War Surgery and Medicine
INFECTIVE hepatitis has for a long time been accepted as an illness common to soldiers on military operations. Cases have been recorded as occurring in all recent wars, and the clinical picture has been well known. The disease is world-wide in distribution, but the Mediterranean littoral has been one of high epidemicity. From October to November 1915 some 25 per cent of a section of British troops on Gallipoli and in Alexandria were affected (Martin, 1917). New Zealand troops were also affected severely, and it was found that the highest incidence was in the winter months of 1915 and 1916, whereas other gastro-intestinal infections reached their height in the summer. Efforts to discover the mode of transmission failed, and Wilcox (1916) concluded that the disease started as a gastro-intestinal infection (see Martin, 1917); but all bacteriological investigations were negative (Hunter, 1922). Kartulis (1916) declared that the pathogenic agent was intimately related to sewers and sea water, because of the decrease in incidence in Alexandria from 1898 to 1916 with the introduction of modern drainage.
At the onset of the Second World War the disease was not considered very seriously. It was thought to be a catarrhal infection with no known methods of treatment or prevention. With the arrival of New Zealand troops in Egypt in 1940 sanitation in base camps was kept at a very high level and very few cases were noted. As 1940 wore on and troops moved to the desert, a few more cases appeared in the late summer and autumn, which time, it was found later, is the time of greatest incidence. This is usually a month after the height of the dysentery epidemic.
It is noteworthy that practically no cases occurred while the Division was on active service in Greece and Crete in 1941, but later in the year 4 Brigade, which had been in Egypt since February 1940, produced cases.
From July to August 1941, 79 cases were notified from New Zealand troops; they were widely scattered and mild—mostly from those in forward areas.
At this stage it was widely accepted that the infection was due to a virus, but the method of spread was disputed. Prior to this page 498 Adler, working in Jerusalem, had failed to isolate any organism or infect any available animal. This work was supported by Van Rooyen and Gordon (1942), but Cameron interjected six human volunteers intravenously with blood from hepatitis cases and produced the disease, thus proving the communicability of the infection.
The first major epidemic among New Zealand troops occurred in 1942 and began in July and August in the Western Desert—again about a month after the height of the dysentery wave.
Between August 1942 and January 1943, 2500 cases occurred among 30,000 New Zealand troops. During September and October 1942 there were 1137 cases, of which 1059 occurred among 7500 men in the Alamein Line and 78 cases among 3900 men in the rear areas within 10 miles of the line.
This epidemic presented several problems:
Manpower: Nearly all cases required a month before returning to duty, and many some weeks more; a few required eventual evacuation to New Zealand. It is easy to see how serious was this problem.
Hospitalisation: Practically all cases were evacuated by ambulance direct to 1 New Zealand General Hospital, which was over 100 miles away. Others found their way to other New Zealand hospitals in the area.
No. 1 New Zealand General Hospital, a 900-bed hospital, found it necessary to expand rapidly, and rose from 900 beds to 1300 in a few weeks, without having extra available staff to meet the situation.
The Study of the Epidemic: An initial survey of the cases arriving at 1 NZ General Hospital soon showed a pattern, and it was decided that there was a possibility of studying the epidemiology and mode of spread of this disease with a reasonable chance of success. This work was undertaken forthwith by Kirk and was eventually published in the Lancet (1945).
It was apparent that most of the cases were coming from units who had been in the New Zealand Box in the Alamein Line a month previously, whereas very few cases came from units in base areas five to ten miles away. This concentrated attention on the site, as the front-line troops occupied an area of five miles square and all units who spent thirty-five to forty days there before the start of the epidemic were involved—units withdrawn after a shorter stay than the remainder were less affected. After the front-line troops left this area the epidemic began to subside. No other troops in the Alamein Line were involved at this time, so that if the site were to page 499 be incriminated it had to be different from the rest of the front line at Alamein. Common factors to all at Alamein were food, water, living conditions, heat, and fatigue, so these could not account for the localised epidemic among New Zealand troops. It is to be noted that New Zealand troops have not at any time exhibited an undue susceptibility to this malady.
Firstly, the possibility of an unknown vector was ruled out. Secondly, spread by droplet infection was unlikely in the front-line units as they were living in dispersed formation with little close contact and no tents or messes. On the contrary the well troops in the rear areas were living in a more congested state, and although the incidence of catarrhal infection was low, opportunities for droplet spread were numerous.
The third possibility, and the one of choice, was that the disease was fly-borne; flies were present in millions everywhere in Alamein, both in front and rear areas, and as the site seemed to be responsible it was thought that in the forward area the insects were infected locally. The New Zealand ground was one of the few parts recently captured from the enemy. It was filthy with excreta and imperfectly buried German and Italian corpses, and it was learned from patrols and prisoners that the enemy were themselves experiencing an outbreak of infective hepatitis.
Thus the epidemic was attributed to local contamination of flies arising from the faeces and cadavers strewn over the battlefield, where food, hands, and mess tins could not be efficiently protected.
This theory of gastro-intestinal infection and spread by excreta explained why the disease did not spread in hospitals to the staff, as all men used well-protected latrines, and why it did not spread in base camps and prisoner-of-war cages where the same conditions existed.
Proof of this theory can be found in publications of work done in America by Havens et al. (1945), and Paul, Havens, Sabin, and Philip (1945); in England by McCallum and Bradley (1944); and in West Africa by Findlay and Willcox (1945).
Of the American work the following quotation summarises the results:
When faecal material from patients with the naturally occurring disease was fed to human volunteers, two out of three contracted the disease in 20 and 22 days respectively. Serum obtained from these two patients in the pre-icteric stage was filtered (Chamberlain 2) and immediately afterwards heated (56 deg. C. for 30 minutes). This heated serum filtrate (M.K.) produced infective hepatitis when fed to 4 out of 5 volunteers with an incubation period ranging from 20 to 31 days. Some of the latter group of volunteers had recovered some months before from serum jaundice, but it did not protect them against an attack of Infective Hepatitis.page 500
Thus, employing one strain of infective hepatitis virus, jaundice was produced in 6 out of 11 subjects when serum was inoculated, 4 out of 5 when serum was fed, and in 2 out of 3 when faeces were fed, and the incubation period was invariably less than thirty-four days in these experiments. It can therefore be said that the virus of infective hepatitis is both present in faeces and possesses powers of viability to enable it to be transmitted by excreta.
Although this fact now is proved, it is not necessarily certain that this is the only means of transmission, but further information may be available in the future. The epidemiological investigations carried out in the Middle East were unable to satisfy all the anomalies that occurred; but it is certain that in the 1942 epidemic among the New Zealand troops the virus was spread by flies from excreta. During 1943 the case incidence dropped during the summer months and did not rise to the expected heights at the end of the year. The 2nd NZEF was in Italy during the winter of 1943–44 and had not received many reinforcements, which may have had some bearing on the number of susceptibles available; however, the greatest incidence was 3·2 per 1000 in October 1943, rising to 6·15 per 1000 in January 1944.
During this time there was little difference in the incidence between forward and base troops. There was a fall in numbers again in 1944, and during this time the Division was moving north in Italy; but by July cases increased, mostly among the divisional troops, and reached 11.15 per 1000. From August 1944 to February 1945, except for a rest period in November, the Division was in the Rimini-Faenza area, and the incidence reached a maximum of 14·55 per 1000 in October to December, 1944. From June 1944 onwards there was considerable movement of locations and the men were living under all types of-conditions. Flies were prevalent in the initial stages of the epidemic, and the sanitation of the local inhabitants, being of a very low standard, made any unit control of little value. There is little doubt that the mode of spread was the same as in the desert, but study in an area of towns and villages made any definite conclusions impossible.
It is significant, however, that in Italy during hepatitis epidemics there was no appreciable incidence among the local population. This is the same as was noticed in Egypt and indicates that the Mediterranean region is an endemic area with a largely immune local population.
In the epidemic in Italy, where 2461 cases occurred from July 1944 to January 1945 among 30,000 men, most of the cases came from front-line troops, and the problems of hospitalisation were again difficult. However, with the 2 NZ General Hospital in the page 501 Naples area and 1 NZ General Hospital on the Adriatic coast at Senigallia, and 3 NZ General Hospital at Bari in the south, lines of evacuation were arranged and hospital treatment was available.
McKinlay and Truelove (1945) carried out detailed investigations of some aspects of epidemiology among New Zealand and Canadian troops in Italy in the 1944 epidemic and their conclusions are as follows:
Infective hepatitis displays striking seasonal variations, incidence being highest in autumn and winter and lowest in spring and summer.
Age exerts great influence on liability to the infection. Within the age limits of an army population, liability decreases progressively with age.
A group which has passed through a major epidemic is less susceptible than a group which has not.
Age standardised incidence rates show that officers are more susceptible than other ranks. British officers showed an incidence of 400 per cent over ORs, whereas New Zealand officers were only 62 per cent.
Since forward troops are much more susceptible than base troops, droplet spread would not appear to be the most important method of transmission in major epidemics.
Though Italian troops suffered heavily from the disease in the Western Desert in 1942, the Italian civil population appears to have been free from any large-scale outbreak, while Allied troops were experiencing major epidemics.