1124 is any more dangerous when cloned in, say, a plasmid. But none of this (Wolstenholme again) would seem to warrant abandonment of either the principles set out in the reports of the Ashby and Williams working-parties
or the G.M.A.G. The G.M.A.G. has lived beyond its first life of two years. How can it, especially in the light of the revised N.I.H. guidelines and the tendency of other countries to
look now to Bethesda rather than London for a lead, make concessions to the changed mood of scientists while not looking complacent to the public? Anyone suggesting that scientists can be left to police themselves in this area is likely to be reminded of the ill-fated scrutiny of the Birmingham smallpox laboratory. What makes the British approach seem, if not old-fashioned, then certainly more bureaucratic and inflexible, is the role of the Health and Safety Executive; a voluntary system of notification which was working well became compulsory last August. Recombinant D.N.A. research holds out exciting prospects for medicine and, especially in the Third World, for agriculture. As experience accumulates, and a lot already has, it will almost certainly become clear that much of this work can be done with less paperwork than was originally feared (perhaps by licensing laboratories rather than projects and by downgrading certain category-i research). What is less certain is whether a statutory Executive designed to make the factory floor safer will be able to respond rapidly to changes in attitudes or facts in an area of research where the risks are not potential but conjectural.
TINNITUS
TINNITUS is usually associated with a hearing defect arising from a disordered neural mechanism of the ear or the auditory pathways. Thus tumours of the cerebellopontine angle, brainstem lesions, and abnormalities of the vascular system must be excluded. Treatable ear disease, such as otosclerosis, chronic otitis media, and labyrinthine lesions, should receive attention. The subjective symptom of tinnitus does not necessarily demand treatment. Explanation of the nature of the symptom, and reassurance that it is not of serious import, enables most patients to live with tinnitus, even to lose it altogether for long periods; but, if treatment is required because of distress and loss of sleep, the choice and the results of therapy are extremely varied, reflecting our limited understanding of this very common symptom. In many cases tinnitus is central, even though the original lesion is commonly in the end-organ and the efferent component of the auditory neural connections may play a part in causing it. Barbiturates are among the more successful medicaments, perhaps because they act on the reticular part of the central nervous system and depress this efferent pathway: amylobarbitone helped most of the forty patients in a recent series. A similar assumption of a central pool of neuronal hyperactivity triggered by a decrease in the afferent impulses from the cochlea has led to the use of intravenous lignocaine. The tinnitus was temporarily controlled in many cases,2 especially in
Meniere’s disease and acoustic trauma where the lesion involved the organ of Corti. Anticonvulsants3 have been tried, to control the abnormal neural activity, and carbamazepine (or, occasionally, phenytoin) relieved the noises in some two-thirds of a small group of patients, while many reported an improvement in their hearing, or at least less distortion. Some patients can control or mask their tinnitus by using background noise from the motor of a fan or from the radio. Pulec and his associates4 analysed the frequency and intensity of the tinnitus in twenty-eight patients, and in twenty-three it proved maskable with a wide-band or high-frequency tinnitus masker, worn behind the ear like a hearing aid, generating the right kind of noise. This could be combined with a hearing aid if necessary. Pulec and others picture a mechanical effect in the cochlea giving rise to tinnitus in many cases without any disturbance in the neural activity of the auditory connections. Undoubtedly tinnitus may be generated in different ways by different méchanisms, and the tinnitus masker is likely to prove a useful, non-invasive method of helping some patients.
SEPSIS, SEPTICÆMIA, AND THE SEA THE isolation of unusual microbes from clinical material tends to be greeted with raised eyebrows. The list is long and the offenders many. Perhaps more often than not such organisms represent opportunist infection in a susceptible host from some environmental source. One such is the sea; indeed, some marine bacteria, especially Vibrio parahæmolyticus (well established as a cause of gastroenteritis associated with seafoods5,6 and widely distributed in British coastal waters3) and its close relation V. alginolyticus, have already been isolated in several countries from soft-tissue and ear infections in bathers, fishermen, and others at risk.7-11Detailed comparison of such isolates received by specialist laboratories can often yield even more information. Thus, in recent study of halophilic vibrios isolated in America, a small group of apparently identical organisms was recognised.12 These strains closely resembled V. parahcemolyticus and V. alginolyticus but were clearly distinguishable by a lower tolerance for salt, by failure to ferment sucrose, and by their ability to ferment lactose, albeit slowly. The separate taxonomic identity of these lactose-positive (L+) vibrios was also supported by D.N.A. hybridisation results." The clinical and epidemiological features of 39 of 48 reported L+ vibrio infections are now described in another paper from the United States.14 They had 3. Melding, P. S., Goodey, R. J., ibid. 1979, 93, 111. 4. Pulec, J. L., Hodell, J. F., Anthony, P. F. Ann. Otol. 1978, 87, 821 5. Sakazaki, R. in The Microbiological Safety of Food (edited by B. C. Hobbs and J. H. B. Christian); p.19, 375. London, 1973. 6. Barrow, G. I., Miller, D. C. in Microbiology in Agriculture, Fisheries and Food (edited by F. A. Skinner, and J. G. Carr); p. 181. London, 1976. 7. Ayres, P. A., Barrow, G. I. J. Hyg., Camb., 1978, 80, 281. 8. Thorsteinsson, S. B., Minuth, J. N., Musher, D. M. Lancet, 1974, ii, 1283. 9. Ryan, W. J. J. clin. Path. 1976, 29, 1014. 10. McSweeney, R. J., Forgan-Smith, W. R. Med. J. Aust. 1977, i, 896. 11. Olsen, H. Acta path. microbiol. scand., Sect. B. 1978, 86, 247. 12. Hollis, D. G., Weaver, R. E., Baker, C. N., Thornsberry, C. J. Clin. Micro-
biol. 1976, 3, 425. 1. Donaldson, I. J. Laryng. Otol. 1978, 92, 123. 2. Melding, P. S., Goodey, R. J., Thorne, P. R., ibid. p.
115.
13. Clark, W. A., Steigerwalt, A. G. Int. J. syst. Bacteriol. 1977, 27, 194. 14. Blake, P. A., Merson, M. H., Weaver, R. E., Hollis, D. G., Heublein, P. C. New Engl. J. Med. 1979, 300, 1.
or the G.M.A.G. The G.M.A.G. has lived beyond its first life of two years. How can it, especially in the light of the revised N.I.H. guidelines and the tendency of other countries to
look now to Bethesda rather than London for a lead, make concessions to the changed mood of scientists while not looking complacent to the public? Anyone suggesting that scientists can be left to police themselves in this area is likely to be reminded of the ill-fated scrutiny of the Birmingham smallpox laboratory. What makes the British approach seem, if not old-fashioned, then certainly more bureaucratic and inflexible, is the role of the Health and Safety Executive; a voluntary system of notification which was working well became compulsory last August. Recombinant D.N.A. research holds out exciting prospects for medicine and, especially in the Third World, for agriculture. As experience accumulates, and a lot already has, it will almost certainly become clear that much of this work can be done with less paperwork than was originally feared (perhaps by licensing laboratories rather than projects and by downgrading certain category-i research). What is less certain is whether a statutory Executive designed to make the factory floor safer will be able to respond rapidly to changes in attitudes or facts in an area of research where the risks are not potential but conjectural.
TINNITUS
TINNITUS is usually associated with a hearing defect arising from a disordered neural mechanism of the ear or the auditory pathways. Thus tumours of the cerebellopontine angle, brainstem lesions, and abnormalities of the vascular system must be excluded. Treatable ear disease, such as otosclerosis, chronic otitis media, and labyrinthine lesions, should receive attention. The subjective symptom of tinnitus does not necessarily demand treatment. Explanation of the nature of the symptom, and reassurance that it is not of serious import, enables most patients to live with tinnitus, even to lose it altogether for long periods; but, if treatment is required because of distress and loss of sleep, the choice and the results of therapy are extremely varied, reflecting our limited understanding of this very common symptom. In many cases tinnitus is central, even though the original lesion is commonly in the end-organ and the efferent component of the auditory neural connections may play a part in causing it. Barbiturates are among the more successful medicaments, perhaps because they act on the reticular part of the central nervous system and depress this efferent pathway: amylobarbitone helped most of the forty patients in a recent series. A similar assumption of a central pool of neuronal hyperactivity triggered by a decrease in the afferent impulses from the cochlea has led to the use of intravenous lignocaine. The tinnitus was temporarily controlled in many cases,2 especially in
Meniere’s disease and acoustic trauma where the lesion involved the organ of Corti. Anticonvulsants3 have been tried, to control the abnormal neural activity, and carbamazepine (or, occasionally, phenytoin) relieved the noises in some two-thirds of a small group of patients, while many reported an improvement in their hearing, or at least less distortion. Some patients can control or mask their tinnitus by using background noise from the motor of a fan or from the radio. Pulec and his associates4 analysed the frequency and intensity of the tinnitus in twenty-eight patients, and in twenty-three it proved maskable with a wide-band or high-frequency tinnitus masker, worn behind the ear like a hearing aid, generating the right kind of noise. This could be combined with a hearing aid if necessary. Pulec and others picture a mechanical effect in the cochlea giving rise to tinnitus in many cases without any disturbance in the neural activity of the auditory connections. Undoubtedly tinnitus may be generated in different ways by different méchanisms, and the tinnitus masker is likely to prove a useful, non-invasive method of helping some patients.
SEPSIS, SEPTICÆMIA, AND THE SEA THE isolation of unusual microbes from clinical material tends to be greeted with raised eyebrows. The list is long and the offenders many. Perhaps more often than not such organisms represent opportunist infection in a susceptible host from some environmental source. One such is the sea; indeed, some marine bacteria, especially Vibrio parahæmolyticus (well established as a cause of gastroenteritis associated with seafoods5,6 and widely distributed in British coastal waters3) and its close relation V. alginolyticus, have already been isolated in several countries from soft-tissue and ear infections in bathers, fishermen, and others at risk.7-11Detailed comparison of such isolates received by specialist laboratories can often yield even more information. Thus, in recent study of halophilic vibrios isolated in America, a small group of apparently identical organisms was recognised.12 These strains closely resembled V. parahcemolyticus and V. alginolyticus but were clearly distinguishable by a lower tolerance for salt, by failure to ferment sucrose, and by their ability to ferment lactose, albeit slowly. The separate taxonomic identity of these lactose-positive (L+) vibrios was also supported by D.N.A. hybridisation results." The clinical and epidemiological features of 39 of 48 reported L+ vibrio infections are now described in another paper from the United States.14 They had 3. Melding, P. S., Goodey, R. J., ibid. 1979, 93, 111. 4. Pulec, J. L., Hodell, J. F., Anthony, P. F. Ann. Otol. 1978, 87, 821 5. Sakazaki, R. in The Microbiological Safety of Food (edited by B. C. Hobbs and J. H. B. Christian); p.19, 375. London, 1973. 6. Barrow, G. I., Miller, D. C. in Microbiology in Agriculture, Fisheries and Food (edited by F. A. Skinner, and J. G. Carr); p. 181. London, 1976. 7. Ayres, P. A., Barrow, G. I. J. Hyg., Camb., 1978, 80, 281. 8. Thorsteinsson, S. B., Minuth, J. N., Musher, D. M. Lancet, 1974, ii, 1283. 9. Ryan, W. J. J. clin. Path. 1976, 29, 1014. 10. McSweeney, R. J., Forgan-Smith, W. R. Med. J. Aust. 1977, i, 896. 11. Olsen, H. Acta path. microbiol. scand., Sect. B. 1978, 86, 247. 12. Hollis, D. G., Weaver, R. E., Baker, C. N., Thornsberry, C. J. Clin. Micro-
biol. 1976, 3, 425. 1. Donaldson, I. J. Laryng. Otol. 1978, 92, 123. 2. Melding, P. S., Goodey, R. J., Thorne, P. R., ibid. p.
115.
13. Clark, W. A., Steigerwalt, A. G. Int. J. syst. Bacteriol. 1977, 27, 194. 14. Blake, P. A., Merson, M. H., Weaver, R. E., Hollis, D. G., Heublein, P. C. New Engl. J. Med. 1979, 300, 1.
