (over 140 degrees F) and cold foods cold (below 40 degrees F).

Four Pediatric Deaths from Community-Acquired Methicillin-Resistant Staphylococcus aureus -- Minnesota and North Dakota, 1997-1999 Methicillin-resistant Staphylococcus aureus (MRSA) is an emerging community-acquired pathogen among patients without established risk factors for MRSA infection (e.g., recent hospitalization, recent surgery, residence in a long-term-care facility [LTCF], or injecting-drug use [IDU]) (1). Since 1996, the Minnesota Department of Health (MDH) and the Indian Health Service (IHS) have investigated cases of community-acquired MRSA infection in patients without established risk factors. This report describes four fatal cases among children with community-acquired MRSA; the MRSA strains isolated from these patients appear to be different from typical nosocomial MRSA strains in antimicrobial susceptibility patterns and pulsed-field gel electrophoresis (PFGE) characteristics.

Case Reports

Case 1. In July 1997, a 7-year-old black girl from urban Minnesota was admitted to a tertiary-care hospital with a temperature of 103 F (39.5 C) and right groin pain. An infected right hip joint was diagnosed; she underwent surgical drainage and was treated with cefazolin. On the third day of her hospital stay, antimicrobial therapy was changed to vancomycin when cultures of blood and joint fluid grew MRSA. The same day, the patient had another hip drainage procedure, but had respiratory failure and was placed on mechanical ventilation. Her course was complicated by acute respiratory distress syndrome, pneumonia, and an empyema that required chest tube drainage. She died from a pulmonary hemorrhage after 5 weeks of hospitalization.

MRSA isolated from her blood, hip joint, and sputum was susceptible to multiple antibiotic classes. An autopsy revealed bilateral bronchopneumonia with abscesses. The patient was previously healthy with no recent hospitalizations. No family members resided in LTCFs or worked in health-care settings.

Case 2. In January 1998, a 16-month-old American Indian girl from rural North Dakota was taken to a local hospital in shock and with a temperature of 105.2 F (40.6 C), seizures, a diffuse petechial rash, and irritability. She was treated with ceftriaxone but developed respiratory failure and cardiac arrest and died within 2 hours of arriving at the hospital. Blood and cerebrospinal fluid cultures drawn immediately postmortem grew MRSA that was susceptible to multiple antibiotic classes. An autopsy revealed multiple small abscesses of the brain, heart, liver, and kidneys; autopsy cultures of meninges, blood, and lung tissue grew MRSA. One month earlier, the patient had been treated with amoxicillin for otitis media. Neither the patient nor family members had been hospitalized during the previous year; no family members resided in LTCFs or worked in health-care settings.

Case 3. In January 1999, a 13-year-old white girl from rural Minnesota was brought to a local hospital with fever, hemoptysis, and respiratory distress. The day before admission she had a productive cough and a 2-cm papule on her lower lip. A chest radiograph revealed a left lower lobe infiltrate and a pleural effusion. She was treated with ceftriaxone and nafcillin. Within 5 hours of arriving at the hospital, she became hypotensive and was transferred to a pediatric hospital, intubated, and treated with vancomycin and cefotaxime. Despite pulmonary and hemodynamic support, the patient's respiratory status deteriorated, and she died on the seventh hospital day from progressive cerebral edema and multiorgan failure.

The patient's blood, sputum, and pleural fluid grew MRSA that was multidrug susceptible. An autopsy revealed consolidated hemorrhagic necrosis of the left lung. The patient had no chronic medical conditions and no recent hospitalizations; no family members were health-care workers or employees of an LTCF or had a history of IDU.

Case 4. In February 1999, a 12-month-old white boy from rural North Dakota was admitted to a tertiary-care hospital with bronchiolitis, vomiting, and dehydration. He had a temperature of 105.2 F (40.6 C) and a petechial rash. Chest radiograph revealed an infiltrate in the right lung consistent with pneumonitis. On the second hospital day, the patient was diagnosed with a large right pleural effusion. He was transferred to the intensive-care unit, a chest tube was inserted, and treatment with vancomycin and cefuroxime was initiated. The patient developed severe respiratory distress and hypotension the following day and died.

The patient's admission blood culture was negative, but his pleural fluid and a postmortem blood culture grew multidrug-susceptible MRSA. An autopsy revealed acute necrotizing pneumonia with extensive hemorrhage and numerous gram-positive cocci in the right lung. The patient had not been hospitalized since birth and had no known medical problems; no family members were health-care workers or employees of an LTCF or known to be IDUs. His 2-year-old sister had been treated for a culture-confirmed MRSA buttock infection 3 weeks earlier. MRSA isolates from the sister and the patient had identical antibiotic susceptibility profiles.

S. aureus can acquire resistance through extrachromosomal plasmids , through additional genetic information delivered by transposons, and through mutations in chromosomal genes. Resistance is achieved through a variety of mechanisms, including enzymatic inactivation of the drug (as with penicillinase , which cleaves the beta-lactam ring of penicillins), alteration of the drug target to prevent binding, and enhanced removal of the drug from the host tissue. A mutation in the MecA gene of Staphylococcus will provide resistance to all beta-lactams. This gene codes for Penicillin Binding Protein --- a mutation in the gene prevents penicillin from effectively binding foreign particles. Resistance to beta-lactams is tested by exposing a bacterial culture to oxacillin. If the bacteria is resistant to oxacillin, it will be resistant to all beta-lactams, and quite possibly also resistant to erythromycin, gentamicin, tetracycline, and clindamycin. Vancomycin resistance has been, to date, documented in enterococci, but not in staphylococcus. Enterococci are gram positive pathogens, listed as the second most common cause of hospital-acquired bacterial infections. They are part of the normal bacterial-makeup of the human gastrointestinal tract, and, like Staphylococci, cause infection when they enter the bloodstream. Enterococci can cause urinary tract infections, wound infections, septicaemia and endocarditis. They are naturally resistant to cephalosporins, aminoglycosides and clindamycin, but were, until recently, susceptible to vancomyciin. j, i, f, j, k. The vanA and vanB genes are responsible for encoding vancomycin resistance in the majority of Enterococci infections. Enterococci are transmitted via person-to-person contact (i.e. on the hands of a health care provider), or through indirect contact (i.e. through contaminated environmental surfaces). The vanA and vanB genes are responsible for resistance transmittance; vanC is a chromosomal gene that cannot be transmitted between gram positive organisms.

Laboratory Summary

MRSA isolates from these four cases were susceptible to all antimicrobial agents tested except beta-lactams. All vancomycin minimum inhibitory concentrations were less than or equal to 2 µg/L. Isolates from all four cases had the mecA gene by PCR assay at MDH. Isolates from cases 1 and 4 shared an indistinguishable PFGE pattern; isolates from cases 2 and 3 differed by two and three bands, respectively, suggesting clonal relatedness among these cases (2). In comparison, these PFGE patterns differed by an average of greater than 10 bands compared with PFGE patterns among nosocomial MRSA isolates from several Minnesota hospitals. Sma I was the restriction enzyme used for PFGE. No isolate produced toxic shock syndrome toxin-1.

Reported by: C Hunt, M Dionne, M Delorme, D Murdock, A Erdrich, MD, Indian Health Svc; D Wolsey, MPH, A Groom, MPH, J Cheek, MD, Indian Health Svc Epidemiology Program; J Jacobson, B Cunningham, MS, L Shireley, MPH, State Epidemiologist, North Dakota Dept of Health. K Belani, MD, S Kurachek, MD, P Ackerman, Children's Hospital and Clinics--Minneapolis; S Cameron, P Schlievert, PhD, Fairview Univ Medical Center; J Pfeiffer, MPH, Hennepin County Medical Center, Minneapolis; S Johnson, D Boxrud, J Bartkus, PhD, J Besser, MS, Minnesota Dept of Health Laboratory; K Smith, DVM, K LeDell, MPH, C O'Boyle, PhD, R Lynfield, MD, K White, MPH, M Osterholm, PhD, K Moore, MD, Acute Disease Epidemiology Section; R Danila, PhD, Acting State Epidemiologist, Minnesota Dept of Health. Div of Applied Public Health Training, Epidemiology Program Office; and EIS officers, CDC.

Editorial Note: Since the first case reports of MRSA infections in the United States in 1968 (3), MRSA has become an increasing problem. The percentage of nosocomial S. aureus isolates that were methicillin resistant increased from 2% in 1974 to approximately 50% in 1997. Methicillin resistance is usually conferred by the chromosomal mecA gene, which encodes an altered penicillin-binding protein (PBP-2A) that causes resistance to all beta-lactam antibiotics, including cephalosporins. However, many nosocomial MRSA strains have acquired resistance to numerous other antibiotic classes through a variety of mechanisms. Approximately 50% of MRSA isolates identified at National Nosocomial Infection Surveillance (NNIS) system hospitals are susceptible only to vancomycin.

Most documented MRSA infections are acquired nosocomially; previously, community-acquired cases were restricted to patients residing in LTCFs and among IDUs. However, both of these groups have extensive exposure to hospitals, and their infections are generally caused by nosocomial MRSA strains. More recently, however, community-acquired MRSA infections have been identified at a Chicago pediatric hospital, in day care centers, and among minority communities in other countries. Unlike nosocomial MRSA isolates, community-acquired isolates from patients without known MRSA risk factors are generally multidrug susceptible (except to beta-lactams) and have distinctive molecular characteristics, as did the four isolates from the fatal cases presented in this report.

These four cases demonstrate the potential severity of community-acquired MRSA infections. Beta-lactam antibiotics (including cephalosporins) are used as empiric therapy for various adult and pediatric infections, but these agents are uniformly ineffective in treating MRSA infections. All patients in this report were initially treated with a cephalosporin antibiotic; the delayed use of antibiotics to which MRSA were susceptible may have contributed to the fatal outcomes. As a result, where such infections exist, obtaining appropriate cultures of infected sites is important. Clinicians should consider MRSA as a potential pathogen in severe pediatric pneumonia or sepsis syndromes in areas where community MRSA infections have been reported. In critically ill patients with invasive infections, empiric treatment with vancomycin (in addition to a third-generation cephalosporin) pending culture results may be necessary to treat cephalosporin-resistant S. pneumoniae or MRSA.

The rural/urban and racial diversity among these cases suggest that MRSA colonization may be widespread, especially in this region of the United States. The extent of community-acquired MRSA infection in the United States is unknown. Few data are available to define the molecular characteristics of these strains. It is also unclear how to limit the spread of MRSA within the community and whether it is feasible to decolonize selected high-risk persons. The role that increased antibiotic use in children--particularly beta-lactams and cephalosporins--has played in selecting for MRSA strains in the community also is unknown. Local or state-based surveillance is needed to characterize and monitor community-acquired MRSA infections and to develop strategies that will improve MRSA treatment and control.

Staphylococci are Gram-positive spherical bacteria that occur in microscopic clusters resembling grapes. Bacteriological culture of the nose and skin of normal humans invariably yields staphylococci. In 1884, Rosenbach described the two pigmented colony types of staphylococci and proposed the appropriate nomenclature: Staphylococcus aureus (yellow) and Staphylococcus albus (white). The latter species is now named Staphylococcus epidermidis. Although nineteen species of Staphylococcus are described in Bergey's Manual (1992), only Staphylococcus aureus and Staphylococcus epidermidis are significant in their interactions with humans. S. aureus colonizes mainly the nasal passages, but it may be found regularly in most other anatomical locales. S epidermidis is an inhabitant of the skin. The staphylococci are in the Bacterial family Micrococcaceae, but they are phylogenetically unrelated to any other genera in the family. Staphylococcus aureus forms a fairly large yellow colony on rich medium, S. epidermidis has a relatively small white colony. S. aureus is often hemolytic on blood agar; S. epidermidis is non hemolytic. Staphylococci are facultative anaerobes that grow by aerobic respiration or by fermentation that yields principally lactic acid. The bacteria are catalase-positive and oxidase-negative. S. aureus can grow at a temperature range of 15 to 45 degrees and at NaCl concentrations as high as 15 percent. Nearly all strains of S. aureus produce the enzyme coagulase: nearly all strains of S. epidermidis lack this enzyme. S. aureus should always be considered a potential pathogen; most strains of S. epidermidis are nonpathogenic and may even play a protective role in their host as normal flora. Staphylococcus epidermidis may be a pathogen in the hospital environment.

Staphylococci are perfectly spherical cells about 1 micrometer in diameter. They grow in clusters because staphylococci divide in two planes. The configuration of the cocci helps to distinguish staphylococci from streptococci, which are slightly oblong cells that usually grow in chains (because they divide in one plane only). The catalase test is important in distinguishing streptococci (catalase-negative) from staphylococci, which are vigorous catalase-producers. The test is performed by adding 3% hydrogen peroxide to a colony on an agar plate or slant. Catalase-positive cultures produce O2 and bubble at once. The test should not be done on blood agar because blood itself contains catalase.

Mastitis caused by Staphylococcus aureus (S. aureus) bacteria is extremely difficult to control by treatment alone. Successful control is gained only through prevention of new infections and cow culling. S. aureus organisms colonize abnormal teat ends or teat lesions. Milkers' hands, wash cloths, teat cup liners, and flies are ways in which the infection can be spread from cow to cow. The organisms probably penetrate the teat canal during milking. Irregular vacuum fluctuations impact milk droplets and bacteria against the teat end with sufficient force to cause teat canal penetration and possible development of new infection. Infected cows must either be culled, segregated from the milking herd and milked last or milked with separate milking units, or teat cup liners must be rinsed and sanitized after milking infected cows. One of the most common types of chronic mastitis is caused by the bacteria, Staphylococcus aureus. Often, it is subclinical, where there is neither abnormal milk nor detectable change in the udder, but somatic cell count has increased. Some cows may flare-up with clinical mastitis, especially after calving. The bacteria persist in mammary glands, teat canals, and teat lesions of infected cows and are considered contagious. The infection is spread at milking time, when S. aureus contaminated milk from infected cows comes into contact with teats of uninfected cows, and the bacteria penetrate the teat canal. Once established, S. aureus usually does not respond to antibiotic treatment, and infected cows eventually must be segregated or culled from the herd. In some herds with somatic cell counts (SCC) below 200,000, dairy managers have not been able to eradicate S. aureus , even when they practiced standard milking time hygiene techniques (Roberson et al., 1994).

Cows infected with S.aureus do not necessarily have high SCC. During 1978-1980, we collected 26,739 aseptic milk samples from cows in 28 herds and found 10% infected with S. aureus (Jones et al., 1984). Only 60% of the infections were found in cows producing milk with more than 200,000 SCC. In several research trials, 3-8% of first lactation cows were found infected with S. aureus at calving. Many remain infected throughout the first lactation and are reservoirs for infecting other cows in the herd. Although as many as half of the cows with high SCC may be infected with S. aureus, somatic cell counts alone are not sensitive enough to positively diagnose S. aureus infections.

S. aureus bacteria produce toxins that destroy cell membranes and can directly damage milk producing tissue. White blood cells (leukocytes) are attracted to the area of inflammation where they attempt to fight off the infection. Initially, the bacteria damage the tissues lining the teat and gland cisterns within the quarter. Then they move up into the duct system and establish deep-seated pockets of infection in the milk secreting cells (alveoli). This is followed by walling-off of bacteria by scar tissue and the formation of abscesses, which is responsible for the poor response to antibiotic treatment. Alveolar and duct cells may be destroyed and milk yield is reduced. These degenerated cells may combine with leukocytes and clog the milk ducts that drain the alveolar areas, contributing to further scar tissue formation. The ducts may reopen and release S. aureus organisms to other areas of the mammary gland. Further abscess formation occurs. Eventually, these become quite large and can be detected as lumps within the udder. Clinically infected quarters often show moderate swelling and visible signs of garget or chunks of milk, especially in forestrippings. Acute S. aureus infections generally develop late in the lactation or just prior to calving . However, the clinical symptoms (udder swelling or hardness, changes in appearance of milk) do not show up until calving or early in the next lactation. It becomes difficult to successfully treat an infection because drugs are not able to penetrate to all infection sites and because the bacteria live inside the white blood cells. S. aureus produces an enzyme that inactivates most penicillin-based treatments, resulting in ineffective antibiotics.

The major reservoirs of these organisms are infected udders, teat canals, and teat lesions, but these bacteria also have been found on teat skin, muzzles, nostrils, and vagina. The bacteria are spread to uninfected quarters by teat cup liners, milkers' hands, wash cloths, and flies. There is some evidence that aerosols play some role in the spread of this organism. Staphylococci do not persist on healthy teat skin but readily colonize teat canals if there are lesions near the teat end. The organisms multiply in infected lesions or colonized teat canals and can readily enter the udder. Infected heifers at calving may represent the most important reservoir to uninfected herdmates. How heifers become infected before calving is unknown at this time. Mastitis control programs need to address the presence of this disease in heifers.

Culture of bulk tank milk is easy, economical, and is an important aid in determining the microbiological cause of mastitis in the herd. This should be conducted in herds where DHI SCC score is 3.3 or above, or the average actual SCC is above 250,000, or more than 0.5 percent of the cows are withheld from the bulk tank on any day because of clinical mastitis. A culture of only one bulk tank sample is not a complete guarantee that contagious mastitis will be detected as S. aureus infected cows may shed the organism intermittently. Sample three consecutive bulk tanks. Freeze the first two samples. Commingle these two with the third for culturing. Check with your State Lab to see if they will conduct cultures and test for bacteria count, lab pasteurized count, preliminary incubation count, and somatic cell count. A small fee probably will be charged, but it should be worthwhile to test bulk tank samples monthly. Some S. aureus herds have histories of gradually increasing SCC but with very few clinical cases. Use the California Mastitis Test (CMT) on cows with elevated DHI SCC to determine which quarters may be infected. In herds with acute mastitis problems, milk samples from clinical mastitis quarters should be collected aseptically and cultured. Early identification of the infection before the bacteria have an opportunity to invade deep within the udder and form abscesses is important.

Infection with vancomycin-intermediate S. aureus, methicillin-resistant S. aureus, and vancomycin-resistant Enterococcus is more frequent in individuals previously treated with vancomycin or an aggressive antimicrobial therapy, individuals with severe underlying disease and immunosuppression, and indivudals recovering from intraabominal surgery. The spread of these pathogens is associated with overuse of antimicrobials (i.e. the prescription of broad-based antibiotics in all situations) and insufficient identification and isolation of contaminated individuals. The emergence of vancomycin resistance has not only been attributed to environmental factors: studies show that prolonged treatment with vancomycin and the prolonged presence of glycopeptides can create a positive selection pressure for vancomycin-resistant strains of S. aureus. The vancomycin eliminates other bacteria, leaving the survivors (those with resistance) a wealth of nutrients on which to survive. In addition, increased antibacterial resistance has been correlated to the widespread use of antibiotics in agriculture. Livestock feeds are often enhanced with low doses of antibiotics which suppress the bacterial flora of the gastrointestinal tract of animals, thereby increasing the possible nutrient uptake. l, c, j, b, h. Antibiotics also enhance growth in livestock. Despite the benefits that such broad-spectrum use of antibiotics affords the agriculture industry, the prolonged usage of antibiotics affords bacteria the opportunity to develop resistance at a quickened pace. These resistant bacteria can be transferred to humans via contaminated food and direct contact.

Control of Staphylococcus aureus Mastitis The most effective control is to prevent new infections by minimizing or eliminating conditions that contribute to the exposure of teat ends through spread of infections from cow to cow and conditions which allow bacteria to contaminate and penetrate the teat canal. In addition, certain nutritional components enhance the animal's resistance to mastitis. Supplementation of the diet with vitamin E and selenium, vitamin A and beta-carotene, and balancing dietary copper and zinc content to meet requirements have reduced mastitis. A. Hygienic Procedures

Milkers should wear rubber gloves. Forestrip 5 powerful squirts of milk from each quarter and check for abnormal milk or flakes. Knock dirt off teats. If teats are very dirty, wash them with a sanitizing solution; use low volumes of water; do not use a common cloth or sponge. Pre-dip with a tested disinfectant, applying with a dipper or cup, not spraying, and allow 30 seconds contact time. Use a separate paper or cloth towel to dry teats and scrub teats five times or 20 seconds (Rasmussen et al., 1991). Towels must not be used on more than one cow. Attach milking unit within 1 to 1.5 mins after beginning of pre-milking preparation. Examine teat ends for chaps, cracks, or lesions that harbor mastitis-causing bacteria. Use an effective post-milking teat dip and cover most of each teat (at least the bottom 1/2 to 2/3). Discard teat dip left in dip cup at end of each milking, rinse cups with water after every milking and dry.

B. Milk First Lactation Cows First if Possible

Uninfected first lactation cows should be milked before older cows carrying subclinical mastitis infections, if possible. If the milking herd can be grouped, a separate group for uninfected first lactation cows is recommended, which can be milked first and fed differently. Since heifers may be infected at calving, aseptic milk samples should be collected shortly after calving and frozen. These samples could be cultured if the cow's DHI SCC score exceeds 4 or clinical mastitis develops. If first lactation cows cannot be separated from infected or high SCC cows, problem cows with clinical mastitis and those receiving antibiotic therapy must be milked last, or milking units must be disinfected with sanitizer after milking infected cows.

C. Milk S. aureus Infected Cows Separately or Last

Cows with clinical mastitis, S. aureus infections or those that have been treated with antibiotics should be milked last, or milked with separate milkers or milking units equipped with backflush to avoid spread of infection via contaminated teat cup liners. Segregation of S. aureus infected cows has been proven to significantly reduce the prevalence of S. aureus mastitis and bulk tank somatic cell counts (Wilson et al., 1995).

D. Milking Equipment

S. aureus infections probably occur during milking when organisms penetrate the teat canal. Irregular vacuum fluctuations, caused by liner slips, flooded lines, etc., may cause a backflow of milk against the teat end with sufficient force to impact any bacteria (from contaminated liners, dirty or wet teats, everted teat ends) deeply into the teat canal and into the teat cistern. Lesions and damage to the teat provide sites for the bacteria to become established and prevent them from being flushed out of the teat.

Try to minimize conditions that are associated with high impact force against the teat end, including liner slips, excessive temporary vacuum losses, low vacuum reserve, inefficient vacuum regulation, and abrupt milking unit removal. Do not remove teatcups from the cow until the vacuum has been shut off. Research has shown that slipping teat cup liners may cause 10-15% of new mastitis infections. Slipping early in milking often results from low vacuum level, blocked air vents, or restrictions in the short milk tube. Slipping in late milking is commonly caused by poor cluster alignment, uneven weight distribution in the cluster, or poor liner condition. Incomplete milking can be caused by poor type or condition of liner, mismatch between claw inlet and short milk tube, clusters too light, clusters that do not hang evenly under the udder, or high milking vacuum levels (Halleron, 1997).

Regular preventive maintenance is essential. Vacuum controllers (regulators), pulsators, and air filters need to be cleaned monthly. Rubber that is cracked, flattened, or otherwise deteriorated should be replaced. Teat cup liners, or short pulsator or milk tubes, should be replaced whenever holes are found in them. The milking system should be evaluated every three months or 500 hours of operation, including the following tests: vacuum reserve, vacuum level, vacuum recovery time, vacuum regulator response, pulsator graphs, and stray voltage.

E. Antibiotic Treatment of S. aureus Cows

Treatment will not control this disease but it may shorten the duration of the infection. Treatment effectiveness decreases as cows become older. Cures were only 34% when 89 cows in 10 Dutch herds were treated for subclinical S. aureus mastitis (Sol et al., 1997). The results showed that probability of cure would be low in older cows with high SCC, infected in hind quarters during early and midlactation. S. aureus infections were found in 36% of clinical mastitis cases in Finish herds (Pyorala and Pyorala, 1997). Of these, only 39% responded to treatment. A SCC < one million was 85% accurate in predicting bacteriological cures. Detect and act on developing mastitis problems early. Successful treatment during lactation is greater if detected and treated early and response is lower when treating chronic infections. Cows whose DHI SCC increases to a score of 5 or actual SCC above 300,000 should be checked with the California Mastitis Test to determine which quarters may be infected. Milk samples from positive quarters should be cultured. Use a strip cup or similar device for detecting abnormal milk. New clinical infections should be treated promptly and appropriately, especially in first lactation cows. Tissue damage can be minimized if treated during early stages of infection. Consult your veterinarian regarding intramammary or other treatments. Use the DHI SCC or CMT to monitor whether treated cows remain low or if infection recurs and becomes chronic.

If a new S. aureus infection is not treated, the bacteria penetrate the mammary gland tissues and the cow attempts to wall off the area, forming an abscess and eventual scar tissue (Belschner et al., 1996). These areas of scar tissue are difficult to penetrate with drugs in effective concentrations. The bacteria also escape the killing effects of some antibiotics in the neutrophils (white blood cells). As these white blood cells attempt to remove bacteria through phagocytosis, many organisms become inactive and are not killed by the neutrophil or by antibiotics which penetrate the cell. The bacteria may remain inactive inside the neutrophil. When the cells die, usually 5-7 days, the bacteria are released to resume cell division and the infection process. The development of antibiotic resistance and formation of L-forms during treatment with some beta-lactam antibiotics (e.g., penicillin) are additional reasons for therapy failures. Chronic S. aureus cows usually have high SCC, abnormal mammary tissue, and recurrent cases of clinical mastitis.

To give an example of the futility of treatment during lactation, pirlimycin is one of the most effective compounds that Pharmacia and Upjohn Co. has found against S. aureus. Its chemical nature allows it to penetrate mammary tissues extremely well. In mastitis data presented to FDA, two tubes were administered 24 hours apart and the cure rate was 36.6%; only 1.1% of non-treated controls recovered spontaneously. The cow cure rate was 49.4% for treatment in field cases. But trials at Louisiana State University and Iowa State University with chronically infected S.aureus cows found cure rates of 12% or less. An extra label treatment duration was experimented with to provide effective drug levels beyond the expected life of the neutrophil. Single quarter extended treatment with repeated label doses of Pirlimycin may not provide adequate drug concentrations for a long enough period of time to effect a bacteriologoical cure on chronically infected animals. Four quarter extended treatment with repeated label doses will provide adequate therapeutic concentrations for many S. aureus bacteria. A cure rate of 50% at 4 weeks after treatment was found in more than 100 treated cows. Whether these cure rates justify the additional expenses and effort (Belschner et al., 1996), not to mention the potential risk of extra label use and antibiotic residue, is unknown.

F. Dry Cow Therapy

Administration of specially formulated dry cow treatments will help prevent new S. aureus infections during the dry period and also will eliminate many existing infections present at drying off. Dry treatment is more effective in eliminating infections than lactating treatment. During the first 2 weeks and the last 7-10 days of the dry period, cows are very susceptible to becoming infected. When cows are not dry treated, spontaneous cures have been very low. Dry cow antibiotic treatment is very cost effective (Kirk et al., 1997). When a cow is dried-off, treat all quarters with a commercial dry cow product. To dry off, cows must be milked out completely, teats dipped in post-milking teat dip and blotted dry after 30 seconds contact time. Scrub teats with alcohol pads before partially inserting tube into teat (one-eighth inch). Teat dip again after treatment. Turn cows into clean, dry environment.

G. Pregnant Heifers

New infections can be found in many heifers, either at calving or in early lactation. As many as one-third of these infections may be caused by S. aureus. Often these S. aureus infections, if untreated, become clinical and recur throughout the first lactation and into the second lactation. Several newly tested procedures can be used on heifers before they calve. Pregnant heifers should not be grouped with dry cows.

Dry Cow Therapy- Louisiana studies have examined the feasibility of giving antibiotic therapy to heifers (Nickerson et al., 1995). A dry cow product containing penicillin and dihydrostreptomycin was administered at the first, second, or third trimester of pregnancy in 35 bred heifers from four herds. Although prevalence of infection and SCC was reduced by treatment in all three groups of heifers, heifers dry-treated during the second trimester of pregnancy demonstrated greater reduction in mastitis and SCC at calving. It is recommended that heifers can be treated with dry cow treatment at 60 days before expected calving date. Properly clean and disinfect teat ends before and after treatment. Check milk for presence of antibiotic residue at 3 to 5 days after calving and before milk is put into milk tank.

Lactating Cow Therapy- In Tennessee, a lactating cow antibiotic treatment containing either cloxacillin or cephapirin was administered to heifers at 7 to 10 days before expected calving (Oliver et al., 1992). Mastitis infections were reduced. Cephapirin gave better treatment results but also resulted in some antibiotic residue in milk at 3 days after calving. The residue was not present when heifers were treated at 14 days before expected calving. It can be recommended that heifers can be treated with lactating cow mastitis treatment at 14 days before expected calving. Use precautions indicated under Dry Cow Therapy.

Milk Heifers Before Calving- Start heifers through milking parlor 2-4 weeks before expected calving (Wilson, 1997). Do not save milk. Calves born to these heifers will need fresh or frozen colostrum from older cows.

Although the vanA and vanB genes are responsible for vancomycin-resistance in MRSA, it appears that VISA strains have a decreased susceptibility to vancomycin due to increased cell-wall material, protecting the bacteria from vancomycin’s ability to disrupt cell wall biosynthesis. Prior to the age of antibiotics and the implementation of penicillin in infectious disease treatment, S. aureus infectious were a serious cause of septic shock and death following surgery. As S. aureus has acquired resistance to penicillin, and then semi-synthetic penicillin derivatives, such as methicillin, vancomycin remains the only drug to which the infection is susceptible. Were vancomycin resistance to be achieved in S. aureus, without an alternative drug therapy, it is likely that septic shock and death would once again be leading causes of mortality in individuals with compromised immune systems. b, d, a, f, e. In addition, the emergence of antibacterial resistant infections are likely to be costly and allow the reemergence of eradicated diseases in new, and more potent forms (such as tuberculosis). Given this threat, and the enormous financial toll that antibiotic resistant diseases already take on the American health care system, there have been a series of recommendations issued on how to deal with the emerging problem of vancomycin resistance in Staphylococcus.

H. Precautions at Calving

Many mastitis infections occur at the time of calving or the preceding 1-2 weeks. A well-drained pasture is preferred as a calving area, with no access to ponds, swampy area, or drainage ditches. A clover-grass sod is desired, in contrast to fescue or muddy, "beaten-up" lots. Lots and pastures should be managed to prevent muddy areas where cattle would lie down. Filthy, damp, or muddy pens, lots, or pastures continually expose the teat end to a barrage of bacteria. Pens should be well bedded, clean, dry, and comfortable. Selenium-vitamin E supplementation or injections at 2-3 weeks before expected calving have been shown to reduce mastitis after calving. However, vitamin E levels of at least 1,000 IU/day during the dry period and 500 IU/d during lactation were more beneficial than National Research Council's recommended 100 IU/d (Weiss et al., 1997). Other minerals and vitamins shown to reduce incidence of mastitis include vitamin A/beta-carotene, copper, and zinc.

Description: The most pathogenic of the staphylococci, this gram-positive, nonmotile, facultative anaerobe grows in perfectly spherical cells (cocci) about 0.5-1.5um in diameter. These cells tend to form in irregular clusters like grapes because the cells divide at random points around their circumference and daughter cells do not completely separate from each other. S. aureus forms large yellow colonies on rich medium at a temperature range from 15-45°C and at NaCl concentrations as high as 15%.

Habitat: Exists in air, dust, sewage, water, milk, and food. Commonly colonizes human hair, skin and mucous membranes, especially in the throat and nasal passages.

Pathogenesis: Expresses many potential virulence factors... 1. Adhesins to promote colonization of host tissues, 2. Invasins leukocidin and hyaluronidase to promote bacterial spread in tissues, 3. Surface factors such as coagulase, protein A, leukocidin, hemolysins, cartenoids, superoxide dismutase, and catalase to inhibit phagocytic engulfment or enhance survival in phagocytes, 4. Immunological disguises like coagulase, protein A and antigenic variation, ... but its pathogenic effects are mainly associated with the toxins it produces. S. aureus uses various membrane-damaging toxins that lyse eukaryotic cell membranes and exotoxins that damage host tissue or otherwise provoke symptoms of disease.

Host Defenses: Phagocytosis is the major mechanism for combating staphylococcal infection. Antibodies are produced which neutralize toxins and promote opsinization. However, the bacterial capsule and protein A may interfere with phagocytosis. No vaccine is available that stimulates active immunity against stapylococcal infections in humans. Infections acquired outside hospitals can usually be treated with penicillinase-resistant b-lactams (nafcillin). Hospital acquired infections are often caused by antibiotic resistant strains and can only be treated with vancomycin.

Diseases: Toxic Shock Syndrome - Originally associated with use of tampons and intravaginal contraceptive devices, but also occurs from infections that follow nasal surgery in which absorbent packing is used, after surgical incisions and in women who have just given birth. The release of toxic shock syndrome toxin (TSST-1) or SE-B and SE-C enterotoxins into the bloodstream causes a sudden onset of fever, chills, vomiting, diarrhea, muscle pains and rash. 5% of all cases are fatal.

Staphyloenterotoxicosis (Food Poisoning) - Contracted by ingestion of undercooked meats, chicken, eggs, or dairy products that have been contaminated with enterotoxins A-G. A dose of <1.0 microgram in contaminated food, reached when S. aureus populations exceed 100,000 per gram, will produce rapid onset of nausea, vomiting, abdominal cramping and prostration. In more severe cases, headache, muscle cramping, and transient changes in blood pressure and pulse rate may occur. Recovery generally takes two days, but may take longer in more severe cases. Death is very rare, although such cases have occurred among the elderly, infants, and severely debilitated persons.

Suppurative (pus-forming) Infections - The portal may be a hair follicle, but usually it is a break in the skin. Leukocidin, which destroys white blood cells and leads to the formation of pus and acne, and hemolysins are the toxins that cause these infections. Symptoms include inflammation characterized by an elevated temperature at the site, swelling, accumulation of pus, and tissue necrosis.

Staphylococcus aureus is a virulent microorganism responsible for many serious infections among the general population. Since recognition of vancomycin-resistant enterococci (VRE), the emergence of vancomycin resistance in S. aureus has been anticipated. This report describes the first documented case of infection caused by S. aureus with reduced susceptibility to vancomycin and includes the initial characterization of this isolate (1); the case occurred in a pediatric patient in Japan. The emergence of reduced vancomycin susceptibility in S. aureus increases the possibility that some strains will become fully resistant and that currently available antimicrobial agents will become ineffective for treating infections caused by such strains.

In May 1996, a 4-month-old boy developed a nosocomial surgical-site infection with methicillin-resistant S. aureus (MRSA). He received treatment with vancomycin (45 mg per kg body weight per day) for 29 days, but fever and surgical-site purulent discharge continued, and the C-reactive protein (CRP) remained elevated (4 mg/dL; normal: less than 1 mg/dL). Treatment was changed to a combination of vancomycin and arbekacin (an aminoglycoside approved for MRSA infection in Japan but not in the United States). After 12 days of this regimen, the purulent discharge subsided, the wound site began to heal, and the CRP declined to 0.9 mg/dL; antimicrobial therapy was discontinued. However, 12 days after antimicrobial therapy was discontinued, fever and surgical-site inflammation recurred, subcutaneous abscesses were detected, and the CRP increased to 3.5 mg/dL. Arbekacin was resumed in combination with ampicillin/sulbactam. After 6 days of this regimen, his fever subsided, and the CRP declined below detectable levels ( less than 0.3 mg/dL). However, during the next several days, the CRP fluctuated between less than 0.3 mg/dL and 1.0 mg/dL, consistent with persistent infection. After debridement of the subcutaneous abscesses and therapy with arbekacin and ampicillin/sulbactam for an additional 17 days, the patient improved, and his CRP remained below detectable levels; his antimicrobial therapy was discontinued, and he was discharged from the hospital.

The MRSA strain that was isolated from the purulent discharge at the surgical site and from the debridement sample demonstrated a vancomycin minimum inhibitory concentration (MIC) of 8 ug/mL (National Committee for Clinical Laboratory Standards breakpoints: susceptible, less than or equal to 4 ug/mL; intermediate, 8-16 ug/mL; and resistant, greater than or equal to 32 ug/mL) by the broth microdilution method performed in Japan and at CDC (2). The organism was negative when tested by polymerase chain reaction for vanA and vanB, the principal genes responsible for vancomycin resistance in enterococci. The mechanism of decreased susceptibility is still under investigation.

The association for Professionals in Infection Control & Epidemiology, Inc. – Greater Omaha Area identified an opportunity for quality improvement and formed an advisory committee with the purpose of addressing key issues regarding MRSA. The committee included representatives from acute care and non-acute care institutions. The goal of the committee was to improve communication among agencies, health care facilities, and health care provides for controlling the spread of MRSA. This goal was accomplished by the development of a document standardizing terminology and providing education on issues related to MRSA.

With the increasing number of patients in Nebraska, health care facilities affected by resistant strains of bacterial {(including methicillin-resistant Staphylococcus aureus (MRSA)}, concern regarding treatment, control and transfer of the patients between institutions is growing. This document is provided as an education resource for facilities in developing/revising their own institutional policies. This document provides minimum basic measures for the care of patients with MRSA. Institutions may implement more stringent isolation precautions as directed by their Infection Control Committee.

Although this document addresses MRSA and its perceived and real problems, the control measures also are applicable to other antibiotic-resistant bacterial such as Pseudomonas aeruginosa. It is extremely important that the concern about MRSA and antibiotic resistant organisms not be exaggerated. Attention and precaution/cohorting practices must be paid to basic infection control principles, including handwashing. Measures such as exclusion from admission to health care facilities are neither necessary nor reasonable.

The World Health Organization and Centers for Disease Control have issued a series of extensive guidelines concerning the containment of vancomycin-resistant infections. The aim of these guidelines is to curb the development of antibacterial-resistant infections before they have evolved total resistance to all currently approved antibacterials. These guidelines are focused around three areas of improvement: 1) education of health care practitioners concerning the appropriate use of vancomycin and other broad-spectrum antibiotics; 2) implementation of systematic procedures for identification and isolation of resistant infections; 3) encourage the prudent use of vancomycin. A key aspect of all guidelines concerning vancomycin-resistance containment is the isolation of individuals with resistance, or intermediate-resistant strains of the pathogen. As it is highly contagious, it is essential that infected individuals be placed in complete isolation, and that the health care practitioners interacting with these individuals be kept at a minimum. A second key point is the prudent use of vancomycin. Numerous studies have reported the correlation between prolonged vancomycin use and the development of vancomycin resistance. i, l, b, c, j. In order to ensure prudent use of the drug, it has been suggested that all health care practitioners receive extensive training on the guidelines for proper use of the drug. The policy approach to combating vancomycin resistance is not the only means by which the medical communicty has chosen to attack this potent pathogen. New drugs, such as “WO9967256A1,” shown below, are being developed which have shown activity against methicillin-resistant S. aureus and VRE. The development of these drugs has been enhanced by new ways of modeling the sites of drug binding on the bacteria.

Health care professionals are facing increasing numbers of patients with MRSA colonization and infection from both acute care and non-acute care facilities. The need for open and frank communication about patient MRSA colonization and infection in and between acute and on-acute care facilities is vital in the effort to control and contain the spread of MRSA. Effective communication is essential early treatment, the identification of risk factors, and the promotion of infection control precautions in both the transferring and receiving institution. It is not acceptable practice to transfer a known MRSA infected or colonized patient without notifying the receiving facility.

S. aureus is a gram positive coccus distinguished by its tendency to cluster under microscopic examination and its positive result on coagulase testing.

It thrives on human skin and mucous membranes, grows rapidly under either aerobic or anaerobic conditions, and can be carried by its host for a long period of time without causing clinical consequences.

Infection caused by S. aureus are cellulitis, pustules, furuncles, carbuncles, impetigo, bacteremia, endocarditis, wound infections, and less commonly, pneumonia. It also produces toxins which can cause gastroenteritis (following ingestion of contaminated foods) and in rare instances, toxic shock syndrome.

S. aureus is transmitted primarily through direct person-to-person contact, especially through the hands of health care workers. Nasal carriage of S. aureus is very common and may be due to hand to nose transmission. A nasal carrier often contaminates his/her own hands by hand to nose contact, then transmits the organism in the course of routine activities. Since skin to skin contract is the most significant mode of transmission, handwashing is of primary importance in preventing its spread.

It can remain viable in the environment for long periods of time in linen, clothing, and dust. However, it is not thought that inanimate objects or environmental surfaces represent significant sources for transmission infection, if appropriately handled.

Airborne spread usually plays little role in the transmission of S. aureus with the exception of burn wound infections in a burn unit, patients with S. aureus pneumonia, or patients with tracheotomies.

This organism was first identified in 1880 by a surgeon, Alexander Ogston, who noted that the majority of abscesses he studied which were inflamed and warm to touch were caused by the same organism. In 1928, penicillin was discovered and was found effective in treating S. aureus.

In 1959, the first semi-synthetic penicillin, methicillin, was produces by altering the chemical composition of penicillin. Two years later, the first methicillin resistant strains of S. aureus were reported.

S. aureus that is resistant to the synthetic penicillins (methicillin, oxacillin, nafcillin) is referred to as methicillin-resistant S. aureus (MRSA). It is also resistant to cephalosporins and sometimes to other antibiotics (erythromycin, clindamycin, aminoglycosides, quinolone).

The first documented nosocomial outbreak of MRSA in the United States occurred at Boston City Hospital in 1968. The investigation of this outbreak supported transmission by the direct contact of hands of personnel to patients in the ward. Since this outbreak, numerous units, intensive care unites, hospital ward, and in the community at large.

MRSA colonization and infection in acute and non-acute care facilities have increased dramatically over the past two decades, evidenced by the increasing number of reported outbreaks in the medical literature. Because of its resistance to antibiotics, management of MRSA infections requires more complicated, toxic, and expensive treatment. MRSA colonization and infections have a significant impact on individual patients and institutions. Many patients with MRSA remain colonized indefinitely, and the majority of hospital and nursing homes that have endemic MRSA never eradicates MRSA from the institution.

Methicillin-Resistant S. Aureus is not a “super bug” and is not more likely to cause serious infection than antibiotic susceptible S. aureus. It is simply resistant to more antibiotics. The mechanisms of transmission of MRSA are virtually identical to those of the usual S. aureus, which is sensitive to methicillin.

DIAGNOSIS/TREATMENT

Identification:

S. aureus colonization of the nares, rectum, or skin can be detected by culture of these areas. Clinical infection caused by S. aureus can be identified by cultures of blood, sputum, urine, percutaneous aspiration, or surgically obtained specimens as appropriate for the particular site.

After S. aureus is identified, antibiotic susceptibilities should be performed. Oxacillin susceptibility testing by the Kirby Bauer technique is the preferred method of identifying MRSA. Resistance to oxacillin also defines resistance to all penicillins. cephalosporins susceptibilities should not be reported on MRSA isolates since all isolated are considered to be resistant in vivo, regardless of in vitro susceptibilities. Reference laboratories should be consulted when questions arise.

Colonization:

It is important for the health care professional to understand the difference between colonization and infection. Colonization indicates the presence of the organism without symptoms of illness. Colonization can occur in the nares, trachea, skin folds, rectum, or in an open wound such as decubitus ulcer. The patient does not symptoms when colonized. 70 % to 90% of all individuals are intermittently colonized with S. aureus (methicillin susceptible or resistant) in the anterior nares. S. aureus permanently colonized the anterior nares of about 20% to 30% of the general population. Hospital workers are more likely to be colonized than persons in the general population, presumably because of increased exposure. Thus, a higher colonization rate with S. aureus is responsibility of the physician to determine if a patient is colonized or infected. Colonization with MRSA is not an indication for hospital admission or for prolonged hospitalization provided appropriate arrangements for disposition can be made (e.g. discharge to home or extended care facility).

Infection:

Infection is defined as tissue invasion by S. aureus with subsequent clinical symptoms. Clinical manifestations of infections caused by S. aureus can range from superficial skin lesions such as boils to deeper infections such as pneumonia which can progress to death. In addition to local symptoms and signs of infection, systemic manifestation of disease such as fever, malaise, and leukocytosis are often present.

Treatment of Infections:

Treatment for an infection due to MRSA may be indication for hospital admission. The standard antibiotic therapy for infections caused by MRSA is intravenous Vancomycin. Vancomycin can have serious side effects, especially in elderly persons. These side effects could include ototoxicity (loss of hearing or other auditory damage), nephrotoxicity (damage to the kidneys or renal system), and allergic reactions such as fever and rash. Infusion of vancomycin, especially when to rapid, can result in flushing, hypotension, and tachycardia known as the “red man syndrome”. Vancomycin given by mouth is not absorbed and is not effective against MRSA.

Decolonization:

Decolonization is the elimination of MRSA carrier state through the use of infection control measures and/or antibiotics. The indications for and efficacy of decolonization vary depending on the unique circumstances surrounding a particular episode or outbreak of MRSA colonization/infection. The effectiveness of permanent decolonization seems marginal, but special circumstances may warrant an attempt. Examples of special circumstances include the following: 1) patients who are immunosuppressed and colonized, and therefore, might develop particularly serious infections, 2) patients who are more likely to spread the organisms, due to behavior (e.g. the mentally retarded), or 30 patients who have repeated infections caused by the MRSA strain that they carry. Decolonization protocols may include the use of oral/topical antibiotics. A physician should assess each situation (an infectious disease specialist may be consulted for decolonization protocol).

ADMISSION/DISCHARGE

The issue of MRSA status (negative culture, colonized, or infected) with regard to hospital and non-acute care facility admission and discharge warrants attention. This issue is of great practical significance in light of the current misinformation, fear and the natural inadequacies of complete, preventive control measures for infection and colonization.

An institution should not deny admission to a person colonized or infected with MRSA if adequate facilities are available to deal with MRSA.

HOSPITAL ADMISSION

Admission Rationale:

Hospital admission because of MRSA infection is acceptable medical practice. However, MRSA colonization does not, by itself, warrant hospital admission. Treatment for infection with MRSA is usually accomplished in an acute-care setting. However, treatment for infection can be accomplished in a non-acute care facility or at home. Such decisions should be based on the clinical judgement of the attending physician.

Room Assignment:

A private room is preferred for MRSA infected of colonized patients. The MRSA colonized patient can be placed with another colonized patient (cohort). If cohorting is not possible, the MRSA colonized patient can be placed with a non-colonized patient. The MRSA-colonized patient should not be placed in a room with a patient who is a high risk for infection (i.e. a patient with a tracheostomy, gastrostomy tube, central line, urinary catheter, open wound, or immunocompromised). A colonized patient with poor hygiene may need to be in a private room.

Infection Control:

Standard infection control guidelines (See Appendix II) should be followed. The facility may employ a stricter infection control policy if so directed by the Infection Control Committee.

HOSPITAL DISCHARGE

Upon completion of appropriate therapy for MRSA infection, and when the clinical manifestation have resolved (even if the patient has a positive culture) hospital discharge may be indicated. A patient colonized with MRSA while hospitalized for another illness may be discharged once that illness is under control. In other words, a patient may be discharged from an acute-care setting with a positive MRSA culture. When this occurs, the hospital should notify, in advance any institution/agency receiving the patent that he/she is colonized with MRSA. A negative culture should not be a prerequisite for transfer to another facility.

NON-ACUTE CARE FACILITY ADMISSION

Admission Rationale:

An institution should not deny admission to a person colonized or infected with MRSA if adequate facilities are available to deal with MRSA. A person colonized with MRSA should be allowed admission to a non-acute care facility.

Under special circumstances, treatment for an MRSA infection can be accomplished in the no-acute care facility. This decision is based on clinical judgment of attending physician and capabilities of the institution, and should be negotiated between the discharging and receiving physicians/facilities.

Room Assignment:

A private room is preferred for MRSA infected or colonized patients. The MRSA colonized patient can be placed with another colonized patient (cohort). If cohorting is not possible, the MRSA colonized patient can be placed with a non-colonized patient. The MRSA colonized person should not be placed in a room with a person at high risk for infection (i.e., a resident with a tracheostomy, a gastrostomy, central line, urinary catheter, open wound or immunocompromised). A colonized person with poor hygiene may need to be in a private room.

Infection Control:

Standard infection control guidelines (see Appendix II) should be followed. The facility may employ a stricter infection control policy if so directed by the Infection Control Committee.

NON-ACUTE CARE FACITLITY

A patient may be discharged to home or hospital while colonized with MRSA. When a MRSA-colonized/infected patients is transferred to and acute care setting, the receiving institution/agency should be notified, in advance, of the patients MRSA status.

DISCHARGE TO HOME:

If the patient is discharged from an acute or non-acute care facility to a private hone, the family should be educated that there is a difference in risk between MRSA infection in the setting of a health care facility versus the home setting. The patient’s family will usually have noted the discharging institutions additional attention to infection control practices and my have questions regarding 1) the need to duplicate these infection control practices in the home setting, and 2) their risk of MRSA infection if they bring the patient home. Information should be conveyed to the patient’s family that additional infection control practices are often employed in the health care facility to reduce the risk of transmission of MRSA to the highly susceptible patients/residents, such as those with open wounds, invasive devices, or server underlying disease.

The patient’s family needs to understand that they rarely need to practice extraordinary infection control measures in the home beyond good handwashing and careful handling of soiled dressings. If there is a highly susceptible family member (e.g., diagnosis of cystic fibrosis, immunosuppressions, or cancer) more extensive precautions might be in order and should be discussed with a physician prior to patient discharge.

What is MRSA?

MRSA is the acronym for methicillin-resistant Staphylococcus aureus. MRSA is distinguished from other bacteria by its resistance to most antibiotics including all penicillins and cephalosporins. MRSA can affect people in different ways. People can carry it in the nose or on the skin without showing any symptoms of illness. This is called MRSA colonization. MRSA can also cause infections such as boils, wound infections, and pneumonia.

How is MRSA transmitted?

MRSA is spread from person-to-person by direct contact. This means that if a person has MRSA on the skin (especially on the hands) and touches another individual, MRSA may be spread. A person may have MRSA on hands as a result of being a carrier or from touching another person who is a carrier or infected with MRSA.

What can I do to prevent the spread of MRSA?

Handwashing, using soap and warm running water, is the single most important measure necessary to control the spread of MRSA. Proper handwashing should be performed after the care of each patient, after handling soiled dressings and clothing, and after wearing gloves. Other measures to prevent becoming infected or transmitting infection to others include avoiding cross-contamination between clean and dirty linen, daily environmental cleaning, wearing gloves for all dressing changes, proper handling of infectious waste and observing isolation procedures. Report illness including unusual skin rashes or boils to your nursing director before working with patients. WASH YOUR HANDS BEFORE AND AFTER CONTACT WITH EACH PATIENT!!!!

Will I take MRSA home to my family?

MRSA can live on linens and clothing but these generally do not transmit the organism. Wear a protective garment at work if you are at risk of contaminating your clothing with wound or other body fluids or drainage. If you have contaminated your clothing with wound drainage or other potentially infectious body fluids or drainage, change clothes. Report any unusual rashes or skin lesions to your physician. Always thoroughly wash your hands before going home from work. Normal healthy people are not usually at risk of serious invasive MRSA disease.

How is MRSA treated?

Persons who carry MRSA, but are not exhibiting symptoms usually do not need to be treated. The antibiotic used to treat persons with MRSA infections is vancomycin given intravenously. Oral vancomycin is not effective against MRSA. Vancomycin can have serious side effects.

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Last modified: May 25, 2005