SEARCH · PubMed Health

Results for “SCALDS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources

PubMed1994

[Changes in blood endotoxin levels after scald in rats].

We quantified the portal blood endotoxin level as well as the systemic blood endotoxin level after scald in rats. The results show that the portal blood endotoxin level is significantly higher than the systemic blood endotoxin level (P < 0.001) in control group. In scald group the portal blood endotoxin level shows double peaks (increase significantly at second hour, decrease to normal at sixth hour and increase significantly again at twelfth hour), but the systemic blood endotoxin level remained low (P > 0.05). The results indicate that there is some endotoxin in the portal blood in normal condition, but large amount of endotoxin escape into portal blood in normal condition, but large amount of endotoxin escape into portal blood from the intestine in early stage after scald, resulting in enterogenous endotoxemia. The origin of systemic endotoxemia is discussed in the present article.

Animals↗

PubMed1975

[The local effect of a silver chelate on standardized scald wounds of the rat].

In rat experiments a new silver chelate salt preparation is tested on scald wounds after standardized infection by Pseudomonas aeruginosa. 30% of the animals survive scalding and infection after treatment with the new cream. This percentage does not reach the gentamycin treated reference group (60%). After combining gentamycin and silver chelate salt in local therapy 75% of the animals survive. Combination of silver chelate salt and gentamycin seems to be a very successful local therapy of scald wounds.

Animals↗

PubMed1993

Abusive scald burns in infants and children: a prospective study.

Between July 1, 1987 and June 30, 1990, 30 consecutive deliberately scalded children were studied prospectively. Purposes of the study were to characterize the scald-abused child and address the management problems specific to this group. Mean age was 22.5 months. Many had preburn growth retardation. Mean burn size was 18.1 per cent of the total body surface area and 37 per cent required a surgical procedure for their scald. All 30 children had burns on the buttocks. Four (13.3%) had other injuries. Eighty per cent of patients had at least one complication. In 30 per cent, diarrhea complicated nutrition support, wound, or autograft care. Four (13.3%) patients with a mean burn size of 32.3 per cent of the total body surface area, diarrhea, and burns involving the buttocks, perineum, and external genitalia died of burn wound sepsis; three of these had Gram-positive bacteremia (Staphylococcus aureus and enterococcus). Burn wounds exposed to the fecal stream (buttocks) should be examined carefully and frequently for signs of infection, particularly in those patients with diarrhea.

Burns↗

PubMed1997

[Electrophoretic mobility and oxidizing status of rat blood erythrocytes at scald trauma].

On model of scald trauma the correlation of electrophoretic mobility of rat blood erythrocytes with intensity of lipid oxidation of erythrocyte membranes and with activity of catalase were studied. It is shown that in dynamics of scald disease development the erythrocyte mobility decreases, the velocity of oxidizing ability of their lipids increases and the protective action of blood antioxidation system is blocked. It is found that there is a close dependence between the level of oxidative processes and electrogenic properties of erythrocytes at the height of manifestation of scald toxaemia. A conclusion was made that the oppressing influence of increasing lipid oxidizing ability a on electrokinetic potential of erythrocytes is of a threshold nature and is realized through change in the membranes' state of these cells.

Animals↗

PubMed1986

Staphylococcal scalded skin syndrome in a homosexual adult.

A homosexual man developed staphylococcal scalded skin syndrome associated with a Staphylococcus aureus septicemia. We discuss the role of prednisone, renal insufficiency, and immunosuppression as predisposing factors to staphylococcal scalded skin syndrome in adults. In particular, our study of the patient's immune function revealed anergy and lymphopenia, with a reduced response to phytohemagglutinin. Studies of T cell subpopulations revealed an elevated percentage of T suppressor cells and a diminished percentage of T helper cells with a depressed T helper/T suppressor ratio. Because of those abnormalities, we suspected acquired immunodeficiency syndrome. A few months after recuperation from the acute disease, the patient has had a normalization of the T helper/T suppressor ratio, but because of persistent polyadenopathy, hypergammaglobulinemia, and a negative sensitization to keyhole-limpet hemocyanin (KLH), we now consider the patient to have an acquired immunodeficiency syndrome-related complex.

Acquired Immunodeficiency Syndrome↗

PubMed1994

Staphylococcal scalded skin syndrome in adults. A clinical review illustrated with a new case.

Staphylococcal scalded skin syndrome is rarely observed in adults; only 32 cases have been reported. In contrast to infant cases, the mortality rate is high. Two major risk factors have been identified: kidney failure and immunosuppression. In adults, clinical features are similar to those of the typical pediatric disease, but blood cultures are often positive for Staphylococcus aureus. Detection of the exfoliative toxin is required for diagnosis; the newborn mouse bioassay is, therefore, usually performed. New immunologic methods allow precise characterization of the toxins and oligonucleotide probes can be used for rapid detection of toxigenic strains. We report a case of staphylococcal scalded skin syndrome in an immunocompetent adult in whom blood cultures were positive; this is the first case in which both exfoliative toxins A and B have been identified in an adult.

Aged↗

PubMed1997

Toxin involvement in staphylococcal scalded skin syndrome.

The production of staphylococcal exfoliative toxin A (ETA) and toxin B (ETB), toxic shock syndrome toxin (TSST-1), and enterotoxins A-E was analyzed in 60 Staphylococcus aureus strains isolated from children with scalded skin syndrome (15 with generalized exfoliative syndrome, 28 with bullous impetigo, and 17 with staphylococcal scarlet fever). All strains isolated from patients with generalized exfoliative syndrome or bullous impetigo produced ETA and/or ETB and caused a Nikolsky's sign when injected subcutaneously into newborn mice. In contrast, exfoliative toxin was detected in an S. aureus strain from only one of 17 case of staphylococcal scarlet fever; the 16 other S. aureus strains produced TSST-1 and/or an enterotoxin. In conclusion, enterotoxins or TSST-1 are more frequently associated with staphylococcal scarlet fever than are exfoliative toxins. Hence staphylococcal scarlet fever may well represent an abortive form of toxic shock syndrome rather than a milder form of staphylococcal scalded skin syndrome.

Animals↗

PubMed1998

Molecular epidemiology of staphylococcal scalded skin syndrome in premature infants.

BACKGROUND: Outbreaks of nosocomial staphylococcal scalded skin syndrome (SSSS) in infants have been well-described associated with the well baby nursery or delivery room. We describe two cases of SSSS in very low birth weight infants in a neonatal intensive care unit (NICU) and the success of infection control strategies used to prevent an outbreak. METHODS: Staphylococcal scalded skin syndrome was diagnosed in two infants in the NICU: Case I (a 47-day-old, formerly 530-g female); and Case II diagnosed 48 h later (a 41-day old, formerly 706-g female). Multiple infection control measures were implemented: (1) isolation and intravenous antibiotic treatment of cases; (2) placement of exposed infants into a cohort; (3) prophylactic mupirocin treatment of the anterior nares of all infants in the NICU and staff colonized with Staphylococcus aureus; and (4) personnel hand washing with hexachlorophene. Detection of exfoliative toxin A and studies to determine the genetic relatedness of S. aureus strains isolated from patients and staff were performed. RESULTS: In addition to the two SSSS cases, S. aureus was isolated from 2 of 12 (17%) exposed asymptomatic infants, 2 of 20 (10%) ancillary staff, 8 of 30 (27%) nurses and 6 of 24 (25%) physicians. Exfoliative toxin A-producing strains were isolated from both cases and one asymptomatic infant. No toxin was expressed by strains isolated from staff. Pulse field gel electrophoresis demonstrated genetically identical strains of S. aureus from the two SSSS cases and the asymptomatic infant, whereas three staff members harbored strains genetically related to the case strain. Unexpectedly two additional unique clusters of genetically related S. aureus strains were identified from the surveillance cultures. CONCLUSIONS: This report documents the rare occurrence of nosocomial SSSS attributed to transmission in the NICU among extremely low birth weight infants. Multiple infection control strategies were effective in limiting the outbreak. Molecular epidemiology investigation supported a unique S. aureus strain responsible for this event and the presence of bidirectional spread between staff and patients of non-toxin-producing strains.

Cross Infection↗

PubMed2001

Development and evaluation of detection systems for staphylococcal exfoliative toxin A responsible for scalded-skin syndrome.

Staphylococcal scalded-skin syndrome is usually diagnosed clinically by its characteristic exfoliating rash. Isolation of Staphylococcus aureus from the patient further supports the diagnosis. Several detection systems have been developed to determine whether the isolated strain produces exfoliative toxin, but none are routinely available in hospital laboratories. In a novel approach, we used computer models to predict the structure of the exfoliative toxins based on other serine proteases and to identify surface epitopes for the production of antibodies that specifically bound the exfoliative toxin A (ETA) serotype. Several rapid immunologically based diagnostic tests for ETA were developed with these antibodies and compared with existing systems. Our results showed that Western blot analysis using these antibodies was in complete correlation with PCR, which has been validated against the "gold standard" mouse model. On the other hand, the double-antibody enzyme-linked immunosorbent assay (ELISA) and Ouchterlony immunodiffusion assay gave unacceptably high false-positive results due to interference by staphylococcal protein A. This problem was successfully overcome by the development of a F(ab')(2) fragment ELISA, which was rapid and reproducible and was as sensitive and specific as PCR and Western blot analysis. The F(ab')(2) fragment ELISA is superior to existing diagnostic systems because it is quantitative, which may be related to the severity of the condition, and can detect amounts of exfoliative toxin in the picogram range directly from serum. This is the first detection system with the potential to confirm the diagnosis of staphylococcal scalded-skin syndrome from a routine blood test within 3 h of presentation.

Animals↗

PubMedDate not supplied

Staphyloccocal scalded skin syndrome in an adult.

We report a case of staphyloccocal scalded skin syndrome due to an oxacillin-susceptible Staphylococcus aureus in an 81-year-old woman. The patient was admitted to the emergency room with arthritis of the left shoulder, ten days after an intra-articular injection of corticosteroids. The shoulder's puncture showed a purulent liquid and gram positive cocci in cluster suggesting the presence of Staphylococcus sp. on the Gram-stain. The culture confirmed the identification of an oxacillin-susceptible Staphylococcus aureus. Before administration of any dose of oxacillin, blisters appeared on the skin, that quickly ruptured, particulary in areas of friction. The exfoliated areas were extensive and resolution of all the lesions was reached after 3 weeks. The skin biopsy showed superficial epidermolysis confirming the diagnosis. Staphyloccocal scalded skin syndrome is usually described in neonates and young children, often in outbreaks. Few cases have been reported in adults, most often associated with severe underlying diseases. The mortality rate is low in children but can reach almost 60% in adults. The most important diagnosis to exclude is Lyell's syndrome which can be done by the skin biopsy.

Aged↗

PubMed2003

Staphylococcal scalded skin syndrome in two very low birth weight infants.

Two premature infants with very low birth weight were diagnosed with staphylococcal scalded skin syndrome (SSSS) during hospitalization in the neonatal intensive care unit. This syndrome which is rare in premature infants, is characterized by blistering and superficial desquamation of the skin and is caused by two epidermolytic toxins (ETA and ETB) produced by Staphylococcus aureus. Staphylococcal scalded skin syndrome usually occurs in young children probably because of inefficient clearance of the epidermolytic toxins from the bloodstream, which causes dysfunction of cell adhesion in the superficial epidermis. Early diagnosis and early treatment with parenterally administered beta-lactamase resistant penicillins are important to prevent life threatening complications of this syndrome.

Birth Weight↗

PubMed2003

Staphylococcal scalded skin syndrome: diagnosis and management.

Staphylococcal scalded skin syndrome (SSSS) is a common disorder that is usually seen in infants and children and rarely seen in adults. SSSS usually presents with a prodrome of sore throat or conjunctivitis. Extremely tender flaccid bullae, which are Nikolsky sign-positive, develop within 48 hours and commonly affect the flexures; occasionally, large areas of the skin may be involved. The bullae enlarge and rupture easily to reveal a moist erythematous base, which gives rise to the scalded appearance. SSSS in adults is a rare disorder, though there are now over 50 documented cases. Usually SSSS occurs in predisposed individuals, but not all adults have an underlying illness. Whereas mortality in childhood SSSS is approximately 4%, the mortality rate in adults is reported to be greater than 60%. SSSS is caused by an infection with a particular strain of Staphylococcus aureus, which leads to blistering of the upper layer of the skin, by the release of a circulating exotoxin. It has recently been demonstrated that the exfoliative exotoxin responsible for SSSS leads to the cleavage of desmoglein 1 complex, an important desmosomal protein. The same toxins that are responsible for causing SSSS also cause bullous impetigo. There appears to be a relationship between the disease extent, the amount of toxin produced and whether the toxin is released locally or systemically. As a result there is likely to be a spectrum of disease and there are likely to be a number of milder cases of adult SSSS that go undiagnosed. Social improvements and hygiene have led to a dramatic fall in the number of cases of SSSS. Treatment is usually straightforward, when there is no coexistent morbidity and the presentation is mild, but can be demanding if the patient is particularly ill. SSSS is still associated with mortality, particularly when it occurs in adults.

Biopsy, Needle↗

PubMed1991

Staphylococcal scalded skin syndrome.

Staphylococcal scalded skin syndrome is a rarely reported superficial desquamating eruption found in patients who have otherwise toxic conditions. Its early recognition and treatment can be lifesaving. A case of staphylococcal scalded skin syndrome is reported in a patient with chronic liver failure.

Adult↗

PubMed1997

Recurrent staphylococcal scalded skin syndrome in children: report of two cases.

A localised "scalded skin syndrome" occurred in two male siblings aged five and ten years old, in Morogoro, Tanzania. This condition recurred in the same children within a period of about 12 months. A haemolytic ampicillin resistant Staphylococcus aureus was isolated from the bullous material, suggesting that the condition was staphylococcal scalded skin syndrome (SSSS). This implies that the bacterial isolate was an exfoliative toxin (ET) producing S. aureus. This infection was, however, striking because SSSS occurs mostly in newborns, and it is rarely recurrent. It is possible that a new strain with particular adaptability, or an inherent susceptibility to the S. aureus of the affected children was the cause of this recurrency.

Administration, Cutaneous↗

PubMed1976

Nursery outbreak of scalded-skin syndrome. Scarlatiniform rash due to phage group I Staphylococcus aureus.

From Aug 6 to 14, 1973, scariatiniform eruptions that were considered to be mild forms of the staphylococcal scalded-skin syndrome developed in four neonates. One infant had mild epidermal peeling. All had generalized, finely papular erythema that cleared rapidly after treatment with antibiotics. Cultures from the umbilical stumps or anterior nares of three of the infants yielded colonies of group I Staphylococcus aureus, phage type 29/52/79/86/D11/81, that were able to produce epidermal exfoliation in suckling mice. These data indicate that the nursery outbreak was caused by phage group I staphylococci rather than group II organisms previously associated with staphylococcal scalded-skin syndrome. The demonstration that a group I Staphylococcus can produce exfoliative toxin suggests that the same mechanism for toxin production may exist for phage groups I and II staphylococci.

Cross Infection↗

PubMed1998

A standardized model of partial thickness scald burns in mice.

BACKGROUND: Large mammal partial thickness wound models were developed primarily for their anatomical similarity to human wounds, yet lack the economy, ease of handling, and statistical power afforded with rodent models. Previous small mammal models of partial thickness burn injury have failed to demonstrate complete reepithelialization in less than 3 weeks. We present a murine partial thickness scald model with a reepithelialization rate comparable to that of porcine wound models. METHODS: Thirty-eight adult male mice were secured in a burn template allowing exposure of a 2 x 3-cm area of the shaved dorsum to 60 degreesC water for 45 s, followed by 4 degreesC water for 45 s. Four wounds were harvested daily on Postburn Days 1-7, 10, and 14 for histologic evaluation. RESULTS: Histologic evidence of partial thickness dermal injury with sparing of dermal appendage epithelial cells was seen in all wounds. Of 134 wound sections evaluated 26 contained some areas of full thickness dermal injury, with only 8 of these 26 sections showing full thickness injury in 50% or more of the cross-sectional area of the wounds. Complete wound reepithelialization was seen between Postburn Days 10 and 14. The viable dermal thickness in all burn cross sections was at least 40-80 micrometers, and up to 1400 micrometers in reepithelialized wounds. CONCLUSIONS: This murine model of partial thickness scald injury provides a standardized thermal wound with consistent depth of injury, low mortality, and a reepithelialization rate between 10 and 14 days. A simple protocol allows easy production of 30-50 wounds daily with one technician.

Animals↗

PubMed1975

The staphylococcal scalded-skin syndrome versus erythema multiforme.

This article reports a case of scalded-skin syndrome in a young child. Characterized by a generalized exfoliative dermatitis resembling scalded skin, the disease may involve the oral mucosa and must be differentiated from Stevens-Johnson syndrome (erythema multiforme). Since the etiology is specific, the disease can be treated with antibiotics with dramatic results.

Administration, Oral↗

PubMed1985

The effect of different cooling temperatures and immersion fluids on post-burn oedema and survival of the partially scalded hairy mouse ear.

One ear of NMRI hairy mice was first scalded and then immediately immersed in cold water or saline at 8 degrees C, 15 degrees C, 20 degrees C, 25 degrees C or 30 degrees C for a period of 30 min in order to study oedema formation and the therapeutic effect at 4 days. Oedema was determined by wet-dry weight measurements of punch biopsies from the ear and expressed as an increase in tissue water content. The therapeutic effects at 4 days were determined by observing the survival of the ear; the area of necrosis was expressed in per cent of the total area of the ear. Significant oedema was found in all scalded ears. A partial (15 per cent) dry necrosis of the untreated burned ear had developed within 4 days. Cooling in 8 degrees C water or saline for 30 min post-burn significantly reduced oedema in this model as determined 2h post-burn. However, 4 days post-burn all cooled ears showed a 15 per cent necrosis.

Animals↗