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. Indīvidual 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 colonīzed with vancomycin-resistant S. aureus should be placed in a private room, and all persons entering the room should wear clean, nonsterīle 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 biologīcal 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 PLAGU