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The quantity of pease-pudding eaten is recorded of two only—G. C. had two teaspoonfuls
and D. E. half-a-pint. The onset in the survivors was similar to that in the
fatal cases, and in all six the first symptoms were observed from 2 or 3 up to 7 hours
after the pease-pudding was eaten (4| and 61 hours in the cases of the two who died).
In the survivors although on the day of admission the maximum pulse rate
in each case was 132 to 156, and the temperature 102° F. to 103-6° F., there was less
circulatory collapse (as shown by better colour and pulse tension, and regular heart
rhythm), and less dehydration, compared with the patients who died. The temperature
returned by lysis to normal in about 72 hours from the onset of the illness,
and, by the same time, the frequency of stools had become almost normal and
convalescence was very rapid.
The infecting organism was isolated from the faeces of each patient on 8th or
9th October, but it very soon became undetectable on careful examination and was
not found in specimens passed later than 48 hours after the onset of symptoms.
The examination was repeated at intervals of a few days during the ensuing
fortnight or three weeks, and no more dysentery bacilli were isolated, although
aperients were given before the last stool tested.
Blood cultures of G. C. and W. C., and of D. E., made on 8t,h October, were
sterile. The urine of all four was cultured on 9th October and no pathogenic
organisms were found.
Leucocyte counts of L. A., G. C. and D. E. were on 8th October, 75,600 per c.mm.
(polymorphs 91 per cent.), 12.000 (polymorphs 85 per cent.), and 14,200 (polymorphs
91 per cent.), respectively. Later counts of L. A. were, on 9th October, 56,800
(polymorphs 92 per cent.) and on the 11th, 14,200 (polymorphs 63 per cent). On
the 11th, also, the corresponding figures for G. C. were 9,600 (polymorphs 68 per
cent.), and for W. C. 12,800 (polymorphs 62 per cent.).
On 16th October, the serum of each patient was tested for agglutinins against
two different strains of B. dysenterice (Sonne), one of which had been isolated from
the patient and the other a stock laboratory strain. No evidence of agglutinins
against either strain was found, although both of them were agglutinable by specific
serum.
A few comments may be offered. In food poisoning due to almost any of
the organisms which may cause it, it is recognised that there may be present in
the poisoned food, at the time it is ingested, living pathogenic bacteria with a varying
amount of toxin formed by them ih the food, or toxins without viable bacteria.
This second possibility is most often realised in the case of foods (especially canned
foods) which have been infected before cooking and in which treatment by heat has
killed the bacteria but not destroyed the toxins already formed which are often thermo
stable under heat conditions which kill the bacteria. Toxins formed in the food
before its ingestion cause all symptoms which arise during the first few hours. In
cases due to a single ingestion of toxin without living bacteria the illness is usually
over within three days if the patient survives the first 24 hours. If the toxin is
in low concentration, insufficient may be absorbed through the wall of the gastrointestinal
tract for symptoms to occur other than those referable to the alimentary
system.
In the cases under review it would appear that although living bacteria were
found in the food the symptoms were mainly due to preformed toxins, as is to be
judged by the early onset of symptoms and the commencement of recovery of those
who survived and the death of the other two within 24 hours of the time the food
was eaten.
The causative organism was not found in the stools of the survivors later than
72 hours after its ingestion, nor in the blood or urine during the acute stage.
A feature of the outbreak is that B. dysenterice (Sonne) is usually associated
with mild dysenteric infections involving a very low rate of mortality as compared
with the Flexner and especially the Shiga type. The high fatality of dysentery
infections brought about by food poisoning is referred to in some of the papers
mentioned above, and, as in the pease-pudding example, is no doubt due to the food
providing a suitable culture medium for a large amount of toxin to be formed.