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Apparently it is the influenza virus itself which doesthe trick ; centrifugation which can throw down thevirus also deposits the agglutinating agent. More-

over, treatment of infected fluids with excess of fowlcells absorbs out the greater part of the virus, whichmust therefore be presumed to act by virtue of

adsorption on the red-cell surface.This finding is not a mere biological curiosity, for

it may prove to have practical application in twodirections. HIRST succeeded on two occasions in

recovering influenza virus from human throat washingsby infecting chick embryos and proving that infectionhad occurred by the aid of the agglutination pheno-menon. If virus could be regularly recovered likethis the necessity for using the ferret would beeliminated, but too much optimism would be unwiseat this stage. Thus BURNET 2 lately described aniethod for infecting chick embryos by the amnioticroute with material of immediate human origin, butworkers using it in this country 3 have not met withsuccess comparable with BURNET’s, and HIRSTindicates that in his hands also the test has proved" rather uncertain." Far more hopeful is the findingthat the agglutination phenomenon is inhibited in thepresence of antiviral serum. It is not yet knownwhether any viruses other than those of influenzacan cause the phenomenon but it seems certain thatthe inhibition by immune serum is a specific effect.Thus the immunologically distinct influenza virusesA and B, as well as that of swine influenza, can besharply separated from one another by this simplein-vitro test, of which the results can be read in an houror so. The agglutination-inhibiting antibodies appar-ently parallel the virus-neutralising ones, as demon-strated by tests in mice, more closely than they dothose concerned in complement fixation. This is prob-ably all to the good, for, though the matter is still indispute, a majority of workers seem to attach moresignificance in influenza studies to measurement ofneutralising antibodies than to the complement-fixation test ; and in any case the vagaries of the lattertest are responsible for more bad language than mostpathological techniques. If HIRST’s results are con-firmed-and they have been reproducible in at leasttwo laboratories in this country-it may prove possibleto diagnose influenza A or B (and perhaps C to Z ifand when they are discovered) by comparing theagglutination-inhibiting titres of

" acute " and con-valescent serum samples, the only unusual reagentsbeing washed fowl red cells and a supply of virus.True, the diagnosis will be only available when thepatient is already out of bed and will not help himmuch, but the new test may prove invaluable inepidemiological and other studies.

MAKING COTTON-WOOL SAFEPUERPERAL tetanus, though long recognised, is a

very rare complication of childbirth. The Registrar-General’s figures for 1927-37 showed that one fatalcase of tetanus occurred in every 700,000 deliveries,an incidence almost identical with that in the femalepopulation as a whole. However, in view of PuLVER-TAFT’S demonstration 4 that sanitary pads may be arich source of both Clostridium tetani and Cl. welchii, a2. Burnet, F. M. Brit. J. exp. Path. 1940, 21, 147 ; see Lancet,

1940, 2, 48.3. Andrewes, C. H., Glover, R. E., Hudson, N. P., Lush, D. and

Stuart-Harris, C. H. Lancet, 1941. In the press.4. Pulvertaft R. J. V. Brit. med. J. 1937, 1, 441.

committee under the chairmanship of Prof. FLETCHERSHAW was set up by the Royal College of Obstetriciansand Gynaecologists at the request of the M.O.H. ofthe London County Council to consider the possibilityof puerperal tetanus or Cl. welchii infection arisingfrom vulvar pads used in the puerperium, and toadvise about ways of making non-infected pads anddressings available. Their valuable report ° is’nowissued. In the maternity departments of a groupof municipal hospitals and four voluntary ones theytraced only one case of fatal tetanus in 244,562deliveries, while data on puerperal infection withCl. welchii from one hospital where full bacteriologicalrecords were available showed 2 fatal and 35 non-fatalinfections among 704 cases of puerperal sepsis. Itshould be pointed out, however, that Cl. welchii maybe present in the genital tract of puerperal cases

without producing any clinical infection. Both

puerperal tetanus and gas-gangrenous infection moreoften follow abortion than full-time delivery, forwhich the greater chance of retained products to actas a suitable pabulum may be partly responsible.That the risk may be specially grave in abortionstherapeutically or criminally induced by the insertionof an unsterile cervical pack is exemplified by theextraordinary experience of BusH,s of Texas, who in afortnight saw 5 cases of post-abortal tetanus, all fromthe practice of one doctor to whom the women hadgone to procure abortion. All cases proved fataldespite intensive serotherapy.As regards infection of dressings, the committee

confirmed earlier investigations that brown cotton-wool, which is not submitted to any chemical treat-ment after it leaves the field where it is grown, isalmost always heavily infected with spore-bearinganaerobes, including the tetanus and Welch bacilli.White cotton-wool, which is boiled with strongalkali and then bleached with an oxidising agent,though not so heavily infected, is seldom free fromanaerobes. Here contamination was found to occurat the drying stage, when large volumes of hot airare blown over it. Infection comes, then, from theair, the wool acting as an efficient filter. Some

change in the manufacturing process to avoid thisgross contamination of a previously sterile substanceis obviously desirable. If this is impracticable thedried material should be resterilised before it is sentout. Until one or other of these steps is taken thepurchaser must himself see that the cotton-wool issterilised before it is applied to an abraded surface.Pyogenic cocci are easily killed, but the destructionof spore-bearing anaerobes in dressings can only beensured by a rigid technique in the use of sterilisingplant, and the committee has done well to detail theexact ritual to be observed in the use of hospitalsterilisers. There is an unfortunate tendency forthe sterilisation of dressings to be left in the hands ofa porter or nurse who does not fully appreciate theprinciples involved, and whose work is not supervisedby one responsible person. In some hospitals itseems to be no-one’s duty to reject a suspected batch.The committee urge the need for loosely packed drums,for sterilisation at a pressure of 20 lb. per sq. in. for20 minutes after preliminary evacuation to a negativepressure of 15-20 in. of mercury, for graphic records

5. J. Obstet. Gynec. June, 1941, p. 394.6. Bush, W. L. J. Amer. med. Ass. July 21, 1941, p. 2750.

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numbered and dated to permit subsequent inspection,and for periodic tests of efficiency with a sporingorganism. They do not consider colour changes intest-capsules placed in the drums satisfactory, andthink there is no substitute for careful bacterio-

logical tests. What is wanted, they say, is not somuch improved apparatus as more rigid supervisionof all the steps involved in the sterilising process.Let us hope that hospitals will take this report toheart, but there will still remain the large quantityof cotton-wool used in doctors’ surgeries and by lay-men with little if any attempt at sterilisation. Therisks of this can only be removed by the manufacturers.

CHRONIC GASTRITISTHAT chronic gastritis exists has long been recog-

nised, but for many reasons it has proved extremelydifficult to study. Its clinical manifestations of

- nausea, flatulence, loss of appetite and vomiting maybe indistinguishable from the reflex effect of somedistant viscus, and little confidence can be placed ina diagnosis based on clinical grounds alone. Indeed,until recently an easy diagnosis of gastritis, so difficultto disprove, has provided a cloak for ignorance alltoo convenient and some rebellious spirits have beeninduced to deny the existence of the condition at all.

, Equally difficult has been the pathological approachto its investigation. Post-mortem specimens of thestomach are damaged by autodigestion soon afterdeath, and in cases of wasting illness shortly beforedeath also. FABER did much to overcome this

difficulty by fixing the stomach in situ by directinjection of formalin immediately after death and inthis way the reality of chronic gastritis was definitelyestablished. But since people do not die from chronicgastritis alone the correlation between the gastricpathology and clinical manifestations has remainedobscure. Moreover, FABER’S investigation was neces-sarily confined to the still picture of the morbidanatomy and histology of the specimen.The further elucidation of gastritis and its effects

has recently been achieved by the application to thestomach of endoscopic methods of examination andthe various stages of the disease process in life can nowbe observed in detail. The endoscopic picture presentsthe characteristic changes of inflmmation found inmucosal surfaces elsewhere. Thus there are oedema,exudation, vascular congestion with petechial heemor-rhages, excessive secretion of mucus, and a hyperplasticor desquamative reaction in the epithelium. These

changes superimposed on the variable contour andrugosity of the gastric mucosa produce a remarkablevariety of appearances. HERMON TAYLOR urgesthe importance of distinguishing between the trueinflammatory effects and those due to the type ofmucosa in the individual stomach. This aspect is

worthy of note, because there seems no doubt of thecorrectness of HURST’S views on the congenitaldifference in the types of mucosa possessed by differentindividuals, whereby under-development or over-

development of the rugosity can occur. LatelyJ:BfiLLER 2 has noted that the rugosity of the stomacharises only in the ninth foetal month, and he observed ahypoplastic mucosa even in one mature infant. Itseems probable that there is an setiological connexion

1. Lancet, 1941, 1, 131.2. Miller, R. A. Arch. Dis. Childh. March, 1941, p. 22.

between such developmental variations in the typeof gastric mucosa and the incidence of gastritis.Moreover, although not in itself a complaint with verydisturbing symptoms, chronic gastritis may promotethe onset of very serious illness. Atrophic gastritisand depression of Castle’s h2emopoietic factor withpernicious anaemia and subacute combined degenera-tion of the cord are an illustration of distant secondarylesions. Locally, HURST has shown that carcinomaof the stomach arises more frequently in patientswith hypoplastic gastritis than in those with normalstomachs. Peptic ulceration, too, can apparentlybe regarded simply as an extension of the diseaseprocess of hyperplastic gastritis, by the inflammatorydepression ofthe resistance of the gastric mucosa tothe digestive activity of its own juice. Erosions,subacute or chronic ulcers may therefore follow

according to the chronicity of the process and theintensity of the gastric acidity.

Gastritis has been subdivided for classification

according to the degree and profusion in which variouschanges present themselves to ,the gastroscopist.Whether this is useful may be questioned, but thesuperficial catarrhal form appears to be distinguishableas a separate entity. This condition is easy to com-

prehend for it occurs in people with chronic diseaseof the mouth, nose or respiratory tract, such as

chronic sinusitis, tonsillitis, pyorrhcea, bronchiectasisand pulmonary tuberculosis. The appearances are

congestion of the tops of the rugae, sticky adherentmucus and lumps of swallowed mucopus floatingabout in the gastric juice ; all suggestive of simplesecondary infection from above. Peptic ulcers maybe associated, but, like the diffuse changes, respondreadily to treatment of the primary disease. Thereseems to be, however, a more insidious form of gastritisindicated only by a diffuse and uniform oedema ofthe gastric mucosa together with some mammillationof the surface, due to true pathological hyperplasia,as distinct from congenital redundancy of the rugae.This condition appears to be distinct from the catarrhalform of gastritis and no reasonable suggestions as toits cause have yet been put forward. It may be a

deficiency disease or due to hormone imbalance, orpossibly an effect of the vagus. Whichever may bethe explanation, it is invariably associated with themore chronic and intractable forms of peptic ulcera-tion. BOWER 3 has treated a series of cases of gastritiswith vitamin-B complex under gastroscopic control.The cases were all atrophic gastritis and a slightimprovement was noticed in 2 out of 7 ; it is a pitythat no cases of hyperplastic gastritis were included.Until the cause of this oedematous hyperplastic formhas been elucidated little progress can be expectedin the reduction of the incidence of peptic ulceration.It has been said that the diagnosis of gastritis can onlyproperly be made by the gastroscope, for -only by thismeans can the congestion, haemorrhages and oedemabe observed. There seems to be little ground for theclaim to make the diagnosis from a study of thebarium-meal film or screen. At most a relief film

might show excess of secretion, but none of the essen-tial minutiae of a diffuse inflammation. Much con-fusion has apparently resulted from descriptions ofvariations in rugosity as evidence not of the congenitaltype of mucosa but of gastritis. Certainly, gastritis

3. Bower, L. L. Rev. Gastroenterol. 1940, 2, 313.