Burns (1991) 17, (4), 309-312
Printed in Greut Britain
Microbiological Hospital, UK
309
aspects of burns at Mount Vernon
L. S. Nakhla’ and R. Sanders2 ‘Department
of Microbiology
and ‘Regional Plastic and Bums Unit, Mount Vernon Hospital, Northwood,
Bactetial infection in 100 burned patienfs over a IO-monfh period has been studied. The commonesf colonizing organism was Staph. aureus (69 per cent), followed by E. coli (35 per cent). Pseud. aeruginosa accounted for only 28 per cenf of isolates. The role of the different bacterial species in burns pathology is discussed. Group G haemolytic streptococci were isolated from 10 per cent of patients and causedgruff failure in some cases. Only 3 per cent of pafients developed septicamiaand all were due to Staph. aureus. Our approach to munagement of infection in burns, especially the policy on systemic antimicrobial chemotherapy, is desm’bed
Introduction Infection is one of the major causes of increased morbidity and mortality in patients with severe bums. Surgeons have known for a long time that patients with severe burns who survived the early phase of hypovolaemic ‘shock’ were apt to develop fatal septic complications. The first line of defence against contamination of the bum consists of topical applications of antimicrobial agents, patient isolation and other methods of preventing cross-infection including the use of occlusive dressings, excision and grafting and the production of a dry eschar. The second line of defence against invasion of tissues and bloodstream from already infected bums consists of selective chemotherapy, immunoprophylaxis and various methods of supporting the natural defences, e.g. control of diabetes and maintenance of nutrition and other physiological norms. Bacteriology of burns The nature of bums which, by definition, contain devitalized tissues, makes these injuries more susceptible to bacterial colonization than most other types of wounds. The moist dead tissue within the bum, together with the surrounding damaged and oedematous tissues, provide a nutrient medium which will support the growth of a variety of bacterial species. In a certain proportion of bums such colonization is a prelude to septicaemia and death.
Methods The standard practice at Mount Vernon Bums Unit is to take bacteriological swabs from wounds and natural carriage 80 1991 Butterworth-Heinemann 0305-4179/91/040309-04
Ltd
Middlesex,
UK
sites (nose, throat and rectum) on admission as a baseline. Swabs from wound sites are repeated at each change of dressing until wound closure has been achieved.
Results Analysis of bacteriological swabs taken from 100 patients admitted to the Unit over a period of 10 months (November 1987 to August 1988) revealed the incidence of different bacteria isolated per patient (T&/e I). The most common organism isolated was Staph. aureus (69 per cent) followed by E. coli and coliforms (35 per cent each). Pselld. ueruginosu was isolated from only 28 per cent of patients. There has been a progressive decline of Psettd. aeruginasa and other Gram-negative bacilli following the introduction of topical silver nitrate in 1964 (Lowbury, 1979) and other effective prophylactic antimicrobial agents such as silver sulphadiazine in 1970 (Babb et al., 1977). A similar pattern of bacterial populations in burned patients has been reported by Lawrence (1985) (Table II).
Discussion Fresh bums are usually sterile but progressively become colonized with one or more bacterial species as the patient’s stay in bum units increases. The mean acquisition time varies from one species of bacteria to another and depends on the extent of the bum. In non-extensive bums it varies from 3.4 days for Sfuapk. uureus to 15.4 days for Klebsiella species: and in extensive bums from 4.3 days for Staph. uureus to 36.0 days for Strep. pyogenes Group A (Lawrence, 1985). The role of the different bacterial species in burns pathology varies from mere colonization, local tissue sepsis and interference with healing and grafting, to invasion of the bloodstream with subsequent septicaemia and death. Sfupk. uureus causes local suppuration and produces alpha toxin (a haemolysin) which rapidly kills skin (Lawrence, 1959). Occasionally it invades the bloodstream and causes septicaemia or produces toxins which cause the toxic shock syndrome. Most staphylococci in our unit are fully sensitive to antibiotics or resistant only to pencillin. From time to time patients are admitted to our unit - usually referred from
Bums (1991) Vol. 17/No. 4
310
Table I, Potentially pathogenic bacteria isolated from 100 patients at Mount Vernon Hospital - 198711988
Table II. Potentially pathogenic bacteria isolated from bum wound swabs during 1983 (from Lawrence, 1985)
Patients Bacterial species
(%)
Staph. aureus Staph. aureus (EMRSA’) Haemolytic streptococci Haemolytic streptococci Haemolytic streptococci Haemolytic streptococci Haemolytic streptococci Haemolytic streptococci Faecal streptococci E. coli
69 12 6 5 2 2 1 10 13 35
Group Group Group Group Group Group
A B C D F G
Klebsiella spp. Proteusspp. Acinetobacter anitratus Other coliform bacilli Ps. aeruginosa Bacreriodes fragilis Bacteriodes melaninogenicus Clostridium perfringens (Welchii) ‘EMRSA,
epidemic methicillin
24 14 21 35 28 1 1 1
resistant Staph. aureus.
other centres - already colonized with the ‘Epidemic Methicillin Resistant Staph. at(reus (EMRSA)‘. These patients are often suffering from extensive bums, are heavily colonized with EMRSA and inevitably spread this infection to other patients in the unit. In the IO-month period of our survey 12 per cent of patients were colonized with this organism. A marked increase in the number of outbreaks of hospital infection due to EMRSA has been reported in Britain, Eire, the USA, Australia and South Africa over the last 8 years (McDonald et al., 1981; Boyce and Causey, 1982; Editorial 1983; Keane and Cafferkey, 1984; Shanson et al., 1985). A notable feature of these strains is the ease with which they spread, hence the terminology ‘Epidemic Methicillin Resistant S&h. aureu.4. These epidemic strains are resistant to many other antibiotics and effective treatment of serious infections has often proved difficult. The antimicrobial agents available against EMRSA are often potentially toxic, limited in number, difficult to administer and expensive. There are also uncertainties in the efficiency of topical antibiotic and antiseptic preparations, although preliminary results with mupirocin (pseudomonic acid) seem to be promising (Casewell and Hill, 1985). Immunocompromised debilitated patients or those with open wounds (as in bums), are particularly at risk from infection with these strains. Psed. aeruginosa delays wound healing and the pigment is toxic to tissues (Lawrence, 1983). Strep. pyogenes of Group A prevents graft ‘take’ (Jackson et al., 1951) and streptococcal haemolysins also kill skin (Lawrence, 1959). The role of other haemolytic streptococci in bums with respect to tissue damage is debatable. Recently there has been an increasing awareness of the effect of Group G streptcocci which was isolated from 10 per cent of our patients. The impression in our patients and that of others (Wilson et al., 1988) is that it is potentially damaging to grafts. Acinetobucteranifrdus is a non-motile, non-fermentative Gram-negative coccobacillus with soil or water as its natural habitat (Henrikson, 1973). It has also been isolated from
Isolates (%)
Species Staph. aureus Ps. aeruginosa Strep. pyogenes Group A Escherichia coli Klebsiella spp. Proteus spp. Acinetobacter anirratus Clostridium perfringens
All burns
Nonextensive burns
Extensive burns
63 32
60 25
74 59
3.7 28 11 19
4.4 20 8 8
1.3 55 22 22
24
18
47
17
12
32
human skin (Al-Khoja and Darrell, 1979). Laboratory isolates from clinical specimens usually reflect colonization rather than infection (Rosenthal and Freundlich, 1977) but serious, sometimes fatal, opportunistic infections have been reported, including septicaemia, endocartitis, meningitis and pneumonia (Glew et al., 1977; Ramphael and Kluge, 197% Retailliau et al., 1979). Increased colonization and infection of hospital patients with this organism has sometimes been reported as epidemic spread (Buxton et al., 1978). In our Bums Unit we have had outbreaks of infection with acinetobacter. In the great majority of patients it was a mere colonization, but in debilitated patients with extensive bums it has caused septicaemia with pneumonia. In the period of the IO-month study reported here this organism was isolated from 21 per cent of patients. Although infection in burns is usually silent (Sevitt, 1976), septicaemic episodes can occur at any time during the treatment of burned patients (Cason,l981); it is considered pertinent to take blood cultures from such patients. The criteria include patients with body temperatures over 39”C, or a lowered blood pressure and high pulse rate. Septicaemia should also be suspected if the patient is disorientated, or the urinary sodium/potassium ratio is reversed. The incidence of positive blood cultures is low -about 10 per cent (Lawrence, 1985). In our 100 patients it was 3 per cent, all due to Stg$. uureus; one was fully sensitive to antibiotics, one was resistant to pencillin only, and a third was an EMRSA (transferred from another unit), consequently antibacterial therapy usually has to be guided by the wound flora. Blood culture results must be interpreted with caution and correlated with the clinical state of the patient. This ensures that the organisms grown are not attributed to septacaemia when in fact they are derived from the surface of the bum skin as a result of inadequate sterilization of the site from which blood samples are taken.
Antimicrobial therapy Invasive infection still occurs in approximately 25 per cent of patients with major bums, although the last 20 years has seen a significant fall in associated mortality from over 60 per cent of those with infective complications in 1965 to about 10 per cent now (MacMillan, 1975; Wilkins and Bennett, 1980). The improved prognosis of these patients may be attributed not only to better use of more potent
Nakhla and Sanders: Microbiological
311
aspects of bums
Certain antibiotics, e.g. aminoglycosides (gentamicin, tobramycin, amikacin, vancomycin, etc.), need to be carefully monitored:
antimicrobials, but to advances in supportive care. In Mount Vernon Hospital bum patients are cared for by a team of doctors, nurses, physiotherapists, dietitians and social workers. A consultant microbiologist is part of the team and advises on antimicrobial chemotherapy and control of infection. Our systemic antibiotic policy is summarized as follows:
1. Systemic
2.
3.
4.
5.
6.
7.
8,
antibiotic prophylaxis is not used routinely. Numerous studies have demonstrated that not only does the indiscriminate use of antibiotics promote colonization of both the environment and the patient with resistant strains of bacteria (Stone, 1966; Wickman, 1970), but also it does not lead to a reduction in the colonization of bums (Cason and Lowbury, 1960; Jones et al., 1966). Tetanus prophylaxis is provided by the usual methods of giving immunoglobulin or tetanus toxoid according to the immune status of the patient. The total failure of skin grafts which almost invariably accompanies Strep. pyogenes (Group A) in bums tissue is an indication for antibiotic therapy regardless of evidence of invasive infection. A short course of erythromycin (5 days) seems to be effective and is preferable to penicillin as the latter is likely to be inactivated by penicillinase produced by staphylococci in the wound. Systemic antimicrobial chemotherapy is given to patients who develop septicaemia manifested clinically. After taking blood cultures and consultation with the microbiologist, antimicrobial chemotherapy is instituted according to the bacterial population in the wound and the prevalence of any particular microorganism and its resistance pattern in the unit. Bacteriologically confirmed septicaemias are treated without question. The treatment is determined by the antibiotic sensitivity and the clinical condition of the patient. Selected patients are given perioperative cover of antibiotics determined by the sensitivity of known colonizing organisms or prevalent bacteria in the unit. Antibiotics are given intravenously an hour before surgery and continued for 24-48 h. An example of such cases are those heavily colonized by bacteria where extensive desloughing has to be undertaken. Generalized sepsis in a patient with extensive bums, especially when it is suspected that the infection is deep, is another indication for systemic antimicrobial chemotherapy. The diagnosis may be difficult to make in the presence of the hypermetabolic state associated with major bums and the leucocyte counts may be raised or suppressed for reasons unrelated to infection. The clinician must have a high awareness of the possibility of invasive infection and the necessity for prompt treatment, but must also avoid the indiscriminate use of broad-spectrum antibiotics which may promote resistant organisms. Chest infection, especially pneumonia, complicating inhalation injury is another indication for systemic antibiotic administration. Urinary infections should also be treated and the antibiotic used should be based on culture and sensitivity. With urinary infections efforts should be concentrated on prevention rather than treatment: unnecessary catheterization should be avoided, indwelling catheters cared for as meticulously and the catheter changed or removed
soon as it is not needed.
a, to ensure that the patient receives adequate therapeutic doses; b, to guard against excessive blood levels which might cause toxicity.
Topical antimicrobial treatment Various agents are used, the common
ones being:
1. Silver sulphadiazine cream. Probably
2.
3.
4. 5.
the most popular topical application for bums in the UK. One per cent silver sulphadiazine cream overcomes many of the problems associated with other silver-containing preparations. The sulphadiazine molecule acts as a carrier of the silver ions which are released gradually in the wound, thus avoiding the systemic effects of the earlier preparations. The occurrence of genuine silver resistance in Ps. aeruginosa is fortunately rare (Bridges et al., 1979). Silver nitrate-cklorkexidine cream (0.5 per cent silver nitrate and 0.2 per cent chlorhexidine) has been found to be of equal efficacy to silver sulphadiazine cream in protecting bums from bacterial colonization (Lowbury et al., 1976). Povidone iodine cream: a controlled comparison with silver sulphadiazine showed disappointingly poor results against both Gram-positive and Gram-negative organisms (Babb et al., 1977). Cklorkexidine: I per cent antiseptic solution. Cklorktxidine gluconafe 4 per cent (Hibiscrub) is used in our unit to bathe the patients.
Control of infection The bacteriological challenge presented by bums requires extra special care by all staff involved in every aspect of treatment. The potential for cross-infection is enormous, consequently thorough attention to all aspects of asepsis and means of infection control are mandatory. It is imperative that all staff are aware of this and are trained accordingly.
References Al-Khoja M. S. and Darrell J. H. (1979) The skin as a source of Acinefobucferand Moraxella species occurring in blood cultures. 1. Clin. Pafhol.32, 497. Babb J. R., Bridges K., Jackson D. H. et al. (1977) Topical chemoprophylaxis: trials of silver phosphate chlorhexidine, silver sulphadiazine and povidone iodine preparations. Bums 3, 65.
Boyce J. H. and Causey W. A. (1982). Increasing occurrence of methicillin resistant staphylococcusuurew in the United States. Infect.Confrol3, 3 77.
Bridges K., Kidson, A., Lowbury E. J. L. et al. (1979) Gentamicin and silver resistant pseudomonas in a burns unit. Br. Med. 1. 1, 446. Buxton A. E., Anderson R. L., Wendegar D. et al. (1978) Nosocomial respiratory tract infection and colonization with Aciwfobacfer calcoaceticus.Epidemiologic characteristics. Am 1. Med. 65, 507.
Burns (1991) Vol. 17/No.
312 Cason J. S. (1981) Treutrnent of Bums. London: Chapman & Hall. Cason J. S. and Lowbury E. J. L. (1960)Prophylactic chemotherapy for bums. Studies on the topical and systemic use of combined therapy. Lancet ii, 501. Casewell M. W. and Hill R. L. R. (1985) In-vitro activity of mupirocin (pseudomonic acid) against clinical isolates of Stuphylococcus uureus. J. Antimicrob. Chernother. 15, 523. Editorial (1983) Methicillin resistant Staphylococcus uureus. J. Hosp. Infect. 4, 327. Glew R. H., Moellering R. C. Jr and Kunz L. J. (1977) Infections with Acinefobucter culcoaceticus. (Herella ouginicoh). Clinical and Laboratory Studies. Medicine 56, 79. Hen&son S. D. (1973) Moraxella, Acinetobacter and Mimeae. Bucferiol. Rev. 37, 522. Jackson D. M., Lowbury E. J. L. and Topley E. (1951) Chemotherapy of Streptococcus pyogenes infection in burns. Lancet ii, 705. Jones R. J., Jackson D. M., and Lowbury E. J. L. (1966) Antisera and antibiotics in the prophylaxis of bums against Pseudomonas asruginosa. Br. J. Plust. Surg. 5, 43. Keane C. T. and Cafferkey M. T. (1984) Re-emergence of methicillin-resistant Staph. uureus causing severe infection. J. Infect. 9, 6. Lawrence J. C. (1959) Some effects of staphylococcal and streptococcal toxins upon mammalian skin in tissue culture. Br. 1. hp. Pufkol. 40, 8. Lawrence J. C. (1983) Bacteriology and wound healing. In: Fox J. A. and Fischer H. (eds), Cudexomet Iodine. Stuttgart: Schattaur, pp. 19-31. Lawrence J. C. (1985) The bacteriology of bums. J. Hosp. Infect. 6, (Suppl. B), 3. Lowbury E. J. L. (1979) Wits versus genes: the continuing battle against infection. J. Trauma 19,33. Lowbury E. J. L., Babb J. R., Bridges K. et al. (1976) Topical chemoprophylaxis with silver sulphadiazine and silver nitrate chlorhexidine creams: emergence of sulphonamide-resistant Gram-negative bacilli. Br. Med. J 1,493.
4
McDonald M. I., Hurse A., and Sim K. N. (1981) Methicillinresistant Stupphylococcusuuretrsbacteraemia. Med. j. Atcsf. 2, 191. MacMillan B. G. (1975) Burn wound sepsis - a ten year experience. Bums 2,l. Ramphael R. and Kluge R. M. (1979) Acinefobucfer calcouceficus variety anitratus: an increasing nosocomial problem. Am. J. Med. Sci. 277, 57. Retailliau H. F., Hightower A. W., Dixon R. E. et al. (1979) Acinefobucfer culcouceticus A nosocomial pathogen with an unusual seasonal pattern. J. Infect. Dis. 139, 371. Rosenthal S. L. and Freundlich L. E. (1979) The clinical significance of Acinefobucfer species. Health Lab. Sci. 14, 194. Sevitt S. (1957) Burns: Pathology and Therapeutic Appliurfions. London: Butterworth. Shanson D. C., Johnstone D. and Midgeley J. (1985) Control of hospital outbreak of methicillin-resistant Stupkylococa~~ uureus infections. Value of an isolation unit. 1, Hosp. Infect. 6, 285. Stone H. H. C. (1966) Review of pseudomonas sepsis in thermal bums. Ann. Surg. 163, 297. Wickman K. (1970) Studies of burns. Acfu Ckir. Scnnd. Suppl. 408. Wilkins T. and Bennett J. E. (1980) The selective use of systemic antibiotics in the treatment of bums. Surg. Gynaecol. Obsfef. 15 I, 404. Wilson G. R., French G. W. and Sully L. (1988) Loss of split thickness skin grafts due to non-group A p haemolytic streptococci. Ann. R. Coil. Surg. Engl. 70, 217.
Paper accepted
15 February
1991.
Correspondence shouti be addressed to: Mr R. Sanders, Department of Research, Mount Vernon Hospital, Northwood, Middlesex HA6 2RN, UK.
4th International ‘Mark0 Godina’ Course 23-2 7 September 1991,Ljubljana, Yugoslavia surgery, hand surgery, head and neck, breast and lower extremity reconstruction and microsurgery. The members of the international faculty are: Graham D. Lister and David L. Dingman, Salt Lake City, Utah, USA; David Soutar, Glasgow, Great Britain; Madeleine Lejour, Bruxelles, Belgium; Zoran M. Amei, Ljubljana and BoriSa Starovic, Sarajevo, Yugoslavia. For further information contact: Zoran M. Amei, MD, PhD, University Department of Plastic Surgery & Bums, University Medical Center Ljubljana, Zalogka 7, YU-61000 Ljubljana, Yugoslavia.
The topics to be covered include aesthetic and reconstructive
Printed in Greut Britain
Microbiological Hospital, UK
309
aspects of burns at Mount Vernon
L. S. Nakhla’ and R. Sanders2 ‘Department
of Microbiology
and ‘Regional Plastic and Bums Unit, Mount Vernon Hospital, Northwood,
Bactetial infection in 100 burned patienfs over a IO-monfh period has been studied. The commonesf colonizing organism was Staph. aureus (69 per cent), followed by E. coli (35 per cent). Pseud. aeruginosa accounted for only 28 per cenf of isolates. The role of the different bacterial species in burns pathology is discussed. Group G haemolytic streptococci were isolated from 10 per cent of patients and causedgruff failure in some cases. Only 3 per cent of pafients developed septicamiaand all were due to Staph. aureus. Our approach to munagement of infection in burns, especially the policy on systemic antimicrobial chemotherapy, is desm’bed
Introduction Infection is one of the major causes of increased morbidity and mortality in patients with severe bums. Surgeons have known for a long time that patients with severe burns who survived the early phase of hypovolaemic ‘shock’ were apt to develop fatal septic complications. The first line of defence against contamination of the bum consists of topical applications of antimicrobial agents, patient isolation and other methods of preventing cross-infection including the use of occlusive dressings, excision and grafting and the production of a dry eschar. The second line of defence against invasion of tissues and bloodstream from already infected bums consists of selective chemotherapy, immunoprophylaxis and various methods of supporting the natural defences, e.g. control of diabetes and maintenance of nutrition and other physiological norms. Bacteriology of burns The nature of bums which, by definition, contain devitalized tissues, makes these injuries more susceptible to bacterial colonization than most other types of wounds. The moist dead tissue within the bum, together with the surrounding damaged and oedematous tissues, provide a nutrient medium which will support the growth of a variety of bacterial species. In a certain proportion of bums such colonization is a prelude to septicaemia and death.
Methods The standard practice at Mount Vernon Bums Unit is to take bacteriological swabs from wounds and natural carriage 80 1991 Butterworth-Heinemann 0305-4179/91/040309-04
Ltd
Middlesex,
UK
sites (nose, throat and rectum) on admission as a baseline. Swabs from wound sites are repeated at each change of dressing until wound closure has been achieved.
Results Analysis of bacteriological swabs taken from 100 patients admitted to the Unit over a period of 10 months (November 1987 to August 1988) revealed the incidence of different bacteria isolated per patient (T&/e I). The most common organism isolated was Staph. aureus (69 per cent) followed by E. coli and coliforms (35 per cent each). Pselld. ueruginosu was isolated from only 28 per cent of patients. There has been a progressive decline of Psettd. aeruginasa and other Gram-negative bacilli following the introduction of topical silver nitrate in 1964 (Lowbury, 1979) and other effective prophylactic antimicrobial agents such as silver sulphadiazine in 1970 (Babb et al., 1977). A similar pattern of bacterial populations in burned patients has been reported by Lawrence (1985) (Table II).
Discussion Fresh bums are usually sterile but progressively become colonized with one or more bacterial species as the patient’s stay in bum units increases. The mean acquisition time varies from one species of bacteria to another and depends on the extent of the bum. In non-extensive bums it varies from 3.4 days for Sfuapk. uureus to 15.4 days for Klebsiella species: and in extensive bums from 4.3 days for Staph. uureus to 36.0 days for Strep. pyogenes Group A (Lawrence, 1985). The role of the different bacterial species in burns pathology varies from mere colonization, local tissue sepsis and interference with healing and grafting, to invasion of the bloodstream with subsequent septicaemia and death. Sfupk. uureus causes local suppuration and produces alpha toxin (a haemolysin) which rapidly kills skin (Lawrence, 1959). Occasionally it invades the bloodstream and causes septicaemia or produces toxins which cause the toxic shock syndrome. Most staphylococci in our unit are fully sensitive to antibiotics or resistant only to pencillin. From time to time patients are admitted to our unit - usually referred from
Bums (1991) Vol. 17/No. 4
310
Table I, Potentially pathogenic bacteria isolated from 100 patients at Mount Vernon Hospital - 198711988
Table II. Potentially pathogenic bacteria isolated from bum wound swabs during 1983 (from Lawrence, 1985)
Patients Bacterial species
(%)
Staph. aureus Staph. aureus (EMRSA’) Haemolytic streptococci Haemolytic streptococci Haemolytic streptococci Haemolytic streptococci Haemolytic streptococci Haemolytic streptococci Faecal streptococci E. coli
69 12 6 5 2 2 1 10 13 35
Group Group Group Group Group Group
A B C D F G
Klebsiella spp. Proteusspp. Acinetobacter anitratus Other coliform bacilli Ps. aeruginosa Bacreriodes fragilis Bacteriodes melaninogenicus Clostridium perfringens (Welchii) ‘EMRSA,
epidemic methicillin
24 14 21 35 28 1 1 1
resistant Staph. aureus.
other centres - already colonized with the ‘Epidemic Methicillin Resistant Staph. at(reus (EMRSA)‘. These patients are often suffering from extensive bums, are heavily colonized with EMRSA and inevitably spread this infection to other patients in the unit. In the IO-month period of our survey 12 per cent of patients were colonized with this organism. A marked increase in the number of outbreaks of hospital infection due to EMRSA has been reported in Britain, Eire, the USA, Australia and South Africa over the last 8 years (McDonald et al., 1981; Boyce and Causey, 1982; Editorial 1983; Keane and Cafferkey, 1984; Shanson et al., 1985). A notable feature of these strains is the ease with which they spread, hence the terminology ‘Epidemic Methicillin Resistant S&h. aureu.4. These epidemic strains are resistant to many other antibiotics and effective treatment of serious infections has often proved difficult. The antimicrobial agents available against EMRSA are often potentially toxic, limited in number, difficult to administer and expensive. There are also uncertainties in the efficiency of topical antibiotic and antiseptic preparations, although preliminary results with mupirocin (pseudomonic acid) seem to be promising (Casewell and Hill, 1985). Immunocompromised debilitated patients or those with open wounds (as in bums), are particularly at risk from infection with these strains. Psed. aeruginosa delays wound healing and the pigment is toxic to tissues (Lawrence, 1983). Strep. pyogenes of Group A prevents graft ‘take’ (Jackson et al., 1951) and streptococcal haemolysins also kill skin (Lawrence, 1959). The role of other haemolytic streptococci in bums with respect to tissue damage is debatable. Recently there has been an increasing awareness of the effect of Group G streptcocci which was isolated from 10 per cent of our patients. The impression in our patients and that of others (Wilson et al., 1988) is that it is potentially damaging to grafts. Acinetobucteranifrdus is a non-motile, non-fermentative Gram-negative coccobacillus with soil or water as its natural habitat (Henrikson, 1973). It has also been isolated from
Isolates (%)
Species Staph. aureus Ps. aeruginosa Strep. pyogenes Group A Escherichia coli Klebsiella spp. Proteus spp. Acinetobacter anirratus Clostridium perfringens
All burns
Nonextensive burns
Extensive burns
63 32
60 25
74 59
3.7 28 11 19
4.4 20 8 8
1.3 55 22 22
24
18
47
17
12
32
human skin (Al-Khoja and Darrell, 1979). Laboratory isolates from clinical specimens usually reflect colonization rather than infection (Rosenthal and Freundlich, 1977) but serious, sometimes fatal, opportunistic infections have been reported, including septicaemia, endocartitis, meningitis and pneumonia (Glew et al., 1977; Ramphael and Kluge, 197% Retailliau et al., 1979). Increased colonization and infection of hospital patients with this organism has sometimes been reported as epidemic spread (Buxton et al., 1978). In our Bums Unit we have had outbreaks of infection with acinetobacter. In the great majority of patients it was a mere colonization, but in debilitated patients with extensive bums it has caused septicaemia with pneumonia. In the period of the IO-month study reported here this organism was isolated from 21 per cent of patients. Although infection in burns is usually silent (Sevitt, 1976), septicaemic episodes can occur at any time during the treatment of burned patients (Cason,l981); it is considered pertinent to take blood cultures from such patients. The criteria include patients with body temperatures over 39”C, or a lowered blood pressure and high pulse rate. Septicaemia should also be suspected if the patient is disorientated, or the urinary sodium/potassium ratio is reversed. The incidence of positive blood cultures is low -about 10 per cent (Lawrence, 1985). In our 100 patients it was 3 per cent, all due to Stg$. uureus; one was fully sensitive to antibiotics, one was resistant to pencillin only, and a third was an EMRSA (transferred from another unit), consequently antibacterial therapy usually has to be guided by the wound flora. Blood culture results must be interpreted with caution and correlated with the clinical state of the patient. This ensures that the organisms grown are not attributed to septacaemia when in fact they are derived from the surface of the bum skin as a result of inadequate sterilization of the site from which blood samples are taken.
Antimicrobial therapy Invasive infection still occurs in approximately 25 per cent of patients with major bums, although the last 20 years has seen a significant fall in associated mortality from over 60 per cent of those with infective complications in 1965 to about 10 per cent now (MacMillan, 1975; Wilkins and Bennett, 1980). The improved prognosis of these patients may be attributed not only to better use of more potent
Nakhla and Sanders: Microbiological
311
aspects of bums
Certain antibiotics, e.g. aminoglycosides (gentamicin, tobramycin, amikacin, vancomycin, etc.), need to be carefully monitored:
antimicrobials, but to advances in supportive care. In Mount Vernon Hospital bum patients are cared for by a team of doctors, nurses, physiotherapists, dietitians and social workers. A consultant microbiologist is part of the team and advises on antimicrobial chemotherapy and control of infection. Our systemic antibiotic policy is summarized as follows:
1. Systemic
2.
3.
4.
5.
6.
7.
8,
antibiotic prophylaxis is not used routinely. Numerous studies have demonstrated that not only does the indiscriminate use of antibiotics promote colonization of both the environment and the patient with resistant strains of bacteria (Stone, 1966; Wickman, 1970), but also it does not lead to a reduction in the colonization of bums (Cason and Lowbury, 1960; Jones et al., 1966). Tetanus prophylaxis is provided by the usual methods of giving immunoglobulin or tetanus toxoid according to the immune status of the patient. The total failure of skin grafts which almost invariably accompanies Strep. pyogenes (Group A) in bums tissue is an indication for antibiotic therapy regardless of evidence of invasive infection. A short course of erythromycin (5 days) seems to be effective and is preferable to penicillin as the latter is likely to be inactivated by penicillinase produced by staphylococci in the wound. Systemic antimicrobial chemotherapy is given to patients who develop septicaemia manifested clinically. After taking blood cultures and consultation with the microbiologist, antimicrobial chemotherapy is instituted according to the bacterial population in the wound and the prevalence of any particular microorganism and its resistance pattern in the unit. Bacteriologically confirmed septicaemias are treated without question. The treatment is determined by the antibiotic sensitivity and the clinical condition of the patient. Selected patients are given perioperative cover of antibiotics determined by the sensitivity of known colonizing organisms or prevalent bacteria in the unit. Antibiotics are given intravenously an hour before surgery and continued for 24-48 h. An example of such cases are those heavily colonized by bacteria where extensive desloughing has to be undertaken. Generalized sepsis in a patient with extensive bums, especially when it is suspected that the infection is deep, is another indication for systemic antimicrobial chemotherapy. The diagnosis may be difficult to make in the presence of the hypermetabolic state associated with major bums and the leucocyte counts may be raised or suppressed for reasons unrelated to infection. The clinician must have a high awareness of the possibility of invasive infection and the necessity for prompt treatment, but must also avoid the indiscriminate use of broad-spectrum antibiotics which may promote resistant organisms. Chest infection, especially pneumonia, complicating inhalation injury is another indication for systemic antibiotic administration. Urinary infections should also be treated and the antibiotic used should be based on culture and sensitivity. With urinary infections efforts should be concentrated on prevention rather than treatment: unnecessary catheterization should be avoided, indwelling catheters cared for as meticulously and the catheter changed or removed
soon as it is not needed.
a, to ensure that the patient receives adequate therapeutic doses; b, to guard against excessive blood levels which might cause toxicity.
Topical antimicrobial treatment Various agents are used, the common
ones being:
1. Silver sulphadiazine cream. Probably
2.
3.
4. 5.
the most popular topical application for bums in the UK. One per cent silver sulphadiazine cream overcomes many of the problems associated with other silver-containing preparations. The sulphadiazine molecule acts as a carrier of the silver ions which are released gradually in the wound, thus avoiding the systemic effects of the earlier preparations. The occurrence of genuine silver resistance in Ps. aeruginosa is fortunately rare (Bridges et al., 1979). Silver nitrate-cklorkexidine cream (0.5 per cent silver nitrate and 0.2 per cent chlorhexidine) has been found to be of equal efficacy to silver sulphadiazine cream in protecting bums from bacterial colonization (Lowbury et al., 1976). Povidone iodine cream: a controlled comparison with silver sulphadiazine showed disappointingly poor results against both Gram-positive and Gram-negative organisms (Babb et al., 1977). Cklorkexidine: I per cent antiseptic solution. Cklorktxidine gluconafe 4 per cent (Hibiscrub) is used in our unit to bathe the patients.
Control of infection The bacteriological challenge presented by bums requires extra special care by all staff involved in every aspect of treatment. The potential for cross-infection is enormous, consequently thorough attention to all aspects of asepsis and means of infection control are mandatory. It is imperative that all staff are aware of this and are trained accordingly.
References Al-Khoja M. S. and Darrell J. H. (1979) The skin as a source of Acinefobucferand Moraxella species occurring in blood cultures. 1. Clin. Pafhol.32, 497. Babb J. R., Bridges K., Jackson D. H. et al. (1977) Topical chemoprophylaxis: trials of silver phosphate chlorhexidine, silver sulphadiazine and povidone iodine preparations. Bums 3, 65.
Boyce J. H. and Causey W. A. (1982). Increasing occurrence of methicillin resistant staphylococcusuurew in the United States. Infect.Confrol3, 3 77.
Bridges K., Kidson, A., Lowbury E. J. L. et al. (1979) Gentamicin and silver resistant pseudomonas in a burns unit. Br. Med. 1. 1, 446. Buxton A. E., Anderson R. L., Wendegar D. et al. (1978) Nosocomial respiratory tract infection and colonization with Aciwfobacfer calcoaceticus.Epidemiologic characteristics. Am 1. Med. 65, 507.
Burns (1991) Vol. 17/No.
312 Cason J. S. (1981) Treutrnent of Bums. London: Chapman & Hall. Cason J. S. and Lowbury E. J. L. (1960)Prophylactic chemotherapy for bums. Studies on the topical and systemic use of combined therapy. Lancet ii, 501. Casewell M. W. and Hill R. L. R. (1985) In-vitro activity of mupirocin (pseudomonic acid) against clinical isolates of Stuphylococcus uureus. J. Antimicrob. Chernother. 15, 523. Editorial (1983) Methicillin resistant Staphylococcus uureus. J. Hosp. Infect. 4, 327. Glew R. H., Moellering R. C. Jr and Kunz L. J. (1977) Infections with Acinefobucter culcoaceticus. (Herella ouginicoh). Clinical and Laboratory Studies. Medicine 56, 79. Hen&son S. D. (1973) Moraxella, Acinetobacter and Mimeae. Bucferiol. Rev. 37, 522. Jackson D. M., Lowbury E. J. L. and Topley E. (1951) Chemotherapy of Streptococcus pyogenes infection in burns. Lancet ii, 705. Jones R. J., Jackson D. M., and Lowbury E. J. L. (1966) Antisera and antibiotics in the prophylaxis of bums against Pseudomonas asruginosa. Br. J. Plust. Surg. 5, 43. Keane C. T. and Cafferkey M. T. (1984) Re-emergence of methicillin-resistant Staph. uureus causing severe infection. J. Infect. 9, 6. Lawrence J. C. (1959) Some effects of staphylococcal and streptococcal toxins upon mammalian skin in tissue culture. Br. 1. hp. Pufkol. 40, 8. Lawrence J. C. (1983) Bacteriology and wound healing. In: Fox J. A. and Fischer H. (eds), Cudexomet Iodine. Stuttgart: Schattaur, pp. 19-31. Lawrence J. C. (1985) The bacteriology of bums. J. Hosp. Infect. 6, (Suppl. B), 3. Lowbury E. J. L. (1979) Wits versus genes: the continuing battle against infection. J. Trauma 19,33. Lowbury E. J. L., Babb J. R., Bridges K. et al. (1976) Topical chemoprophylaxis with silver sulphadiazine and silver nitrate chlorhexidine creams: emergence of sulphonamide-resistant Gram-negative bacilli. Br. Med. J 1,493.
4
McDonald M. I., Hurse A., and Sim K. N. (1981) Methicillinresistant Stupphylococcusuuretrsbacteraemia. Med. j. Atcsf. 2, 191. MacMillan B. G. (1975) Burn wound sepsis - a ten year experience. Bums 2,l. Ramphael R. and Kluge R. M. (1979) Acinefobucfer calcouceficus variety anitratus: an increasing nosocomial problem. Am. J. Med. Sci. 277, 57. Retailliau H. F., Hightower A. W., Dixon R. E. et al. (1979) Acinefobucfer culcouceticus A nosocomial pathogen with an unusual seasonal pattern. J. Infect. Dis. 139, 371. Rosenthal S. L. and Freundlich L. E. (1979) The clinical significance of Acinefobucfer species. Health Lab. Sci. 14, 194. Sevitt S. (1957) Burns: Pathology and Therapeutic Appliurfions. London: Butterworth. Shanson D. C., Johnstone D. and Midgeley J. (1985) Control of hospital outbreak of methicillin-resistant Stupkylococa~~ uureus infections. Value of an isolation unit. 1, Hosp. Infect. 6, 285. Stone H. H. C. (1966) Review of pseudomonas sepsis in thermal bums. Ann. Surg. 163, 297. Wickman K. (1970) Studies of burns. Acfu Ckir. Scnnd. Suppl. 408. Wilkins T. and Bennett J. E. (1980) The selective use of systemic antibiotics in the treatment of bums. Surg. Gynaecol. Obsfef. 15 I, 404. Wilson G. R., French G. W. and Sully L. (1988) Loss of split thickness skin grafts due to non-group A p haemolytic streptococci. Ann. R. Coil. Surg. Engl. 70, 217.
Paper accepted
15 February
1991.
Correspondence shouti be addressed to: Mr R. Sanders, Department of Research, Mount Vernon Hospital, Northwood, Middlesex HA6 2RN, UK.
4th International ‘Mark0 Godina’ Course 23-2 7 September 1991,Ljubljana, Yugoslavia surgery, hand surgery, head and neck, breast and lower extremity reconstruction and microsurgery. The members of the international faculty are: Graham D. Lister and David L. Dingman, Salt Lake City, Utah, USA; David Soutar, Glasgow, Great Britain; Madeleine Lejour, Bruxelles, Belgium; Zoran M. Amei, Ljubljana and BoriSa Starovic, Sarajevo, Yugoslavia. For further information contact: Zoran M. Amei, MD, PhD, University Department of Plastic Surgery & Bums, University Medical Center Ljubljana, Zalogka 7, YU-61000 Ljubljana, Yugoslavia.
The topics to be covered include aesthetic and reconstructive
