2
321 have studied the distribution of bacteria in a bath, and since the load of bathers varies rapidly in size and distribu- tion one might doubt whether a single sample taken anywhere gives a reliable estimate of the bacterial flora. Not much more is known of the nature and number of the bacteria which are shed from the skin, respiratory tract, and private parts of the healthy bather. A recent paper from the U.S.A. tries to answer this question.2 A bath was constructed to hold 150 gallons of sterile water and large enough to allow a simulated swimming action. In this five ladies, in turn, performed a schedule of natatory exercises, and the water in which they had bathed was then examined by a variety of methods for coliform organisms, fxcal and salivary streptococci, and staphylococci. Included in these experiments were observations on the effects of menstruation and of a preliminary shower- bath. The results of much careful work are not very striking, but they may be useful. Menstruation seems to have little effect. The beneficial results of a shower before bathing are not obvious. The girls who habitually used soap containing hexachlorophene seemed to get rid of fewer coliform bacilli than the others. In general, faecal organisms were shed in numbers insufficient to be much use as indicators of pollution. The organisms shed most consistently and in the largest numbers were staphylo- cocci. Because these organisms seem to be more resistant to chlorination than coliform bacilli and because super- ficial staphylococcal infection may be a likely consequence of bathing, other workers have suggested that these might replace coliform bacilli in the routine examination of swimming-bath water.3 With membrane filters, quantita- tive estimation presents no real difficulty. We would be interested to see these experiments repeated with staphylococci alone as indicators of pollu- tion, but with many more subjects and with varying times of immersion. There is a suggestion in the figures that shedding bacteria in the bath is a personal habit-to be deprecated but probably unpreventable. ANTIBIOTICS, CELL WALLS, AND MUCOPEPTIDASE ANTIBIOTICS can be broadly divided into those which act primarily on the cell wall, such as penicillin, and those which interfere with the synthesis of D.N.A., R.N.A., and protein, such as chloramphenicol and tetracycline. The first group are usually bactericidal, directly killing bacteria, and the second may be classed as bacteriostatic, inhibiting the vital processes of the organisms and enabling the defence mechanisms of the host to overcome them. Bactericidal antagonism may sometimes arise when a bactericidal drug is combined with one that is only bacteriostatic.5 5 The antagonism between penicillin and tetracycline has been demonstrated in vitro 6; and Lepper and Dowling 7 showed that benzylpenicillin plus tetracycline was less effective than benzylpenicillin alone in the treatment of bacterial meningitis. A reason- able explanation would be that the penicillins inhibit the formation of the bacterial cell wall, so that when growth 2. Robinton, E. D., Wood, E. W. J. Hyg., Camb. 1966, 64, 489. 3. Favero, M. S., Drake, C. H., Randall, G. B. Publ. Hlth Rep., Wash. 1964, 79, 61. 4. See Lancet, 1966, ii, 484. 5. Barber, M. Proc. R. Soc. Med. 1965, 58, 990. 6. Garrod, L. P., Waterworth, P. M. J. clin. Path. 1962, 15, 328. 7. Lepper, M. H., Dowling, H. F. Archs intern. Med. 1951, 88, 489. takes place the cells die by lysis, but when the cells are not growing (the tetracycline effect) they are not killed.5 But this explanation may be too simple. As a bacterial cell grows, its mucopeptide wall has to extend to contain its increased cytoplasmic volume. This change is accomplished by the laying down of new mucopeptide externally and the autolysis of inner mucopeptide layers, so allowing remoulding of the cell wall. The autolysis is carried out by mucopeptidases-enzymes which are receiving increased attention.8 9 All bacteria produce these enzymes, and it may be that they are important in destroying the cell wall and leading to cell death when penicillin is inhibiting further synthesis of the wall. While penicillins, even in high doses, do not inhibit protein formation a bacteriostatic agent, such as chlor- amphenicol, which interferes with protein synthesis may inhibit the production of mucopeptidase and so prevent cell lysis. Rogers 11 has demonstrated that the lysis and death of staphylococci when methicillin is added to cultures of this organism can be prevented by chlor- amphenicol, provided it is added not later than 15 minutes after the penicillin. This indicates that irre- versible damage to the cell is not caused by the inhibition of mucopeptide synthesis, provided that protein synthesis is switched off within a time that corresponds to about a fifth of a generation-time in the medium used. Further evidence of disparity in time between the effect of penicillin on cell-wall synthesis and the secondary factors leading to death or lysis of the cells is provided by Pennington and O’Grady. 12 They found that the activity of benzylpenicillin solutions on a strain of Staphylococcus aureus had to be maintained for almost 100 minutes before appreciable lysis was observed. With- drawal before the end of this critical period resulted in the rapid resumption of growth by the organism. Despite the almost immediate action of penicillin on cell-wall mucopeptide synthesis, therefore, the cells remain viable for some considerable time before lysis begins. Thus it is reasonable to suppose that interruption of cell-wall synthesis and death of the cell are separate events. While there may be several different mechanisms by which lysis is brought about, the widespread presence of mucopeptidases in bacteria suggests that they play an important part in events leading to the death of some microorganisms when penicillin is preventing the synthesis l of the cell wall. HOW NOT TO DO IT THE universities have been infuriated by the Govern- ment’s decision 13 to raise fees for overseas students from E70 to E250 a year-though with exemption of those holding scholarships from British Government agencies or already taking courses at the expense of their own Governments, and with a graded increase for others already studying here. Of the 31,000 overseas students at present taking higher- education courses of one kind or another in the United Kingdom, some 11,000 rely on private resources for their fees; and these will include a few who will have difficulty in finding the annual increment of C50 in each successive 8. Perkins, H. R. Bact. Rev. 1963, 27, 18. 9. Shockman, G. D. ibid. 1965, 29, 345. 10. Rogers, H. J., Jeljaszewicz, J. Biochem. J. 1961, 81, 576. 11. Rogers, H. J. Nature, Lond. 1967, 213, 31. 12. Pennington, J. H., O’Grady, F. ibid. p. 34. 13. House of Commons Hansard, written answer, Dec. 21, 1966, col. 375.

HOW NOT TO DO IT

Embed Size (px)

Citation preview

Page 1: HOW NOT TO DO IT

321

have studied the distribution of bacteria in a bath, andsince the load of bathers varies rapidly in size and distribu-tion one might doubt whether a single sample takenanywhere gives a reliable estimate of the bacterial flora.Not much more is known of the nature and number of thebacteria which are shed from the skin, respiratory tract,and private parts of the healthy bather. A recent paperfrom the U.S.A. tries to answer this question.2 A bath wasconstructed to hold 150 gallons of sterile water and largeenough to allow a simulated swimming action. In thisfive ladies, in turn, performed a schedule of natatoryexercises, and the water in which they had bathed was thenexamined by a variety of methods for coliform organisms,fxcal and salivary streptococci, and staphylococci.

Included in these experiments were observations onthe effects of menstruation and of a preliminary shower-bath. The results of much careful work are not verystriking, but they may be useful. Menstruation seems tohave little effect. The beneficial results of a shower before

bathing are not obvious. The girls who habitually usedsoap containing hexachlorophene seemed to get rid offewer coliform bacilli than the others. In general, faecalorganisms were shed in numbers insufficient to be muchuse as indicators of pollution. The organisms shed mostconsistently and in the largest numbers were staphylo-cocci. Because these organisms seem to be more resistantto chlorination than coliform bacilli and because super-ficial staphylococcal infection may be a likely consequenceof bathing, other workers have suggested that these mightreplace coliform bacilli in the routine examination of

swimming-bath water.3 With membrane filters, quantita-tive estimation presents no real difficulty.We would be interested to see these experiments

repeated with staphylococci alone as indicators of pollu-tion, but with many more subjects and with varying timesof immersion. There is a suggestion in the figures thatshedding bacteria in the bath is a personal habit-to bedeprecated but probably unpreventable.

ANTIBIOTICS, CELL WALLS, AND

MUCOPEPTIDASE

ANTIBIOTICS can be broadly divided into those whichact primarily on the cell wall, such as penicillin, and thosewhich interfere with the synthesis of D.N.A., R.N.A., andprotein, such as chloramphenicol and tetracycline. Thefirst group are usually bactericidal, directly killingbacteria, and the second may be classed as bacteriostatic,inhibiting the vital processes of the organisms and

enabling the defence mechanisms of the host to overcomethem.

Bactericidal antagonism may sometimes arise when abactericidal drug is combined with one that is onlybacteriostatic.5 5 The antagonism between penicillin andtetracycline has been demonstrated in vitro 6; and

Lepper and Dowling 7 showed that benzylpenicillinplus tetracycline was less effective than benzylpenicillinalone in the treatment of bacterial meningitis. A reason-able explanation would be that the penicillins inhibit theformation of the bacterial cell wall, so that when growth2. Robinton, E. D., Wood, E. W. J. Hyg., Camb. 1966, 64, 489.3. Favero, M. S., Drake, C. H., Randall, G. B. Publ. Hlth Rep., Wash.

1964, 79, 61.4. See Lancet, 1966, ii, 484.5. Barber, M. Proc. R. Soc. Med. 1965, 58, 990.6. Garrod, L. P., Waterworth, P. M. J. clin. Path. 1962, 15, 328.7. Lepper, M. H., Dowling, H. F. Archs intern. Med. 1951, 88, 489.

takes place the cells die by lysis, but when the cells arenot growing (the tetracycline effect) they are not killed.5But this explanation may be too simple. As a bacterialcell grows, its mucopeptide wall has to extend to containits increased cytoplasmic volume. This change is

accomplished by the laying down of new mucopeptideexternally and the autolysis of inner mucopeptide layers,so allowing remoulding of the cell wall. The autolysisis carried out by mucopeptidases-enzymes which arereceiving increased attention.8 9 All bacteria producethese enzymes, and it may be that they are important indestroying the cell wall and leading to cell death whenpenicillin is inhibiting further synthesis of the wall.While penicillins, even in high doses, do not inhibit

protein formation a bacteriostatic agent, such as chlor-amphenicol, which interferes with protein synthesis mayinhibit the production of mucopeptidase and so preventcell lysis. Rogers 11 has demonstrated that the lysis anddeath of staphylococci when methicillin is added to

cultures of this organism can be prevented by chlor-amphenicol, provided it is added not later than 15minutes after the penicillin. This indicates that irre-versible damage to the cell is not caused by the inhibitionof mucopeptide synthesis, provided that protein synthesisis switched off within a time that corresponds to abouta fifth of a generation-time in the medium used.

Further evidence of disparity in time between theeffect of penicillin on cell-wall synthesis and the secondaryfactors leading to death or lysis of the cells is providedby Pennington and O’Grady. 12 They found that the

activity of benzylpenicillin solutions on a strain of

Staphylococcus aureus had to be maintained for almost 100minutes before appreciable lysis was observed. With-drawal before the end of this critical period resulted inthe rapid resumption of growth by the organism. Despitethe almost immediate action of penicillin on cell-wall

mucopeptide synthesis, therefore, the cells remain viablefor some considerable time before lysis begins. Thus it isreasonable to suppose that interruption of cell-wall

synthesis and death of the cell are separate events. Whilethere may be several different mechanisms by whichlysis is brought about, the widespread presence of

mucopeptidases in bacteria suggests that they playan important part in events leading to the death of somemicroorganisms when penicillin is preventing the synthesis

l of the cell wall.

HOW NOT TO DO IT

THE universities have been infuriated by the Govern-ment’s decision 13 to raise fees for overseas students fromE70 to E250 a year-though with exemption of thoseholding scholarships from British Government agenciesor already taking courses at the expense of their ownGovernments, and with a graded increase for othersalready studying here.Of the 31,000 overseas students at present taking higher-

education courses of one kind or another in the United

Kingdom, some 11,000 rely on private resources for theirfees; and these will include a few who will have difficultyin finding the annual increment of C50 in each successive

8. Perkins, H. R. Bact. Rev. 1963, 27, 18.9. Shockman, G. D. ibid. 1965, 29, 345.

10. Rogers, H. J., Jeljaszewicz, J. Biochem. J. 1961, 81, 576.11. Rogers, H. J. Nature, Lond. 1967, 213, 31.12. Pennington, J. H., O’Grady, F. ibid. p. 34.13. House of Commons Hansard, written answer, Dec. 21, 1966, col. 375.

Page 2: HOW NOT TO DO IT

322

year during the rest of their course. A dean of one largemedical school estimates that two or perhaps three of hisundergraduate students will need help to complete theircourse-help that will have to come from the university’scoffers.

In medicine the effect of the increase on numbers

coming from overseas is likely to be most evident in entriesfor full-time postgraduate courses-notably courses forthe diploma in tropical medicine and hygiene. Of 47

attending the present course for this diploma at the Lon-don School of Hygiene and Tropical Medicine, 37 havepaid their own fees. At one of the other centres runningcourses for this diploma, an informal census of those whohave paid their own fees has suggested that half wouldcertainly have been unable to attend under the new feesystem, and another quarter would have found it hard toso do. An orderly decline in numbers taking this diplomain the United Kingdom would not strike everyone as

catastrophic-if there is to be such a diploma, it is prob-ably best taken in the tropics. But an orderly decline ismuch different from the problematical but probably sub-stantial fall in numbers at the next intake. The LondonSchool of Hygiene offers many postgraduate courses be-sides that for the D.T.M. & H.; and, as Dr. Spooner, theSchool’s dean, points out in a letter on a later page, a dropin the numbers of the fairly senior people coming fromabroad for any of these courses would represent a real lossto this country. In faculties of medicine and, morenotably, of science, heads of departments predict grosscurtailment in numbers of PH.D. students from the UnitedStates and the Commonwealth-an especially gloomyprospect, since these students often contribute both to

teaching and to running the department.University teachers, like their students, resent the

discriminatory character of the proposed increase. Theyare, moreover, anxious lest, by preventing potential under-graduate students from applying, this increase may hinderthe pursuit of universality in the universities. In medicine,as in other faculties, not all the overseas students comefrom the tropics. For instance, universities in the North-East have long accepted each year a few from Norway:not all obtain a scholarship or have long purses; but theseScandinavian visitors, like others from beyond these

shores, make a contribution which the universities are lothto forgo.The Government’s best course would be to acknowledge

that it has made a gaffe and rescind its decision. Failingthis, it might devote the additional revenue from theincrease to scholarships for the needy; 2 or it might extendthe increase to all. For United Kingdom students, underthe comprehensive system of grants such an extensionwould entail increased payment only by the fairly well-to-do ; but it would have the merit of stilling the charge ofApartheid-and, for the universities, it might bring a realgain in flexibility with a lessened sense of threat fromGovernmental encroachment.

SHOE DERMATITIS

THE diagnosis and treatment of skin diseases of the feetis not quite as simple as it might seem to those who regardfungal infection as responsible for the vast majority ofcases. Ideas about the aetiology of even such a commoncondition as " toe-rot " have had to be revised since theadvent of griseofulvin, which, while specific in the controlof true mycelial infection, leaves interdigital maceration

2. See Lancet, Feb. 4, 1967, p. 262.

quite unchanged-apparently because of the part playedby yeast organisms in this continually moist flexural area.Possibly the most important effect of the wearing of shoesis the creation of a warm and humid subtropical environ-ment, especially when non-porous rubber soles are used.True sensitivity to allergens in shoe material has beenrecognised for many years. Bloch was the first in the

English literature to describe a case in which a patch testto the leather was positive, and when the shoes werechanged the patient recovered. Since then, shoedermatitis has been closely studied to try to eliminate theallergens.

Shoes are normally made of an upper and a sole. The

upper is most commonly leather, which is chrome or

vegetable tanned, but usually there is also a lining oflinen, paper, or vegetable-tanned leather. The sole is

generally vegetable-tanned leather or rubber. (In Americaand Scandinavia, an added item is the thermoplastictoecap, which is seldom seen in this country.)

Calnan and Sarkany 2 reviewed 102 cases of shoedermatitis seen over six years at St. John’s Hospital,London. 63% had positive patch tests to leather, and36% to rubber (in each case, the patient’s actual shoematerial was used). But whereas further patch tests

showed that in the rubber-sensitive cases the vast majoritywere sensitive to mercapto-benzthiazole or tetramethyl-thiuram sulphide (chemicals commonly used in themanufacture of rubber), in the leather-sensitive patientsonly about 13% reacted to potassium dichromate.Cronin 3 has based a follow-up report to the Calnan

and Sarkany series on a further 111 cases between 1960and 1965. It seems that since 1959 the incidence of rubber

sensitivity has been increasing, and vegetable-tannedleather (especially East Indian) is now a much commonercause of trouble than the chrome-tanned variety. This

may be partly due to the fact that the leather manu-facturers are careful to process their material in such a

way that chrome salts cannot easily be leached out (bysweat, for example), and also in most shoes a protectivelining prevents much sweat reaching the upper. Thenature of the allergen in vegetable-tanned leather isundetermined.That chrome sensitivity can arise at times on quite a

large scale was demonstrated by Scutt.4 Over 100 navalratings were invalided home from the tropics withdermatitis of the dorsum of the foot after they had beenwearing unlined chrome-tanned leather sandals. About

70% had a positive patch test to potassium dichromate.Trauma and sweating were thought to play a large partin preparing the way for sensitisation. Once chrome

sensitivity is established, only minute quantities ofchrome salts need be leached out to keep the eczematousprocess smouldering. Clearly the moist environmentcaused by rubber soles is liable to foster such a process.When sensitivity to shoe materials has been acquired,

cure depends on how far the patient can avoid the offend-ing substance. But he will not find it easy to determinefrom the retailer whether or not such-and-such an allergenis present in the finished article. There is a strong casetherefore for requiring the manufacturer to state for

every type of shoe whether the leather is full-chrome,semi-chrome, or vegetable-tanned, and whether any ofthe well-known sensitisers are present in the rubber.1. Bloch, B. Archs Derm. Syph. 1929, 19, 175.2. Calnan, C. D., Sarkany, I. Trans. St. John’s Hosp. derm. Soc., Lond.

1959, 43, 8.3. Cronin, E. Br. J. Derm. 1966, 78, 617.4. Scutt, R. W. B. ibid. p. 337.