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PubMed1988

Detection of staphylococcal exfoliative toxin by slide latex agglutination.

A simple and rapid method in which slide latex agglutination was used was developed to detect the exfoliative toxin (ET) elaborated by clinical isolates. ET types A and B (ET-A and ET-B) were purified by plate gel isoelectrofocusing, and anti-ET sera were obtained by immunizing rabbits. A specific immunoglobulin G antitoxin was then prepared from the immunized rabbit sera by fast protein liquid chromatography, and latex particles were coated with the antitoxin. Of 74 staphylococcal strains isolated from patients with staphylococcal scalded skin syndrome, 61 strains were found to produce ET by the newborn mouse bioassay. All 61 strains were shown to be positive for ET-A and ET-B production by the slide latex agglutination method. The lowest concentration of ETs detected by the latex agglutination method was 0.5 microgram/ml, which was much lower than that detected by the double immunodiffusion method, with a sensitivity of 50 micrograms/ml. It is crucial to prove ET production by clinical isolates for the diagnosis and surveillance of staphylococcal scalded skin syndrome. The latex agglutination method is a sensitive, simple, and rapid test which can be used as an alternative to the newborn mouse bioassay.

Animals↗
PubMedDate not supplied

An inhibitor of Staphylococcus aureus exfoliative toxin.

We describe here an inhibitor of Staphylococcus aureus exfoliative toxin. The toxin was extracted from an S. aureus strain isolated from a case of staphylococcus scalded skin syndrome. The activity of the toxin was compared in tryptic soy broth and brain heart infusion broth. Both supported growth of S. aureus but the culture filtrate of brain heart infusion broth lacked exfoliative toxin activity. Furthermore it appeared to contain a substance that neutralized the action of exfoliative toxin. This suggests the possibility of a treatment for staphylococcal scalded skin syndrome and bullous impetigo.

Animals↗
PubMed1990

The causes, cost, and prevention of childhood burn injuries.

In 1985, fire and/or burn injuries killed 1461 children aged 0 to 19 years in the United States; an estimated 23,638 children were hospitalized and 440,000 were treated for burns. More than 101,000 life years were lost. A "cost of burn injury" model suggests a dollar value of societal losses from childhood burn deaths and injuries at approximately $3.5 billion. Very young children (0 to 4 years) dying in house fires accounted for 47% of these deaths. Preventing fire deaths through residential sprinklers, smoke detectors, fire-safe cigarettes, and child-resistant lighters would prevent more than three quarters of all childhood fire/burn deaths. While interventions exist for tap water scalds, solutions to the problems of "kitchen" scald and gasoline-involved flame burns are less apparent.

Accident Prevention↗
PubMed1993

Impact of exogenous insulinlike growth factor 1 on hepatic energy metabolism in burn injury.

BACKGROUND: Insulinlike growth factor 1 (IGF-1) has previously been demonstrated to improve the nutritional status of burned animals. The method by which it achieves this result has not yet been fully elucidated, but may be the result of alterations in hepatic metabolism. OBJECTIVE: To determine if IGF-1 is able to correct the burn-induced impairments in hepatic metabolic function. DESIGN: Seventy-two Sprague-Dawley rats were subjected to a sham burn (n = 24), or a 50% total body surface area scald burn (n = 48). Half the scald burn group received 3 micrograms/kg per day of IGF-1. The remainder received a placebo. The rats were sequentially assayed for multiple components of hepatic function. RESULTS: Insulinlike growth factor 1 corrected the burn-induced decrease in hepatic adenosine triphosphate concentration and prevented the burn-induced increase in hepatic ketone body levels. Insulinlike growth factor 1 was also able to prevent the burn-induced decrease in the hepatic acetoacetate-beta-hydroxybutyrate ratio. Since this ratio is directly proportional to mitochondrial redox potential this indicates that IGF-1 is also able to prevent the burn-induced impairment in hepatic redox potential. CONCLUSIONS: These data indicate that part of the previously demonstrated beneficial effect of IGF-1 in burn injury may be due to its ability to improve multiple components of hepatic metabolism.

Adenosine Triphosphate↗
PubMed1978

H2-receptors and traumatic oedema.

The effects of the H2-antagonists, metiamide and cimetidine, on the oedema following limb ischaemia or scald have been investigated in two strains of rat. No inhibition of oedema formation was found except when large doses of cimetidine were given before scalding. This effect was attributed to the fall in body temperature. Our results do not support the view that H2-receptors are concerned in the vascular response to injury.

Animals↗
PubMed2001

Effect of varying burn sizes and ambient temperature on the hypermetabolic rate in thermally injured rats.

BACKGROUND: Small animals with scald covering 50% of their total body surface area (TBSA) have been used to study the hypermetabolic burn response. In the 50% TBSA burn rat model, the area of normal skin that is available for animal instrumentation is restricted and the mortality rate has been high. The purpose of this study was to determine whether a smaller burn size can induce a similar hypermetabolic response with mortality rates lower than those of the 50% TBSA model. METHODS: Rats were randomly divided into four groups to receive a 0% (sham nonburned), 30%, 40%, or 50% TBSA third-degree scald burn. The hypermetabolic response was determined by measuring changes in body weight and oxygen consumption at ambient temperatures of 21, 26, and 31 degrees C for each burn size. Weight measurements were made daily while oxygen consumption was measured 7, 11, and 14 days after thermal injury. RESULTS: All thermally injured rats lost body weight; however, there were no significant differences between the 30, 40, and 50% TBSA burn groups. Burn induced a hypermetabolic response as indicated by an increase in oxygen consumption from 130 to 200% that of sham nonburned rats. No significant difference in oxygen consumption could be shown over the study period between the three burn sizes at different ambient temperatures. Mortality was 0% in the sham and 30% group, 10% for the 40% group, and 50% for the 50% TBSA burn group. CONCLUSIONS: From our study we conclude that a burn size covering 30% of the TBSA induces the same hypermetabolic response as a 50% TBSA burn.

Animals↗
PubMed1978

Heat injuries to the respiratory system.

A steam-tube of the main boiler exploded on a ship lying in the harbour of Hamburg. The steam temperature was 283 degrees C. Cutaneous and severe inhalational scalding occured in the 27 fatalities, the men dying after different intervals. This paper deals with the pathological findings in the respiratory passages and the lung, describing the topographical extent of direct thermal injury and the temporal course of tissue reactions. In cases of instantaneous death coagulation necrosis of the tracheal and bronchial wall was found to extend to alveolar ducts in central parts of the lung. The lung parenchyma showed marked congestion, alveolar edema and desquamation of alveolar epithelial cells. Death occured due to acute pulmonary dysfunction and shock. Lethal complications following the period of primary shock consisted of fulminant confluent bronchopneumonia, the hyaline membrane syndrome or the onset of desquamative interstitial pneumonia. These changes rendered it difficult to evaluate the effects of the heavy cutaneous scalding on the pathological course of inhalational injuries in those surviving for longer periods.

Adult↗
PubMed1977

The effect of thermal injury on plasma carnitine in rats.

The plasma concentration of L-carnitine in scalded rats was determined to be greater (p less than or equal to 0.05) than that of control rats at 6 h following the administration of a 20% body surface, full-thickness burn produced by scalding in a 100 degrees C water bath for 15 sec.

Animals↗
PubMed1987

Acute epidermal necrolysis or Lyell syndrome.

Acute epidermal necrolysis may be caused by staphylococcal toxins (staphylococcal scalded skin syndrome and toxic shock syndrome) or may be related to usually drug-induced hyper-sensitivity mechanisms (toxic epidermal necrolysis). Diagnostic certainty can only be obtained by histologic localisation of a cleavage plane which is intraepidermal in staphylococcal scalded skin syndrome but situated at the dermo-epidermal junction in toxic epidermal necrolysis. Steroid therapy is indicated in toxic epidermal syndrome. This report of two cases of acute epidermal necrolysis emphasizes the importance of an early skin biopsy for accurate diagnosis and appropriate treatment.

Child↗
PubMed2006

Associations between DNA markers and resistance to diseases in sugarcane and effects of population substructure.

Association between markers and sugarcane diseases were investigated in a collection of 154 sugarcane clones, consisting of important ancestors or parents, and cultivars. 1,068 polymorphic AFLP and 141 SRR markers were scored across all clones. Data on the four most important diseases in the Australian sugarcane industry were obtained; these diseases being pachymetra root rot (Pachymetra chaunorhiza B.J. Croft & M.W. Dick), leaf scald (Xanthomonas albilineans Dowson), Fiji leaf gall (Fiji disease virus), and smut (Ustilago scitaminea H. & P. Sydow). By a simple regression analysis, association between markers and diseases could be readily detected. However, many of these associations were due to the effects of embedded population structure and random effects. After taking population structure into account, we found that 59% of the phenotypic variation in smut resistance ratings could be accounted for by 11 markers, 32% of variation for leaf scald and pachymetra root rot rating by 4 markers, and 26% of Fiji leaf gall by 5 markers. The results suggest that marker-trait associations can be readily detected in populations generated from modern sugarcane breeding programs. This may be due to special features of past sugarcane breeding programs leading to persistent linkage disequilibrium in modern parental populations.

Genetic Linkage↗
PubMed1986

Hepatic and skeletal muscle phospholipid metabolism in recovering burned rats.

Liver and soleus muscles of control animals and rats recovering from a single hindlimb scald were analyzed for diphosphatidyl glycerol, phosphatidyl ethanolamine, phosphatidyl choline, sphingomyelin, lysophosphatidyl choline, phosphatidyl inositol, and phosphatidyl serine. Liver of 4-hr postburn rats exhibited decreased contents of diphosphatidyl glycerol (-20%), phosphatidyl ethanolamine (-11%), and phosphatidyl choline (-7%). At 3 days after the burn, only an 11% decrease in hepatic phosphatidyl inositol was observed. Soleus muscle of the unburned limb of burned rats showed at 3 days postburn an 11% decrease in sphingomyelin content but the other measured phospholipids were at control level. In contrast, soleus muscle from the contralateral burned limb exhibited increased contents of sphingomyelin (+29%), lysophosphatidyl choline (+145%), and phosphatidyl serine (+27%) compared to control uninjured animals. It also showed a 25% higher phosphatidyl inositol level than the contralateral uninjured counterpart. It is concluded that recovery from a single hindlimb scald is associated with alterations in phospholipid metabolism in the liver and in the region of the wound. The local response to thermal injury may be mediated, in part, by stimulated activity of phospholipase A2.

Animals↗
PubMed1992

Alterations in levels of plasma phenylalanine and its catabolism in the liver of stressed rats.

This study examined the relationship between elevation of blood phenylalanine (Phe) concentrations often observed in trauma or infected patients without hepatic dysfunction and alterations of liver Phe catabolism. Rats underwent pathophysiologically different stresses, either sepsis or scald injury. The catalytic activity of hepatic Phe hydroxylase (PH) in the septic rats, as measured after preincubation with Phe, decreased to 60% of the control values; this in vitro result suggests a reduction of enzyme species activated by its substrate. Phe was degraded in the septic rats to a similar extent to that in controls, when measured by pulse administration of [1-14C]-Phe. In the scalded rats whose plasma Phe level showed a comparable but transient increase, no significant alterations occurred in Phe catabolism and enzyme activities. The changes in plasma glucagon and catecholamine levels were consistent with those of the enzyme activities involved in Phe and tyrosine (Tyr) catabolism in the stressed groups. These results indicate that inadequate activation of native PH by regulatory mechanisms involving Phe in vivo was also associated with the accumulation of plasma Phe in infected rats during massive mobilization of amino acids from muscles under conditions of enhanced and sustained catabolism.

Animals↗
PubMed1982

Burn toxin and its competitin.

A "toxic factor' has been isolated and purified from scalded normal human skin; it is lethal to mice and toxic to HeLa and HEP2 cell lines in tissue culture. The toxic factor in both crude and purified form is antigenic in rabbits, producing an antisera that neutralizes the in vivo and in vitro effects of "burn toxin', similar to that of the convalescent sera of burned human subjects. The sonicate of the toxic glycoprotein named competitin is relatively non-lethal and protects against the lethal effect of the toxic factor. The action of the purified burn toxic factor and its competitin is at the ATP site of actomyosin preparations. The data presented suggests that the purified burn toxic factor and its competitin compete for the same receptor sites in the myocardium. A thesis is presented that states that it is vital to neutralize the toxic effects of burn breakdown tissue products in severely burned subjects before the vicious cycle of depressed immunological function and malnutrition ensues. Competitin produced in vitro from toxic factor(s) generated scalded normal human skin is offered as a means of neutralizing the toxic factors(s).

Actomyosin↗
PubMed1987

Experimental study on topical antimicrobial agents in burns.

Numerous organic silver salts have been tested against a virulent strain of Pseudomonas aeruginosa which had been deliberately applied to the scalded tails of mice and deeper scald wounds on the backs of rabbits. Silver pipemidate was found to be more effective than silver sulphadiazine in treating these infected wounds.

Administration, Topical↗
PubMed1987

Epidemiology of adults' and childrens' burns in a Turkish burn center.

From 1 January 1979 to 1 January 1985, 4094 patients were treated for burn injury in our centre. Of these, 84.9 per cent were treated as outpatients and 617 (15.1 per cent) were hospitalized. Of the 617 patients, 56.7 per cent were under 15 years of age (birth to 6 years: 67.7 per cent; 7-15 years, 32.3 per cent) and 43.3 per cent were over 15 years. The causes of burns in the over 15 years group were: flame, 36.3 per cent; electrical, 28.0 per cent; scalding, 18.4 per cent; liquefied petroleum (LP) gas explosion, 11.0 per cent; and others, 6.3 per cent. The burn cases in the under 15 years group were: scalding, 58.0 per cent; flame, 24.6 per cent; electrical, 10.0 per cent; hot meals, 5.2 per cent; and others, 2.0 per cent. After being resuscitated, these patients were treated with systemic antibiotics, local chemotherapy and silver-nitrate-incorporated amniotic membrane. Despite all medical efforts, 217 (35.7 per cent) of the hospitalized patients died as a result of various complications. At the same time, 3477 patients were treated as outpatients: 72.0 per cent of these were under 15 years old (birth to 6 years, 82.9 per cent, 7-15 years, 18.8 per cent) and 28.0 per cent patients were over 15 years of age. The causes of burn injury in these patients were: hot liquids, 61.7 per cent; flame, 17.0 per cent; hot meals, 8.4 per cent; hot metal, 5.8 per cent; electrical, 3.6 per cent; and chemical, 1.7 per cent.

Adolescent↗
PubMed1987

Burns: epidemiology and the effect of a prevention programme.

Epidemiological data concerning 1391 patients hospitalized at the Burns Unit, Odense University Hospital during a 17-year period are presented. The annual incidence showed a steady downward trend of 3 per cent per year. Scald and fire were the most important causes of burn injuries. Among children a significant reduction in burns due to scalds and electrical or corrosive injuries was noted. The rate of injury among adults and the elderly was constant. These results might reflect an intensive information campaign in the media, revisions of laws and regulations and improvements in the safety of household products, especially directed towards thermal injuries among smaller children.

Adolescent↗
PubMed1987

Hand burns in children under 5 years of age.

In order to evaluate the epidemiology and functional results of hand burns in young children, 92 consecutive patients (126 hand burns) under age 5 years admitted to a Burn Center were reviewed. Scald burns (49 per cent) were most common, followed by flame (34 per cent), contact (14 per cent) and electrical burns (3 per cent). The child was left unattended by an adult in 53 per cent of cases and documented abuse was present in 6 per cent. The mean total body surface area (TBSA) burned was 17 per cent, and 77 patients (85 per cent) had additional burns in other areas (arms 34 per cent, legs 31 per cent, chest 29 per cent and face 27 per cent). Palmar burns occurred in 24 hands (19 per cent), dorsal in 41 (33 per cent), while both surfaces were burned in 61 (48 per cent). Joints involved included the MP in 96 (76 per cent), PIP in 87 (69 per cent) and DIP in 80 (63 per cent). The depth was superficial partial thickness in 53 (47 per cent), deep partial in 55 (44 per cent), and full thickness in 18 hands (14 per cent); a total of 29 hands were grafted (15 deep partial and 14 full thickness). Escharotomies were required in 12 hands (9 per cent) (9 flame and 3 scald) and partial amputation of digits was required in 3 (2 per cent). Follow-up was available in 46 hands from 7 to 120 months (mean 39 months). Partial thickness burns (34) healed with normal (32) or near-normal (2) hand function and developmental delay occurred in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Burn Units↗
PubMed1988

Burns in adults in Zaria, Nigeria.

From 1971 to 1981, 245 adults with burn injuries were admitted to the Ahmadu Bello University Hospital, Zaria. The burns were major in 197 patients, moderate in 28 and minor in 20. Socioeconomic factors contributing to the injuries included the use of wood fires for cooking, for warming the body and the dwelling during the cool harmattan season, loose indigenous garments, thatch-roofed huts, petrol hoarding and epileptic seizures. Flame burns exceeded scalds with a high seasonal frequency in both men and women during the harmattan. Scalds occurred predominantly among the women, puerperal hot baths being a major cause. The overall mortality rate of 22 per cent is excessive. General economic development, architectural improvements, proper handling of petrol and kerosene, modification or abandonment of the puerperal ritual of hot baths, the maintenance of chronic epileptics on anticonvulsants and a programme of universal active immunization against tetanus would contribute to the prevention of burns and complications in adults and decrease the mortality rate.

Adolescent↗