271 immunofluorescent staining which antigen ofL. pneumophila. Direct fluorescent antiserum
was
specifically recognises
the
kindly provided by the Center for
Disease Control, Atlanta, Georgia, U.S.A.
Rijksinstituut voor de Volksgezondheid, Bilthoven, Netherlands
J. L. DE FREITAS J. BORST
Department of Infectious Diseases, University Hospital, Leiden
P. L. MEENHORST
characteristics is most readily seen in high-tension electrical injury of an extremity, where non-viable muscle near the centrally located bone may underlie more superficial viable muscle and the extent of skin injury at the contact points offers little indication of the actual extent of trauma. This situation demands thorough surgical examination of the extremity, particularly of the periosseous muscles, to determine the extent of debridement or amputation necessary. Army Institute of Surgical Research, Brooke Army Medical Center,
U.S.
LEGIONELLA PNEUMOPHILA SEROTYPES to our paper on the isolation of a serotype of Legionella pneumophila (Dec. 2), we reported a preliminary finding regarding the stability of cellular antigens of the Los Angeles 1 serotype in formalin. I have been unable to duplicate this experiment, and now concur with Center for Disease Control investigators that prolonged formalin fixation of this strain does not alter its reactivity with either homologous or heterologous antisera.
SIR,-In the addendum
Fort Sam Houston, Texas 78234, U.S.A.
BASIL A. PRUITT, JR ARTHUR D. MASON, JR
FIBRE AND DIABETES
new
Division of Infectious Diseases, V. A. Wadsworth Medical Center, Los Angeles, California 90073, U.S.A.
PAUL EDELSTEIN
LEGIONNAIRES’ DISEASE AND CEREBRAL DISTURBANCE
SiR,—The difficulty of establishing a diagnosis of legionnaires’ disease solely on serological tests have been the subject of recent editorial comments.’,2 Consequently, sporadic instances of patients with unexplained pulmonary infiltrates represent a diagnostic dilemma. The patients described by Dr Lees and Dr Tyrrell (Dec. 23/30) could very well not have had legionnaires’ disease. The legionnaires’ bacillus has been successfully isolated from a transtracheal aspirate.’ Thus without cultural confirmation, Lees and Tyrell have not established the diagnosis of legionnaires’ disease. The diagnosis in the second reported patient was based initially on clinical response to erythromycin; such reasoning is untenable. Department of Infectious Diseases, Geisinger Medical Center, Danville, Pennsylvania 17821, U.S.A.
GARY R. PLOTKIN
HIGH-TENSION ELECTRICAL INJURY
SIR,-Your editorial4 properly emphasises the risk of deep tissue damage in patients with high-tension electrical injury, but the mechanism of that damage appears to be related more to the configuration of the tissue involved than to its resistarice properties. In high-voltage trauma, heat is the principal mediator of tissue injury; the differences of tissue resistance are so small that the body acts as a volume conductor. Heat is generated in this conductor as a function of voltage drop and current flow per unit cross-sectional area, or current density. This dependence upon cross-sectional area accounts for the frequency of severe injury to the extremities and the rarity of major injury to the trunk in high-tension electrical injury. At the points of contact, where density is greatest, the skin is severely injured and chars; when this occurs resistance rises sharply, limiting further passage of current and heating. The heated conductor cools, the deeper portions cooling more slowly than the superficial. Since thermal injury of tissue is dependent upon both the temperature achieved and the duration of exposure to that temperature, the deeper tissues are more liable to severe injury. The clinical reflection of these 1 British Medical Journal, 1978, ii, 1319. 2 Tsai T. F., Fraser, D. W. Ann. intern. Med, 1978, 89, 413. 3 Lattimer, G. L., McCrone, C., Galgon, J. New Engl. J. 1172.
4 Lancet, 1978, ii, 978.
Med.
1978, 299,
SIR,-Mr Wolever and colleagues have reported
on the the reducequivalent gelled non-gelled guar tion in post-prandial blood-glucose in healthy volunteers given an oral glucose load. We have been investigating the properties of several fibre compounds taken in powder form by diabetics, and as part of this study we compared the effects of guar and pectin taken in gelled and non-gelled forms. There was little difference in the effect on post-prandial glucose between 10 g guar taken in an adequately hydrated form as a blancmange and a similar dose taken in powder form. However, the meal supplied on both occasions to our subjects consisted of food items often consumed for breakfast-i.e., cornflakes (30 g), milk (200 ml), bread (35 g), butter (8 g), marmalade (25 g), tea (150 ml), and sugar (15 g). The use of normal meals is a more appropriate test of the likely effect of fibre when added to normal diets for diabetics; the addition, to a liquid test meal, of any substance, even of non-fibre origin, might affect plasmaglucose if it delayed gastric emptying and slowed glucose
effects of
and
on
absorption. Not only was the effect of gelling unimportant but the effect of the guar as such was unremarkable (see figure). Although some reduction in plasma-glucose seems to have been achieved, this reduction was not, in our subjects, statistically significant, and we doubt whether the effect in many other trials23 can be claimed to be therapeutically relevant. This limited response does not mean that dietary fibre given in a different form will not be effective, but the demonstration in diabetics that glycosuria can be reduced during a trial period with extra dietary fibre23 cannot be taken as proof that the 1. Wolever, T. M. S., Taylor, R., Goff, D. V. Lancet, 1978, ii, 1381. 2. Jenkins, D. J. A., and others. ibid. 1977, ii, 779. 3. Jenkins, D. J. A., and others. Br. med. J. 1978, ii,1744.
Increment in post-prandial plasma-glucose in four maturityonset diabetics after test breakfast supplemented with 10 g gelled or non-gelled guar.
was
specifically recognises
the
kindly provided by the Center for
Disease Control, Atlanta, Georgia, U.S.A.
Rijksinstituut voor de Volksgezondheid, Bilthoven, Netherlands
J. L. DE FREITAS J. BORST
Department of Infectious Diseases, University Hospital, Leiden
P. L. MEENHORST
characteristics is most readily seen in high-tension electrical injury of an extremity, where non-viable muscle near the centrally located bone may underlie more superficial viable muscle and the extent of skin injury at the contact points offers little indication of the actual extent of trauma. This situation demands thorough surgical examination of the extremity, particularly of the periosseous muscles, to determine the extent of debridement or amputation necessary. Army Institute of Surgical Research, Brooke Army Medical Center,
U.S.
LEGIONELLA PNEUMOPHILA SEROTYPES to our paper on the isolation of a serotype of Legionella pneumophila (Dec. 2), we reported a preliminary finding regarding the stability of cellular antigens of the Los Angeles 1 serotype in formalin. I have been unable to duplicate this experiment, and now concur with Center for Disease Control investigators that prolonged formalin fixation of this strain does not alter its reactivity with either homologous or heterologous antisera.
SIR,-In the addendum
Fort Sam Houston, Texas 78234, U.S.A.
BASIL A. PRUITT, JR ARTHUR D. MASON, JR
FIBRE AND DIABETES
new
Division of Infectious Diseases, V. A. Wadsworth Medical Center, Los Angeles, California 90073, U.S.A.
PAUL EDELSTEIN
LEGIONNAIRES’ DISEASE AND CEREBRAL DISTURBANCE
SiR,—The difficulty of establishing a diagnosis of legionnaires’ disease solely on serological tests have been the subject of recent editorial comments.’,2 Consequently, sporadic instances of patients with unexplained pulmonary infiltrates represent a diagnostic dilemma. The patients described by Dr Lees and Dr Tyrrell (Dec. 23/30) could very well not have had legionnaires’ disease. The legionnaires’ bacillus has been successfully isolated from a transtracheal aspirate.’ Thus without cultural confirmation, Lees and Tyrell have not established the diagnosis of legionnaires’ disease. The diagnosis in the second reported patient was based initially on clinical response to erythromycin; such reasoning is untenable. Department of Infectious Diseases, Geisinger Medical Center, Danville, Pennsylvania 17821, U.S.A.
GARY R. PLOTKIN
HIGH-TENSION ELECTRICAL INJURY
SIR,-Your editorial4 properly emphasises the risk of deep tissue damage in patients with high-tension electrical injury, but the mechanism of that damage appears to be related more to the configuration of the tissue involved than to its resistarice properties. In high-voltage trauma, heat is the principal mediator of tissue injury; the differences of tissue resistance are so small that the body acts as a volume conductor. Heat is generated in this conductor as a function of voltage drop and current flow per unit cross-sectional area, or current density. This dependence upon cross-sectional area accounts for the frequency of severe injury to the extremities and the rarity of major injury to the trunk in high-tension electrical injury. At the points of contact, where density is greatest, the skin is severely injured and chars; when this occurs resistance rises sharply, limiting further passage of current and heating. The heated conductor cools, the deeper portions cooling more slowly than the superficial. Since thermal injury of tissue is dependent upon both the temperature achieved and the duration of exposure to that temperature, the deeper tissues are more liable to severe injury. The clinical reflection of these 1 British Medical Journal, 1978, ii, 1319. 2 Tsai T. F., Fraser, D. W. Ann. intern. Med, 1978, 89, 413. 3 Lattimer, G. L., McCrone, C., Galgon, J. New Engl. J. 1172.
4 Lancet, 1978, ii, 978.
Med.
1978, 299,
SIR,-Mr Wolever and colleagues have reported
on the the reducequivalent gelled non-gelled guar tion in post-prandial blood-glucose in healthy volunteers given an oral glucose load. We have been investigating the properties of several fibre compounds taken in powder form by diabetics, and as part of this study we compared the effects of guar and pectin taken in gelled and non-gelled forms. There was little difference in the effect on post-prandial glucose between 10 g guar taken in an adequately hydrated form as a blancmange and a similar dose taken in powder form. However, the meal supplied on both occasions to our subjects consisted of food items often consumed for breakfast-i.e., cornflakes (30 g), milk (200 ml), bread (35 g), butter (8 g), marmalade (25 g), tea (150 ml), and sugar (15 g). The use of normal meals is a more appropriate test of the likely effect of fibre when added to normal diets for diabetics; the addition, to a liquid test meal, of any substance, even of non-fibre origin, might affect plasmaglucose if it delayed gastric emptying and slowed glucose
effects of
and
on
absorption. Not only was the effect of gelling unimportant but the effect of the guar as such was unremarkable (see figure). Although some reduction in plasma-glucose seems to have been achieved, this reduction was not, in our subjects, statistically significant, and we doubt whether the effect in many other trials23 can be claimed to be therapeutically relevant. This limited response does not mean that dietary fibre given in a different form will not be effective, but the demonstration in diabetics that glycosuria can be reduced during a trial period with extra dietary fibre23 cannot be taken as proof that the 1. Wolever, T. M. S., Taylor, R., Goff, D. V. Lancet, 1978, ii, 1381. 2. Jenkins, D. J. A., and others. ibid. 1977, ii, 779. 3. Jenkins, D. J. A., and others. Br. med. J. 1978, ii,1744.
Increment in post-prandial plasma-glucose in four maturityonset diabetics after test breakfast supplemented with 10 g gelled or non-gelled guar.
