IV. INVESTIGATION OF C. DIPHTHERIAE
75
In this respect the interested research worker is referred to Loeffler’s
(1 884) early review concerning the pathogenicity in animals.
In guinea pigs, the following clinical symptoms may occur: the animal
appears to be suffering and sits crouched in its cage; a soft swelling occurs
at the site of inoculation, within 24 h, and death usually occurs within
48-92 h. The time to death may be shorter with larger doses of toxin.
At necropsy of a guinea pig that died within 4 days, the following three
typical signs were noted: (i) gelatinous haemorrhagic oedema at the site
of inoculation (subsequently developing to necrosis) ; (ii) swelling and
congestion of the adrenal glands; (iii) serous or haemorrhagic exudates in
the pleural and abdominal cavities with intensive congestion of the abdominal viscera. Degenerative changes can always be demonstrated in the
heart, liver and kidneys. Sublethal doses cause late paralysis similar to
that observed in man.
All toxic effects described, as well as death, can be specifically neutralised
and prevented by a previously administered specific diphtheria antitoxin.
By intradermal inoculations on the shaved skin of a rabbit, diphtherial
toxin or toxigenic strains promote a typical erythematous reaction which may
also be neutralised by a previously administered antitoxin.
An experimental model was achieved (Calalb et al., 1963) by conjunctival infection of the guinea pig with C. diphtheriae strains. Bonciu
et al. (1965, 1966), and Meitert et al. (1972a, b) established clear-cut
differences in the pathogenic effects of the three biotypes : graais, intermedius,
mitis, tox+ and tox-.
(c) Clinical aspects. I n man the first obvious sign of infection is the occurrence of a greyish, extensive, adherent membrane, in most cases on the
fauces. It may also be localised on the nasal mucosae, where there is a thick,
sero-sanguinous rhinorrhoea, sometimes on skin wounds, leg ulcers, on
the fingers, ears, eyes, vagina.
Diphtheria bacilli multiply at the site of infection and the toxin produced
is carried by the blood stream to the rest of the body. It produces lesions
mainly in the heart and nervous system, possibly leading to death. Paralysis
of the palate muscles and of other muscles are common complications.
How toxin reaches the nervous system is as yet uncertain.
When a general specific level of immunity has been acquired in large
sections of the population, circulating toxinogenic C. diphtheriae may give
rise to atypical clinical forms of diphtheria, characterised by pharyngeal
redness and slight fever, situations that have to be differentiated from
common colds.
8. Virulence and toxinogeny
With Freeman’s discovery (1951) that pairs of toxigenic (tox+) and non-
75
In this respect the interested research worker is referred to Loeffler’s
(1 884) early review concerning the pathogenicity in animals.
In guinea pigs, the following clinical symptoms may occur: the animal
appears to be suffering and sits crouched in its cage; a soft swelling occurs
at the site of inoculation, within 24 h, and death usually occurs within
48-92 h. The time to death may be shorter with larger doses of toxin.
At necropsy of a guinea pig that died within 4 days, the following three
typical signs were noted: (i) gelatinous haemorrhagic oedema at the site
of inoculation (subsequently developing to necrosis) ; (ii) swelling and
congestion of the adrenal glands; (iii) serous or haemorrhagic exudates in
the pleural and abdominal cavities with intensive congestion of the abdominal viscera. Degenerative changes can always be demonstrated in the
heart, liver and kidneys. Sublethal doses cause late paralysis similar to
that observed in man.
All toxic effects described, as well as death, can be specifically neutralised
and prevented by a previously administered specific diphtheria antitoxin.
By intradermal inoculations on the shaved skin of a rabbit, diphtherial
toxin or toxigenic strains promote a typical erythematous reaction which may
also be neutralised by a previously administered antitoxin.
An experimental model was achieved (Calalb et al., 1963) by conjunctival infection of the guinea pig with C. diphtheriae strains. Bonciu
et al. (1965, 1966), and Meitert et al. (1972a, b) established clear-cut
differences in the pathogenic effects of the three biotypes : graais, intermedius,
mitis, tox+ and tox-.
(c) Clinical aspects. I n man the first obvious sign of infection is the occurrence of a greyish, extensive, adherent membrane, in most cases on the
fauces. It may also be localised on the nasal mucosae, where there is a thick,
sero-sanguinous rhinorrhoea, sometimes on skin wounds, leg ulcers, on
the fingers, ears, eyes, vagina.
Diphtheria bacilli multiply at the site of infection and the toxin produced
is carried by the blood stream to the rest of the body. It produces lesions
mainly in the heart and nervous system, possibly leading to death. Paralysis
of the palate muscles and of other muscles are common complications.
How toxin reaches the nervous system is as yet uncertain.
When a general specific level of immunity has been acquired in large
sections of the population, circulating toxinogenic C. diphtheriae may give
rise to atypical clinical forms of diphtheria, characterised by pharyngeal
redness and slight fever, situations that have to be differentiated from
common colds.
8. Virulence and toxinogeny
With Freeman’s discovery (1951) that pairs of toxigenic (tox+) and non-