1044

No-one working with these protozoa in the laboratory canfail to be impressed by the many wide differences theyexhibit. T. hominis has entirely different growth require-ments from T. vaginalis, and fails to grow in media whichsupport a profuse growth of T. vaginalis.

Uncritical acceptance of the view that the infectionoriginates in the bowel can only obscure the true factsand postpone fuller investigation of the actual meansof transmission of this troublesome infection.

Liverpool. M. G. McENTEGART.M. G. MCENTEGART.

1. Barr, M., Glenny, A. T., Howie, J. W. J. Path. Bact. 1953, 65, 155.2. Barr, M., Glenny, A. T., Randall, K. J. Lancet, 1950, i, 6.

DIAGNOSIS OF ACUTE MENINGITIS ININFANCY

W. P. SWEETNAMConsultant Pædiatrician.Halifax General Hospital.

SiR,-Dr. Haworth, in his article of May 9, rightlycalls attention to the frequent absence of the " classicalsigns " of meningitis in infancy and to the necessity forearly lumbar puncture. Recent emphasis in your leadingarticle of April I on the hazards of lumbar punctureshould not deter us from the use of this valuable diag-nostic aid. The wide range of antibiotic and chemo-therapeutic agents now available should further reducethe mortality. But how often is the hospital clinicianneedlessly handicapped by the indiscriminate use ofthese drugs which, in many cases, only result in disguisingthe clinical signs and making the identification of thecausal organism difficult or impossible ? In these difficultcases a full history from the general practitioner is

always helpful, but what is probably more importantis a detailed account of the treatment given prior toadmission.

DIET AND IMMUNITY

MOLLIE BARR.Wellcome Research Laboratories,Beckenham, Kent.

SiR,-Your leading article of May 9 ends with a

statement for which there is surely little evidence. Thisstatement reads :

"... we can learn from the Scottish blackface ewes and theirlambs that ... the most effective interval between injectionsof the antigen [A.P.T.] is two months, ... and that routineimmunisation with A.P.T. should not be applied to infants

during the first few months of life."In one of the papers under review 1 it was shown that,

with the particular dosage used in ewes, an interval ofnine weeks between injections was definitely better thanan interval of four weeks ; but no other interval wastried. The optimum interval depends on the size of thedose and perhaps on the species of animal, and it isprobable that an interval of three months can be regardedas best in the immunisation of young babies with A.P.T.2It was also shown that a rough correlation existedbetween the total passive maternally conferred diph-theria antitoxin of lambs, and their response to the firstand to the second injection of A.P.T. given in a course ofactive immunisation. Considerable if not total inter-ference with the primary response was caused by thepresence of sufficient antitoxin to neutralise half theA.P.T.

Evidence had previously, however, been published 2

showing that babies can be successfully immunised bytwo doses, each 0-5 ml. of A.P.T., if the titre of maternallyconferred antitoxin is below 0.04 unit per ml. at the timeof the first injection.

In recent unpublished work carried out at theselaboratories and in collaboration with Dr. N. R. Butlerof University College Hospital, we have been investi-gating the efficiency of three prophylactics in the immu-nisation of babies. All consisted of purified toxoid,partially or totally adsorbed on mineral carriers. Of 167babies receiving the first injection at the age of about 1week and the second injection either at 6 or 14 weeks,161 (96-3%) had active antitoxin titres above the Schicklevel when measured at the aa-e of 9 or 12 months. Of

115 babies receiving injections at the ages of 6 and 14weeks, all but 1 had titres above the Schick level when 9or 12 months old. This population was a random sample,6-4% of whom had cord-blood titres of 1.0 unit per ml. ormore, compared with 7-1% in 3000 samples of cord-bloodtested here during the last few years.From the evidence available, it would appear that a

very high proportion of babies born at the present timecan be satisfactorily immunised against diphtheria duringthe first few months of life, so long as a precipitated oradsorbed prophylactic is used. Attention has, however,been drawn to the fact that a large proportion of failuresmight follow the use of plain fluid purified toxoid, if thefirst of three injections were given at or before the ageof 10 days.3

3. Barr, M., Glenny, A., T. Hignett, S., Randall, K. J., Thomson, A.Ibid, 1952, ii, 803.

4. Fetcher, E. S., Hall, J. F., Shaub, H. G. U.S. Air ForceMemorandum. March, 1949.

5. Pickering, G. W., Hess, W. Clin. Sci. 1933, 1, 213.6. Lewis, T., Pickering, G. W. Heart, 1931, 16, 33.

INVOLVEMENT OF AUTONOMIC NERVE-FIBRESIN DIABETIC NEUROPATHY

A. MCPHERSON.Physiology Department,

St. Mary’s Hospital Medical School,London, W.2.

SiR,-As Dr. Allwood and Mr. Burry (April 18) pointout, it is not necessary to have a rate of heat loss as greatas 240 kg. cal./hr./m2 if only gross changes in blood-floware to be estimated by means of skin-temperaturemeasurements. It is sufficient if the extremity of a nudesubject is placed in a cold box or if the extremity of thewarmly dressed subject is exposed in a cold room.4 Evenunder these conditions, however, the estimation of blood.flow changes in the feet by skin-temperature measurementmay be especially difficult. In my own experience 25%of normal subjects show only a twofold increase in footblood-flow (measured plethysmographically) in responseto prolonged heating of the forearms and hands in water-baths at 45°C, and this increase may be too small todetect by means of skin-temperature measurement.

Pickering and Hess 5 found that it was sometimesdifficult to produce vasodilatation in the feet, and theydescribed one normal subject in whom they completelyfailed to produce vasodilatation (estimated by skin-

temperature measurement). Because of this, failure toproduce a marked increase in the skin-temperature of thefeet, in response to warming the body elsewhere, has tobe regarded with circumspection before it is interpretedas being due to autonomic involvement.Even if one assumes that the skin-temperature measure-

ments of patients with diabetic neuropathy are a reason.able reflection of the limb blood-flow, failure to producevasodilatation in response to warming cannot be inter.preted as being due to disease of the autonomic nervoussystem unless certain other possibilities are excluded. Forexample, occlusive vascular disease may be responsiblefor this effect, and the fact that Priscol’ (tolazoline)may produce vasodilatation in patients suffering fromdiabetic neuropathy is not adequate evidence of theabsence of vascular disease. It is quite conceivable thatpriscol may dilate a diseased artery although physiologicalstimuli will not. Disuse of the limbs with a consequentdecrease in their metabolic activity and increase in theirvenous pressure may also affect the vasomotor reactions.Lewis and Pickering 6 have shown that the relative disuseof one limb even for half an hour will produce differencesin the skin-temperature of the limbs which persist after j:warming the body. Similar differences are produced if the initial temperature of one limb is lower than thatof the other.

It is for these and similar reasons that I suggested that IDr. Martin’s conclusions (March 21) should be examined

with caution. ’