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systemic zygomycete infections and, while there is nocompletely reliable rapid diagnostic test,8 some simpleprocedures may help. Direct microscopy of specimensfrom pus, contact smears taken from the cut surface of

biopsies,9 or histology of frozen sections may confirmthe diagnosis within a few hours. In tissue, zygomycetehyphae are characteristically broad and produce right-angled branching. In doubtful sections, other methodsof recognition, not based on morphology, can be used.These methods include labelling of tissues withfluorescein or peroxidase conjugates of specific anti-zygomycete antibodies,lO application of fluorescein-conjugated lectins,l1 or use of the cresyl-fast violetstain," which stains zygomycete hyphae red and othermycelial fungi blue or purple. Computerisedtomographic scanning, which has proved invaluable inrhinocerebral disease for demonstrating the true extentof infection,13 may also be useful.The usual treatment for mucormycosis is intravenous

amphotericin Bl,2 in a daily dose of at least 08-10mg/kg. In many cases, however, surgical excision ofinfected tissues in addition to antifungal chemotherapyhas been life saving.3 To be of benefit, surgery has to beradical; persistence of unsuspected areas of infectionmay lead to serious postoperative complications such ashaemorrhage. Despite the development of a number ofnew azole antifungals for systemic use, there is littleevidence that they are useful in this condition eventhough ketoconazole is effective in some subcutaneouszygomycete infections. 14 Generally the prognosis in

many patients with mucormycosis remains poor despitetreatment, while other cases are only recognised postmortem. Attention has therefore focused on preventiveaspects, when the source of infection can be

identified-eg, occasionally clusters of cases are seen inthe same hospital,15 suggesting common exposure to theinfecting organisms (for instance, from a contaminatedventilation system). R rhizopodiformis infection has beenassociated with the use of comtaminated surgicaldressing materials.8 Development of other preventivemeasures depends on detailed knowledge of factorspredisposing to zygomycete infection. Two areas havelately been highlighted-the role of unsaturatedtransferrin in inhibiting zygomycete growth 16 and, indiabetic animals, defective alveolar macrophageinhibition of spore germination.l’ Understanding ofsuch mechanisms may provide a basis for new

approaches to the management of mucormycosis byaltering patient susceptibility.8. Marchevsky AM, Bottone EJ, Geller SA, Giger DK. The changing spectrum of

disease, etiology and diagnosis of mucormycosis. Hum Pathol 1980; 11:457-64.

9. Hay RJ, Campbell CK, Marshall WM, Rees BI, Pincott J. Disseminatedzygomycosis (mucormycosis) caused by Saksenaea vasiformis. J Infect 1983;7: 162-65.

10. Chandler FW, Watts JC, Kaplan W, Hendry AT, McGinnis MR, Ajello L.Zygomycosis: report of four cases with formation of chlamydoconidia intissue. Am J Clin Pathol 1985; 84: 99-103.

11. Benbow BW, Delamore IW, Stoddart RW, Reid H. Disseminated zygomycosisassociated with erythroleukaemia. Confirmation by lectin stains. J Clin Pathol1985; 38: 1039-44.

12. Rolph L, Austwick PKC. Differential staining of fungi in tissues. J Sci Tech1973; 17: 22-26.

13. Anderson D, Matick H, Naheedy MH, Stein K. Rhinocerebral mucormycosiswith CT scan findings: a case report. Comput Radiol 1984; 8: 113-17.

14. Drouhet E, Dupont B. Laboratory and clinical assessment of ketoconazole indeep seated mycoses. Am J Med 1983; 74: 1B 30-47.

15. Gutierrez Diaz A, Palacio Hernanz A, del Larregla S, Sanz Lopez A. Orbitalphycomycosis. Ophthalmologia 1981; 182: 165-70.

16. Artis WM, Fountain JA, Delcher HK, Jones HE. A mechanism of susceptibilityto mucormycosis in diabetic ketoacidosis: transferrin and iron availability.Diabetes 1982; 31: 1109-14.

17. Waldorf AR, Levitz SM, Diamond RD. In vivo bronchoalveolar defense againstRhizopus oryzae and Aspergillus fumigatus. J Infect Dis 1984; 150: 752-60.

LESSONS FROM STAFFORD

THE first recorded, and still the largest, outbreak oflegionnaires’ disease was centred on a Philadelphia hotelin 1976. The latest, and second in scale, happened in anew hospital in Stafford in 1985, and it was judgedworrying enough to warrant an official inquiry. Themedical aspects of this investigation are summarised onp 1374. Sir John Badenoch and his colleagues recognisethe dangers of passing judgment with hindsight. Never-theless, they were called together at a time whenoutsiders were wondering if the response locally to theStafford outbreak had been as effective as it should havebeen. Rightly, when criticism is justified, they do notshirk from saying so; nor, when blame has been

misplaced, do they fail to correct the balance.Before the ward round on April 22, the day on which

the alarm bells sounded, a medical registrar had takenblood samples for legionella antibody testing, thoughthis was not the only diagnosis under consideration. Hadthe district microbiology laboratory been on the spot,had it been able (as few such laboratories would be) totest for antibody to Legionella pneumophila, and hadthere been a better working relationship between

microbiology and the bedside via an infectious diseasesspecialist or otherwise, the correct clinical and ecologicaldiagnoses might have been reached sooner. And thesame could be said of calling earlier on theCommunicable Diseases Surveillance Centre. Having amedical emergency committee to handle the crisis,another recommendation from the Badenoch commit-

tee, might have made the response look better, but thefortunate fact remains that long before the diagnosis wasor could have been reached, the outbreak of infectionhad ceased: dissemination, to patients and visitors, ofL pneumophila serotype Pontiac la stopped, for reasonswe may never know, on or around April 19.

If monoclonal antibodies to legionella’ antigensbecome widely available as a diagnostic test or ifbronchoalveolar lavage (not mentioned by the

committee) were to be regarded as acceptable as a

routine in apparently atypical pneumonia, legionnaires’disease might be diagnosed more quickly. In other

circumstances, however, clinicians are going to have towait-though not, it is to be hoped, for as long as theStafford physicians did-for laboratory diagnosis. Forthis reason it is a pity that the Badenoch inquiry does notoffer advice on the place and dosage of intravenouserythromycin in the immediate management of atypicalpneumonia. A clear picture does not emerge from thereport when it is read side by side with the Staffordphysicians’ own preliminary account.1

Should L pneumophila be in a hospital’s water-cooledair-conditioning system at all and should it be able tospread to, for example, an outpatient department?L pneumophila is a ubiquitous organism, and warmwater sprays and people whose resistance to infection isalready lowered are some of the ingredients for anoutbreak. All three are found in hospitals with water-cooled ("wet") air conditioning. The committee’s

experts and hospital engineers focused on the "plumetheory" and a "backflow theory". Contaminated plumesfrom within the cooling tower could have strayed outsideand been entrained with air or, as in other outbreaks in

hospitals, re-entered through windows. At Staffordthere was a gap in the floor of the cooling tower above the

1. Rashed K, Mason A, Gibson J, Francis J, Fairfax A, Daggett P. Legionnaires’disease in Stafford: Management of an epidemic. Lancet 1986; i: 197-99.

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air intake level; although it was not the upper floors thatwere affected, this is the route the committee favours.Other investigations revealed design and/orconstruction faults elsewhere in the system: it was

clearly possible for contaminated water to flow back to atray collecting condensate from a chiller battery.However, the report finds it unlikely that bacteria-ladenaerosol could have reached patients and visitors fromthis source.

So, what is the future of water cooling in the airconditioning of hospitals? None at all, says the Ministerof Health, Mr Barney Hayhoe. His department,criticised by Badenoch for not more urgently upgradingguidance issued in 1980 on the avoidance of legionella inhospitals, does not know how many wet systems it has.The West Midlands Regional Health Authority does,and on June 6 it announced that all fifteen, includingStafford (whose offending tower has already gone), willbe demolished and replaced by air-cooled systems, at atotal cost of [It million. The inquiry recommends that"urgent consideration should be given to replacing anywet cooling tower [in existing hospitals] with an air-cooled system". The replacement of such cooling"towers", which take up one extra room on top of ahospital, is not as spectacular or disruptive as thedemolition of cooling towers in some othercircumstances. All the same, Health Departments willhesitate before ordering that this be done everywhere;nor will this message from the Badenoch inquiry bewelcome in other countries, many of which dependheavily on water cooling. The Badenoch committee maybe overly pessimistic when it doubts the ability ofanyone, with or without biocides, to guarantee thathospitals which use such systems will be free fromlegionella. Air-to-air systems are more expensive to putin and cheaper to run but they are heavy and would addto the perils of multistorey hospitals. Clinicians andothers may have to wait for the second report forelaboration of the recommendation that "The extent towhich the design of future hospitals ,should includereliance on air conditioning should be subject to

scrutiny."

TISSUE EXPANSION

SKIN stretches to accommodate the growth of massesbeneath it, as witnessed by natural phenomena such asbreast development, pregnancy, and tumour enlarge-ment. Primitive societies exploit this expansion fordecorative purposes-eg, the platter-lipped women ofChad. Neumann is credited with the first application ofskin stretching or tissue expansion to modernreconstructive surgery; in 1956, he inflated a rubberballoon in the subcutaneous tissue adjacent to an avulsedear remnant to create enough skin excess to allowreconstruction of the ear. The technique of skin

expansion was later refined by Radovan,2 whose

expanders remain the basis of clinical practice in mostcentres. The expander, a spherical or rectangularsilicone bag, connected by a silicone tube to a self-sealinginjection port, is inserted surgically. The expander itselfis placed in the subcutaneous fat whilst the injection port

1. Neumann CG. The expansion of an area of skin by progressive distensionof a subcutaneous balloon. Plast Reconstr Surg 1957; 19: 124-30.

2. Radovan C. Development of adjacent flaps using a temporary expander. ASPRSPlast Surg Forum 1979; 2: 62.

is placed in subcutaneous fat at a discrete distance and ata site where it is easily palpable through the skin. After ahealing period of two to six weeks, the expander isinflated by percutaneous injection of sterile saline intothe injection port. Inflation is usually undertaken as anoutpatient procedure once or twice a week withoutanaesthesia. On each occasion, saline is injected until thepatient feels the skin overlying the expander becominguncomfortably tight; further inflation will compromisethe blood supply of the expanded skin. Under mostcircumstances, this simple clinical guide is an adequatemonitor for safe inflation.3 Complete inflation usuallytakes one to three months, although optimum andmaximum rates of expansion are unknown.The increased demand for breast reconstruction after

mastectomy has been a considerable impetus to thedevelopment of tissue expansion. When too little skinremains on the anterior chest wall after mastectomy toaccommodate a gel-filled prosthesis, tissue expansionwill usually stretch the available skin sufficiently-up to700 or 800 ml is possible-to create an appropriatebreast mound.4,S The expander is replaced later by apermanent prosthesis. Congenital breast hypoplasiamay also be corrected by tissue expansion: Argenta andhis colleagues have described insertion of expanders infive patients with Poland’s syndrome soon after puberty;periodic inflation maintained symmetry over the

ensuing four to five years of breast development.6Tissue expansion finds its other and wider application

as an alternative to distant flaps for closure of skindefects that are either not amenable to closure by directsuture or local flaps, or are unsuitable for split-skingrafting.7 In effect, expansion of the skin adjacent to adefect or lesion destined for surgical excision createssufficient skin to allow local flap closure. Use of thetechnique in this way confers the benefits of local overdistant flaps-simplicity, localisation of scarring, and anideal match of skin consistency, colour, and hair-bearingproperties. The potential applications of this kind fortissue expansion are large, its use being precluded onlywhen immediate skin cover is necessary, the defect is too

large relative to the adjacent skin available for expansion,or the technique is unacceptable to the patient. To avoidneedle punctures, the injection port can be exteriorised,extending the acceptability of the technique to children.Moderate-sized areas of scalp alopecia,"-10 burn

scarring, naevi, and superficial haemangiomas have allbeen treated successfully and more ambitious

applications are being reported with increasingfrequency.11,12 Nevertheless, many defects remain more

3. Hallock GG, Rice DS. Objective monitoring for safe tissue expansion. PlastReconstr Surg 1986; 77: 416-20.

4. Birnbaum L, Olsen JA. Breast reconstruction following radical mastectomyusing custom designed implants. Plast Reconstr Surg 1978; 61: 355-63.

5. Radovan C. Breast reconstruction after mastectomy using the temporary

expander. Plast Reconstr Surg 1982; 69: 195-206.6. Argenta LC, Vanderkouk C, Friedman RJ, Marks M. Refinements in

reconstruction of congenital breast deformities. Plast Reconstr Surg 1985; 76:73-80.

7. Radovan C. Tissue expansion in soft-tissue reconstruction. Plast Reconstr Surg1984; 74: 482-90.

8. Nordstrom REA, Devine JW. Scalp stretching with a tissue expander for closureof scalp defects. Plast Reconstr Surg 1985; 75: 578-81.

9. Leonard AG, Small JO. Tissue expansion in the treatment of alopecia. Br J PlastSurg 1986; 39: 42-56.

10. Roberts AHN, Dickson WA, Dickson MG, Cary A. The correction of scalp hairdefects by tissue expansion. Ann R Coll Surg Engl 1986; 68: 89-92.

11. Oneal RM, Rohrich RJ, Izenberg PH. Skin expansion as an adjunct to

reconstruction of the external ear Br J Plast Surg 1984; 37: 517-19.12. Rees RS, et al. Tissue expansion: Its role in traumatic below-knee amputations.

Plast Reconstr Surg 1986; 77: 133-37.