War Surgery and Medicine
SECOND WORLD WAR
SECOND WORLD WAR
Dysentery being endemic in Egypt, it was only natural that New Zealand troops in 2 NZEF in Egypt would contract the disease in some form despite good sanitation arrangements and hygiene education within the Force. As it happened, up to 4 per cent annually of the 2 NZEF were hospitalised with dysentery. In addition it was thought likely by many medical officers that the vast majority of cases of acute diarrhoea occurring in troops in the Middle East were, in reality, cases of bacillary dysentery, because the clinical features were the same in those patients from whom bacilli were not isolated as in those from whom they were.
Probably nearly every soldier in the Middle East had at least one attack of acute diarrhoea, usually soon after arrival, and only a page 481 proportion of those reporting sick were sent to hospital. New Zealand troops had had no opportunity to develop an immunity to the infection, and suffered from the disease in common with other Commonwealth troops, no matter how high the standards of camp hygiene. Some immunity seemed to be developed in Egypt, however, as in the second summer recurrences of diarrhoea were not nearly as common as initial attacks among newly arrived troops. The seasonal incidence tended to show two main peaks—in early and in late summer—the drop in mid-summer being associated with the diminution in the number of flies. This was not true of 2 NZEF in 1942; the Division was holding the Alamein line in mid-summer, and the presence of swarms of flies spread the infection at that period.
In April and May of 1940, at the beginning of the summer, there was a period of high incidence among First Echelon troops, among whom there were 140 cases. By June there were very few cases, but in October and November 1940 there were 278 cases. The Third Echelon had arrived in Egypt on 29 September, and 60 per cent of the cases were from these newly-arrived troops. The First Echelon at this stage was in the Western Desert; there the incidence of dysentery was higher than in Maadi Camp, where steady improvement in camp sanitation had taken place.
In the 505 cases in 2 NZEF in Egypt up to the end of November bacteriological examination revealed that the types of dysentery were Flexner 22.4 per cent, Shiga 4.5 per cent, Schmitz 1.4 per cent, Sonne 0.4 per cent, amoebic 2 per cent, bacillary exudate 38.4 per cent, and indefinite exudate 30.9 per cent. In November there was an increase in the relative incidence of bacillary dysentery due to infection by the Shiga bacillus. This applied to British troops as well as to New Zealanders, and the medical authorities kept a careful watch for these infections owing to the risk of a true epidemic occurring. These cases were more serious than the average Flexner dysentery, and of the three deaths caused in 2 NZEF by dysentery between February and November 1940, one at least was due to Shiga infection.
In a British hospital in Egypt the analysis of a large number of dysentery cases over two years revealed that the types of bacilli isolated occurred in the following proportions: Flexner 70 per cent, Shiga 19 per cent, Sonne 6 per cent, Schmitz 5 per cent, amoebic 1 per cent. Of the total dysenteries, 56 per cent did not pass blood and mucus, and their average stay in hospital was ten days; 20 per cent of the cases, though passing mucus, were mild, while 22 per cent were moderately severe and 2 per cent severe. Those passing mucus stayed in hospital an average of twenty days. page 482 It is likely that 2 NZEF experience with the disease was somewhat in conformity with this.
At the base hospital at Helwan special wards were constructed, apart from the main building and near the laboratory, to prevent cross infection in the wards and the spread of the disease to the rest of the hospital.
In May and June 1941 there was a rise in incidence again following the evacuation of Greece and Crete, where dysentery was also endemic, and where during the withdrawal there could not be the normal standard of control in hygiene and sanitation. Again in November 1941, when the New Zealanders were in Libya, there was an increase in the number of cases. This was thought to be in some measure due to dust-storms which swept over areas contaminated by natives and by the enemy, whose incidence of dysentery was found in the second Libyan campaign to be much higher than that of the Allies, as instanced in a prisoner-of-war camp.
In 1940 and early 1941 the dysentery cases were treated with sodium sulphate eliminative treatment, but in 1941 a new drug, sulphaguanidine, became available. It was most effective and became the standard treatment when full supplies were available. First supplies were used by 2 NZEF in June 1941. It was noted that sulphaguanidine brought marked amelioration of symptoms in cases where sodium sulphate treatment had failed. The new drug reduced the possibility of death from the disease. Of the eight deaths in 2 NZEF, only one occurred after sulphaguanidine was introduced.
In 1942 the incidence of dysentery in 2 NZEF in the summer was fairly uniform, being between 3 and 4 per thousand per month. In 1943 there was a marked increase in the number of cases in June, July, and September. In June and July the troops mostly affected were the 9th Reinforcements, who were quartered in a camp at Mena prior to the departure of the furlough drafts. The large number of gastro-intestinal complaints at Mena was considered to be due to the milk supply. The issue of fresh milk was stopped and the incidence of diarrhoea diminished. The 10th Reinforcements arrived in August, and in September there was an appreciable increase in the incidence of dysentery, the troops concerned being mainly from that reinforcement. The rates of 10.6 and 13.5 per thousand per month in July and September, together with that of 14 per thousand in April 1940, were the highest in the history of 2 NZEF.
In Italy dysentery did not account for as many cases as had been expected, though the morbidity rate was nearly double that for the page 483 British and Canadian forces. Hygiene was better, contamination less, and flies fewer than in Egypt. All New Zealand troops going to Italy had been in Egypt and were to some extent immunised. The highest incidence in June 1944 cannot be assigned to any particular cause, seemingly being due to the arrival of unseasoned troops as much as to the fact that divisional troops were on leave in Rome and other cities.
Cases continued to occur, of course, in the base units and reinforcements in Egypt. There was a sudden increase in May 1945 with the arrival of the last of the reinforcements in Egypt, but at no stage did the disease reach epidemic proportions. All fluctuations in the figures for dysentery were closely observed, and any increases were the subject of immediate inquiry and correction if possible. Seldom was dysentery found to be the result of defective hygiene and sanitation, and the Division's record as regards dysentery was particularly creditable. The highest, and almost unavoidable, incidence in 2 NZEF occurred when reinforcements with no immunity to the disease arrived in Egypt at the beginning or end of the summer, when flies were most numerous and infection most common.
In the Pacific force dysentery was much less serious a problem than in the Middle East as flies, which play such an important part in transmission, were fewer. Outbreaks of bacillary dysentery in the Pacific coincided with the establishment of new camps, and were found to be Flexner in type. Lack of flyproof latrines and cookhouses, together with inadequate fly measures, were inevitable in the early days of camp construction.
In May 1943 the average dysentery sick rate was stated to be 5 per cent per month. At Guadalcanal in September mild outbreaks of dysentery occurred in some units, and at Vella Lavella in October many cases were reported and ascribed to the poor sanitary practice of the individual soldier.
The cases seen in the Solomon Islands were stated by Major C. G. Riley to be milder than those seen in the Middle East, and the stay in hospital was short. So-called ‘tropical diarrhoea’, like ‘gyppy tummy’, was a dysenteric infection so mild that no blood and little mucus was passed. Chronic diarrhoea following an acute attack of bacillary dysentery was occasionally observed, but complications of bacillary dysentery were not common. Some mild cases of arthritis with effusion were seen, all recovering completely.page 484
Treatment of Bacillary Dysentery
In the Second World War, due to the discovery that certain of the sulphonamide drugs exercise a specific action on dysentery bacilli, it was possible to bring about rapid cure in all cases, however severe, which came under early treatment. Sulphaguanidine was used and this became available in the Middle East in the middle of 1941. Before that the treatment was a dose of 1 oz. of castor oil at night followed by sodium sulphate in 1 dram doses two-hourly, beginning at 6 a.m., for eight doses. Fluids were given for twenty-four to forty-eight hours and then a gradually increasing diet.
The sulphaguanidine treatment given, at first for the severe cases and then for all cases, was as follows: Sulphaguanidine by mouth (a) 4 grammes on admission, (b) 2 grammes four-hourly till the stools were reduced to six to eight daily (usually in 48 hours); (c) 2 grammes six-hourly until the stools were formed; (d) 2 grammes eight-hourly till motions were free from blood and mucus. The average course lasted four to five days. Anti-dysenteric serum, in doses of 50,000–100,000 units, was at first given to all severe toxic cases if seen before the third or fourth day. Shiga anti-serum was given when Shiga infection was present, and polyvalent serum when the bacillus was not identified. The efficacy of the serum was difficult to assess.
After the introduction of sulphaguanidine there were very few seriously ill patients and only one death amongst some five thousand cases admitted to hospital in the Middle East, though there were six deaths in fewer cases before that time. Sulphaguanidine was always available to the Pacific force and was given early in all cases, whether admitted to hospital or not, and there were no deaths from bacillary dysentery.
Diet (as given in New Zealand hospitals): No milk was given.
Stage 1: Water with glucose or cane sugar; barley or rice water, tea with sugar, clear chicken broth, Bovril.
Stage 2: Orange juice, soups, marmite, calves-foot jelly; arrowroot biscuits; apple puree, sago, arrowroot, ground-rice puddings.
Stage 3: Toast and butter; bread and butter; eggs; junket; fish; chicken; well-boiled potatoes; stewed fruit.
Extra vitamin B was given if the course had been protracted.
Symptomatic: If there was severe colicky pain in the early stages, the following were tried:
1st: Hot water bottles or antiphlogistine.
2nd: Starch or opium enemas.
3rd: Tr Opii M xv by mouth, or Morphia gr. ¼.
If patient was very dehydrated and unable to drink, intravenous saline (.85 per cent) with glucose 5 per cent was given intermittently or by continuous drip.
Amoebiasis is often insidious, and chronic and persistent in type. There may be few or no acute bowel symptoms, but chronic signs develop in the liver as hepatitis or abscess, and in the large bowel as caecal or rectal amoebiasis. Dyspeptic and general vague abdominal symptoms associated with debility and psychoneurosis are often present.
The diagnosis of intestinal amoebiasis was dependent partly on a combination of symptoms and physical signs, partly on sigmoidoscopy, but essentially on the discovery of Entamoeba Histolytica in the stools. It proved very difficult to find the amoeba, and it became necessary to ‘wring the amoebae out of the bowel’ by strong purgation by calomel and salts, with the production of six fluid stools in one day. The specimens were examined immediately, at the same time being kept warm. The characteristically mobile amoeba with ingested red blood corpuscles established the diagnosis.
Sigmoidoscopy was of great value in diagnosis, and in amoebic dysentery showed (a) small superficial ulcers about 1–2 mm. in diameter on the valves of the lower four inches of the bowel, (b) pitting of the mucosa at sites of healed ulcers, (c) granular proctitis with mucus and often submucosal haemorrhages.
It was essential in the indefinite chronic cases to make an exact diagnosis by demonstrating the amoeba before embarking on a long unpleasant course of treatment.
In hepatic lesions less than half the cases gave positive results on stool examination, and the diagnosis had to be made first on clinical grounds, and finally by a therapeutic test. The high incidence of infective hepatitis in Italy increased the difficulty of diagnosis in the hepatic cases.
In Egypt amoebic dysentery was diagnosed in only a small percentage of the cases investigated. A marked increase was noted in September 1942, when 33 cases were treated at 1 General Hospital and 19 at 2 General Hospital. This increase was ascribed to infection arising in Syria. In Italy the relative incidence was much higher, and chronic amoebic infection became an important problem at the base hospital.
The figures in Italy were boosted by the intensive examinations carried out on patients at 3 General Hospital, Bari, even on a number of patients admitted primarily for other diseases. Lieutenant-Colonel G. W. Hayward made a survey of patients page 486 admitted to the medical division of 3 General Hospital from July 1944 to June 1945. Of the 4601 patients, there were 2016 with infective hepatitis; 252 with intestinal amoebiasis; 6 with acute hepatic amoebiasis; 109 with diarrhoea; 104 with bacillary dysentery; 108 with malaria; and 2006 with other diseases. Thus amoebiasis accounted for over half the admissions in the diarrhoea-dysentery group. Of the 252 cases of intestinal amoebiasis, 82 were admitted primarily for other diseases such as infective hepatitis, peptic ulcer, ascariasis, or anxiety neurosis, and the disease was in a latent or a chronic stage. These cases were difficult to diagnose. Once diagnosed the response to treatment was good and the relapse rate low. The duration of symptoms in all cases before admission varied from a few days to 18 months, with an average of three to four months. The disease was characterised either by recurrent attacks of diarrhoea or by persistent malaise with vague abdominal symptoms. Dysenteric symptoms were unusual. Tenderness and thickening in the region of the caecum were the most important physical findings. Seventy per cent of the cases showed abnormal findings on sigmoidoscopy, and it was stated that this figure would have been higher had it been realised earlier that the type and extent of the ulceration seen in Syria and North Africa were uncommon in Italy and that the changes were much less marked but none the less characteristic. Considerable difficulty in demonstrating the vegetative forms of E. Histolytica was encountered until the routine was adopted of examining all stools passed after vigorous purgation. After treatment 226 men returned to full duties, 7 were down-graded for base duties, and 19 were graded unfit for further overseas service, chiefly because of persistent hepatomegaly or the presence of some associated condition such as coronary artery disease or duodenal ulcer. Only 9 cases were known to have relapsed.
It is interesting to note that at several large military hospitals in Canada in 1944 a survey for amoebiasis was carried out among soldiers who had returned from the Mediterranean theatre. These men had been hospitalised for wounds and not for tropical disease, yet Entamoeba Histolytica was found in 11 per cent of the 259 men examined, whereas a previous study of soldiers who had not left Canada had shown an incidence of only 1 per cent.1
In the Pacific area there were comparatively few cases of amoebic infection hospitalised. The majority of the patients gave a history of repeated mild attacks of diarrhoea and complained of general page 487 ill-health and loss of weight. In some cases the onset was acute, owing very often to a superimposed bacillary infection.
From March to September 1943, 15 cases of amoebiasis, including one case of hepatitis, were treated at 4 General Hospital, New Caledonia. Carriers and active cases were found in a Field Bakery unit. The occurrence of chronic amoebiasis came under increasing notice during 1943 and 1944, and investigations of the accessible hospital staff disclosed a number of cases. In February 1944 two nursing sisters, three medical officers, and one laboratory technician were treated for the disease. It is apparent that had investigations been more widespread in the Force, the number of positive cases would almost certainly have been much higher. Up to the end of May 1944 there were 27 cases of amoebiasis diagnosed in 2 NZEF (IP)—10 from the Solomons and 17 from New Caledonia. The total number of dysentery cases admitted to medical units from June 1943 to July 1944 was 281.
Treatment for Amoebiasis
The standard treatment for amoebiasis in the Middle East Force was (a) emetine 1 gr. daily with quinoxyl 2½ per cent enemata for ten days; (b) carbarsone .25 gm. twice daily for eight days; (c) emetine bismuth iodide 3 gr. for twelve days.
In Italy the standard course became (a) emetine 1 gr. daily for three days; (b) emetine bismuth iodine 3 gr. concurrently with quinoxyl 2½ per cent retention enemata for ten to twelve days; (c) carbarsone .25 gm. twice daily for eight days. All cases with liver enlargement or in which there was any suspicion of amoebic hepatitis were given 10 gr. of emetine during their initial course of treatment and a further course of 6–10 gr. after three weeks at the convalescent depot.
Lieutenant-Colonel Hayward reported that the immediate results of the treatment in Italy were good and that only two cases out of 252 had positive stools three weeks after the course of treatment. Only nine cases in the group were known to have relapsed. Three of them with persistent diarrhoea, extensive ulceration of the colon, and positive stools were given a five-day course of sulphasuxidine (80 gm.) and penicillin (1,200,000 units) before being given a second course of emetine bismuth iodide and quinoxyl, with immediate good results. It was stressed that every effort should be made to eradicate the infection during the first course of treatment as the relapse rate from inadequate courses of treatment would be high.
The routine treatment adopted in the Pacific force was: emetine hydrochloride gr. 1 subcutaneously daily for five days, with the page 488 patient in bed. Carbarsone .25 gm. thrice daily for seven days, beginning on the third day of the emetine injections. Interval of seven days if either of the above produced gastro-intestinal irritation or other toxic effects. Chiniofon 1.0 gm. thrice daily for seven days. Another interval of seven days if necessary. Carbarsone .25 gm. thrice daily for seven days. Both carbarsone and chiniofon were given by mouth, and if they did not produce toxic symptoms, the interval between their administration could be eliminated.
Major Riley stated that the course of treatment gave better results than the standard MEF course.
For amoebic hepatitis and liver abscess emetine gr. 1 was given daily for ten days, followed by the standard combined course of carbarsone and chiniofon to clear up the infection in the bowel. If emetine did not clear up the symptoms, exploratory puncture and aspiration was carried out, with operation as a last resort.
Late Results of Amoebiasis
In a lecture to medical officers of 2 NZ Division on 31 October 1944 Colonel Boyd, Consultant Physician, expressed the opinion that amoebiasis would be a main problem in New Zealand regarding infections contracted overseas. He emphasized that doctors should not be put off in a suspicious case by a man's statement that he had never had either diarrhoea or dysentery. In a number of cases the primary bowel infection remained symptomatically completely quiescent and the first evidence was a metastatic lesion. The disease might show itself as amoebic hepatitis and abscess, caecal or rectal amoebiasis. It had to be remembered that E. Histolytica was by no means easy to find—some cases of diarrhoea after repeated negative stool and sigmoidoscopic examinations eventually proved to be cases of amoebiasis. Colonel Boyd's opinion has unfortunately proved to be correct and chronic amoebiasis has been increasingly recognised as a cause of disability in returned servicemen.
This point is borne out by a survey made by Dr I. S. Wilson of the War Pensions Branch in 1949. Between 1 April 1946 and 30 September 1949 there were 148 cases accepted for pensions suffering from chronic amoebiasis, none of whom were considered to be infected on their arrival in New Zealand. Fifty-two of the cases had been classed as Grade I on their final medical board in New Zealand. Most of the cases (134) were from the Army. Operational regions in which the men served were: Middle East (including Italy), 108; Middle East and Pacific, 8; Pacific, 21; page 489 Far East, 2; Middle East and Far East, 3; Navy overseas, 6; 26 were ex-prisoners of war. The number of cases accepted for pensions year by year was 29 in year ended March 1947, 47 in year ended March 1948, 53 in year ended March 1949, and 19 in six months ended September 1949. The increase in 1947–48 was thought to be partly due to the increasing awareness by medical practitioners of the possibility of amoebiasis.
The average period between return to New Zealand and diagnosis of amoebiasis was thirty-three months, the longest being six years one month, and the shortest two months. There were 22 cases who were diagnosed and adequately treated overseas for amoebiasis and who appeared quite recovered on their return to New Zealand. The average time interval before their relapse was just over four years, the longest interval being seven and a half years and the shortest eighteen months. There were 17 cases of amoebic hepatitis, of whom the stools of 10 were negative for E. Histolytica, and 3 of amoebic abscess.
Entamoeba Histolytica was found in all but 10 per cent of the cases, and in these the diagnosis was proved by the therapeutic test. In only one case when Entamoeba Histolytica was not found did sigmoidoscopy suggest the diagnosis.
Of the 148 cases, 78 had been diagnosed as suffering from various disabilities which were in reality due to, or closely related with, the amoebic infection—dyspepsia (4 per cent), anxiety neurosis (14 per cent), recurrent diarrhoea, debility, chronic appendicitis, etc. (In 17 cases there were recurrent attacks of definite pain in the right iliac fossa which might have led to a diagnosis of chronic appendicitis.) In the series 24 cases had been quite well since return and the onset of illness was comparatively sudden.
Thirty-nine of the cases showed anxiety neurosis in some degree, and residual symptoms following treatment were more frequent and prolonged in these cases. Only three had been cured both of their neurosis and their amoebiasis and were not on pension. Yet in 100 cases not showing a neurosis, 36 were considered cured of their amoebiasis and their pension ceased. The cure rate for amoebiasis in cases showing a neurosis was 20 per cent.
The results of treatment of the 148 cases were: apparently cured, 44 (32 per cent); much improved, 48 (35 per cent); some improvement, 35 (25 per cent); no improvement, 12 (9 per cent); too early to assess result, 9.
Pension had ceased in all the apparently cured, except 5 who were still pensioned for some degree of anxiety neurosis. The 48 cases could be considered well on the way to recovery and were mostly on a small pension of 10–15 per cent. In the 35 cases with some page 490 improvement a proportion were in the early stages of treatment and supervision, a matter usually of many months, while the remainder were resistant cases or with residual symptoms such as ‘irritable bowel’. In the cases where no improvement in symptoms and health occurred after adequate treatment and with stools remaining negative, the infection could be considered to be in an inactive state and playing no part in the illness, or else the patient had really been a carrier. In such cases the diagnosis was usually reviewed. The average duration of treatment and supervision from diagnosis to apparent cure was just over fifteen months, the longest period being thirty-five months, and the shortest two months. Fourteen of the 17 cases of amoebic hepatitis were cured or showed marked improvement.
This survey suggested that amoebiasis will be a continuing problem for some years at least, with fresh cases arising from time to time.
Chronic amoebiasis has proved to be the major problem associated with infective disease contracted during the Second World War.
A further review was carried out by Dr J. V. Cable at the Wellington Hospital in 1951. In the period since 1946 there had been 135 ex-service men and women treated at the hospital for amoebiasis, of whom 111 men and 4 women had vegetative forms of E. Histolytica in the stools and 20 were diagnosed on clinical grounds when efforts to isolate the parasite failed. The majority had served in the Army and there were many former prisoners of war.
Some patients had received treatment for amoebiasis overseas, but the majority had developed bowel symptoms in North Africa or Italy which had persisted or become worse on return to New Zealand. Symptoms usually complained of were recurring bouts of diarrhoea often provoked by minor dietary excesses, flatulence, a sense of fullness after meals, and rectal flatus. A proportion of cases had colicky abdominal pain, and a few complained of soreness in the right hypochondrium. More difficult to assess were complaints of lack of energy, tiredness, and general slackness.
The diagnostic procedures included, in addition to a routine physical examination, strong purgation and the examination of a series of six warm stools. For some time all cases were examined sigmoidoscopically, but as it became realised that significant findings were most exceptional this was not used as a routine in later cases. It was thought that the explanation of this lay in the fact that the disease was chiefly in the caecal region which was often tender and gave a sense of resistance or ‘thickness’ on palpation. page 491 Slight liver enlargement with tenderness was very common, but liver abscess was diagnosed twice only.
For four years the treatment was that usually employed in the Army, viz., emetine injections, emetine bismuth iodide by mouth, and carbarsone in addition. Enemata of chiniofon were used in addition for some time, but were discontinued when diodoquin became available for oral administration. In addition to this course relapsed cases received courses of penicillin and pthalyl sulphathia-zole. Later emetine bismuth iodide was not used and this, in addition to avoiding much gastro-intestinal upset, shortened the period in hospital from three weeks to one. Relapsed cases were then treated with aureomycin in addition to emetine injections and diodoquin and carbarsone.
A large proportion of cases required more than one course of treatment to give relief from symptoms and eliminate the protozoa from the stools. Even among those in whom it was not possible to isolate the parasite at successive examinations commencing some weeks after treatment, there were a number in whom minor disabilities persisted, chiefly some flatulence and some colonic irritability.
With regard to the question of the infectivity of the disease, the only evidence that could be produced was that only three cases with proved intestinal amoebiasis were treated who were close contacts of ex-service personnel. It was not suggested that this necessarily represented a true picture of the infectivity of the disease, because in a civilian population the possibility of the disease might not be kept in mind.
Two cases of intestinal amoebiasis in returned servicemen of the First World War were treated in the period under consideration. One of these was employed in a large camp in New Zealand during the Second World War and was in contact with returned men of the recent war who were also working in the camp. Three cases were known to have developed pulmonary tuberculosis subsequent to a diagnosis of amoebiasis being made. There was a steady decrease in the number of cases being treated, but in 1951 a few cases were still being met with in whom the disease had not been diagnosed before.
It would appear that the recognition of the problem led to efficient diagnosis and treatment with resultant success, which the discovery of new drugs has accentuated. There seems to be no danger of any spread of the disease to the civilian population of New Zealand.
(Reports from the Pensions Department late in 1952 show that few cases have been seen during the last year and that the problem is not now a serious one.)