in the production of dysentery from the earliest times. Aretæus
mentions acrid foods, and Aëtius crudities, as directly causing the
disease; and unripe fruits have been especially stigmatized from the
days of Galen down. Decomposing, fermenting food and drink cause
diarrhoea much more frequently than dysentery, but if the irritation be
severe or prolonged, or be superimposed upon a catarrhal state, a
diarrhoea, it is claimed, may pass over into dysentery. Impurities in
drinking-water were charged with causing dysentery by Hippocrates
himself, with whom Avicenna fully coincided; and the view that
epidemics of the disease are caused in this way has been abundantly
advocated ever since. So far as running water is concerned, the
researches of Pettenkofer have shown that all impurities are speedily
destroyed, for even at the distance of a few rods from the reception of
sewage the water is perfectly safe. Nor does standing water lack the
means of purification, provided it be sufficiently exposed to the air.
The observations of Roth and Lex have shown that the water of the wells
of fifteen churchyards in Berlin contained nitrates in less quantity
than the average wells in the city; and Fleck made a similar statement
with regard to the wells of Dresden. But no one in our day would rely
upon a mere chemical analysis in the detection of the organic poisons
or particles of disease. It is the physiological test which remains the
most conclusive, and the evidence in favor of the production of
dysentery by the ingestion of drinking-water poisoned by the reception
of excrementitious matter, especially the dejecta of disease, is as
positive as in the case of typhoid fever. Thus, De Renzy found that the
number of cases of dysentery "immediately decreased at Sibsagor (India)
so soon as better drinking-water was obtained from wells deeply sunk
and lined with earthenware glazed pipes;" and Payne found that the
cases of dysentery (as well as diarrhoea and lumbrici) almost
disappeared from the asylum at Calcutta as soon as the habit of
drinking water from the latrines was stopped. In face of such facts,
which might be infinitely multiplied, one would hesitate to subscribe
to the statement of Fergusson that "true dysentery is the offspring of
heat and moisture, of moist cold in any shape after excessive heat; but
nothing that a man could put into him would ever give him a true
dysentery."
The relation of the action of the dejecta must be studied from the
double standpoint of the development and the dissemination of the
disease, as originating the catarrhal form by mechanical or chemical
irritation of the intestinal mucosa, and as spreading the specific form
by direct or indirect infection.
By the time the contents of the alimentary canal have reached the colon
they have become, through absorption of their fluids, more or less
inspissated, and hence as hard, globular masses fill the sacculi of the
large intestine. Mechanical irritations by crude, indigestible residue
of any kind of food, more especially of vegetable food, or chemical
irritations, as by fermenting food, accumulate in this region, fret the
mucous membrane into a state of inflammation, even ulceration, and
produce the anatomical picture and the clinical signs of dysentery. If
there be a superadded or {792} pre-existent catarrhal condition of the
mucosa or a defective peristalsis of the muscular coat, which is
sluggish enough at best, the development of a pathological state is
much facilitated. And there is no doubt that the dysentery of the
tropics is increased by the bulky, indigestible, feces-producing
character of the food.
The anatomical construction of the colon may also favor these processes
by its mere abnormal length or size or by duplicatures in its course.
The protracted constipation of the insane, in whom the transverse colon
is often found elongated or displaced--to assume the well-known M-form,
for instance--may partially account for the frequency of dysentery in
these cases (Virchow), though the neglect which comes of preoccupation
of the mind, with the general inhibition of peristalsis, is a more
frequent cause of the constipation.
Wernich (1879) sums up the action of the feces, independently of a
specific cause, in attributing the dysentery of the tropics, aside from
the great changes of temperature, to (1) bad aborts, the dejecta being
deposited in all parts of the towns or into an opening made in the
floor of the hut, with which is associated total lack of personal
cleanliness; (2) to the diet, which causes a large amount of feces; and
(3) to the relaxation of the intestine in general, permitting
accumulations of infecting matter.
Upon the question of the propagation of the disease by the dejecta rest
in great measure the all-important problems of a specific virus and of
the contagiousness of the disease.
It is the almost universal opinion of those who have had the
opportunity of widest observation that epidemic dysentery arises from,
or is due to, a specific cause, a miasm, a malaria (in its wide
etymologic sense, bad air), which emanates from the soil. The
simultaneous sudden attack of great numbers under the most diverse
surroundings admits of explanation in no other way. But the precise
nature of the morbific agent is still unknown. The similarity of
epidemic dysentery to malaria would indicate the existence of a low
form of vegetable life, a schizomycete, as the direct cause of the
disease. But the proof of the presence of a specific parasite or germ
is still lacking, and though its speedy disclosure by means of the
solid-culture soils may be confidently predicted, it cannot, in the
light of existing knowledge, be declared as yet.
Especial difficulty is encountered in the study of micro-organisms in
diseases of the alimentary canal because of the myriad variety in
enormous numbers found in healthy stools. Decomposition and
fermentation both begin in the large intestine, so that the feces swarm
with the bacteria and torulæ productive of these processes. Woodward
declares that his own observations have satisfied him that "a large
part of the substance of the normal human feces is made up of these low
forms in numbers which must be estimated by hundreds of millions in the
feces of each day," bacteria, micrococci, and torulæ being found
"floating in countless multitudes along with fragments of
partly-digested muscular fibres and other débris from the food;" but
while the torulæ are increased, the other micro-organisms, bacteria,
etc., do not appear to be more numerous in the stools of dysentery than
in healthy feces.
The doctrine that dysentery depends upon parasites is very old in
medicine, and included animal as well as vegetable growths. Langius
(1659) declared that swarms of worms could be found in dysenteric
stools, and {793} Nyander (1760) went so far as to call dysentery a
scabies intestinorum interna; which extravagant conception would have
speedily met with merited oblivion had not his preceptor, the great
Linnæus, incorporated the Acarus dysenteriæ into his _Systema Naturæ_.
Sydenham about this time (1670) expressed a much clearer conviction of
the cause of the disease when he spoke of "particles mixed with the
atmosphere which war against health and which determine epidemic
constitutions."
Baly (1849) first proclaimed the idea of a vegetable fungus, similar to
that described by Brittan and Swayne in cholera, as the parasite of the
disease; and Salisbury (1865) described algoid cells and species of
confervæ as occurring abundantly in all well-marked cases. Klebs (1867)
found spore-heaps and rod-like bacteria in the stools of dysentery as
in cholera, but maintained that those of dysentery were larger and
thinner than those of cholera. Hallier (1869) maintained that although
there was no morphological difference in the micro-organisms of the
stools of dysentery, typhoid fever, and cholera, he was able by
culture-experiments to develop the micrococcus of dysentery into a
special fungus, which he called Leïosporium dysentericum. Busch (1868)
demonstrated nests and colonies of micrococci, as well as mycelium, in
the villi and among the glands of the mucous and submucous tissues in
the cases of dysentery from Mexico which he examined, but Heubner
(1870) was able to disclose them in equal numbers in preserved
preparations or fresh contents of healthy intestines. Dyer[4] (1870)
believes that the parasites constituting the mildew or sweat which
forms a viscous pellicle upon fruit is the agent which directly
produces and propagates the disease. Mere immaturity of fruit gives
rise only to diarrhoea. This parasite occurs in some years more than
others, which accounts for the irregularity of occurrence of the
disease. He avers that it is only necessary to clean fruit, more
especially plums, to prevent the disease. This suggestion merits place
only as a curiosity in the history of the mycology of dysentery.
[Footnote 4: _Journal f. Kinderkrankheiten_, No. 317.]
More important are the results of the experiments of Rajewski (1875),
who found the lymph-spaces filled with bacteria, and who was able to
produce a diphtheritic exudation upon the surface and in the substance
of the mucous membrane of the colon by the injection of fluids
impregnated with bacteria into the bowels or blood of rabbits; but this
result was only obtained when the mucous membrane had been previously
irritated or brought into a catarrhal state by the introduction of
dilute solutions of ammonia. It remains for subsequent investigation to
confirm these highly significant conclusions, which, when properly
interpreted, may explain the action of the predisposing and exciting
causes of the disease. Rajewski's bacteria, it is needless to state,
were simply the bacteria of common putrefaction. Lastly, Prior (1883)
describes a micrococcus as the special micro-organism of dysentery, and
Koch (1883), in prosecuting his studies of cholera in Egypt, remarks
incidentally upon a special bacillus which he encountered in the
intestinal canal in dysentery, though he is as yet by no means prepared
to ascribe to it pathogenetic properties.
The question of contagion hinges upon the specificness of the disease,
and cannot be definitely determined until this problem is finally
solved. The old writers believed in the contagion of dysentery.
Helidæus {794} declared that he "had often seen it communicated by the
use of clyster-pipes previously used in the treatment of those
suffering with the disease, and not properly cleaned;" and Horstius and
Hildanus speak of the communicability of the disease from the latrines
contaminated by dysenteric excreta. Van Swieten maintained that
washerwomen contract it, and that physicians and nurses might be
affected. Degner saw the disease spread from street to street in
Nimeguen, while every one who came in contact with the disease became
affected. Pringle observed it spread from tent to tent in the same way;
and Tissot went so far as to declare, "Sil ya une maladie veritablement
contagieuse c'est celle ci." Ziemssen believed that the disease is only
contagious when the element of crowd-poisoning is superadded; and
Heubner states that trustworthy army surgeons in the Franco-Prussian
War frequently saw infection occur when many severe cases were heaped
together in a small space. Under these circumstances thorough
disinfection of the privies checked the spread of the disease. But it
was the universal testimony of these surgeons, as also of our own
surgeons of the Civil War, that the disease was never transported to
the civil population by any of the tens of thousands of cases on their
return to their homes.
By most modern writers dysentery is given a place, in respect to
contagion, between the exanthematous maladies, typhus and scarlatina,
which are without doubt contagious, and the purely miasmatic diseases,
malarial and yellow fevers, which are without doubt not contagious.
Dysentery is ranked with typhoid fever, which is contagious, not by
contact with the body, but with the discharges. It is not a question in
dysentery of epithelial drift or pulmonary exhalations, but of
ingestion or reception of the dejecta of the disease. By this
observation it is intended to convey the impression that dysentery,
like typhoid fever, is mostly spread in this way, but the reverse may
be true; it may be spread, like yellow fever and malaria, by poisons in
the air. But dysentery, as has been repeatedly remarked, is only a
clinical expression of a disease which may be caused in many ways; and
among these causes, least potent perhaps, but present nevertheless, is
contagion. For, not to mention the epidemics which were undoubtedly
spread in this way, as among the Allies at Valmy in 1792, among the
French in Poland in 1807, and in the hospital at Metz in 1870,
dysentery has been directly communicated by the use of clysters,
bed-pans, and privies in a most unmistakable way.
According to Eichhorst, the poison of dysentery is endowed with
extraordinary persistence of duration or tenacity of life in the
stools; for "observations are recorded where dysenteric stools have
been emptied into privies, and individuals employed to clean them out
after the lapse of ten years have been infected with the disease. These
observations go to prove, of this as of other similar affections
(typhoid fever), that the virus or microbe of the disease finds its
most favorable nidus in vaults, cesspools, sewers, etc. When the poison
is exposed to the air it is much more speedily destroyed, but is in the
mean time of course a possible conveyer of the disease." Fayrer quotes
from an anonymous writer, "whose views are as remarkable for their
force as for their originality," the rather extravagant assertion that
"if human excrement be not exposed to the air there can be no
dysentery."
{795} Knoewenagel has recently[5] opened up a new series of reflections
in his suggestion of a possible direct infection of the large intestine
per rectum, where the disease usually begins and is mostly best
expressed. He calls attention to the fact that people who suffer with
constipation indulge in longer sessions at stools and induce in
straining efforts a degree of relaxation of the rectal mucosa. The
mucous membrane at its orifice may become at the same time abraded by
hardened fecal masses, to leave open surfaces or crevices upon which
germs may lodge. Moreover, aspiration follows the efforts at expulsion,
and the air with its particles is drawn directly into the rectum, thus
affording all the conditions for immediate or direct infection.
[Footnote 5: _Schmidt's Jahrbucher_, Sept. 25, 1882.]
At any rate, it must be admitted that the evidence in favor of
contagion is in some cases too strong to be ignored. A single instance
may suffice for illustration: Flügel reports that the towns of
Nordhaben and Reichenbach, containing together twenty-two hundred
inhabitants, were visited by dysentery in 1873, when nearly four
hundred people were attacked. The visit of a relative carried the
disease from Reichenbach to the daughter of an innkeeper at Tauchnitz,
and from this house the disease spread over the whole place, so that in
a short time more than one hundred people fell ill. Four to six,
sometimes as many as eleven, members of one family were successively or
simultaneously affected. The use of the same bed was the surest means
of contagion.
The duration of the poison was proven in an exquisite case, which is,
however, not entirely free from objection: Two children of an officer
were severely affected in September and October, 1872. In January,
1873, the house was vacated and occupied by a successor in office,
whereupon in April, six months after dysentery had disappeared from the
place, the wife and child of the second officer were affected with the
disease.
To sum up the etiology of dysentery in a few words, it may be said that
few chapters in medicine are so thoroughly unsatisfactory, as the
prospect of reconciling the accumulated discordant facts is very
discouraging. Because of the singular uniformity in the symptoms and
lesions the temptation is strong to look for a common cause, and to
ascribe all cases to this cause, explaining differences by degree
rather than by kind. Such a view would find solid support in the
assumption of a specific germ, and would ally dysentery with typhoid
fever, a disease which has likewise, in all cases, uniform symptoms and
lesions, and which prevails in both sporadic and epidemic form. The
advocates of this view would fix the poison of the disease in the air
and alimentary canal (but not in the blood), and explain the existence
of individual cases, as well as the prevalence of epidemics, by
meteorological conditions as affecting the growth or dissemination of
specific germs. Nor would the adoption of this view exclude the
possibility of producing the catarrhal (sporadic) cases by many kinds
of noxious germs, including those of common putrefaction. Hot air and
wet air are notorious bearers and breeders of germs, and the law of
gravity keeps them near the surface of the earth--conditions which
coincide with the prevalence of the disease in the tropics and among
individuals (soldiers) who sleep upon the ground. If the contagion of
the disease be admitted, the existence of a {796} contagium animatum is
implied at once, for no chemical poison has the power of propagation.
But the germ of dysentery has not been found as yet, and until it has
been found, cultivated in suitable soil, and inoculated to produce the
disease, the evidence of its existence remains merely presumptive.
So that at the present time dysentery must be regarded as a malady
which stands in closer relation to, or finds a better analogue in,
cholera than typhoid fever; for cholera is a disease which has the same
geography, has likewise nearly uniform symptoms and lesions, so far as
it leaves any, and certainly has two distinct forms of origin--one
clearly specific, cholera Asiatica, and the other catarrhal, cholera
morbus.
PATHOLOGY.--Dysentery is a local malady, but, like every local malady
if sufficiently severe, it may show constitutional effects. It is
usually gradually ushered in from a lighter form of gastro-intestinal
catarrh. After a stage of incubation which lasts from a few hours to a
few days symptoms of dyspepsia and diarrhoea set in or increase,
attended with anorexia, heartburn, nausea, eructation or borborygmi,
pain in the abdomen, and copious fluid discharges. Hereupon ensue the
pains and the discharges characteristic of the disease. Violent griping
and colicky pains (tormina) traverse the abdomen, with sickening
sensations of depression. The desire of evacuation of the bowels
(tenesmus) becomes intense and more or less constant, and the discharge
itself is attended with little or no relief. At the same time the
region of the rectum, intensely inflamed, is the seat of intolerable
burning pain, which becomes excruciating with the introduction of a
speculum or the finger.
The discharges may be copious, dark-brown, thin, and highly offensive
(bilious dysentery), may contain occasional hard round fecal casts of
intestinal sacculi (scybalæ), or may become more and more scant, until
with the most violent efforts only the minutest quantity is extruded of
mucus, generally streaked or tinged with blood (rose mucus) like the
rusty sputum of pneumonia. Later, all effort at emptying the alimentary
canal may be futile (dysenteria sicca), or the mucus may be pure or
commingled with pus to remain perfectly colorless (dysenteria alba), or
with blood in larger quantity (dysenteria rubra). In other cases, or at
other periods in the same case, the discharges consist of fleshy masses
composed of inspissated mucus or pus, blood, and tissue-débris (lotura
carnea). Sometimes, though rarely, the discharges consist of pure
blood, but oftener of a copious turbid fluid, which on standing
separates into a clear upper layer of serum and a sediment of
disintegrated lotura carnea. Or, lastly, the sediment is composed of
small round vitreous masses, evidently swollen by maceration to look
like sago-grains, which have been erroneously supposed to represent the
liberated contents of the intestinal follicles.
The general condition of the patient suffers correspondingly. There may
be fever or there may be none throughout the whole course of the
disease, but the pain and discharges quickly exhaust the strength of
the patient, and in severe or long-continued cases lead to emaciation
and profound prostration.
The skin is hot and dry; the tongue is heavily coated; the face wears
an anxious expression. The abdomen is tumid with gases, or in more
advanced cases sunken, discolored, and tender, especially in the course
{797} of the colon, whose thickened walls may often be felt beneath the
emaciated surface. The anus is spasmodically constricted, or in the
worst cases paralyzed, patulous, and livid or blue. Prolapse of the
rectum is common in children, and excoriation of the perineum by the
acrid discharges is not infrequent.
Finally, a typhoid state may set in or a pyæmia occur, when the
discharges may become involuntary or unconscious, and brain
symptoms--insomnia, stupor, delirium, and coma--supervene; or the
patient may linger long enough to perish by simple exhaustion or
marasmus.
Under favorable hygiene the great majority of cases of catarrhal
dysentery recover without special treatment in the course of from three
to ten days, but specific dysentery has no definite duration and but
little tendency to spontaneous cure. The worst cases are often quickly
controlled by appropriate interference, and the most surprising results
may be sometimes obtained in cases of even years' duration. On the
other hand, a certain percentage of cases is characterized by a
defiance to every kind of treatment, including the last resort, a
change of climate.
An acute case of catarrhal dysentery generally subsides without
lesions, and the natural duration of the attack may be much abbreviated
by proper treatment. Specific or epidemic dysentery lasts from two to
four weeks, or, becoming chronic, continues for years or for life, with
exacerbations and remissions.
Various complications are liable to occur in the course of the disease.
Three deserve especial mention--viz. affection of the joints
(rheumatism), paralysis, and abscess of the liver. Perforation and
peritonitis, always possibilities, and deformities of the colon,
thickenings, and constrictions, are not infrequently left.
MORBID ANATOMY.--The lesions of dysentery are the ordinary signs of
inflammation of a mucous membrane and its subjacent structures. They do
not differ in any essential way from those of any mucous surface in a
state of inflammation, the minor variations being due to differences in
the anatomy and physiology of the part affected. Thus, a description of
the pathological process in inflammation of the pharynx, bronchi, or
uterus would answer upon the post-mortem table for the same process in
the large intestine, and the finer microscopic lesions could be
differentiated in any case only by the histology of the part affected.
A slight lesion of any mucous membrane constitutes what is known as a
catarrhal process; a more grave affection, a diphtheritic process; a
more chronic inflammation, a hypertrophic or hyperplastic process.
Hence an easy distinction between sporadic and epidemic cases might be
based upon the character of the lesion found. But, as has been stated
already, it is impossible to draw a line between catarrhal and specific
cases, the same lesions being found in either form. The difference, so
far as the morbid anatomy is concerned, is wholly in degree or stage,
and not at all in kind, the specific (epidemic) form presenting the
graver lesion as a rule. So most cases of sporadic dysentery show only
catarrhal lesions, while most cases of epidemic dysentery show
diphtheritic lesions.
Catarrhal dysentery shows as its first obvious alteration a hyperæmia
of the mucous surface. It is limited exclusively to the large intestine
in the vast majority of cases, and only in rare exceptions affects the
small intestine, though cases have been mentioned as curiosities in
which the {798} process has reached the stomach in its upmost
prolongation. The hyperæmia is most marked, as a rule, in the lowest
parts of the large intestine, the rectum and descending colon, but
there is, as Virchow has pointed out, a peculiar predisposition to
affection at the seat of all the flexures, the iliac, hepatic, splenic,
sigmoid, where the additional element of fecal arrest or impaction is
superadded to the cause of the disease.