IN the Middle East diphtheria occurred as a seasonal disease during the months of November to March. Among New Zealand troops the incidence was low, except for two epidemics at 1 NZ General Hospital, at Helwan, Egypt, in December 1942, and at Senigallia, Italy, in the winter of 1944–45. In addition there were increased admissions at 2 NZ General Hospital in December 1941 and at 3 NZ General Hospital in February 1944. In the most serious epidemic, that at Senigallia in 1944, when over 150 cases were diagnosed, routine swabbing revealed four carriers on the hospital staff. In connection with the outbreak it was noted that many Italian children were suffering from diphtheria and were in close contact at times with New Zealand troops who were living in houses in the divisional sector. These epidemics involved both faucial and cutaneous diphtheria. In the Middle East true cutaneous diphtheria was rarely found, except in units where faucial infection was also present. Therefore, when diphtheria appeared in a medical unit, carriers (faucial and nasal) had to be sought and wound-dressing technique carefully scrutinised. Preparatory to invaliding to New Zealand by hospital ship in December 1942, a convoy of 161 cases was submitted to routine swabbing of wounds. Twenty-two swabs were returned positive for KLB (Klebs-Loeffler bacilli), but virulence tests were positive in only two cases. These latter cases were temporarily retained in Egypt.

On other occasions, and notably in the outbreak at Senigallia, a number of gunshot wounds were infected and the healing process protracted.

A possible complication in diphtheria cases was post-diphtheritic polyneuritis, of which there were in 2 NZEF 2 cases in 1942, 4 in 1943, 5 in 1944, and 13 in 1945. Though infection of gunshot wounds with the bacillus of diphtheria was rare, except at Senigallia, it was not uncommon to find various skin lesions with an infection of this nature. The organism responsible for the paralysis was found on various occasions in desert sores, the lesion of scabies, or even in an infected pile or ingrowing toenail. page 571 Apart from possible paralysis, it was found the cutaneous diphtheria caused a very great delay in the healing of a wound or lesion. Diphtheria bacilli in wounds caused more than local effects; when toxin was absorbed, paresis and death might follow unless full doses of anti-toxin were given at an early stage.

A full bacteriological examination, including a virulence test of any diphtheria-like organism that might be recovered, was essential in every case before a diagnosis of cutaneous diphtheria could be made. Diphtheroids or diphtheria-like bacilli were commonly found in a variety of superficial skin lesions, and it was most important, therefore, that the virulence of all such organisms should be checked.

On some occasions diphtheritic ulcers could be distinguished by oedema round the wound edges and blackened or yellowish-grey crusts or membrane in the wound, associated with blood-stained sero-purulent discharge and regional lymphadenitis. But clinical appearances were variable and the possibility of diphtheria had always to be remembered, when, after apparent initial healing, a wound developed a serous discharge and became necrotic. In some serious burn cases diphtheritic infection occurred without the characteristic wound appearances.

The incidence of diphtheria among New Zealand troops in the Pacific was low and complications were rare, but tropical ulcers had to be considered a potential diphtheria hazard until proved innocent by appropriate cultures, and, whenever possible, by virulence tests. Several cases of cutaneous diphtheria were diagnosed among patients admitted to 2 NZ CCS from Vella Lavella in January 1944.