predisposition to diseases, as there are others in whom,
notwithstanding ample exposure, infection does not easily take place.
Yet in the families in which diphtheria is of frequent occurrence it
cannot always be attributed to enlarged tonsils and a tendency to
pharyngeal or nasal catarrh.
{682} Still, catarrh and the vulnerability of mucous membranes must be
considered as a frequent source of diphtheria; children will get
numerous relapses often after a nasal or pharyngeal catarrh. Sudden
changes in the temperature of the atmosphere or of the surface of the
body are therefore dangerous in predisposed persons. And thus it is
that while severe epidemics have spared no climate or land known to
us, the majority of cases have occurred in winter and spring; in other
words, at a time when catarrhal disorders are of most frequent
occurrence. In my experience at New York, the first quarter of the
year yielded more cases than any other. Still, they are frequent
enough in warm seasons. Krieger insists upon the injurious influence
of hot summers and dry hot rooms. I do not doubt the correctness of
his views, which cannot but be strengthened by the damaging results of
our furnace-heating. But the influence of season on the invasion and
course of diphtheria is but indirect and conditional, and may be,
perhaps, after all, compared with that exerted by filth--a term which
is lately used to express all sorts and forms of nastiness, from
filthy bodies of men to their clothes, their habits, their food, and
the air they breathe, whether polluted by carbonic acid, by
excrementitious gases, or by exhalations of sewers.
Cases of diphtheria which are traced to exhalations from sewers (or
even to filthy habits of life) are very frequent. Yet typhoid is
attributed to the same causes. So is dysentery. Can, then, foul
exhalations produce alike diphtheria, typhoid, and dysentery? Do these
diseases arise from a common poison? Or is the poison of a treble
character, so that a part may give origin to diphtheria, another part
to typhoid, a third to dysentery?[18] Have we to deal, in such
occurrences, with specific influences, or only with a lowering of the
standard of health, thereby affording other morbid influences an
opportunity to exercise their power? These questions are still
involved in darkness, and constitute problems the solution of which
still engages the minds of both individual writers and authorities. A
report of the Board of Health of Massachusetts, closely adhering to
the results of exact observations,[19] leaves them doubtful, and the
affirmative reports of some modern writers do not bear scrutiny.[20]
[Footnote 18: In regard to the causal connection of the two latter
diseases with sewer exhalations we can be more positive than in regard
to the former.]
[Footnote 19: Author's _Treatise on Diphth._, p. 35.]
[Footnote 20: M. A. Avery, _Med. Jour. and Obst. Rev._, Feb., 1882.]
Air polluted by bad drainage or leaky sewers has been considered
responsible for diphtheria as well as for typhoid fever and dysentery.
Not only the impairment of general health, but the direct and
unmistakable disease, has been attributed to it. Thus Bayley refers,
in the endemic of Bromley,[21] the first cases to unventilated sewers
and cesspools. School-children multiplied the disease. Thursfield
attributes the diphtheria at Ellesmere[22] to the accumulation of
excrements under the school-room, and to deficient supply of water,
which, moreover, was of bad quality. Tripe (like Railton, Bailey,
Russell, Bell) accuses sewer gas;[23] others polluted waters or bad
drainage.[24] I have not been convinced, however, that diphtheria can
be considered a sewer-gas disease, in the same way as typhoid fever.
The deterioration of the general health resulting from the inhalation
of foul air is sufficient to explain the outbreak of the individual
attack during a prevailing epidemic.
[Footnote 21: _Sanit. Record_, Aug. 10, 1877.]
[Footnote 22: _San. Rec._, 158, 1877.]
[Footnote 23: _Ibid._, June 14, 1878.]
[Footnote 24: _Ibid._, April 18, May 2, 1879.]
{683} In regard to polluted water, I do not think that pathologists
who attribute infectious diseases to bacteria only are justified in
condemning it. It may not be so guilty, after all, for the admixtures,
inorganic and organic, minerals, admixtures of wood and plants, also
lower fungi and their products--algæ, infusoria--would render water
rather disagreeable, but not exactly unhealthy. The latter effect can
be accomplished--always assuming the bacteria theory correct, for the
sake of argument--by bacteria only. But when they arrive in the
stomach, their doom is sealed; they are decomposed. The only places
where, possibly, they could take root would be diseased or ulcerated
places in either the oral cavity or the upper portion of the
oesophagus.
Not only water, but the milk of animals also, has been accused of
being the direct cause of diphtheria. Powers concludes, though a
connection between diphtheria and the consumption of milk have not
been proven as yet, that it is very probable indeed. His careful
investigations into the causes of some local epidemics in North London
exclude any other source from which the people could have been
affected. Perhaps one of the forms of garget, cow mammitis, is of an
infectious character. His reasoning, however, is not accepted by A.
Dowrus,[25] who still believes that the milk which gave rise to
diphtheria at a distance may have been soiled and infected. For though
the connection between milk and scarlatina and typhoid fever had been
known for years and variously studied, no observation of the kind had
yet been made in regard to diphtheria. Besides, where the young, in
England, drink much milk--viz. in the cities--diphtheria was very much
less frequent than where little or no milk was taken--viz. in the
country. Even in the country the well-to-do classes, who drink milk,
had but little diphtheria, while the children of the poor, who
obtained none, suffered a great deal from it.
[Footnote 25: "Diphtheria and Milk-Supply," _Brit. Med. Journ._, Feb.
1, 1879.]
In regard to this transmission of diphtheria by means of milk O.
Bollinger[26] hesitates to express any opinion, except that the matter
is very doubtful indeed. Probably the possibility of contracting
diphtheria directly from animals is very much greater than the danger
from water or milk. On a Pomeranian farm, during the winter 1875-76,
every newly-born calf died of diphtheria. The superintendent of the
farm and the woman who attended to the calves were taken with
diphtheritic angina.[27] Similar occurrences have been recorded.
Bollinger reports a mycotic disease of the trachea and lungs in birds.
[Footnote 26: _D. Z. f. Thiermed. u. vergleich. Pathol._, vi., 1879,
p. 7.]
[Footnote 27: Damman, in _D. Zeitsch. f. Thiermed._, 1876, p. 1.]
Friedberger's report,[28] presented to the Veterinary Society of
Munich, on croup and diphtheria of domestic fowls, leaves no doubt as
to its frequency, particularly amongst the nobler varieties.
[Footnote 28: _D. Zeitsch. f. Thiermed._, v., 1879, p. 16.]
Nicati[29] studied an epidemic diphtheria amongst hens which had
similar symptoms and a course very much like that in man; it could be
inoculated into other animals, and was contemporaneous with the
outbreak of the epidemic amongst the human population of Marseilles.
Trasbot[30] succeeded in inoculating a healthy hen from a diphtheritic
one, but the {684} attempts at transmission to dog, pig, and man were
unsuccessful. The _Med. and Surg. Journal_[31] contains the following:
In a house at Ogdensburg, N.Y., five children were ill with
diphtheria. Three kittens who had been playing with them from time to
time took the disease and died. Post-mortem examination showed
diphtheritic membranes in their throats.[32]
[Footnote 29: _Revue d'Hygiène et de Police sanitaire_, 1879, p. 3.]
[Footnote 30: "De la transmission de la Diphth. des Animaux à
l'Homme," _Gaz. hebdom._, 1879 Avril 25.]
[Footnote 31: _Med. Rec._, Nov. 8, 1879.]
[Footnote 32: An elaborate description of the croupo-diphtheritic
inflammations of mucous membranes in hens, turkeys, pheasants, and
pigeons may be found in _Zürn. Krankh. d. Hausgeflügels_, 1882, p.
104.]
Gerhardt[33] reports the following: 2600 hens were imported from
Verona, Italy, into a village, Messelhausen, in Baden. Some of these
hens were affected with diphtheria when they arrived. Within six weeks
600 of their number died of diphtheria, and 800 more soon after. In
the following summer 1000 chickens were raised by artificial breeding,
all of which died of diphtheria within six weeks. Five cats kept in
the place also died of diphtheria; a parrot fell sick with it, but
recovered. An Italian cook, suffering from diphtheria, in the month of
November, 1881, while being subjected to local treatment with carbolic
acid, bit the head-nurse's left foot and hand. Both these wounds
became diphtheritic, the man falling sick with high fever, and
requiring three weeks for his gradual recovery. Besides, four of the
six workingmen employed in taking care of the hens of the
establishment were taken with diphtheria. Not a single case, however,
occurred in the neighboring village. Thus, it is safe to assume that
the diphtheritic disease of hens can be transmitted to man.
[Footnote 33: _Verhandlungen des_ (ii.) _Congresses für Innere
Medicin_, Wiesbaden, 1883, p. 129.]
Diphtheria may be also produced by outside influences. In this regard
the attempts at generating pseudo-membranes by artificial means are
very interesting indeed. As early as 1826, Bretonneau, by the
introduction of tincture of cantharides and olive oil into the
trachea, succeeded in producing a "dense, elastic, reed-like
membranous concretion." Delafond called croup into existence by the
use of ammonia, oxygen, chlorine, corrosive sublimate, arsenic, and
sulphuric acid. On the other hand, H. Mayer asserts that it is
impossible, by means of ammonia, to produce a croup in the windpipes
of animals which in the slightest degree resembles that occurring in
human beings. Trendelenburg, however, after producing membranes in the
trachea by the use of a solution of corrosive sublimate (1:120),
succeeded in hardening the entire mass with bichromate of potassium,
which it was impossible to do with the most tenacious mucus.
Rey observed croup in horses that inhaled smoke in a burning
stable.[34] In the collection of the veterinary school of Zurich there
is a croup membrane from a heifer which had been exposed to a fire; at
Munich, one from the trachea of a horse, produced by forcibly
injecting medicines into the nose. Hahn made an observation on cows,
W. Ammon on horses, of long croup membranes after the animals had been
exposed to smoke and fire; and Oertel constantly insists on there
being "no actual difference between croup as it ordinarily occurs and
that excited in the windpipe of a rabbit by means of ammonia. The
color and texture, the physical, chemical, and histological
characteristics, are identical."
[Footnote 34: _Journ. de méd. vét. de Lyon_, 1850, p. 249.]
{685} MORBID ANATOMY.--Either the membrane or the granular
infiltration is characteristic of diphtheria. The statement that the
former occurs only when atmospheric air can gain access thereto, as A.
d'Espine and C. Picot still hold,[35] is plainly contradicted by its
appearance on the mucous membrane of the lower intestines. The
condition of the membrane is not unalterable, any more than the
clinical symptoms of the disease, for, according to different
circumstances, epithelium, mucus, blood, and vegetable parasites are
added thereto. The membrane can either be lifted from the mucous
membrane on which it lies or is imbedded into and underneath it. In
the first instance, it consists to a great extent of fibrin, the
result either of epithelial changes or derived directly from the
exuded blood-serum. E. Wagner, who makes no anatomical distinction
between croup and diphtheria, considers epithelial changes the
principal source. The pavement epithelium becomes altered in a
peculiar manner. It becomes turbid, larger, dentated, and dissolves
into a network; it is at first uninhabited, but serves later as the
vehicle of newly-formed cells; there also occurs a considerable
infiltration of the mucous membrane pus-cells and granules; besides,
the cellular tissue is studded with granules, the granular
degeneration resulting sometimes in necrotic destruction, which is
looked upon by Virchow as the most important element in severe forms
of diphtheria. The several conditions or degrees may occur independent
of each other, associated or in succession. Classen shares Wagner's
views, but, according to Boldygrew, the pseudo-membrane consists of
successive coagulations of a fibrinous fluid which exudes from the
diseased surface. Steudener also opposes the views of Wagner. He does
not believe in the probability of an exclusively endogenous origin of
the cellular elements of croup membrane; in fact, he doubts the
occurrence of an endogenous formation of pus-globules in epithelium.
Croupous membrane, according to him, is formed by the migration of
numerous white blood-globules through the walls of the vessels in the
mucous membrane, and by a direct formation of fibrin from the
transuded plasma. In addition to this, the mucous membrane is stripped
of its epithelium (except at the mouths of the acinous glands) and
infiltrated with migrating cells. Fresh croupous membrane consists of
a delicate network of homogeneous structure and shining appearance, in
which numerous cells and the epithelium of the various layers of the
trachea are imbedded. In old membranes the cells are destroyed by
granular degeneration and general maceration. Tenacious mucus with
pus-cells and detritus are then found. C. Weigert looks upon the
deposits as analogous to those on serous membranes. Every inflammation
yields an exudation which may coagulate when the coagulating ferment
is added. This latter is probably produced by the white blood-cells
when in disintegration. But he does not say why it is that there is no
such coagulation in suppurative processes, where the leucocytes are
more numerous. He believes himself justified in establishing
pathological differences of croup, pseudo-diphtheria, and diphtheria.
A croupous inflammation means destruction of epithelium, which gives
rise to a fibrinous exudation upon the surface, while the cellular
tissue remains intact. The only difference between it and the
pseudo-diphtheritic inflammation is looked for in the larger number of
emigrated white {686} blood-cells. The superficial deposit consists,
to a great part, of them and the fibrinous exudation. When there are
but few leucocytes the deposit is a network of fibrillæ (croup). When
there are many, the masses are more solid and voluminous
(pseudo-diphtheritis). When, however, the tissue is changed into a
hard substance resembling coagulated fibrin, when the exudation does
not exist on the surface, but takes place into the mucous membrane,
the process is diphtheria. Zahn also establishes three varieties--viz.
1st, such as result from a peculiar degeneration of pavement
epithelium; 2d, such as originate in the solidification of a
muco-fibrinous, and, 3d, of a fibrino-purulent, exudation. Each of
these varieties may contain colonies of micrococci, but these
organisms are neither essential nor are they constantly found.
[Footnote 35: _Man. prat. des mal. de l'enfance_, 1877, p. 81.]
The diphtheritic process does not merely consist of the membranous
changes in the pharynx and air-passages. Its fatal cases have afforded
marked evidence of the implication of most of the organs. Reimer's 17
cases give the following post-mortem results: the lungs were hyperæmic
in 8 cases, twice the seat of pneumonia, and three times of embolic
infarctions; in addition, emphysema in 12, oedema in 6, atelectasis in
7, subpleural ecchymoses in 7, pericardial ones in 4. The heart-muscle
had undergone fatty degeneration in 6, and was the seat of ecchymoses
of the size of a pin's head in 3. In addition to frequent hyperæmic
conditions of the abdominal viscera, emboli of the liver in 3 (with
capillary hemorrhages of the peritoneal covering in 1), emboli of the
spleen in 5, desquamative nephritis in 7 (in 6 of which there were
colonies of micrococci in the uriniferous tubules), cellular
hyperplasia of the cervical and mediastinal glands in 14 (complicated
in 6 with capillary hemorrhages in the glandular tissue). The blood
was frequently normal, very often watery and dark, at times
leucocythæmic. Thus the disease exerts its influence everywhere.
Rindfleisch defines diphtheritic inflammation as that form of
inflammation which produces a coagulating necrosis in the tissues by
the immigration of schizomycetæ. The coagulating necrosis differs from
the usual form of necrosis in this, that the change from life to death
is accompanied with the coagulation of fluid albuminoids. This process
takes place mainly in the interior of cells and other parts of
tissues, and therein differs from the coagulation of fibrin. In the
cells there is taking place a peculiar homogenization of protoplasm;
at the same time the nuclei disappear, and are changed into irregular
masses liable to cohere and form membranous conglomerates, which owe
their peculiar wax color to the invasion of a solid albuminoid endowed
with a strong tendency to refract the light. Coagulating necrosis is
found in circumscribed localities, and gives rise, in the
neighborhood, to a marked amount of inflammation and suppuration,
which leads to the expulsion of the necrotic part, with more or less
loss of substance--either mild or phagedenic ulceration.
Leyden describes a gray degeneration of the muscular tissue which he
believes to be truly inflammatory, and Unruh has lately published an
account of some cases in which myocarditis occurred. In Leyden's
cases, the muscular nuclei were increased, became atrophied, and
underwent fatty degeneration, giving rise thereby to extravasations,
softening, dilatation and debility of the heart, with general
debility, collapse, {687} and--probably by reflex action on other
branches of the pneumogastric--vomiting. Micrococci he found neither
in the heart nor in the kidneys.
In the heart, particularly on the right side, numerous thrombi are
frequently found in various stages of development; its muscular tissue
is often in a state of fatty degeneration or the seat of
parenchymatous inflammation and hemorrhages. Bridges first called
attention to the occurrence of endocarditis in diphtheria.[36] This
complication, which, however, occurs more frequently with rheumatism,
puerperal fever, diphtheria of wounds, pyæmia, and old valvular
affections than in the course of an acute diphtheria, does not, as
found in the latter affection, consist simply of a fatty degeneration
and subsequent ulceration, but is considered a genuine diphtheritic
process (Virchow), affecting the mitral valve more frequently than the
tricuspid or pulmonary valves. It begins with hyperæmia and the
exudation of plasma in the cellular elements, so that they appear
larger and darker. The granulations which form are frail and easily
destroyed, so that ulcers form on which fibrin is deposited, and
whence it is conveyed as emboli into the terminal arteries (Cohnheim)
of the spleen, nerves, brain, and eye. Infarctions may also occur in
the valveless veins of these organs, giving rise rather to small
multiple abscesses than to large purulent collections. Suppuration but
rarely takes place in the heart; the granular mass found there resists
the action of æther and alcohol, and spreads throughout the cardiac
parenchyma, so that perforation of the septum and of the right auricle
and aorta has been observed.
[Footnote 36: _Med. Times and Gaz._, ii. p. 204.]
Bouchut and Labadie-Lagrave, out of 15 cases of diphtheria, met in 14
with a plastic endocarditis, which became the source of emboli. Thus,
there were infarctions of the lungs, at times in their centre
colorless, at other times in a state of purulent degeneration;
superficial thrombi of the small veins of the heart, subcutaneous
connective tissue, pia mater, brain, and liver; and in addition,
moderate leucocytosis.
The lungs exhibit (post-mortem) all sorts of inflammatory and
congestive conditions, with their consequences, as oedema, catarrh,
broncho-pneumonia, atelectasis, emphysema, ecchymoses, and large
infarctions.
The spleen (and occasionally the liver) is frequently large,
congested, and friable, and studded with infarctions to a greater or
less extent.
The kidneys are either simply congested or the seat of nephritis or
infarctions. The same forms of inflammation which accompany
scarlatina--to wit, the desquamative and the diffuse--are here
observed. The diffuse form is not of so frequent occurrence as in
scarlatina, but is sometimes extensive and dangerous.
The muscles occasionally exhibit ecchymoses, and are at times the seat
of parenchymatous inflammation, gray degeneration, and atrophy.
The lymphatic glands are frequently inflamed and swollen, either hard
or doughy, oedematous or congested. Large abscesses are rare. It is
more especially the gland tissue, and less the connective tissue of
the glands, which takes part in the pathological process. The
periglandular tissue very soon becomes involved, however. Necrotic
foci have been described by Bizzozero. When the entire surface of the
mucous membrane of the mouth and of the air-passages, from the nose to
the trachea, is the seat of the disease, there is an impregnation of
the mucous membrane, from the epithelial surface to the submucous
tissue, of the entire {688} tongue, borders of the lips, and
frequently of the lips and cheeks, as well as of the tonsils, the
lower portion of the nasal cavities and the upper, and especially the
anterior, portion of the larynx. The fossæ Morgagni and the posterior
aspect of the soft palate are more frequently affected in the same way
than the anterior aspect. Small isolated spots are found on the
tonsils and occasionally on the posterior wall of the pharynx. The
so-called croupous form--that is to say, the one in which the
membranes deposited may either be removed in large patches or lie
macerated in the profuse secretion of subjacent mucous glands--is
found partly in the nasal cavities, on the posterior surface of the
soft palate, and also in the trachea and its subdivisions.
The character of the mucous membrane varies with the locality. Its
different elements, as the epithelium, the basement membrane, the
connective tissue mingled with elastic fibres, the blood-vessels, the
nerves from the cerebro-spinal and sympathetic systems, and the
papillæ and ducts of numberless glands, all influence the pathological
process going on upon the surface. Their distribution in the oral
cavity and the respiratory organs is a very interesting study, and in
a table already published,[37] I have exhibited it in a condensed
tabular form.
[Footnote 37: _Treatise on Diphtheria_, p. 126.]