Staph is short for Staphylococcus, a type of bacteria. There are over 30 types, but Staphylococcus aureus causes most staph infections, including
Skin infections
Pneumonia
Food poisoning
Toxic shock syndrome
Blood poisoning (bacteremia)
Skin infections are the most common. They can look like pimples or boils. They may be red, swollen and painful, and sometimes have pus or other drainage. They can turn into impetigo, which turns into a crust on the skin, or cellulitis, a swollen, red area of skin that feels hot.
Anyone can get a staph skin infection. You are more likely to get one if you have a cut or scratch, or have contact with a person or surface that has staph bacteria. The best way to prevent staph is to keep hands and wounds clean. Most staph skin infections are easily treated with antibiotics or by draining the infection. Some staph bacteria are resistant to certain antibiotics, making infections harder to treat.
Conditions known as staph infections are those caused by the bacteria Staphylococcus aureus. Many healthy people carry staph bacteria in their noses without getting sick. But when the skin is punctured or broken, staph bacteria can enter the wound and cause infections, which can lead to other health problems.
You can help prevent your child from developing a staph infection by encouraging regular hand washing, keeping your child’s skin clean with a daily bath, and keeping areas that have been cut clean or covered.
How Staph Infections Spread
Staph can spread through the air, on contaminated surfaces, and from person to person. A child can carry staph bacteria from one area of the body to another on dirty hands and under dirty fingernails. Staph can pass from person to person the same way. So hand washing is the most important way to prevent staph infections.
You can also help prevent staph skin infections by keeping your child’s skin clean with a daily bath or shower. If your child has a skin condition such as eczema that makes frequent bathing difficult, speak with your child’s doctor for advice.
Keep areas of the skin that have been injured - such as cuts, scrapes, and rashes caused by allergic reactions or poison ivy - clean and covered, and use any other treatments that your doctor suggests.
Complications of Staph Infections
Staph bacteria can cause folliculitis, boils, scalded skin syndrome, impetigo, toxic shock syndrome, cellulitis, and other types of infections.
Impetigo
Impetigo is a skin infection that can affect skin anywhere on the body but commonly occurs in the area around the nose and mouth.
Impetigo usually affects preschool- and school-age children, especially in the summer months. Impetigo caused by staph bacteria is characterized by large blisters containing fluid that is first clear, then cloudy. The blisters may burst, ooze fluid, and develop a honey-colored crust. Impetigo may itch, and it can be spread by scratching. Typically, impetigo is treated with a topical ointment prescribed by a doctor and, depending on the severity, oral antibiotics may be added.
Folliculitis and Boils
Folliculitis is an infection of hair follicles, tiny pockets under the skin where hair shafts (strands) grow. In folliculitis, tiny white-headed pimples appear at the base of hair shafts, sometimes with a small red area around each pimple. Children with fine hair that is often worn tightly pulled back in barrettes or braids are particularly susceptible to folliculitis.
Without treatment, folliculitis can either heal within 1 week or progress to become boils. With a boil, the staph infection spreads deeper and wider, often affecting the skin’s subcutaneous tissue (deeper tissue under the skin) and the oil-producing glands, which are called sebaceous glands. In the first stage, which parents and kids often miss, the area of skin either begins to itch or becomes mildly painful. Next, the skin turns red and begins to swell over the infected area. Finally, the skin above the infection becomes very tender and a whitish “head” may appear. The head may break, and the boil may begin to drain pus, blood, or an amber-colored liquid. Boils can occur anywhere on the skin, especially under the arms or on the groin or buttocks in children.
To help relieve pain from a boil, try warm-water soaks, a heating pad, or a hot-water bottle applied to the skin for about 20 minutes, three or four times a day. Boils are occasionally treated with oral antibiotics and in some cases need to be surgically drained.
Without treatment, boils may heal once they open up and drain, but treatment makes them heal faster and may prevent the staph infection from spreading to other skin areas.
Scalded Skin Syndrome
Scalded skin syndrome (SSS) most often affects newborns and children under age 5. The illness usually starts with a localized staph skin infection, but the staph bacteria manufacture a toxin that affects skin all over the body. The child has a fever, rash, and sometimes blisters. The rash begins around the mouth, then spreads to the trunk, arms, and legs. As blisters burst and the rash passes, the top layer of skin is dislodged and the skin surface becomes red and raw, like a burn.
Scalded skin syndrome is a serious illness that needs to be treated and monitored in a hospital. It affects the body in the same way as serious burns. After treatment, most kids make a full recovery from SSS.
Treating Staph Infections
Most localized staph skin infections can be treated by washing the skin with an antibacterial cleanser, applying an antibiotic ointment prescribed by a doctor, and covering the skin with a clean dressing. To keep the infection from spreading, use a towel only once when you clean an area of infected skin, then wash it (or use disposable towels).
For most serious staph skin infections, your child’s doctor may prescribe an antibiotic for your child. If so, give the antibiotic on schedule for as many days as your doctor directs.
Call the doctor whenever your child has an area of red, irritated, or painful skin, especially if you see whitish pus-filled areas or your child has a fever or feels sick. Also, call the doctor if skin infections seem to be passing from one family member to another or if two or more family members have skin infections simultaneously.
Staphylococcus aureus /?stæf.?.lo?ko.k?s ?o??i.?s/, literally “Golden Cluster Seed” and also known as golden staph, is the most common cause of staph infections, is a spherical bacterium, frequently living on the skin or in the nose of a person, that can cause a range of illnesses from minor skin infections, such as pimples, impetigo, boils, cellulitis and abscesses, to life-threatening diseases, such as pneumonia, meningitis, endocarditis, Toxic shock syndrome (TSS), and septicemia. Abbreviated to S. aureus or Staph aureus in medical literature, S. aureus should not be confused with the similarly named (and also medically relevant) species of the genus Streptococcus.
S. aureus was discovered in Aberdeen, Scotland in 1880 by the surgeon Sir Alexander Ogston in pus from surgical abscesses.[1] Each year some 500,000 patients in American hospitals contract a staphylococcal infection. [2]
Microbiology
Gram stain of S. aureus.S. aureus is a Gram-positive coccus, which appears as grape-like clusters when viewed through a microscope and has large, round, golden-yellow colonies, often with ?-hemolysis, when grown on blood agar plates.[3] The golden appearance is the etymological root of the bacteria’s name: aureus means “golden” in Latin.
S. aureus is catalase positive and thus able to convert hydrogen peroxide (H2O2) to water and oxygen, which makes the catalase test useful to distinguish staphylococci from enterococci and streptococci. A large percentage of S. aureus can be differentiated from most other staphylococci by the coagulase test: S. aureus is primarily coagulase-positive, while most other Staphylococcus species are coagulase-negative.[3] However, while the majority of S. aureus are coagulase-positive, some may be atypical in that they do not produce coagulase. Incorrect identification of an isolate can impact implementation of effective treatment and/or control measures.[4] It is medically important to identify S.aureus correctly as S.aureus is much more aggressive and likely to be antibiotic-resistant. Coagulase-negative S. aureus appears to be an increasing problem that clinical laboratories should be aware of. They are as virulent as those producing coagulase and can colonize, cause infections and spread among patients.[5]
S. aureus has about 2,600 genes and 2.8 million base pairs of DNA in its chromosome. Plasmids can also comprise part of the species’ genome.
The species has been subdivided into two subspecies: S. aureus aureus and S. aureus anaerobius. The latter requires anaerobic conditions for growth, is an infrequent cause of infection, and is rarely encountered in the clinical laboratory.
Role in disease
S. aureus may occur as a commensal on human skin (particularly the scalp, armpits and groins); it also occurs in the nose (in about 25% of the population) and throat and less commonly, may be found in the colon and in urine. The finding of Staph. aureus under these circumstances does not always indicate infection and therefore does not always require treatment (indeed, treatment may be ineffective and re-colonisation may occur). It can survive on domesticated animals such as dogs, cats and horses, and can cause bumblefoot in chickens. It can survive for some hours on dry environmental surfaces, but the importance of the environment in spread of S. aureus is currently debated. It can host phages, such as the Panton-Valentine leukocidin, that increase its virulence.
S. aureus can infect other tissues when normal barriers have been breached (e.g. skin or mucosal lining). This leads to furuncles (boils) and carbuncles (a collection of furuncles). In infants S. aureus infection can cause a severe disease Staphylococcal scalded skin syndrome (SSSS).[6]
S. aureus 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.
Deeply situated S. aureus infections can be very severe. Prosthetic joints put a person at particular risk for septic arthritis, and staphylococcal endocarditis (infection of the heart valves) and pneumonia, which may be rapidly fatal.
Staphylococcus aureus and influenza
S. aureus superinfection is an uncommon complication of influenza. However, in the last three influenza pandemics (1918, 1957–58, and 1968), added infection with S. aureus was a common complication.
Toxic Shock Syndrome
Certain strains of S. aureus are also the causative agent for Toxic Shock Syndrome.
Mastitis in cows
S. aureus is one of the causal agents of mastitis in dairy cows. Its large capsule protects the organism from attack by the cow’s immunological defenses.[7]
Virulence factors
Toxins
Depending on the strain, S. aureus is capable of secreting several toxins, which can be categorized into three groups. Many of these toxins are associated with specific diseases.
Pyrogenic toxin superantigens (PTSAgs) have superantigen activities that induce toxic shock syndrome (TSS). This group includes the toxin TSST-1, which causes TSS associated with tampon use. The staphylococcal enterotoxins, which cause a form of food poisoning, are included in this group.
Exfoliative toxins are implicated in the disease staphylococcal scalded-skin syndrome (SSSS), which occurs most commonly in infants and young children. The protease activity of the exfoliative toxins causes peeling of the skin observed with SSSS.
Staphylococccal toxins that act on cell membranes include alpha-toxin, beta-toxin, delta-toxin, and several bicomponent toxins. The bicomponent toxin Panton-Valentine leukocidin (PVL) is associated with severe necrotizing pneumonia in children. The genes encoding the components of PVL are encoded on a bacteriophage found in community-associated MRSA strains.
Role of pigment in virulence
The vivid yellow pigmentation of S. aureus may be a factor in its virulence. When comparing a normal strain of S. aureus with a strain modified to lack the yellow coloration, the pigmented strain was more likely to survive dousing with an oxidizing chemical such as hydrogen peroxide than the mutant strain was.
Colonies of the two strains were also exposed to human neutrophils. The mutant colonies quickly succumbed while many of the pigmented colonies survived. Wounds on mice were swiped with the two strains. The pigmented strains created lingering abscesses. Wounds with the unpigmented strains healed quickly.
These tests suggest that the yellow pigment may be key to the ability of S. aureus to survive immune system attacks. Drugs that inhibit the bacterium’s production of the carotenoids responsible for the yellow coloration may weaken it and renew its susceptibility to antibiotics.[8]
Diagnosis
Depending upon the type of infection present, an appropriate specimen is obtained accordingly and sent to the laboratory for definitive identification. A Gram stain is first performed to guide the way, which should show typical gram-positive bacteria, cocci, in clusters. Secondly, culture the organism in Mannitol Salt Agar, which is a selective medium with 7%-9% NaCl that allows S. aureus to grow producing yellow-colored colonies as a result of salt utilization and subsequet drop in the medium’s pH. Furthermore, for differentiation on the species level, catalase (positive for all species), coagulase (fibrin clot formation), DNAse (zone of clearance on nutrient agar), lipase (a yellow color and rancid odor smell), and phosphatase (a pink color) tests are all done.
Treatment and antibiotic resistance
Wikinews has related news:
Supergerm deaths soar, surpass AIDS in the United StatesFor more details on this topic, see Methicillin-resistant Staphylococcus aureus (MRSA).
Antibiotic resistance in S. aureus was almost unknown when penicillin was first introduced in 1943; indeed, the original petri dish on which Alexander Fleming observed the antibacterial activity of the penicillium mould was growing a culture of S. aureus. By 1950, 40% of hospital S. aureus isolates were penicillin resistant; and by 1960, this had risen to 80%.[9]
Mechanisms of antibiotic resistance
Staphylococcal resistance to penicillin is mediated by penicillinase (a form of ?-lactamase) production: an enzyme which breaks down the ?-lactam ring of the penicillin molecule. Penicillinase-resistant penicillins such as methicillin, oxacillin, cloxacillin, dicloxacillin and flucloxacillin are able to resist degradation by staphylococcal penicillinase.
The mechanism of resistance to methicillin is by the acquisition of the mecA gene, which codes for an altered penicillin-binding protein (PBP) that has a lower affinity for binding ?-lactams (penicillins, cephalosporins and carbapenems). This confers resistance to all ?-lactam antibiotics and obviates their clinical use during MRSA infections.
Glycopeptide resistance is mediated by acquisition of the vanA gene. The vanA gene originates from the enterococci and codes for an enzyme that produces an alternative peptidoglycan to which vancomycin will not bind.
Staph infections lead to rapid weight loss and muscle depletion. Even after fully cured, it will still take months to recuperate fully.
Today, S. aureus has become resistant to many commonly used antibiotics. In the UK, only 2% of all S. aureus isolates are sensitive to penicillin with a similar picture in the rest of the world, due to a penicillinase (a form of ?-lactamase). The ?-lactamase-resistant penicillins (methicillin, oxacillin, cloxacillin and flucloxacillin) were developed to treat penicillin-resistant S. aureus and are still used as first-line treatment. Methicillin was the first antibiotic in this class to be used (it was introduced in 1959), but only two years later, the first case of methicillin-resistant S. aureus (MRSA) was reported in England.[10]If the bacteria produces the enzymes ?-lactamase or penicillinase, these enzymes will break open the ?-lactam ring of the antibiotic, rendering the antibiotic ineffective
Despite this, MRSA generally remained an uncommon finding even in hospital settings until the 1990s when there was an explosion in MRSA prevalence in hospitals where it is now endemic.[11]
MRSA infections in both the hospital and community setting are commonly treated with non-?-lactam antibiotics such as clindamycin (a lincosamine) and co-trimoxazole (also commonly known as trimethoprim/sulfamethoxazole). Resistance to these antibiotics has also lead to the use of new, broad-spectrum anti-Gram positive antibiotics such as linezolid because of its availability as an oral drug. First-line treatment for serious invasive infections due to MRSA is currently glycopeptide antibiotics (vancomycin and teicoplanin). There are number of problems with these antibiotics, mainly centred around the need for intravenous administration (there is no oral preparation available), toxicity and the need to monitor drug levels regularly by means of blood tests. There are also concerns that glycopeptide antibiotics do not penetrate very well into infected tissues (this is a particular concern with infections of the brain and meninges and in endocarditis). Glycopeptides must not be used to treat methicillin-sensitive S. aureus as outcomes are inferior.[12]
Because of the high level of resistance to penicillins, and because of the potential for MRSA to develop resistance to vancomycin, the Centers for Disease Control and Prevention have published guidelines for the appropriate use of vancomycin. In situations where the incidence of MRSA infections is known to be high, the attending physician may choose to use a glycopeptide antibiotic until the identity of the infecting organism is known. When the infection is confirmed to be due to a methicillin-susceptible strain of S. aureus, then treatment can be changed to flucloxacillin or even penicillin as appropriate.
Vancomycin-resistant S. aureus (VRSA) is a strain of S. aureus that has become resistant to the glycopeptides. The first case of vancomycin-intermediate S. aureus (VISA) was reported in Japan in 1996;[13] but the first case of S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.[14] Three cases of VRSA infection have been reported in the United States.[15] as of 2005.
Infection control
Spread of S. aureus (including MRSA) is through human-to-human contact, with environmental contamination thought to play a relatively unimportant part. Emphasis on basic hand washing techniques are therefore effective in preventing the transmission of S. aureus. The use of disposable aprons and gloves by staff reduces skin-to-skin contact and therefore further reduces the risk of transmission. Please refer to the article on infection control for further details.
Alcohol has proven to be an effective topical sanitizer against MRSA. Quaternary ammonium can be used in conjunction with alcohol to increase the duration of the sanitizing action. The prevention of nosocomial infections involve routine and terminal cleaning. Nonflammable alcohol vapor in CO2 NAV-CO2 systems have an advantage as they do not attack metals or plastics used in medical environments, and do not contribute to antibacterial resistance.
An important and previously unrecognized means of community-associated methicillin-resistant S. aureus colonization and transmission is during sexual contact. [16]
Staff or patients who are found to carry resistant strains of S. aureus may be required to undergo “eradication therapy” which may include antiseptic washes and shampoos (such as chlorhexidine) and application of topical antibiotic ointments (such as mupirocin or neomycin) to the anterior nares of the nose.
March 2007: The BBC has reported promising experiments in UK where a vaporizer spraying some essential oils into the atmosphere reduced airborne bacterial counts by 90% and kept MRSA infections at bay. This may hold promise in MRSA infection control.