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HOW DO ANTIBIOTIC-RESISTANT STAPHYLOCOCCI ARISE?
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usually impossible, and many of them become demoralised. Simple measures are of no avail, and for this group Chevalier and Simon advocate a step-by-step approach, with infiltration of the preaortic plexus with procaine or ligation of the internal mammary artery under local anxsthesia
If these measures fail, the first stage. myxcedema is induced with radioactive iodine; only if this is unsuccessful is one of the cardiac revascularisation operations advised-usually the Harken or Beck-1 type. Finally, if all else fails, bilateral section of the upper four posterior thoracic nerve-roots is recommended, solely to abolish pain. Whilst this is claimed to be a rational approach, it would seem more logical to determine which measure offers the best chance of success with the least risk, and to advise this in all cases; but this is easier said than done, for accurate comparison is notoriously difficult in angina pectoris, and, as we have already indicated,3 no single procedure is at present clearly preferable to all others. The enthusiasm following recent claims 4-6 that iproniazid greatly reduces angina has been tempered by the high incidence of side-effects and occasional jaundice. Shoshkes et al. have obtained good results in a small series of patients with far smaller doses than those previously advocated. 50 mg. or less per day proved effective and was associated with considerable reduction in sideeffects : liver damage was not encountered, but this is no guarantee that it cannot occur at this level. as
HOW DO ANTIBIOTIC-RESISTANT STAPHYLOCOCCI ARISE?
Waisbren and Strelitzerset out to discover whether administration of an antibiotic caused a change in the sensitivity of the staphylococci infecting the patient. They studied 50 patients from whom coagulase-positive staphylococci were isolated before and after treatment with one or more of all the common antibiotics. The differences between the two cultures in their sensitivity to the antibiotics were ascertained, and an attempt was made to correlate these differences with the antibiotics that were given. These workers also sought to discover whether giving more than one antibiotic at a time reduced the risk that the infecting bacteria would acquire resistance. They recognised the difficulties inherent in their study. Without phage-typing, which they applied to only 4 pairs of cultures, they did not know whether the second isolate was of the same type as the first or could have been acquired by the patient as a new infection from the hospital environment. In each of the 4 pairs on which phagetyping was done-in all of which resistance to penicillin had increased-the second isolate was of a different type In the 14 patients from whom only from the first. isolated from the blood were compared, staphylococci there was no change in resistance. From all their sensitivity tests on the organisms from their 50 patients, Waisbren and Strelitzer had 152 instances in which bacterial sensitivity tests were made before and after In 53, the sensitivity of the antibiotics were given. staphylococci remained the same to the antibiotic that was administered; in 57, the second isolate was more resistant; and in 42 it was more sensitive. In 17 patients to whom a single antibiotic was given, 5 instances of 3. 4. 5. 6. 7.
Lancet, Oct. 24, 1959, p. 653. Cesarman, T. Arch. Inst. Cardiol. Mex. 1957, 27, 563. Cossio, P. Amer. Heart J. 1958, 56, 113. Master, A. M. ibid. p. 570. Shoshkes, M., Rothfeld, E. L., Becker, M. C., Finkelstein, A., Smith, C. C., Wachtel, F. W. Circulation, 1959, 20, 17. 8. Waisbren, B. A., Strelitzer, C. L. Amer. J. med. Sci. 1959, 238, 202.
increased resistance were found; and in 27 who received two antibiotics 14 instances of increased resistance were observed. Without full details it is hard to assess the authors’ conclusion that these figures show that combinations of antibiotics do not apparently affect the subsequent development of resistance. They consider that these results show that the administration of an antibiotic to a patient does not greatly influence the antibiotic sensitivity of infecting staphylococci. In the light of this, they explain the present dominance of antibiotic-resistant staphylococci in hospitals by invoking the organism’s great capability of variation, which will continually make antibiotics obsolete. They regard this explanation as independent of the factor of antibiotic usage and a constant stimulus for the development of new anti-
staphylococcal drugs. Such development
is certainly important, but it does not seem to need to be pressed in existing circumstances. On the other hand, it would be unfortunate if this interesting paper caused doctors to look away from the importance of infection of patients in hospitals with the resistant staphylococci already well established there. Moreover, the resistance pattern of the staphylococci carried by the staff of hospitals accurately indicates which antibiotics have been used in that hospital. The organisms in a patient’s lesion are not the only, or perhaps the important, ones in the spread of resistant staphylococci. Sensitive staphylococci may be eliminated from the patient’s nasopharynx leaving that area ready for colonisation by the resistant organisms already there or acquired from his nurse or another patient. Nor should we forget that aerosols of antibiotic may be inhaled and directly eliminate sensitive organisms from the nasopharynx.9 Certainly we must encourage the search for new antibiotics, but we must continually plead for the wise and restrained use of those we already have. (Barber et al.10 reached the important conclusion that the use of two antibiotics in combination might be of value. In particular, they found that the use of novobiocin might prevent the emergence of erythromycin-resistant staphylococci.) Nor must we take a defeatist attitude in the difficult matter of eventually understanding and controlling the spread of infection in our hospitals. Accurate ascertainment of its extent is an important first step, and further progress in thought and action on that aspsct is fortunately apparent.ll Williams et al.12 have made a very intensive study of the relationship between nasal staphylococci and sepsis in hospital patients. Their work shows clearly the increasing colonisation of the noses of patients with resistant strains during their stay in hospital. They established, moreover, that the incidence of postoperative staphylococcal wound sepsis was 2% in 342 patients who were never nasal carriers of staphylococci, and 7’1% in 380 who were carriers at some time. THE
next
session of the General Medical Council will
Tuesday, Nov. 24, at 2.15 P.M., when Sir DAVID CAMPBELL, the president, will deliver an address. The Medical Disciplinary Committee will sit on Wednesday, Nov. 25, at
open
on
10.30
A.M.
9. Gould, J. C. Lancet, 1958, i, 489. 10. Barber, M., Csillag, A., Medway, A. J. Brit. med. J. 1958, ii, 1377 11. Coles, R. B. Mon. Bull. Minist. Hlth Lab. Serv. 1959, 18, 132. 12. Williams, R. E. O., Jevons, M. P., Shooter, R. A., Hunter, C. J. W., Girling, A., Griffiths, J. D., Taylor, G. W. Brit. med. J. Oct. 10, 1959,
J.
p. 658.
usually impossible, and many of them become demoralised. Simple measures are of no avail, and for this group Chevalier and Simon advocate a step-by-step approach, with infiltration of the preaortic plexus with procaine or ligation of the internal mammary artery under local anxsthesia
If these measures fail, the first stage. myxcedema is induced with radioactive iodine; only if this is unsuccessful is one of the cardiac revascularisation operations advised-usually the Harken or Beck-1 type. Finally, if all else fails, bilateral section of the upper four posterior thoracic nerve-roots is recommended, solely to abolish pain. Whilst this is claimed to be a rational approach, it would seem more logical to determine which measure offers the best chance of success with the least risk, and to advise this in all cases; but this is easier said than done, for accurate comparison is notoriously difficult in angina pectoris, and, as we have already indicated,3 no single procedure is at present clearly preferable to all others. The enthusiasm following recent claims 4-6 that iproniazid greatly reduces angina has been tempered by the high incidence of side-effects and occasional jaundice. Shoshkes et al. have obtained good results in a small series of patients with far smaller doses than those previously advocated. 50 mg. or less per day proved effective and was associated with considerable reduction in sideeffects : liver damage was not encountered, but this is no guarantee that it cannot occur at this level. as
HOW DO ANTIBIOTIC-RESISTANT STAPHYLOCOCCI ARISE?
Waisbren and Strelitzerset out to discover whether administration of an antibiotic caused a change in the sensitivity of the staphylococci infecting the patient. They studied 50 patients from whom coagulase-positive staphylococci were isolated before and after treatment with one or more of all the common antibiotics. The differences between the two cultures in their sensitivity to the antibiotics were ascertained, and an attempt was made to correlate these differences with the antibiotics that were given. These workers also sought to discover whether giving more than one antibiotic at a time reduced the risk that the infecting bacteria would acquire resistance. They recognised the difficulties inherent in their study. Without phage-typing, which they applied to only 4 pairs of cultures, they did not know whether the second isolate was of the same type as the first or could have been acquired by the patient as a new infection from the hospital environment. In each of the 4 pairs on which phagetyping was done-in all of which resistance to penicillin had increased-the second isolate was of a different type In the 14 patients from whom only from the first. isolated from the blood were compared, staphylococci there was no change in resistance. From all their sensitivity tests on the organisms from their 50 patients, Waisbren and Strelitzer had 152 instances in which bacterial sensitivity tests were made before and after In 53, the sensitivity of the antibiotics were given. staphylococci remained the same to the antibiotic that was administered; in 57, the second isolate was more resistant; and in 42 it was more sensitive. In 17 patients to whom a single antibiotic was given, 5 instances of 3. 4. 5. 6. 7.
Lancet, Oct. 24, 1959, p. 653. Cesarman, T. Arch. Inst. Cardiol. Mex. 1957, 27, 563. Cossio, P. Amer. Heart J. 1958, 56, 113. Master, A. M. ibid. p. 570. Shoshkes, M., Rothfeld, E. L., Becker, M. C., Finkelstein, A., Smith, C. C., Wachtel, F. W. Circulation, 1959, 20, 17. 8. Waisbren, B. A., Strelitzer, C. L. Amer. J. med. Sci. 1959, 238, 202.
increased resistance were found; and in 27 who received two antibiotics 14 instances of increased resistance were observed. Without full details it is hard to assess the authors’ conclusion that these figures show that combinations of antibiotics do not apparently affect the subsequent development of resistance. They consider that these results show that the administration of an antibiotic to a patient does not greatly influence the antibiotic sensitivity of infecting staphylococci. In the light of this, they explain the present dominance of antibiotic-resistant staphylococci in hospitals by invoking the organism’s great capability of variation, which will continually make antibiotics obsolete. They regard this explanation as independent of the factor of antibiotic usage and a constant stimulus for the development of new anti-
staphylococcal drugs. Such development
is certainly important, but it does not seem to need to be pressed in existing circumstances. On the other hand, it would be unfortunate if this interesting paper caused doctors to look away from the importance of infection of patients in hospitals with the resistant staphylococci already well established there. Moreover, the resistance pattern of the staphylococci carried by the staff of hospitals accurately indicates which antibiotics have been used in that hospital. The organisms in a patient’s lesion are not the only, or perhaps the important, ones in the spread of resistant staphylococci. Sensitive staphylococci may be eliminated from the patient’s nasopharynx leaving that area ready for colonisation by the resistant organisms already there or acquired from his nurse or another patient. Nor should we forget that aerosols of antibiotic may be inhaled and directly eliminate sensitive organisms from the nasopharynx.9 Certainly we must encourage the search for new antibiotics, but we must continually plead for the wise and restrained use of those we already have. (Barber et al.10 reached the important conclusion that the use of two antibiotics in combination might be of value. In particular, they found that the use of novobiocin might prevent the emergence of erythromycin-resistant staphylococci.) Nor must we take a defeatist attitude in the difficult matter of eventually understanding and controlling the spread of infection in our hospitals. Accurate ascertainment of its extent is an important first step, and further progress in thought and action on that aspsct is fortunately apparent.ll Williams et al.12 have made a very intensive study of the relationship between nasal staphylococci and sepsis in hospital patients. Their work shows clearly the increasing colonisation of the noses of patients with resistant strains during their stay in hospital. They established, moreover, that the incidence of postoperative staphylococcal wound sepsis was 2% in 342 patients who were never nasal carriers of staphylococci, and 7’1% in 380 who were carriers at some time. THE
next
session of the General Medical Council will
Tuesday, Nov. 24, at 2.15 P.M., when Sir DAVID CAMPBELL, the president, will deliver an address. The Medical Disciplinary Committee will sit on Wednesday, Nov. 25, at
open
on
10.30
A.M.
9. Gould, J. C. Lancet, 1958, i, 489. 10. Barber, M., Csillag, A., Medway, A. J. Brit. med. J. 1958, ii, 1377 11. Coles, R. B. Mon. Bull. Minist. Hlth Lab. Serv. 1959, 18, 132. 12. Williams, R. E. O., Jevons, M. P., Shooter, R. A., Hunter, C. J. W., Girling, A., Griffiths, J. D., Taylor, G. W. Brit. med. J. Oct. 10, 1959,
J.
p. 658.