War Surgery and Medicine
There was, as expected, a definite relationship between the incidence of pneumonia and the wetness of the season. In March and April 1940 the incidence reached 2.8 per 1000 among troops of the First Echelon in Egypt. There were 49 cases during January and February 1941, of whom 2 died. Between 1 July 1941 and 31 March 1943 there were in all 218 cases of pneumonia, of which 164 were classified as lobar and 54 as bronchopneumonia. Six of the 164 cases of lobar pneumonia died (3.6 per cent). Many cases developed a serous effusion, but only in three did this proceed to empyema (1.8 per cent). The reduction of complications and the improved prognosis were directly attributable to the effective use of sulphonamides. In the earlier cases sulphapyridine was used: later sulphathiazole was preferred on account of its equal effectiveness with lesser toxicity. The dosage given was four tablets as soon as diagnosis was made and thereafter two tablets page 579 every four hours till the temperature dropped (usually thirty-six to forty-eight hours). Then two tablets t.i.d. till the temperature had been normal for two days. (Total was usually 18–24 gms. Each tablet equals .5 grammes.) The rapid symptomatic response to chemotherapy contrasted with the slowness of complete clinical and radiological resolution.
In July and August 1943, following the Nile flood, there were 258 cases of pneumonia. These cases were very toxic, with a tendency to more patchy distribution of consolidation.
Between January and June 1944, when 2 NZEF were exposed to the rigours of an Italian winter in the Cassino area and the mountain sectors, the incidence of pneumonia reached its highest figure (4.6 per 1000 in March 1944). Similarly in March and April 1945, as the Division prepared to launch the final spring offensive in Italy, an increased incidence was observed. In both these years the majority of the cases were classified as ‘primary atypical pneumonia’. A consecutive series of these cases, mainly in British troops, was closely studied at 2 NZ General Hospital during 1945. The clinical features and later agglutination studies showed that these epidemics of ‘atypical pneumonia’ were in fact Q fever due to infection with Rickettsia burneti. (See Chapter 15.) These cases ran a toxic course virtually uninfluenced by chemotheraphy or by penicillin, which became available to a limited extent at this stage.
In many cases of short-term pyrexia, classified clinically as ‘influenza’, radiological examination revealed small and slowly resolving areas of pneumonitis.
The recorded incidence of pleurisy was closely related to that of pneumonia. The number of cases was usually between 10 and 20 per cent of the number of cases of pneumonia.
It is of particular interest to compare this record of pneumonia in 2 NZEF with that of 1 NZEF during the First World War. From 1941 to 1945 there were in 2 NZEF 2012 cases of pneumonia, of whom 10 died. These figures include atypical pneumonia and Q fever, but even so the mortality (.5 per cent approximately) is in striking contrast with that observed in 1 NZEF, when of 1579 deaths from disease in 92,860 New Zealand troops, 578 were from pneumonia, 20 from pleurisy, and 152 from influenza, often with complicating pneumonia during the epidemic of 1916–17. This gives a grand total of 750 deaths from acute respiratory disease—almost 50 per cent of all deaths from disease. The conditions of active service in France in 1914–18 undoubtedly favoured respiratory infections, and the 1916–17 epidemic of influenza which heralded the pandemic of 1918 was of extreme virulence. page 580 The highest incidence of pneumonia in 2 NZEF was 4.6 per 1000 in March 1944, whereas the overall incidence in 1 NZEF was 6.1 per 1000. Even allowing for an increased incidence and greater virulence, the transformation in the mortality rate from pneumonia in the two forces is noteworthy and may reasonably be attributed largely to chemotherapy.