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54
was partially neutralised by either scarlatinal or erysipelas serum ; and vice versa
in the same proportion of cases puerperal streptococcal serum neutralised the
scarlatinal and erysipelas toxins.
Directly concerned with the question of the relationship of throat infection
to scarlet fever is a paper (by F. A. Stevens and A. R. Dochez of New York) (J. A. M.A.
April 10th, 1926, p. 1110) which describes an epidemic of hæmolytic streptococcus
infection among the nursing staff and patients at a certain hospital giving rise
for several months to cases of scarlet fever and of sore throat without rash.
The authors quote the evidence of several writers 50 to 60 years ago to show
that scarlet fever had long been suspected to occur unaccompanied by any rash.
As the result of their observations they consider that there is sufficient justification
for this belief; further, they found that the type of throat infection concerned
might affect individuals who gave negative skin reactions to scarlatinal-toxin and
were, therefore, presumably insusceptible to true scarlet fever.
Their investigations included the isolation of hæmolytic streptococci from
the throats of the contacts suffering from pharyngitis, as well as of the cases of
scarlet fever, and the testing of the strains with the sera from types of the two groups
respectively, as regards agglutination and absorption and the neutralisation of
toxin. The scarlatinal sera agglutinated five out of 17 of the pharyngitis strains
of hæmolytic streptococci and neutralised their toxins; thus showing that the
toxin production of the pharyngitis streptococci and agglutinating properties of
the scarlatinal sera were in some cases closely parallel.
An important observation arising from their work confirmed that of Rosenow,
namely, that the skin reaction following intracutaneous inoculation of scarlatinal
toxin was an index of antitoxic immunity, but not of immunity of the throat to
streptococcal infection, as shown by the fact already mentioned that cases of scarlatinal
angina actually occurred in individuals giving a negative skin reaction.
They refer to the wide distribution of streptococcus scarlatinæ, from the observations
of Dr. Anna Williams, who reported the presence of scarlatinal-toxin-producing
strains in osteomyelitis, endocarditis and in chronically inflamed tonsils,
without any of the usual manifestations of scarlet fever. It was not surprising,
therefore, that five of the strains of streptococci obtained in cultures from the cases
of acute pharyngitis, occurring in the epidemic of scarlatina and angina, showed
both the agglutinative and toxin-producing properties of streptococcus scarlatinae.
Reference has already been made to the doubtful reliability of the cutaneous
reaction as a specific index of scarlatinal susceptibility (v. p. 52). This has also been
observed by Gerbasi of Naples (Pediatria Naples, February 1st, 1926. p. 119), who
found that injection of toxins from hæmolytic streptococci, derived from other
sources than scarlet fever, produced in children reactions similar to those with the
Dick toxin, and therefore possibly destroying or reducing the value of the specificity
of the scarlet fever streptococcus and the Dick reaction.
Stevens and Dochez are also inclined to share this view and utter a word of
caution against drawing too strict an analogy between scarlet fever and diphtheria.
Whereas in diphtheria the infecting organism is essentially a toxin-producer and
the Schick test is apparently an accurate index of susceptibility to diphtheria infection,
in scarlet fever the streptococcus scarlatinæ is both a toxin producer, and,
by dissemination through the circulation, is productive of secondary bacterial infection.
Therefore, although the Dick test may be regarded as an index of antitoxic
immunity, they hold that it is no index of bacterial (streptococcal) immunity. This
dual combination of the bacterial and toxic factors may possibly serve to explain
the varying individual susceptibility mentioned on p. 53; giving rise, in one
individual, to simple acute pharyngitis or angina without any rash due to
bacterial susceptibility, but a sufficient antitoxic immunity,—yet causing in
another, true scarlet fever from lack of both antitoxic and antibacterial immunity.