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05.12.2015, admin
Staphylococcal Scalded Skin Syndrome (SSSS) is a skin disorder caused by two exotoxins released from the toxigenic strains of Staphylococcus aureus bacteria. The clinical features of SSSS were first described by Baron Gottfried Ritter von Rittershain in the year 1878 who studied 297 cases of children being affected by this skin disorder in a Czechoslovakian children’s home and recorded them over a period of 10 years.
The condition is mostly detected in children below 5 or 6 years of age, especially neonates. SSSS begins from a localized staphylococcal infection that produces two causative exotoxins, namely, the epidermolytic toxins A and B. The condition normally starts with a fever, sensations of irritability and a widespread redness of skin. Wrinkling of the skin that has a tissue paper-like look, followed by appearance of large bullae in armpits, groin and other body orifices like the ears and nose (nasopharyngeal infection). Peel off in sheets of the topmost layer of the skin, thereby leaving a moist, reddish and tender surface.
The affected children might feel feverish and miserable; they might also detest being held or touched. While diagnosing SSSS, a doctor first evaluates the personal medical history of sufferers and conducts a thorough physical examination. There are a number of skin disorders which show signs and symptoms similar to that of SSSS.
The mainstay of SSSS treatment is eradication of primary infection along with supportive care.
The moist, bare areas of the skin should be lubricated by using a bland emollient cream to alleviate signs of pruritus and tenderness.
Physiotherapy is essential as SSSS normally tends to affect the limb flexures severely and the patients will intentionally restrict movement due to pain and discomfort. Most cases of SSSS are mild, and the prognosis for children affected with this disorder is excellent. Staphylococcal Scalded Skin Syndrome responds well to treatment and patients can recover fully within a short period of time.
Staphylococcus aureus colony morphology and microscopic appearance, basic characteristic and tests for identification of S.aureus bacteria. This program is funded through Health Resources and Services Administration, US Department of Health and Human Services.
Which one of the following statements is TRUE regarding community-acquired skin and soft tissue MRSA infections in HIV-infected persons? Resistance to methicillin and cephalexin results from production of an altered penicillin-binding protein by Staphylococcus aureus that has reduced affinity for binding to beta-lactam antibiotics.CorrectThe resistance to methicillin and cephalexin results from the production of an altered penicillin-binding protein (penicillin binding protein 2a) that has reduced affinity for binding to beta-lactam antibiotics. More than 30% of the isolates from skin and soft tissue infections have shown resistance to trimethoprim-sulfamethoxazole (Bactrim, Septra).IncorrectResistance rates of community-acquired MRSA to trimethoprim-sulfamethoxazole have been low, certainly much less than 30%. Ciprofloxacin (Cipro) is one of the preferred oral regimens.IncorrectCommunity-acquired isolates of MRSA also frequently show resistance to fluoroquinolones, such as ciprofloxacin, and thus ciprofloxacin is not considered a preferred regimen. In a patient allergic to trimethoprim-sulfamethoxazole (Bactrim, Septra), azithromycin (Zithromax) is considered the preferred alternative.IncorrectThe rates of MRSA resistance to macrolides are high and empiric use of macrolides, such as azithromycin, is not recommended for the empiric treatment of MRSA, even in a patient who is allergic to trimethoprim-sulfamethoxazole. Figure 1Figure 1 - Scanning Electron Micrograph of Methicilin-Resistant Staphylococcus aureus (MRSA)This colorized scanning electron micrograph shows abundant clumps of MRSA. Figure 2Figure 2 - Incidence of Community-Acquired MRSA Skin and Soft Tissue Infections Among HIV-Infected PatientsSource: Popovich KJ, et al.
Figure 6Figure 6 - MRSA Abscess and Surrounding Cellulitis in Right Arm in HIV-Infected PatientSource: Image courtesy of Timothy Dellit, MD, Harborview Medical Center, University of Washington. Figure 10Figure 10 - Antibiotic Resistance in Staphylococcus aureus-Containing Cutaneous abscesses of Patients with HIVKrucke GW, Grimes DE, Grimes RM, Dang TD. Figure 11Figure 11 - Antimicrobial Therapy for MRSA Skin and Soft Tissue Infections legendSource: Liu C, Bayer A, Cosgrove SE, et al.
Figure 12Figure 12 - Body Sites for MRSA ColonizationIllustration from David Ehlert, Cognition Studio. Figure 13Figure 13 - Efficacy of Mupirocin in Nasal Decolonization of MRSASource: Martin JN, et al. Staphylococcus aureus is a gram-positive bacteria that grows in grape-like clusters (Figure 1). Patients with a MRSA skin and soft tissue infection most often present with a localized inflammatory abscess.
When fluctuance is present (a fluid-filled cavity is palpable), incision and drainage should be performed.
Extend the incision to a length sufficient to adequately drain the abscess; the opening should be large enough to allow insertion of a hemostat and packing material. Express additional material remaining from within the abscess that did not spontaneously drain after the incision.
Use a curved hemostat to perform blunt dissection to break up loculations and fully open the abscess cavity; the dissection should proceed in a circular direction around the abscess cavity.
Irrigate the wound with normal saline until the fluid becomes clear, making sure to use a splash shield during this process. Pack the inside of the wound with a packing strip, but avoid packing the wound too tightly. Some patients initially present with a tense inflammatory lesion that does not contain a softer, fluid-filled region amenable to incision and drainage. In January 2011, the Infectious Diseases Society of America (IDSA) published guidelines on the management of community-acquired skin and soft tissue infection in the current era of MRSA infections.[14] For a simple abscess or boil, incision and drainage is considered the primary treatment and often provides a good clinical response even without antimicrobial therapy. When choosing antimicrobial therapy, clinicians should consider prior results from the same patient as well as local resistance data, if known.


In patients who have nonpurulent cellulitis (and no abscess), use of trimethoprim-sulfamethoxazole alone to target MRSA is problematic, since S. The desmosomes are a part of skin cell that is responsible for attaching to adjacent skin cell. Application of lifelong antibodies against the staphylococcal exotoxins has reduced the chances of this skin disease greatly in adults and older children. Fluid-filled blisters are formed within the first 24 to 48 hours which rupture easily, thereby leaving areas of moist erythematous base that have a burn-like, scalded appearance. In newborns, the lesions are frequently found around the diaper area as well as in and around umbilical cord (infected umbilicus). If larger areas of the skin are shed, patients would lose valuable amounts of body fluids and salts thereby developing dehydration.
Samples of pus or surface fluid may be taken with the help of a skin swab to check the presence of bacteria.
Hence, while diagnosing SSSS, it is essential to differentiate it from such similar conditions in order to facilitate the development of an optimum treatment plan. Patients often need to be admitted to a hospital, although in some cases treatment can be carried out at home. Supportive care can be given by administering fluids and electrolytes that helps in ensuring a rapid recovery.
A complete resolution of the condition can be expected within 10 days after the start of treatment without signs of any significant scarring. The golden appearance of colonies of some strains is the etymological root of the bacteria's name; aureus meaning "golden" in Latin. MRSA) often have only weak or no beta-hemolysis and special cultivation media with oxacillin, mannitol and NaCl for their isolation are used. He describes having a pimple-like lesion on the dorsal surface of his left hand that has now progressed with erythema surrounding the initial lesion.
The mecA gene has been identified as the gene responsible for the formation of the altered penicillin-binding protein; the mecA gene is part of a mobile genetic element known as the staphylococcal cassette chromosome mec (SCCmec) that is inserted into the staphylococcal chromosome. Preferred antimicrobials for community-acquired skin and soft tissue MRSA infections include trimethoprim-sulfamethoxazole (Bactrim, Septra), doxycycline, minocycline, clindamycin, and linezolid (Zyvox). Role of Penicillin Binding Protein in the Cross-Linking of Bacterial Cell Wall Figure 3Figure 3 - Mechanism of Action of Beta-Lactam AntimicrobialsImage B. Antibiotic resistance in Staphylococcus aureus-containing cutaneous abscesses of patients with HIV.
Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. In the past decade, medical providers in the United States have witnessed an epidemic of community-acquired methicillin-resistant Staphylococcus aureus (MRSA) infections. The skin lesions often begin as a simple pimple or boil, but then typically expand into a larger erythematous, swollen, and painful lesion (Figure 6).
Most clinicians have becomes familiar with the characteristic clinical appearance of MRSA skin abscesses. On physical examination, it may be difficult to determine whether the skin lesion requires exploratory incision and drainage. Evolution of virulence in epidemic community-associated methicillin-resistant Staphylococcus aureus. Incidence of and risk factors for clinically significant methicillin-resistant Staphylococcus aureus infection in a cohort of HIV-infected adults. Community-associated methicillin-resistant Staphylococcus aureus and HIV: intersecting epidemics. Recurrence of skin and soft tissue infection caused by methicillin-resistant Staphylococcus aureus in a HIV primary care clinic.
Staphylococcus aureus colonization in a community sample of HIV-infected and HIV-uninfected drug users. Increasing rates of community-acquired methicillin-resistant Staphylococcus aureus infections among HIV-infected persons. Emergence of multidrug-resistant, community-associated, methicillin-resistant Staphylococcus aureus clone USA300 in men who have sex with men. Risk factors for community-associated methicillin-resistant Staphylococcus aureus skin infections among HIV-positive men who have sex with men. Prevalence of and risk factors for methicillin-resistant Staphylococcus aureus (MRSA) nasal colonization in HIV-infected ambulatory patients.
The toxins adhere themselves to a molecule within desmosome known as Desmoglein 1 and thereby break it up making the skin cells unstuck. Immunocompromized individuals or people having renal failure are as a group more prone to this disorder. These are known as Nikolsky’s sign-positive and they commonly affect the patient’s flexures.
Iatrogenic injury to the skin can cause unnecessary pain and may occur when anesthetic creams are applied beneath occlusive dressings before intravenous cannulation. As this condition disturbs the thermoregulatory functions of the skin, monitoring the body temperature is essential at regular intervals.
However, the outcome is poor in adults and rests on various factors like the duration of treatment, host immunity as well as other additional comorbidities. Identification of the childcare worker, healthcare worker, visitor or parent infected or colonized with the Staphylococcus aureus bacteria is essential for the management of the problem.
The production of beta-lactamase causes resistance to penicillin, but it does not result in methicillin resistance.


These infections have been predominantly caused by the highly virulent infectious strain of S.
The center of the lesion often has a yellow or white color (Figure 7) and usually softens as abscess formation progresses; spontaneous drainage of pus may occur. Any clinician who performs an incision and drainage of a skin lesion should send the abscess material for culture; the goal is to identify the causative organism, and if S. If the benefit of incision and drainage is not clear, anesthetize a small region of the skin lesion and attempt to aspirate fluid with a 16- or 18-gauge needle attached to a syringe; obtaining purulent material would suggest proceeding to incision and drainage, whereas a "dry" aspirate indicates that incision and drainage is unlikely to yield a significant amount of purulent material. For patients with purulent cellulitis (absence of a drainable abscess), empiric antimicrobial therapy should cover MRSA until culture results are known.
In this author's opinion, clindamycin is less preferable than trimethoprim-sulfamethoxazole or a tetracycline because of the required three times daily dosing, risk of developing Clostridium difficile-associated colitis, and potential for development of inducible clindamycin resistance. The frequency and role of MRSA in nonpurulent cellulitis remains poorly define; the use of antimicrobials to treat MRSA in this setting is recommended if a patient does not respond to treatment with a beta-lactam alone and initial empiric MRSA treatment should be considered in patients with systemic toxicity.
Compared to other ethnic groups, the Caucasian people have a greater tendency to be affected by this disorder. They are proteases which cleave the desmoglein-1 that generally holds the spinosum and granulosum layers together. Hence, it is best to apply these creams beneath an appropriate non-adherent dressing that can be aided by gauze or bandage, or a cling-film wrap. The ambient temperature of the room where the patient rests should also be adjusted accordingly. Some patients present with lesions that have marked induration, erythema, and tenderness, but without a detectable soft abscess.
Patients with a nonpurulent cellulitis (and absence of an abscess) often have infection with a streptococcal species, such as Streptococcus pyogenes (group A streptococcus); since incision and drainage is not an option in nonpurulent cellulitis, antimicrobial therapy is the primary therapy. In addition, this author notes that although linezolid is a highly effective agent against MRSA, it is extremely expensive and should be reserved for patients with severe infections or those who have antimicrobial allergies that prohibit them from taking first-line agents. If the toxin is not removed by the immune system, it can circulate through the blood and infect most of the body surface.
The Staphylococcus aureus bacteria produce a poison that lead to skin damage, thereby causing blistering and scaling of the skin. Medical experts prefer an opioid infusion instead of non-steroidal anti-inflammatory drugs (NSAIDs) as the damaged skin surface is already vulnerable to bleeding.
Community-acquired MRSA infections have predominantly consisted of skin and soft tissue infections, but other clinical manifestations have included pneumonia, bacteremia, and endocarditis. Penicillin, as well as other beta-lactam antimicrobials (penicillins, cephalosporins, carbapenems, and monobactams), exert their mechanism of action by binding to the bacterial penicillin binding protein (and rendering it ineffective), thereby disrupting the penicillin binding protein's ability to cross-link the peptidoglycan components of the bacterial cell wall (Figure 3). The skin lesions can have a punched-out necrotic appearance.[8] Some patients state that they have recently suffered a "spider bite", though few have actually seen a spider. If the clinician is considering using clindamycin to treat the infection, it is important to ensure the laboratory performs a "D zone test" to rule out inducible clindamycin resistance. Some clinicians have used rifampin as adjunct therapy in this setting, but the IDSA guidelines recommend against the use of rifampin, either as a single agent or as an adjunct agent for the treatment of a MRSA abscess or cellulitis.
Emollient creams should be applied as long as the skin has healed fully, eventually feeling smooth and supple.
Among HIV-infected persons, community-acquired skin and soft tissue infections caused by MRSA have become a significant clinical problem.[2] Accordingly, the following discussion will focus on skin and soft tissue infections in HIV-infected individuals. If additional coverage for group A streptococcus is desired, the best options are to use clindamycin or linezolid alone, or to add a beta-lactam agent, such as amoxicillin (500 mg PO TID), to trimethoprim-sulfamethoxazole or a tetracycline.
Renal excretion of these exotoxins makes it vital that the patient can make the maximum use of optimum renal functions. Among HIV-infected patients with MRSA skin and soft tissue infections, fewer than 10% develop bacteremia.[2,3] The role of MRSA in cellulitis without abscess formation remains unclear, since cultures are rarely obtained in this setting. Oral antimicrobial therapy is usually sufficient in this setting, but patients with severe skin and soft tissue infections may require hospitalization and intravenous therapy; preferred options for intravenous therapy recommended in the IDSA guidelines include vancomycin, linezolid, daptomycin, and telavancin. In 1959, the anti-staphylococcal antimicrobial methicillin was introduced as an new agent to treat penicillin-resistant S. In general, decontamination strategies do not required the use of systemic antimicrobials, except in the presence of an active infection. Staphylococcal methicillin resistance resulted from the acquisition of the mecA gene, which is part of a larger mobile genetic element known as the staphylococcal chromosomal cassette (SCCmec)--a genetic element that integrates into the staphylococcal chromosome. However, there is increased risk for this complication among the elderly, small children, and people with weakened immune systems.
The mecA gene encodes for an altered penicillin binding protein known as penicillin binding protein 2a (Figure 5), which has reduced affinity for methicillin binding and thus confers resistance to methicillin and other similar beta-lactam agents. Although methicillin is no longer used, the term methicillin-resistant Staphylococcus aureus (MRSA) has persisted since methicillin was the most common anti-staphylococcal agent used when this resistance was discovered.
These bacteria have a high salt tolerance, and as such can grow in ham and other meats, as well as in dairy products. The most common causes of SFP include contaminated milk or cheeses, or through contact with food workers who carry the bacteria. Foods that required a lot of handling and that are stored at room temperature are frequently involved with this type of food poisoning, including: sandwiches puddings cold salads, such as tuna, chicken, macaroni or ham salad sliced deli meats cream-filled pastries Symptoms of Staphylococcus Aureus FoodPoisoning SFP causes symptoms similar to a severe case of gastroenteritis (inflammation of the digestive tract).
However, children, the elderly, and those with weakened immune systems may experience severe dehydration that requires treatment in a hospital.



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