by the nuclear structure as shown in stained specimens. In _E.
coli_ the nucleus is vesicular with a thick nuclear membrane
and the chromatin chiefly deposited on the under surface of the
nuclear membrane. This chromatin often seems deposited in quadrant
aggregations. The karyosome is eccentric.
For the pathogenic amoeba we recognize a _histolytica_ type of
nucleus, which is found in dysenteric stools, and a _tetragena_ type,
which is found in diarrhoeal or more or less normal stools. Dobell
does not recognize this differentiation.
[Illustration: FIG. 60.—The more important intestinal amoebae of man
showing nuclear structure when stained. 1. _E. histolytica._ 1(a).
_E. histolytica_ cyst. 2. _E coli._ 2(a). _E. coli_ cyst. 3. _E.
nana._ 3(a). _E. nana_ cyst. 4. _I. bütschlii._ 4(a). _I. bütschlii_
cyst. (After Dobell.)]
The histolytica nucleus has a thin nuclear membrane and is poor in
chromatin while the tetragena nucleus has more chromatin, showing
radial projections from the inner surface of the nuclear membrane,
and a loose central spherical karyosome, which contains a central
chromatin dot or centriole, with a clear halo surrounding it.
Dobell states he has not been able to note this centriole.
The preëncysted _E. histolytica_ has a nucleus resembling that of _E.
coli_. The smaller size and chromidial bodies are differentiating.
Animal experimentation upon kittens with _E. coli_ by Schaudinn,
Craig and Wenyon have been unsuccessful as to production
of dysenteric manifestations. On the other hand all of
these experimenters produced typical lesions and dysenteric
manifestations in kittens injected rectally or fed with material
containing pathogenic amoebae.
Wenyon as previously stated produced a liver abscess in one of his
experiments.
Darling has been so successful in his experimental work with
kittens that he compares the colon of a kitten to a test tube and
suggests the procedure of rectal injections of material containing
amoebae as a means of differentiating the two human amoebae.
On the other hand Walker was unable to infect kittens and
monkeys with material containing pathogenic amoebae and he makes
the statement that such failures would indicate the greater
susceptibility of man to infection, as he was able to infect 17 out
of 20 men with one feeding of such material.
Sellards and Baetjer note that inoculation of kittens per rectum
or by feeding dysenteric stools rich in amoebae has resulted in
infection in about 50% of experiments.
By inoculating the material directly into the caecum they were
able to infect every one of their kittens. They were also able
to propagate a strain of amoebae through a series of animals for
several months.
The intracaecal inoculations yielded positive results in diagnosis
of human amoebiasis when the clinical manifestations were obscure
and the amoebae in the discharges so few and atypical as to make
such an examination unsatisfactory.
_Other Intestinal Amoebae._—It is a remarkable fact that one of
the most common of the intestinal amoebae, _Endolimax nana_, has
only recently been reported (Wenyon and O’Conner in 1917). In the
examination of the stools of American soldiers Kofoid found it
present in 28% of his examinations while _E. coli_ was present
in 23% of cases and _E. histolytica_ in 9.3%. In examining 156
British soldiers Dobell noted its presence in 33% of them. The
general view is that it is not pathogenic but its great importance
is in the possibility of its being mistaken in its cyst form for
_E. histolytica_. The living amoeba averages about 8 microns but
in stained specimens it is somewhat smaller. In freshly passed
faeces the amoeboid motion is sluggish and the nucleus indistinct.
This amoeba is best identified by haematoxylin stained specimens
when the nucleus shows a measurement of about 2 microns with a
large eccentric karyosome which exhibits a variety of form. Unless
perfectly fresh material is stained the degenerative changes in the
amoebae may give a signet ring appearance of karyosome and ring
nucleus. Such an appearance may suggest the limax nucleus. The
mature cysts are usually oval, but sometimes round, and contain
4 nuclei, but when newly formed may only have one nucleus. The
nucleus is large in the uninucleate form (up to 3 microns) but
in the quadrinucleate forms it is about 1.2 microns with a large
eccentric mass of chromatin. Chromidial bodies are rarely, if ever,
present in these cysts.
_Iodine Cysts._—These bodies which stain a deep brown colour when
treated with iodine are now recognized as amoebae and have been
named _Iodamoeba bütschlii_. They are most probably nonpathogenic.
It is a small amoeba (9 to 13 microns, rarely up to 20 microns)
and shows the sluggish movements of _E. coli_. The nucleus is very
difficult to discern, thus differing from _E. coli_. In stained
specimens it has a vesicular nucleus about 2 microns in diameter
with a fairly large central karyosome. The cysts are spherical
or oval, often of irregular outline and are about 10 microns in
diameter. The nucleus is large and eccentrically placed and has a
karyosome which tends to show as a peripherally placed mass. There
is almost always present a large glycogen mass in the cyst which
stains intensely with iodine.
_Dientamoeba Fragilis_ (Jepps and Dobell 1918).—A rare binucleate
amoeba averaging 8-9 microns in size. Nuclei show a fairly large,
central granular karyosome and no peripheral chromatin. Strands
of linin may be seen radiating from karyosome to nuclear wall.
This organism is said to be frequently mistaken for Blastocystis
when the vacuoles coalesce leaving a thin ring of cytoplasm. Cysts
unknown. Considered nonpathogenic. Recently Kofoid and Swezy
reported another species of amoeba parasitic in man, _Councilmania
lafleuri_. The adult and cystic stages resemble in many respects
the _E. coli_. Adult said to ingest red blood cells. Stated to be
pathogenic but that more evidence is needed on this point.
=Human Experiments.=—Recently Walker and Sellards have published a
most important paper.
The experiments were made in men who had been under observation
for years at Bilibid Prison, whose food was cooked and the water
they drank distilled. Moreover, there were complete records of
examination for intestinal parasites, including entamoebae. They were
under complete control and the existence or possibility of natural
infection with amoebae was reduced to a minimum. All the men fed
pathogenic amoebae were volunteers and each signed, in his native
dialect, an agreement to the conditions of the experiment.
The first series of experiments was with cultural amoebae, in
order to refute statements that amoebae cultivated from water or
other nonparasitic sources, as well as from dysenteric stools, are
capable of living in man parasitically or of producing dysenteric
symptoms. Twenty feeding experiments on ten men were made by Walker
and Sellards with cultures of amoebae without the development in a
single instance of dysentery or the finding of such amoebae in the
stools upon microscopical examination. In 13 cases they recovered
the amoebae in cultures from the faeces from the first to the sixth
day, but never afterwards. They stated definitely that cultural
amoebae are nonpathogenic.
The next experiments were with _Entamoeba coli_. In the 20 cases
fed with material containing _Entamoeba coli_ there was a uniform
failure to recover them culturally and in no instance was dysentery
produced. Seventeen became parasitized as the result of a single
feeding in from one to eleven days, the entamoebae being found
in the stools and persisting in their appearance in the stools
for extended periods. They concluded that _Entamoeba coli_ is an
obligate parasite, nonpathogenic, and cannot be cultured.
The third series of 20 feedings, carried on by Walker alone, was
with _Entamoeba histolytica_. The material was mixed with powdered
starch or magnesium oxide and given in gelatin capsules. In these
experiments they obtained tetragena cysts in the stools of men
fed only motile _Entamoeba histolytica_, and motile _Entamoeba
histolytica_ in the stools of men who were fed only tetragena
cysts and, finally, an alternation of motile _E. histolytica_ and
tetragena cysts in the stools of a man having a recurrent attack of
amoebic dysentery.
=Results.=—Seventeen of the men became parasitized after the first
feeding; 1 required three feedings, and 2, who did not become
parasitized at the first feeding, were held as controls. The
average time for parasitization was nine days. Only 4 of the 18
parasitized men developed dysentery, which came on after twenty,
fifty-seven, eighty-seven, and ninety-five days, respectively,
after the ingestion of the infecting material.
In 4 cases fed with material from acute dysenteric stools or
from amoebae-containing pus from liver abscess, and containing
motile amoebae, there was no resulting dysentery, the 4 cases of
experimental dysentery resulting from feeding of material from
normal stools of carriers.
As regards the cases which became parasitized, but did not develop
dysentery, it is suggested that the amoebae live as commensals in
the intestine of the host and only penetrate the intestinal mucosa
and become tissue parasites when there occurs depression of the
natural resistance of the host or as the result of some lesion of
the intestine. That the pathogenic amoebae are more than harmless
commensals, however, is shown by the fact that they alone, and not
the nonpathogenic _Entamoeba coli_, are capable of penetrating a
possibly damaged intestinal mucosa.
=Epidemiology.=—The chief factor in the spread of amoebic dysentery
would seem to be the encysted amoebae in the stools of convalescents,
or symptomless carriers, rather than the motile amoebae in dysenteric
stools. When such carrier has to do with the preparation of food, he
becomes a particular source of danger.
This probably explains the endemic rather than the epidemic
characteristics of the spread of amoebic dysentery because, if the
innumerable vegetative amoebae in dysenteric stools were equally
operative with the more sparsely eliminated cysts, there would
be epidemics of amoebic dysentery similar to those of bacillary
dysentery. The old idea that water, fruit or vegetables, from
which one can isolate amoebae on culture, are sources of infection
must be abandoned, as such cultural amoebae are known to have no
pathogenic relation to man.
Vegetative amoebae undergo disintegration in a short time after
the stool is passed, so that they are probably rarely concerned in
amoebic infections but the resisting cysts may be washed from a
dried stool into a water supply or even be transported in dust to
lodge on unprotected foodstuffs.
Flies may possibly act as transmitting agents. As bearing on the
probable importance of such flies as _Musca domestica_ and _Fannia
canalicularis_ in transmitting amoebic infections may be noted
the findings of Wenyon that the faeces of such flies, as well as
_Lucilia_ and _Calliphora_, after feeding on cyst-containing human
faeces, teem with such cysts. In a dissection of 1027 house flies
caught in Mesopotamia Buxton found ova of parasites of man in
4.09%. The percentage of infection with _E. histolytica_ cysts was
O.3%.
PATHOLOGY
Wenyon thinks that the pathogenic amoebae work their way into the
tubular glands of the intestines and multiply and subsequently,
either by pressure of their pseudopodia or through the disintegrating
action of some toxic substance elaborated by them, they force their
way into the underlying submucosa. In this location they produce a
gelatinous, oedematous necrosis, which shows a marked absence of
polymorphonuclears, but a proliferation of connective tissue cells.
The process is regenerative rather than inflammatory.
Small hemispherical elevations of the overlying mucosa mark
the location of the deeper-lying necrotic process. With the
multiplication of the amoebae and the extension of the necrotic
process in the submucosa we have thrombi formed in the terminals of
the portal vein and possibly in those of the mesenteric arteries,
which in the former case may result in emboli being swept up the
portal vein to lodge in the liver and form a starting point for a
similar necrosing process there or, as the result of interference
with the blood supply of the overlying mucosa, cause this to
undergo necrosis and be cast off as a slough, leaving an oval or
irregular ulcer with deeply undermined edges and a floor formed by
the muscular coat. The ulcers may be no larger than a pin’s head or
they may be 1 or 2 inches in diameter or by coalescence be still
larger. The gelatinous necrosis in the submucosa always extends
beyond the limits of the necrosis of the mucosa, thus explaining
the undermining. At times the muscular coats of the intestines are
involved thus leading to a slough which involves all coats except
the serous one. Bacterial infection, with coagulation necrosis of
the mucosa overlying the amoebic process, is also responsible for
some of the tissue destruction.
The amoebic ulcerations rarely extend above the ileo-caecal valve but
may involve the entire large intestine. Rogers and Lafleur found the
lesions most often in the caecum and ascending colon, often limited
to this area.
The appendix was involved in 7% of the Manila autopsies. Often mild
cases may only show lesions in the caecum. When there is a tendency
to perforation the omentum will often be drawn over to the location
of the threatened perforation. There is often thickening of the
intestine in one place with cicatricial contraction of the lumen
and thinning in another, so that there is an appearance of great
irregularity.
SYMPTOMATOLOGY
The great majority of cases of amoebic dysentery run a chronic course
with periods of improvement alternating with recurrences of pains and
dysenteric stools. From Walker’s experiments the period of incubation
would appear to be from one to three months. The onset in such cases
is very insidious and the patient may complain more of diarrhoeal
than dysenteric manifestations. Such patients often give a history
of passing three or four pultaceous stools daily and complain of
tenderness in the region of the caecum or along the course of the
large intestine. One may determine some thickening of the colon in a
thin subject.
Fever is absent and there are very few of the toxic manifestations
which often accompany bacillary dysentery, such as headache, nausea
and a mildly delirious state. There is progressive loss of weight
and strength with the development of neurasthenic symptoms. The
skin becomes dry and earthy and we have the picture of a more or
less marked secondary anaemia. It is in these cases that we should
be on the lookout for grayish green or grayish brown mucoid masses
which can usually be found during an exacerbation. Sloughs of the
gelatinous-like necrosis in the submucosa usually contain amoebae.
The X-ray has been utilized to give location of amoebic ulcerations.
Bismuth is used for several days prior to taking the photograph and
fills the sites of ulceration.
Such cases usually show a moderate leucocytosis in which the
percentage of large mononuclears is increased and a very
important point is that with tenderness about the caecum, plus a
leucocytosis, one may diagnose appendicitis and operate on a normal
appendix. Autopsy records however have shown that the appendix is
not infrequently invaded by amoebae but in some of these cases,
other than finding amoebae in the lumen of the appendix, I have
been unable to note any change. Cases of amoebiasis confined to
caecum and ascending colon may only show symptoms of slight anaemia.
Besides the more common insidious chronic type we may have amoebic
dysentery setting in quite acutely with severe griping and frequent
scanty grayish green to reddish brown mucoid stools.
Such cases may show anorexia and nausea with some fever but there
is not present the manifestations of toxemia one associates with a
severe case of bacillary dysentery in the tropics.
Very confusing cases are those in which a bacillary dysentery
sets in upon an amoebic one and this possibility should always be
thought of when a severe bacillary dysentery does not respond to
serum therapy or an amoebic one to emetine.
Gangrenous lesions may occur in amoebic dysentery although more
common in bacillary infections. Such cases will show extreme
prostration and even give the clinical picture of cholera.
=Complications.=—By far the most important and serious complication
of amoebic dysentery is liver abscess, which occurs in about 20%
of cases. This condition is treated of separately. Besides liver
abscess quite a number of cases of amoebic abscess of the brain
have been reported, 26 such cases occurring in Egypt alone. These
abscesses almost always occur in those cases which have developed
liver abscess and may appear after the liver abscess has healed.
The pus of such abscesses is viscid and blood-tinged, resembling
liver abscess pus. The amoebae are found in the abscess wall.
The symptoms are those of brain tumor, meningitis not occurring.
Necrotic processes of skin and muscles have also been reported in
which amoebae have been found.
Perforation of the large intestine is not rare, Strong having noted
12 perforations in 77 autopsies. These usually occur in the region
of the sigmoid flexure.
Adhesions are common complications of amoebic dysentery.
DIAGNOSIS
=Clinical Diagnosis.=—In the clinical diagnosis it is well to
remember that many cases of chronic tropical diarrhoeas are really
due to amoebic ulcerations of the intestines.
We can as a rule differentiate bacillary from amoebic dysentery by
the more sudden and acute onset of the former together with fever
and other evidences of toxaemia. The pulse rate is more rapid in
bacillary than amoebic dysentery. Again the number of stools in
bacillary dysentery is usually greater and the amount of each
stool less in quantity. The stool of bacillary dysentery is of a
milky whiteness from the large number of pus cells or composed
of gelatinous, reddish mucus, while that of amoebic dysentery is
tinged with disintegrated blood giving it a grayish-green or brown
color. The mucopurulent mass in bacillary dysentery may be flecked
or streaked with blood. The therapeutic results following emetine
injections are of value in diagnosis.
Gangrenous types of dysentery are similar whether due to bacillary
or amoebic infection. Chronic dysentery of bacillary origin is much
like amoebic dysentery clinically.
Manson-Bahr and Gregg recommend the use of the sigmoidoscope in
the diagnosis of chronic amoebic ulcerations. In the evening the
patient takes ½ ounce of castor oil and the next morning a soap and
water enema is given followed by 15 minims of laudanum. The patient
is put in the lithotomy position. No anaesthetic is used. The pain
in introducing the instrument is greater in chronic bacillary
ulceration cases than in amoebic ones. Scrapings can be made for
microscopic examinations. Nisbet has reported the diagnosis of a
case of balantidial ulceration by use of the sigmoidoscope.
=Laboratory Diagnosis.=—The mucoid mass of amoebic dysentery is
often brownish. The pathogenic amoeba shows active finger-like
processes and in acute attacks often shows contained red cells.
In the fresh specimen of the milky mucopurulent mass of bacillary
dysentery one observes large numbers of pus cells and particularly
very large phagocytic cells which greatly resemble amoebae. Upon
staining with Gram’s stain one may find numerous Gram-negative
bacilli in the cytoplasm of this cell.
These large cells which resemble amoebae are often vacuolated, thus
intensifying the similarity. They are nonmotile, however, and do
not show the small ring nucleus which is so characteristic of the
vegetative human amoebae. The nucleus of the confusing cells is
also larger, approximating one-fourth the size of the cell.
Bacillary dysentery stools show an absence of Charcot-Leyden
crystals which are often present with amoebic stools.
For bringing out the nuclear characteristics of human amoebae
Walker recommends fixation of thin moist smears in Giemsa’s
sublimate alcohol (absolute alcohol 1 part, sat. aq. sol.
bichloride 2 parts) for 10 to 15 minutes. These smears are then
well washed with water and stained with alum haematoxylin for five
minutes. The nuclear characteristics are noted under etiology. In
such staining the preparations, which are best made on cover-slips,
should never be allowed to become dry.
An excellent iron haematoxylin method is that of Rosenbusch:
Rapidly smear out with a toothpick a small particle of faeces or
other material containing protozoa and, while still moist, fix by
Giemsa’s method and, after getting rid of the mercury with iodine
solution followed by 95% alcohol, treat smears with a 3.5% solution
of iron-alum in distilled water for one-half hour or overnight,
then wash thoroughly in distilled water.
Then stain from five to twenty minutes in the following
haematoxylin stain: (1) 1% solution of haematoxylin in 95% alcohol.
It takes at least ten days to ripen. (2) A saturated solution of
lithium carbonate. Add to 10 cc. of the haematoxylin solution
5 to 6 drops of the lithium carbonate one. Next wash well and
differentiate with about 1% solution of the iron-alum. Again wash
in water, pass through alcohols to xylol and mount in balsam. With
vegetative amoebae I have obtained beautiful results with vital
staining which can best be done by tinging the faeces emulsion with
a 1% aqueous solution of neutral red. I have also had good results
by emulsifying the faeces in a drop of 1 or 2% formalin and then
adding a drop of 2% acetic acid. The mixture is then tinged with
either neutral red or methyl green.
For distinguishing the encysted form of _Entamoeba coli_ one can
obtain excellent results by emulsifying the faeces in Gram’s iodine
solution. Owing to the glycogenic reaction given by _E. coli_, the
round amoeba, with its 8 nuclei stands out very distinctly.
For diagnosing the 4-nucleated cyst of the pathogenic amoeba one
gets better results with haematoxylin as this brings out not only
the 4 nuclei but the chromidial bodies as well. It was formerly
customary to recommend the administration of salts prior to examining
for amoebae. Walker warns that such a procedure gives us amoebae
which are difficult to differentiate, the nuclear characteristics of
_E. coli_ and the tetragena nucleus of _E. histolytica_ being much
alike as they both contain much chromatin. In a dysenteric stool the
histolytica type of nucleus, containing but little chromatin, does
not resemble the nucleus of _E. coli_.
He prefers the examination of formed stools obtained without a
purgative.
DIFFERENTIATING CHARACTERISTICS OF PATHOGENIC AMOEBAE
(AFTER DOBELL AND O’CONNOR). MOTILE STAGE
-----+----------------+-----------------+----------------+----------------
| Entamoeba | Entamoeba coli | Endolimax nana | Iodamoeba
| histolytica | | | bütschlii
-----+----------------+-----------------+----------------+----------------
Size | 20-30µ | 20-30µ | 6-12µ | 9-13µ
-----+----------------+-----------------+----------------+----------------
Moti-|Very character- |Usually sluggish |Slow progressive|Slight motility
lity| istic. Flows in| but may show | movement when | with movements
| almost straight| considerable | freshly passed.| similar to
| line across | activity when | Later slight | E. coli.
| field. Later | freshly passed. | changes of | Quickly
| becomes less |The movement | shape. Soon | degenerates
| active pushing | consists chiefly| rounds and | and dies.
| out a few, | in changes of | dies. |
| large blunt, | shape without | |
| blade-like | progression. | |
| pseudopodia | | |
| which are per- | | |
| fectly hyaline | | |
| being composed | | |
| entirely of | | |
| ectoplasm. | | |
-----+----------------+-----------------+----------------+----------------
Cyto-|Endoplasm finely|Endoplasm had a |Endoplasm finely|Endoplasm finely
plasm| granular and | bulky granular | granular with | granular and
| uniform in | appearance and | numerous minute| homogeneous.
| appearance. May| contains numer- | food vacuoles |Usually contains
| contain red | ous food | containing | numerous food
| blood cells but| vacuoles charged| bacteria. |vacuoles charged
| bacteria | with bacteria |No sharp line as| with minute
| probably never | and vegetable | a rule between | bacteria. Cysts
| seen in normal | débris. Never | the endoplasm | of this amoeba
| individuals. | contains red | and ectoplasm. | have previously
|Ectoplasm clear | blood cells. No | | been described
| and well | sharp line be- | | been described
| developed. | tween endoplasm | | as “iodine
| | and ectoplasm. | | cysts.”
-----+----------------+-----------------+----------------+----------------
Nuc- |4-7µ. A delicate| 4-7µ. |1-3µ. Vesicular |2-3.5µ. Small
leus | vesicle incon- | Distinguishable.| with delicate | vesicle with
| spicuous or | Stained shows | membrane. | distinct mem-
| invisible. | larger beads of |Stained shows | brane. Stained
|Stained shows | chromatin lining| wall free from | shows wall free
| fine beads of | wall. Karyosome | chromatin. All | from chromatin
| chromatin | spherical, | chromatin cont-| as a rule.
| lining wall. | eccentric and | ained in large,|Typically
|Karyosome small,| larger than | irregular, | chromatin cont-
| spherical and | that of | eccentric | ained in large,
| central. | E. histolytica. | karyosome. | central
| | |Variations in | spherical
| | | shape of | karyosome. Zone
| | | karyosome | between nuclear
| | | characteristic.| wall and
| | | | karyosome
| | | | filled with
| | | | single layer of
| | | |small granules.
-----+----------------+-----------------+----------------+----------------
(Part 1 of 2)
-----------------------------------------------------------------
ENCYSTED STAGE
-----------+------------------------+---------------------------+
| Entamoeba histolytica | Entamoeba coli |
-----------+------------------------+---------------------------+
Size | 7-15µ | 15-20µ |
-----------+------------------------+---------------------------+
Shape | Round. | Round. |
-----------+------------------------+---------------------------+
Wall | Thin. | Thicker than E. |
| | histolytica. |
-----------+------------------------+---------------------------+
Nuclei |Typically shows four |Typically shows eight |
|nuclei. May show one to |nuclei. May show one to |
|four. Nuclei at rest |twenty. Structurally |
|structurally similar to |similar to adult nucleus. |
|that of adult nucleus. | |
| | |
-----------+------------------------+---------------------------+
Chromatoids|Large chromatoids |Large chromatoids may be |
|common. |present but usually absent.|
-----------+------------------------+---------------------------+
Glycogen |Diffuse but not |Relatively abundant in the |
|abundant. |early stages. Scanty or |
| |absent in mature cysts. |
-----------+------------------------+---------------------------+
(Part 2 of 2)
-----------------------------------------------------------------
ENCYSTED STAGE
-----------+---------------------------+-------------------------
| Endolimax nana | Iodamoeba bütschlii
-----------+---------------------------+-------------------------
Size | 7-9µ | 9-12µ
-----------+---------------------------+-------------------------
Shape | Usually oval. | More or less rounded.
-----------+---------------------------+-------------------------
Wall | Thin. | Relatively thick.
| |
-----------+---------------------------+-------------------------
Nuclei |Very small. May show from |One relatively larger
|one to four nuclei. Rarely |nucleus. Differs struct-
|eight. Structurally similar|urally from the adult
|to adult type of nucleus. |type in that the granules
| |in the clear zone become
| |massed at one pole giving
| |an eccentric karyosome.
-----------+---------------------------+-------------------------
Chromatoids|Absent. |Absent.
| |
-----------+---------------------------+-------------------------
Glycogen |Rarely present. |Dense glycogen mass is
| |characteristic.
| |
-----------+---------------------------+-------------------------
Walker also notes the advantages of examining a specimen with a
⅔ inch objective as encysted amoebae are easily picked up. In
opposition to the usual recommendation of text-books to report
only on motile amoebae, he recommends the making of a differential
diagnosis on nonmotile encysted forms. This however is now
generally accepted by experienced workers as true.
The preëncysted _E. histolytica_ has a nucleus much resembling that
of _E. coli_. The presence of the same chromidial bodies one notes
in the cysts is an aid in recognizing this stage. The 4 nuclei of
the cysts are much smaller than the nucleus of the preëncysted or
vegetative stage.
PROPHYLAXIS AND TREATMENT
=Prophylaxis.=—The main consideration is a knowledge of the
importance of the carrier problem. The stools of all persons
preparing food in localities where amoebic dysentery is prevalent
should therefore be examined for the 4-nucleated cyst of the
pathogenic amoeba. It must be remembered that while emetine controls
the dysenteric manifestations of amoebiasis it does not seem to cause
the disappearance of the parasite, so that patients who have had
amoebic dysentery tend to become carriers.
As a matter of fact there is a question as to the possibility
of the emetine treatment acting as a factor for the increase of
carriers.
Vedder considers that while emetine will kill the amoebae deeply
placed in the submucosa it has no effect on the more superficially
located cysts and suggests that it may be possible to treat
carriers by colonic irrigations with quinine or silver salts.
Emetine bismuth iodide has recently been highly recommended as our
best agent for eradication of _E. histolytica_ cysts of carriers.
=Treatment.=—The emetine treatment may now be considered as the
specific one for amoebic dysentery. In Brazilian ipecac about
72% of the total alkaloids is emetine, so that it is better than
Carthagena ipecac which contains only about 40% of emetine. Emetine
was recommended for dysentery as long ago as 1817, but owing to
the impossibility of differentiating between bacillary and amoebic
dysentery, until recently, this method of treatment was little
advocated.
In 1910 Vedder found that emetine was practically without power in
its action on dysentery bacilli but that it would kill amoebae,
even in dilutions of 1 to 100,000. He also found that deëmetized
ipecac was quite inert in its action on amoebae.
In 1912, Rogers, who had for years been an ardent advocate of
the ipecac treatment of amoebiasis, took up the treatment of
amoebic dysentery and its liver complications with emetine.
Reports from all over the world now attest the value of this drug
in the treatment of the acute manifestations of amoebiasis but
unfortunately note the inefficacy of this treatment on the encysted
forms of amoebae.
It is usual to give from ⅓ to ⅔ grain of emetine hydrochloride,
dissolved in sterile saline, by hypodermic injection into the
subcutaneous tissues. Some now give as high as 1 grain daily for
about ten days, but Vedder prefers ⅓ grain repeated 3 times daily. In
these doses there is practically no nausea.
It was found by Baermann and Heinemann that subcutaneous injections
of from 2 to 2½ grains daily caused indisposition and anorexia. The
subcutaneous injections are less painful than the intramuscular
ones.
Rogers has used emetine intravenously in doses of 1 grain without
bad effect.
Vedder calls attention to the fact that the minimal fatal dose
of emetine is several times less when administered to rabbits
intravenously than when given subcutaneously, so that after seeing
rabbits die with what was apparently centric paralysis immediately
after intravenous doses of comparatively small amounts of emetine
hydrochloride he would hesitate before administering 1 grain
intravenously in a human case.
Levy and Rowntree think emetine should not be given intravenously
except in extreme cases. Among ill effects of emetine they note
peripheral neuritis. Kilgore has reported such cases where even
wrist-drop was seen.
Low has treated cases successfully with keratin-coated tabloids of
emetine hydrochloride, giving ½ grain every night. Vedder has not
obtained satisfactory results with the drug by mouth.
Rogers considers that 15 grains of emetine is the fatal dose for
an adult man and as there is possibly a cumulative action it would
seem safer to continue the drug only for ten days and then later
repeat the course of hypodermics. Of course emetine cannot cure the
ulcerative lesions of amoebic colitis and as bacillary infections
are apt to set in when damaged tissues are present and, as such
infections do not yield to emetine, one must be prepared for failure
in treatment of symptoms in such cases.
Recognizing the great importance of immediate treatment to prevent
extension of the ulcerative process, as well as against abscess, the
rule was adopted in the medical care of the English forces, in the
Mediterranean, to give emetine so soon as a case of dysentery was
seen, not waiting for a determination of etiology. The treatment
ordered was 1 grain of emetine, hypodermically, every day for ten
days, or ½ grain morning and evening for ten days. There must not be
any intermission of a single day.
Before the introduction of emetine the usual treatment was with
ipecac.
It was customary to give 20 to 50 grains of powdered ipecac in
capsule, cachet or keratin-coated pills to a patient with an empty
stomach and who had had a dose of morphine or laudanum about 20
minutes before the time for giving the ipecac. The salol-coated
ipecac pills are generally used in America. The patient should be
in bed and should try to yield to the soporific influences of the
opiate. Any flow of saliva should be removed with gauze as its
swallowing would provoke nausea. Some use a mustard poultice to the
epigastrium. It is remarkable the change which this treatment will
effect in the number and character of the stools.
Many now think it advisable to give emetine hypodermically to reach
the amoebae deeply seated and, at the same time, to give ipecac by
mouth to destroy more superficially situated ones, or those in the
lumen of the gut. Alcresta ipecac has been recommended as a good
method of giving ipecac by mouth.
We do not have now the same confidence in emetine injections that
we formerly entertained. In Egypt the combination of emetine
injections with ½ grain keratin coated tablets of emetine by
mouth seemed to give better results in the more chronic stages of
amoebiasis.
Very favorable reports have come from the use of emetine bismuthous
iodide. This drug is given by mouth in doses not exceeding 3 grains
in a day. It is put up in gelatine capsules and a course of treatment
is one 3 grain capsule each night for 12 nights. It is supposed that
there is no action on the drug in the stomach as it is insoluble in
dilute acid but as a matter of fact nausea and vomiting frequently
occur and slight purging is common after its administration. During
the twelve-day course of treatment the patient should remain in bed
and be given a milk diet.
We have recently had success with the administration of ipecac by the
duodenal tube and it might be that bismuthous emetine iodide could be
given in the same way.
Ross thinks that the flushing action of salines, thus washing away
amoebae and necrotic material, is of advantage in amoebic as well as
in bacillary dysentery. He also thinks liquid petrolatum of value.
Some advise the bismuth treatment recommended by Deeks of giving a
large teaspoonful of bismuth subnitrate, in a glass of water, 3 or 4
times during the day.
A decoction made by boiling for 15 minutes one teaspoonful of
powdered chaparro in 8 ounces of water and given one-half hour before
each meal has been reported on favorably. The powdered roots, stems
and leaves of “Chaparro amargosa” are used. This is a plant of Texas
and is named _Castela nicholsoni_. A decoction of about one-half
strength of that taken by mouth is recommended for enemata. Simaruba
bark is recommended by some practitioners. Its action is similar to
chaparro. Benzyl benzoate is recommended for the pains and tenesmus
of amoebic dysentery as well as bacillary dysentery. Twenty drops of
the 20% alcoholic solution are given three times daily.
Many drugs have been recommended for colon irrigation of which the
favorite is probably quinine muriate in dilution of 1 to 1000 or 1
to 2500. Inject 2 or 3 pints slowly by gravity. Protargol in 1 to
500 solution is better than silver nitrate in 1 to 2000. Emetine
enemata do not seem to be of much value.
In very serious cases, particularly when gangrenous change in
the mucosa may be present, the operation of appendicostomy seems
indicated, following which a catheter is inserted and the large
intestine irrigated with a 1% solution of bicarbonate of soda to wash
away the mucus and later with a boracic acid solution of 1 to 125 or
1 to 10,000 of potassium permanganate.
In a discussion as to certain surgical considerations in connection
with appendicostomy Muller notes that the right rectus incision
is to be avoided on account of danger of gangrene from pressure
of rectus on the stitched-up appendix. He also thinks that
appendicostomy is much safer than caecostomy on account of the
frequent thinning of the walls of the caecum. For irrigation he
prefers a 1 to 500 solution of collargol.
In treating dysentery cases rest in bed and the use of a
nonirritating diet are advisable.
The return of the increase of large mononuclears to normal may be
used as an index to cure.
Walker and Emrich have recently reported success in treatment of cyst
carriers by giving oil of chenopodium in 3 hourly doses of 16 minims,
followed by castor oil and preceded by a dose of magnesium sulphate.
CHAPTER XI
LIVER ABSCESS
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—Although Hippocrates noted the method of evacuating
abscess of the liver by caustics there was very little known about
the condition until during the last century.
The history in connection with the finding of amoebae in liver
abscesses is of very recent date (1887) and is taken up under the
history of amoebic dysentery.
=Geographical Distribution.=—Concisely one may state that the
distribution of liver abscess is in relation to the existence of
amoebic dysentery. It is particularly prevalent in those centers
of amoebic infection where there are many white men having little
knowledge of the conditions necessary for the maintenance of health
in the tropics.
In liver abscess, as with blackwater fever, it is education rather
than acclimatization that brings about a diminution of these
tropical diseases.
For several years subsequent to the American occupation of the
Philippines amoebic dysentery and liver abscess were common but in
more recent years liver abscess has become rare in Americans and
amoebic dysentery much reduced in prevalence.
More temperate living results in less storing up of fat in the
liver and an organ more resistant to infection.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—The dislodgment of amoebae-containing material from
amoebic intestinal ulcerations and the plugging of the portal
capillaries by such emboli give us the starting point of a liver
abscess. The exciting cause is _Entamoeba histolytica_ which in the
liver continues the same production of a gelatinous necrosis as is
carried on in the submucosa of the large intestine or appendix.
This pathogenic amoeba is fully described under amoebic dysentery.
As to obtaining a history of amoebic dysentery in liver abscess
cases we have the following statistics:
500 cases with dysentery findings in 60% (Kartulis).
444 cases with dysentery findings in 59% (Zancarol).
500 cases with dysentery findings in 85% (Kelsch and Kiener).
63 cases with dysentery findings in 90.5% (Rogers).
38 cases with dysentery findings in 85% (Seamen’s hospital
autopsies).
Amoebic liver abscess is exceedingly rare among children and
probably 10 times less common among women than men.
Of 40 cases of liver abscess Waring noted intemperance in 67.5% and
authorities generally insist upon the importance of the abuse of
alcohol as a predisposing factor.
Natives of India very rarely develop liver abscess but it has been
noted that when they begin to follow the customs of Europeans, as
to eating and drinking, such lesions become more common in them.
As to the proportion of cases of amoebic dysentery which give
rise to liver abscess only the statistics of those who have
differentiated between bacillary and amoebic dysentery are of any
value. Such statistics would indicate that about 20% of the cases
of amoebic dysentery are complicated by liver abscess.
Liver abscess may be present without demonstrable lesions in the
large intestines, such lesions having healed or the intestinal
involvement having been so slight as not to have caused other than
microscopic changes.
It is a well-known fact that liver abscess may set in years after a
patient has left the tropics and years after the occurrence of any
dysenteric manifestations.
PATHOLOGY
There seems little doubt but that the amoebae in the thrombosed
terminals of the portal vein are carried by way of the upward current
into the liver where they lodge in the liver capillaries, Councilman
and Lafleur having found amoebae in such emboli.
Another view is that the amoebae may wander across the abdominal
cavity and enter the liver in this way. This seems as improbable as
that view which considers a possible entrance by way of the bile
duct. Bile is toxic to amoebae and it would be difficult to explain
their presence in the small intestines.
In 639 cases Roux found the abscess in the right lobe in 70% of the
cases.
Other statistics give about 75% for the right lobe, 10% for the
left lobe, 4% for the lobus Spigelii and in about 10% of cases
abscesses are found in both right and left lobes.
In 562 cases Zancarol found a single abscess in 60% of the cases.
In 288 cases Waring found a single abscess in 61.5%, double abscesses
in 11.5% and multiple abscesses in 27%. The favorite site of liver
abscess is the superior and posterior part of the right lobe and near
its surface.
The abscesses vary enormously in size, some being no larger
than a walnut while others may contain a quart or more of pus,
exceptionally as much as a gallon. The pus is typically of a
chocolate color and contains degenerated liver cells, granular
débris and often haematoidin and Charcot-Leyden crystals. There is
an absence of polymorphonuclears. It may however be creamy in color.
In Strong’s cases about 50% of the abscesses showed bacteria upon
culturing, the organisms noted being staphylococci, streptococci,
_B. coli_ and _B. pyocyaneus_.
The walls of liver abscesses are rather shaggy and the amoebae are
found deeply located.
It is probable that the necrotic process, set up by the amoebae,
begins in the interlobular capillaries although it may at times
begin within the lobule.
Microscopically, the necrotic abscess wall shows amoebae in its
depths but necrosis of the surrounding tissue beyond the zone of
the amoebae is noticeable which would suggest the elimination
by the amoebae of some toxic substance. There is an absence of
polymorphonuclear infiltration around the abscess.
Surrounding the abscess wall there is a zone of marked hyperaemia.
Amoebae may be found in this area as well as in the abscess wall.
If the liver abscess is not treated by emetine or with this drug
and some surgical procedure the tendency is for rupture to occur
and Cyr’s statistics show that of 159 cases rupture occurred
as follows: lungs 59, pleural cavity 31, peritoneal cavity 39,
intestines 8, stomach 8, vena cava 3, kidneys 2, bile ducts 4,
pericardium 1 and externally 2.
SYMPTOMATOLOGY
Although the statistics would indicate that a history of amoebic
dysentery has been obtained in only from 60 to 90% of cases of liver
abscess, yet, when we consider that amoebic lesions of the large
intestines have been frequently noted at autopsy in those who had
never shown symptoms of dysentery during life, we are forced to
believe that amoebic lesions of the appendix or large intestines are
necessary factors in the production of liver abscess. Consequently, a
history of amoebic dysentery is one of the most important points to
consider in the making of a diagnosis of tropical liver abscess.
=Tropical Liver.=—There is also much evidence to be obtained from
statistics and otherwise to support the view that the amoebic
infection of the liver is only possible in a person whose liver
has been functionally impaired. To this condition the designation
tropical congestion of the liver or simply tropical liver has been
applied. There is much to support the view that, in the tropics,
the intestines and liver take the place of the thoracic organs
in being subject to congestion. In temperate climates excesses
and exposure to debilitating influences result in coryza or
pneumonia. In the tropics we have diarrhoea and congestion of the
liver. Tropical liver is recognized by vague digestive troubles,
high-colored urine, loss of energy, irritability, with a sensation
of fullness in the region of the liver which is generally described
by the patient’s statement that he feels his liver. There may be
pain referred to the right shoulder and the liver may be tender on
palpation.
By the discontinuance of alcohol and highly spiced foods, with
treatment by phosphate of soda or sodium sulphate, together with
general care of the health, the patient may recover completely.
Rogers recognizes a condition which he terms the _pre-suppurative
stage of amoebic hepatitis_ in which the amoebae from dysenteric
lesions have lodged in the portal terminals of the liver but in
which abscess formation has not taken place.
At this stage we have a leucocytosis in which the
polymorphonuclears are but little increased in percentage with a
low remittent fever. At this time Rogers considers that the disease
may be cured by emetine or ipecac and liver abscess avoided.
=A Typical Case of Liver Abscess.=—Following a case of amoebic
dysentery, during the period of convalescence or subsequently, a
rather irregular type of fever is noted, which shows an evening rise
with sweatings which tend to become colliquative. From a marked
feeling of weight in the region of the liver there may later develop
tenderness or pain upon palpation of the liver. Of importance is
the fact that there is no associated splenic enlargement. In the
majority of cases the right side of the liver enlarges in an upward
direction. A tape-measure will often show enlargement of the right
side. Pain referred to the right shoulder is often complained of when
the abscess is located in the upper convex part of the liver but,
when nearer the inferior concave surface, there may be pain referred
to the region of the appendix. When located in the left lobe the
symptoms may be considered as of gastric origin.
The upward enlargement of the liver as shown by X-rays is of great
value in diagnosis, but an abscess located in the center of the liver
is not indicated by such rays.
There is a marked tendency to splint the liver so that the patient
tends to lie towards the right side and when walking applies his
right arm and forearm to his side, which led Koch to remark, “It is
as if he carried his abscess under his arm.” The right rectus often
shows rigidity.
Auscultation of the base of the right lung reveals a moist
crepitation which, together with a dry cough (tussis hepatica),
the fever, evening sweats, anaemia and emaciation, may suggest
tuberculosis. The respirations are shallow as deep inspiration tends
to cause pain. It must be remembered that cases of liver abscess
have been reported where there were practically no symptoms.
Insomnia is a marked feature in many cases. Jaundice is rare,
but an earthy color or subicteroid tinging is often noted. The
superficial veins may be enlarged.
The urine is scanty and high-coloured, frequently with a marked
increase in the ammonia nitrogen. Urobilin may be present in
considerable amount.
There is a rather constant but low leucocytosis of from 12 to 20
thousand, which shows only about 70% of polymorphonuclears with an
increase in large mononuclears up to 10 to 15%.
The final proof is the obtaining of the chocolate-coloured or anchovy
sauce-like pus by exploratory puncture.
[Illustration: FIG. 61.—Temperature chart of liver abscess.]
This pus does not contain pus cells but only granular débris,
cholesterin crystals and is often bacteriologically sterile. The
amoebae, being in the abscess wall, are not apt to be found when
pus is at first withdrawn. Owing to the tendency of liver abscess
to rupture into the lungs the first indication of the true nature
of a prolonged hectic fever may be obtained when the characteristic
pus is expectorated by the patient.
Attended with progressive emaciation and exhaustion the patient,
as a rule, after a prolonged illness, dies, unless operative
procedures cure him or some intercurrent disease brings about his
death.
Symptoms in Detail
_Onset and the Fever Chart._—The onset is at times so insidious
that there may be no symptoms and yet a liver abscess be found at
autopsy. Usually following convalescence after amoebic dysentery an
irregular fever sets in which becomes hectic in character. Profuse
sweats accompany the evening rise. The morning temperature is
frequently normal and there may be frequent apyretic intervals.
_The Respiratory System._—Crepitation at the right base, a dry
cough (tussis hepatica) and shallow respirations are features of
the disease.
_The Nervous System._—Pains in the right shoulder are connected
with irritation of the branches of the phrenic nerve.
The patient is irritable and often complains of insomnia.
The right rectus tends to be somewhat rigid and decubitus is dorsal
or toward the right side.
_The Liver and Spleen._—The liver is tender and as the abscess in
nine-tenths of the cases is located in the right lobe and generally
toward the upper convex surface we have an enlargement upward.
There is very rarely any jaundice.
The urine shows an excess of urobilin and of nitrogen eliminated
as ammonia. When the abscess is in the left lobe the condition is
apt to be considered as some gastric disturbance. The spleen, as a
rule, shows no enlargement.
_Examination of the Blood._—There is usually a moderate
leucocytosis with normal polymorphonuclear percentage and increase
in the large mononuclears.
[Illustration: FIG. 62.—Liver abscess. X-ray photograph taken from
the side and showing upward enlargement of liver. (Ruge and zur Verth
after Béclére.)]
DIAGNOSIS
=Clinical Diagnosis.=—Of greatest importance is a history of a
previous dysentery although it must be remembered that liver abscess
may appear in one who has never had dysenteric symptoms. Fever
of a hectic type with crepitation at right base, pain and upward
enlargement of the liver are most significant.
The X-ray may confirm the diagnosis of upward enlargement which may
be as high as the angle of the scapula. The majority of conditions
causing enlargement of the liver give a downward enlargement.
The amelioration of symptoms by giving emetine hypodermically for two
or three days is diagnostically exceedingly important.
Syphilitic gummata may give the picture of liver abscess,
especially as regards the fever and loss of weight. Iodide of
potash is said to be of use in differentiating, as it controls the
fever of syphilis. The gummatous enlargement, however, is irregular
and projects downward.
Suppurative pylephlebitis generally arises from infections of the
colon or appendix. This condition as well as pyaemic (multiple)
abscesses of the liver is apt to show jaundice.
In suppurative cholangitis and cholecystitis we get a history of
biliary colic, jaundice and usually a marked point of tenderness
at the tip of the ninth rib and a tumor in the region of the gall
bladder. Abscess of the left lobe may give the symptoms of gastric
trouble.
In differentiating empyema we usually have a history of pleurisy or
pneumonia.
Suppurating hydatid cyst which may be confused with liver abscess
is most surely differentiated by finding echinococcus hooklets.
Then too the complement fixation test for hydatid disease will
differentiate.
Tuberculosis is often thought of, particularly when a liver
abscess ruptures through the lungs. Malaria is also usually
suspected. Abscess in the kidney or perinephritic region may be
very confusing. In an abscess of the abdominal wall an exploring
needle does not move up and down with respiration as it does when
penetrating a liver abscess cavity.
=Laboratory Diagnosis.=—The chocolate-colored pus of a liver
abscess, when there has been no bacterial contamination, shows an
absence of polymorphonuclears and does not at first show amoebae.
These appear in the pus coming from the drainage tube about the
third day. Cholesterin and haematoidin crystals may be found in the
granular débris of a fresh drop of pus used for examination for
amoebae.
Liver abscess usually shows a moderate leucocytosis with a normal
polymorphonuclear percentage and an increase of large mononuclears
and transitionals to about 12 to 20%.
According to Schilling-Torgau we may have a perfectly normal white
count and polymorphonuclear percentage and yet have evidence of the
presence of liver abscess in his modification of Arneth’s index, so
that in an apparently normal differential count we may find that
½ or more of the polymorphonuclears are of a less mature type and
in cases where there are many immature polymorphonuclears we have
indications which force a very cautious or unfavorable prognosis.
Thus a differential count of 33% band-form polymorphonuclears
and 39% of normal nucleated ones would make us give a cautious
prognosis, while one with 1% myelocytes, 22.5% immature
polymorphonuclears, 21% band-form nucleated ones and 30% of normal
ones would make for a very bad prognosis. We have a displacement to
the left. Normally there are 63% of normal polymorphonuclears, 4%
of band-form and no immature ones or myelocytes.
One may find an iodophilia in liver abscess.
Of the functional liver tests we may determine the ammonia
quotient, the percentage of N eliminated as ammonia being increased
in abscess of the liver. The same is true of the lipase test.
Probably the most specific test for disturbances of the hepatic
function is that for urobilinogen. The test is made by adding 5 to
10 drops of Ehrlich’s aldehyde reagent to 5 cc. of perfectly fresh
urine when a positive reaction gives a fine cherry-red color.
PROPHYLAXIS AND TREATMENT
=Prophylaxis.=—The prophylaxis is the same as that for amoebic
dysentery plus avoidance of anything which reduces the functional
power of the liver, such as overfeeding, alcoholic excesses, etc.
It is well to remember that abscesses may occur months or even two
or three years after an attack of amoebic dysentery, consequently
it is well to give a grain of emetine on two or three successive
days of each month following an acute attack.
=Treatment.=—Leaving out of consideration the pre-suppurative stage
of amoebic hepatitis which, according to many authorities, responds
to injections of emetine, it may be stated that the treatment of
liver abscess is entirely surgical and such treatment should be
instituted the moment the diagnosis is made. The earlier a liver
abscess is drained the less run down will be the patient, the more
rapid the convalescence and the better the prognosis.
Until recently surgical authorities condemned severely the trocar
and cannula method of operation, but with the introduction of
emetine there are now those who believe that such a procedure may
suffice and a more radical operation not be necessitated.
Prior to introducing the trocar and cannula the usual procedure
is to use an aspirating needle of about ⅛ inch bore and 3½ inch
length. If the needle happens to be longer it should not be passed
deeper than 3½ inches, in a person with a 32-inch chest, in order
surely to avoid the vena cava. If there are no distinct localizing
signs the needle should first be introduced in the eighth or ninth
interspaces in the anterior axillary line and pushed backward,
inward and slightly upward. Manson recommends at least 6 punctures
before abandoning exploration. Cantlie does not think that a
moderate degree of haemorrhage from the puncture of the liver will
do harm in a case which is simply a liver congestion. One should
always be ready to operate in case pus be found in the exploring
needle. Leaving the needle in situ a small skin incision is made
and a 4 or 5 inch by ⅜ inch trocar and cannula introduced along
the line of the needle. Withdrawing the trocar some of the pus is
allowed to escape through the cannula and there is then introduced
a 6 × ½ inch piece of strong rubber drainage tubing, one end of
which has lateral fenestrations but a closed tip in order that a
long steel pin may put the tubing on the stretch so that it passes
the smaller lumen of the cannula.
The cannula is then slipped out over the tubing and the external
stretched end of the tubing released so that the contracting rubber
fills the puncture. The steel pin used for introducing the rubber
tube is then withdrawn and the tubing transfixed close to the skin
with a safety pin.
After the cavity has drained of pus a dressing is applied. There
are some who advocate aspiration alone without subsequent drainage.
The dressing should be changed frequently and a connecting tube,
draining into an antiseptic-containing bottle, should be attached
to the tube in the cavity in order to obtain a syphoning action.
Some aspirate and inject into the cavity about 2 ounces of 1 to
1000 emetine solution.
Some report favorably from the use of 1 to 1000 quinine
irrigations. At present the hypodermic use of emetine will probably
obviate the necessity of any irrigation.
There are those who think that a preliminary aspiration, followed
by incision, after a few days of improvement in general condition,
is the best method in serious cases.
It is usual to recommend a general anaesthetic when introducing the
aspirating syringe or trocar and cannula. Local anaesthesia with
quinine and urea hydrochloride, however, will usually suffice and
lessen the dangers of shock in bad cases. Rib resections and even
intra-abdominal procedures are best done under local anaesthesia
provided the operator is familiar with the technic.
Newman has recently warned against the use of the small aspirator
for diagnosis, pointing out that it is unreliable and that the
diagnosis should be made by other diagnostic aids, including
hypodermic use of emetine. He notes the occurrence of death from
internal haemorrhage, the interference of the needle with the
surgical incision and, further, the obscuration of the field of
operation by pus where no adhesions exist and, finally, the danger
of general peritoneal infection from a leak. He notes that the
cavity may be under tension and that the pus may force itself along
the track of the needle. He recommends incision and packing with
gauze where adhesions do not exist and the exploration of the liver
with dressing forceps instead of cutting into the liver with the
knife.
USUAL OPERATION FOR LIVER ABSCESS
Either a vertical incision about the middle of the right rectus
(Bevan) or a Kocher incision, parallel with the costal margin, may
be used. The latter incision favors hernia if prolonged drainage is
required. The hand is introduced into the abdominal cavity and the
liver palpated. Often the borders of the site of a liver abscess give
a hard feeling on palpation. If adhesions are not present the area
should be packed off with gauze and the cavity opened by a dressing
forceps, haemostat or thermo-cautery. It is often advisable to
introduce a trocar and cannula and to drain off the excess of pus.
Where the abscess is situated far back or high up in the liver
the transpleural route is to be preferred to the abdominal one.
Make a 3 or 4 inch incision over the 9th rib with its center in
the line of the angle of the scapula. Excise about 2 inches of
rib subperiosteally. An assistant presses a roll of gauze against
the tissues above the line of incision to prevent air entering
the pleural cavity. Later the upper flap may be sutured to the
endothoracic fascia. Even if the pleural cavity should be opened
and air enter no serious result will follow although it is an
accident to be avoided if possible. The diaphragm is now cut
through and the liver exposed and after packing gauze around the
area to be opened, the abscess cavity is entered and drained as
previously described.
McDill prefers to resect 2 or 3 inches of both 9th and 10th ribs
in the midaxillary line. The muscle wounds made in resection are
then closed by catgut. This movable wall is now forced against the
diaphragm with a roll of gauze pressed inward by an assistant.
A 3-inch incision is now made through this bone-free wall near
the upper border of the 11th rib, going through diaphragm and
exposing the liver. The edges of the wound in the thoracic wall
and diaphragm are now clamped together by haemostats to close off
the pleural cavity. Later catgut sutures are substituted for the
forceps. The liver often bulges into the wound. Finding the abscess
by a palpating finger as a rather firm area in a less resistant
liver surface we introduce a forceps or aspirating needle or trocar
and proceed as above noted.
There are indications that the use of emetine subcutaneously may
make the more radical operations unnecessary. In a recent symposium
on liver abscess many of the papers would indicate a preference for
aspiration without drainage coupled with emetine subcutaneously.
Rogers, in a recent article, notes that a case of liver abscess was
cured by emetine without any form of operation. Recent experience,
however, would indicate that it is necessary to evacuate the pus to
effect a cure.
SECTION II
DISEASES DUE TO BACTERIA
CHAPTER XII
BACILLARY DYSENTERY
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—Epidemics of dysentery have been noted since ancient
times, the widespread and fulminating nature of such outbreaks in
times of war and famine having impressed observers in all ages. The
disease is mentioned in the Ebers Papyrus (1600 B. C.).
Herodotus referred to an epidemic of dysenteric nature in the
Persian Army and Hippocrates described the dysenteric syndrome. It
has been known in India since remote times.
While the etiology of amoebic dysentery was thoroughly investigated
and its connection with amoebae fairly well established during the
decade from 1880 to 1890 it was not until 1898 that Shiga isolated
the causative organism of bacillary dysentery. It is true that
Chantamesse and Widal drew attention to a bacillus isolated from
large intestines, mesenteric glands and spleen of cases of tropical
dysentery but the organism was not clearly differentiated from
_Bacillus coli_. Celli isolated an organism which coagulated milk
and produced gas in glucose media. This organism which Celli called
_B. coli dysentericus_, differs culturally from _B. dysenteriae_.
=Geographical Distribution.=—Bacillary dysentery differs from the
amoebic form in that it tends to appear in extensive epidemics
spreading over temperate as well as tropical and subtropical parts
of the world.
It is peculiarly liable to follow the movements of armies in any
part of the world and like typhoid fever its distribution is one of
hygienic rather than geographical influence.
Infections with various strains of dysentery bacilli are important
factors in morbidity among infants and young children in whatever
part of the world the question has been investigated. The disease
is prone to prevail in lunatic asylums whether in temperate or
tropical parts of the world.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—During a very fatal epidemic of dysentery in Japan
Shiga isolated an organism, _Bacillus dysenteriae_, from dysenteric
stools of 36 cases, which bacillus he found to be agglutinated by the
serum of the patients. He reported this work in 1898. In 1900, Kruse
isolated an organism from patients in an epidemic of dysentery in
Germany which corresponded to that of Shiga. In 1900, Flexner, Strong
and Musgrave, working in Manila, not only encountered an organism
similar to that of Shiga but also an organism of wider fermentative
action. Dysentery has resulted from accidental laboratory infections
and Strong produced dysentery in a prisoner condemned to death
through ingestion of cultures.
In 1903, Hiss and Russell isolated an organism from a fatal case of
diarrhoea in a child to which they gave the name “Y”.
On the whole, dysentery bacilli correspond culturally with the
typhoid bacillus except in showing slightly weaker fermentative
action on carbohydrates. The main point of difference however is
their absolute nonmotility.
The characteristic of nonmotility is of greatest differentiating
value and the reports of slight motility are probably from
misinterpretation of molecular movement as motility. The dysentery
bacilli do not form those thread or whip-like filaments so
characteristic of typhoid cultures and are somewhat plumper. The
dysentery bacillus is not found in the blood and hence is not
eliminated in the urine, although recently there have been reported
rare cases where dysentery bacilli were isolated from the blood. It
is found in mesenteric glands. In dysentery patients agglutination
phenomena do not show themselves until about the tenth day from
the onset. Hence, this procedure is of no particular value in
diagnosis. It is of value, however, to identify an organism
isolated from the stools at the commencement of the attack, using
serum from an immunized animal or a human convalescent for the
agglutination test.
There seems to be only moderate agglutination power in the serum
of convalescents from Shiga strains. Flexner strains give higher
agglutinations, but early in convalescence the serum is not apt to
have a titre of more than 1-150.
Dysentery bacilli produce a coagulation necrosis of the mucous
membrane of the large intestine and occasionally of the lower
part of the ileum. Polymorphonuclears are contained in the fibrin
exudate.
It was formerly thought that these lesions were of local origin,
but the present view is that toxins are produced which, being
absorbed, are eliminated by the large intestine with resulting
necrosis. Flexner, by injecting rabbits intravenously with a toxic
autolysate, produced characteristic intestinal lesions. The toxin
withstands a temperature of 70°C. without being destroyed. The
toxin may cause joint trouble.
There are two main types of dysentery bacilli:
1. Those producing acid in mannite media—the acid strains
(Flexner-Strong types).
2. Those not developing acid in mannite (Shiga-Kruse types). The
Shiga type is very toxic in cultures, while the Flexner type seems to
be less so. An organism resembling the Shiga bacillus but producing
indol is the Schmitz bacillus. It does not appear to be pathogenic.
In immunizing horses for the production of antidysenteric serum it
is customary to use both Flexner and Shiga strains, thus producing
a polyvalent serum.
Lentz recognizes 4 types of dysentery bacilli for the
differentiation of which he uses mannite, maltose and saccharose
bouillon with litmus as an indicator.
------------+-------------+---------+--------+-------
| Shiga-Kruse | Flexner | Strong | “Y”
------------+-------------+---------+--------+-------
Mannite | Blue | Red | Red | Red
Maltose | Blue | Red | Blue | Blue
Saccharose | Blue | Blue | Red | Blue
------------+-------------+---------+--------+-------
The following table gives the more important cultural
characteristics of the intestinal bacilli which might be confused
with the various strains of dysentery bacilli.
Key for column headings:
A - Motility
B - Milk coagulation
C - Glucose
D - Maltose
E - Lactose
F - Mannite
G - Saccharose
H - Glucose neutral red bouillon
I - Butt
J - Slant
K - Indol
------------------+---+---+-------+---+---+---+---+---+----+--------+---
| | |Litmus | | | | | | |Russel’s|
| | | Milk | | | | | | | Medium |
| | |-------| | | | | | |--------|
| | |1st|3d | | | | | | | |
| A | B |day|day| C | D | E | F | G | H | I | J | K
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. faecalis | | | | | | | | | | | | |
alkaligines | + | - |Alk|Alk| O | O | O | O | O | O | O | O | -
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. typhosus | + | - | A | A | A | A | O | A | O | O | A |Alk | -
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. dysenteriae | | | | | | | | | | | | |
(Shiga-Kruse) | - | - | A |Alk| A | O | O | O | O | O | A |Alk | -
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. dysenteriae | | | | | | | | | | | | |
(Flexner-Strong) | - | - | A |Alk| A | A | O | A | O | O | A |Alk | -
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. dysenteriae | | | | | | | | | | | | |
“Y” | - | - | A |Alk| A | O | O | A | O | O | A |Alk | +
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. Morgan No. 1 | + | - | O | O |A G| O | O | O | O | G | | | +
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. paratyphosus A | + | - | A | A |A G|A G| O |A G| O | G |A G|Alk | -
------------------+---|---+---+---+---+---+---+---+---+----+---+----+---
B. paratyphosus B | + | - | A |Alk|A G|A G| O |A G| O |G Fl|A G|Alk | -
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. enteriditis | | | | | | | | | | | | |
(Gaertner.) | + | - | A |Alk|A G|A G| O |A G| O |G Fl|A G|Alk | -
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. coli | + | + | A | A |A G|A G|A G|A G| O |G Fl|A G| A | +
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. lactis | | | | | | | | | | | | |
aerogenes | - | + | A | A |A G|A G|A G|A G|A G|G Fl|A G| A | -
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. cloacae | + | + | O | A |A G|A G|A G|A G|A G|G Fl|A G|Alk | +
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
B. proteus | | | | | | | | | | | | |
vulgaris | + | | O |Alk|A G|A G| O | O |A G| G |A G|Alk | -
------------------+---+---+---+---+---+---+---+---+---+----+---+----+---
Of the above tabulated nonspore bearing, Gram-negative, intestinal
bacilli only _B. lactis aerogenes_ shows capsules and only _B.
cloacae_ and _B. proteus vulgaris_ liquefy gelatin. In the table +
= positive, - = negative, O = no change, A = acid, Alk = alkaline,
G = Gas and Fl = fluorescence in neutral red bouillon.
=Epidemiology.=—There is probably no disease, with the possible
exception of cholera, where those attending a patient are so liable
to have their hands contaminated with infectious material.
The terrible frequency of the stools and the tendency of the
mucilaginous mucoid mass to become smeared over the buttocks and
clothing of the patient make it onerous for an attendant to carry
out methods of personal protection. In a family, where the mother
may have to care for a sick child, and prepare food for the other
children and herself, the opportunities for the spread of the
infection in the family are great. In military barracks, as well
as in other institutions where large numbers make use of the same
water-closet accommodations, the chances of contamination of the seat
by a patient responding to the frequent and imperious demands for
evacuation are most probable, with subsequent transference of the
infectious material to others. Bacillary dysentery is peculiarly an
institutional disease and tends to spread in jails, orphan asylums
and the like. A carrier is a particular source of danger in such an
institution.
Not only is there the danger from a patient ill with bacillary
dysentery but as well that from the convalescent or chronic
carrier. Such carriers are particular sources of danger where they
take part in the preparation of food for others. It is now thought
that the striking prevalence of the disease in insane asylums is
associated with the difficulty of making such patients observe the
proper care of their hands as well as their persons.
Friedmann has recently noted an outbreak of dysentery due to the
Shiga type of bacillus which was instituted by a soldier returning
to the barracks from a furlough.
There resulted 86 cases in the man’s regiment of which 49 belonged
to his own squadron. The spread of the disease was traced to the
latrines. The epidemic was suppressed by the enforcement of the
most rigid rules of cleanliness especially as regarding washing of
the hands after leaving the latrines.
The stools of the convalescents were examined and no man was
discharged from hospital until his stools were negative for
dysentery bacilli upon 3 successive tests in fourteen days.
Isolation of the bacilli from convalescents was obtained in 40
patients only for periods under fourteen days while with 27 others
such carrying of bacilli lasted from two weeks to one month.
As the dysentery bacillus does not invade the blood stream we do
not find it in the urine so that to a certain extent the dysentery
bacillus carrier is less dangerous than the typhoid one.
There have been reports of isolation of Flexner and “Y” type
bacilli from monkeys and rabbits but there is nothing to indicate
that any other host than man is of importance.
Flies are undoubtedly of as much importance in the spread of
bacillary dysentery as of typhoid.
The possibility of infection through the medium of soiled clothes,
sent out for washing, is to be thought of.
There have been several instances of transference of the disease by
the water supply.
In times of war, with large forces of soldiers, bacillary dysentery
tends to become the most important disease encountered by military
surgeons. During the Civil War there were 285,000 cases of dysentery
in the Federal army.
It is possible that infectious material may be disseminated as dust
and thus contaminate food.
PATHOLOGY
Injection of dysentery bacilli into the peritoneal cavity of guinea
pigs causes a muco-sanguinolent diarrhoea with congestion of and
haemorrhage into the caecum. There is also a haemorrhagic peritoneal
exudate.
In the rabbit lesions similar to those in man are obtained as well
as paralysis of the limbs.
It is therefore thought that there are two toxins concerned in the
pathology of bacillary dysentery, one a neurotoxin which may cause a
peripheral neuritis or joint trouble and the other a toxin which acts
on the lower bowel, especially the caecum, with the production of
congestion and coagulation necrosis of the mucosa.
Cases have been reported where the adrenals showed congestion and
necroses, as if subjected to the action of a toxin.
In man we have an acute inflammation of the mucosa of the large
intestines and, in the tropics, we frequently find the lower
third of the ileum involved as well. In amoebic dysentery the
process rarely extends beyond the ileo-caecal valve. A catarrhal
process with hyperaemia and sero-purulent exudate is first noted,
to be succeeded by fibrin formation in the mucosa, a process of
coagulation necrosis. When the process invades the ileum there
is no involvement of Peyer’s patches. Virchow noted the greater
intensity of the process in the region of the rectum, sigmoid
flexure and ileo-caecal valve.
As a rule, however, the entire large intestine is grayish red,
looking like lustreless red velvet. Later on we may have irregular
islands of grayish membrane formation surrounded by the red swollen
congested gut. The solitary glands are usually swollen and may
soften and ulcerate, having the submucosa as a base. Ulceration in
bacillary dysentery is superficial rather than deep as with amoebic
dysentery. The ulcers of bacillary dysentery involve the free folds
of the intestine and extend transversely while amoebic ulcers run
longitudinally. The intervening mucosa is unaffected in amoebic
ulcerations while in bacillary ones it is inflamed.
Microscopically we note marked congestion of the blood vessels
of the mucosa and submucosa with dilated lymph spaces full of
polymorphonuclear cells.
In the mucosa we find an outpouring of pus cells which are
entangled, along with the glandular structures of the mucosa, in a
fibrinous exudate which causes necrosis of the mucosa (coagulation
necrosis).
In chronic bacillary dysentery, according to Rogers, the lesions
are limited to the lower portion of the large gut and rarely extend
above the descending colon.
In this region one finds serpiginous ulcerations separated by
islands of mucosa. Willmore and Savage have noted autopsy findings
of what was practically a large granulating surface over the whole
large intestine, in cases which had apparently recovered, with the
exception of a prolonged convalescence.
SYMPTOMATOLOGY
Bacillary dysentery usually runs an acute course, rarely relapsing
and but occasionally going on to a chronic condition. The period of
incubation is usually from two to seven days although accidental
infection with bacilli in the laboratory has given an incubation
period approximating twenty-four hours. Periods of incubation longer
than a week can probably be explained as for cholera, such cases
being in those who are healthy carriers, but by reason of some
gastro-intestinal upset the quiescent bacilli take on pathogenic
activity.
In temperate climates and in particular when the infecting organism
is a Flexner type the case may appear as a watery diarrhoea
associated with colicky pains and anorexia. The stools soon become
more scanty in amount, frequent in number and associated with
straining. This is followed by mucous stools more or less tinged
with blood. The temperature is normal or but slightly elevated and
the patient does not seem ill.
In the tropics and in temperate climates where the Shiga type
bacillus is the infecting organism the onset is usually rather
sudden with malaise, abdominal pain and a diarrhoea, which only
temporarily relieves such pain. This initial diarrhoea is soon
followed by the characteristic dysentery stool and the pains, which
latter tend to centre about the umbilicus and to become continuous.
There is usually loss of appetite and slight nausea and the patient
may at times show a very slight tendency to flightiness. The mind
however is usually clear. Fever of moderate degree is not uncommon
and it may be quite marked,—up to 104°F. Ingestion of food or
drink or any movement of the body brings on a desire for defecation.
The number of stools, which in mild cases number 15 to 30, may become
excessive, even more than one hundred in twenty-four hours, and the
tenesmus most torturing, so that excoriations around the anus and
at times prolapse of the bowel intensify the distressing clinical
picture. In acute cases the stool may be almost pure blood with only
an admixture of mucus.
Vesical tenesmus may be present and the urine may be diminished in
amount.
There is a toxic effect on the heart so that the pulse tends to
become accelerated and weak. Bacillary dysentery may show a moderate
leucocytosis with increased polymorphonuclear percentage instead of a
large mononuclear one as with amoebic dysentery.
At times, however, the lymphocytes may be the leucocytes showing
the greatest relative increase.
_Collapse Types._—In the most severe types of dysentery we may have
an abrupt onset with rigors and vomiting and a high fever. This fever
gives way to a subnormal temperature and the patient shows signs of
collapse and such a case may die without having passed dysenteric
stools. The abdomen is rigid and very tender on palpation.
_Entero-dysentery._—In those cases where the process extends to
the lower portion of the small intestine the general symptoms are
much more severe although the tenesmus is less and the stools less
frequent and more voluminous. They contain much blood and mucus mixed
with feculent material. Shiga calls such cases entero-dysentery.
In severe cases of the more typical dysentery or colodysentery, as
designated by Shiga, the stools may change from the mucopurulent
mass to a serous discharge which is very rich in albumin and of an
albuminous odor. In such cases emaciation of the patient is very
rapid. Such cases may show signs of collapse with cold clammy skin
and the clinical picture one associates with cholera.
It has been suggested that such cases may be due to action of the
dysentery toxins on the adrenal.
This serous fluid may contain the flesh-like particles which the
French liken to gut scrapings. During convalescence there may be an
arthritis, which however does not impair the function of the joint.
=Complications.=—In addition to the arthritis there may be neuritis,
which, in severe cases, may go on to muscular atrophy. In the
arthritis the knee joint is that most frequently involved. This
complication appears late in the course of the attack. Arthritis may
be frequent in one epidemic and absent in another. The joint swelling
usually clears up completely. Some of the reported joint involvements
are undoubtedly serum reactions from antidysenteric serum treatment.
Rarely in Shiga infections we may have an irido-cyclitis. Subnormal
temperature may follow severe attacks.
In some epidemics of dysentery gangrenous manifestations have been
common. This is a very fatal type and is recognized by the passage
of dark-brown serous discharges containing ashy gray to black
sloughs or even tubules of gangrenous mucosa, the stool having a
putrid odor. The general symptoms are pronounced, there being a dry
glazed tongue, and low muttering delirium with a thready pulse. It
is the typhoid state.
It is usual to consider bacillary dysentery as a self-limited
disease, running on to convalescence within ten days or two weeks.
Rogers has called attention to the importance of bearing in mind
a chronic condition as well as the acute one. In these chronic
cases the ulcerations are usually located in the descending
colon, sigmoid flexure or rectum and give rise to frequent stools
containing blood and mucus and causing a progressive loss of
strength and weight. There is marked digestive disorder and the
patient becomes weak, anaemic and neurasthenic.
DIAGNOSIS
In the presence of the dysenteric syndrome of tormina, tenesmus,
frequent scanty stools of muco-purulent or muco-sanguinolent
character, one must keep in mind the various conditions which may
give rise to such manifestations of dysentery and not diagnose a
bacillary dysentery until we have excluded tuberculous, cancerous and
syphilitic processes as well as those connected with schistosome or
other helminthic infections.
=Clinical Diagnosis.=—Amoebic dysentery is differentiated clinically
from bacillary dysentery by the usual absence of manifestations of
toxaemia and by its insidious onset and chronic course.
It is important however to remember that either bacillary or
amoebic dysentery may show gangrenous manifestations and in such
cases the clinical picture of the typhoid state is the same
whether the process is amoebic or bacillary. Fulminant bacillary
dysenteries may greatly resemble cholera in its algid stage.
Tropical liver abscess is a complication exclusively occurring in the
amoebic form of dysentery while joint manifestations and evidences
of multiple neuritis may be noted in some epidemics of bacillary
dysentery. Again, the toxins of the dysentery bacilli have a tendency
to damage the myocardium. At present we consider the good effects
of the administration of emetine as important in the diagnosis of
amoebic dysentery.
It is important to remember that chronic dysentery may result from
bacillary as well as amoebic infections, although a chronic process
is more a feature of amoebic dysentery.
The muco-purulent stool of bacillary dysentery is more of a milky
whiteness and flecked or streaked with blood or a very viscous bright
blood-tinged mucus rather than the homogeneous, grayish brown,
gelatinous mixture of disintegrated blood and mucus of the amoebic
one. The odour is apt to be foetid in amoebic stools but rather
albuminous with bacillary dysentery ones.
=Laboratory Diagnosis.=—The chief point is to determine whether we
are dealing with an amoebic or bacillary infection. While these two
kinds of dysentery may coexist it is practical to consider a case in
which amoebae with long, rapidly extruded, finger-like pseudopodia
and containing red blood cells are found, as one of amoebic dysentery.
A fresh specimen of the muco-purulent stool of bacillary dysentery
shows, in addition to pus cells, numerous large, phagocytic
cells, which may show vacuolation and strikingly resemble
amoebae. Such cells never show motility but, under conditions of
lowered temperature of specimen or from prolonged standing and
beginning disintegration, the amoebae too fail to show motility.
If mounted in Gram’s iodine solution these large cells show a
much larger nucleus than that of amoebae and take the yellow
staining of iodine more intensely. The best method, however, is
to make a smear, fix it by heat and stain by Gram’s method or
with Loeffler’s blue or dilute carbol fuchsin. These confusing
cells stain easily and perfectly and in the Gram specimen we note
the Gram-negative bacilli in the cytoplasm. Giemsa’s stain, with
methyl alcohol fixation, or the usual Wright or Leishman technique
answer equally well. On the other hand it is rather difficult to
obtain satisfactorily stained amoebae in this way, it usually
being necessary to fix moist thin smears of the stool with some
bichloride fixative, as Zenker’s fluid, and then carry out the
staining with haematoxylin.
_The Stained Smear._—The presence of pus cells as well as
endothelial cells in a stained smear of material from a bacillary
dysentery stool is of value in differentiating from an amoebic
stool smear in which pus cells are rarely seen. The amoebic
dysentery smear gives more the picture of granular débris.
We should always examine a stool as soon after it is passed as
possible.
If the microscopical examination indicates a bacillary infection
we should take a small mass of the stool, wash it in sterile
water and then drop it in a tube of sterile bouillon or salt
solution. After emulsifying in this tube of bouillon we take up 2
or 3 loopfuls of the emulsion and deposit them on a poured plate,
later smearing out with a glass rod, either by successive parallel
strokes or by revolving the plate while smearing the surface with
the glass rod. It is in the first two or three days of an attack
of acute dysentery that we obtain the best cultural results, often
noting a pure culture of dysentery bacilli from proper material
taken at the onset. Manson-Bahr states that he has never recovered
true dysentery bacilli from a purely faecal stool. Even faecal
contamination of the mucoid mass makes it difficult to recover the
organism. Dysentery bacilli rapidly die out if the stool is acid so
that it has been recommended to make the stool strongly alkaline
where it has to be sent to a laboratory from a distance.
It has seemed to me that litmus lactose agar gives results more
surely than the more restraining faeces-plating media. Still I
generally use Endo’s fuchsin agar because it is always at hand
for typhoid or paratyphoid culturing and gives good results. The
dysentery bacillus colonies on this medium are like those of
typhoid—grayish white. In England they prefer MacConkey’s neutral
red bile salt agar while others use the Conradi-Drigalski medium.
We are now using the Teague medium, which is taken up in the
chapter on Faeces. On all these media the colonies resemble those
of typhoid and the differentiation is most easily made by examining
for motility. At the same time one not infrequently finds lack of
motility in bacilli from colonies just isolated on Endo’s medium
which later on in subculture show motility and are found to belong
to the typhoid or paratyphoid group. For the sure determination
of dysentery bacilli or for differentiating the Flexner and Shiga
strains one should carry out agglutination tests.
The isolation of dysentery bacilli from chronic cases or from
convalescents is more difficult as a rule and agglutination tests may
be more practical. A trouble is that an agglutinating effect may be
connected with a prior infection.
Although some observers have noted the appearance of agglutinins
in the serum of cases of acute bacillary dysentery within three or
four days from the onset of the disease, yet it is usual not to
obtain agglutination with the patient’s serum before the tenth day.
With the Shiga strains agglutinating power in 1 to 50 is usually
accepted as evidence of specificity but for Flexner strains we
generally have a higher titre so that a dilution of 1 to 150 should
be required for the test.
Ritchie has recently tested the sera of 792 normal persons and found
that 30% of these individuals agglutinated Shiga bacilli in 1 to 32,
while with Flexner strains 41% agglutinated in 1 to 64 and 30% in 1
to 128. For comparison Ritchie’s results with typhoid showed that
only 6% agglutinated such bacilli in 1 to 16. There is some evidence
that typhoid vaccination increases the agglutinating power of the
serum against dysentery organisms. These findings are remarkable, as
the usual advice is to consider an agglutination of 1 to 30 as fairly
specific for Shiga infections and 1 to 100 for Flexner ones.
Willmore and Savage tried heating serum to 56°C. for thirty
minutes, but found that such a procedure was of no practical
value with dysentery, thus differing from Malta fever serum where
such a procedure is of value in destroying coagglutinins and thus
increasing the specific action. The work of Ohno would indicate
that we should trust to the acid-producing effect on mannite
for differentiating Flexner and Shiga strains rather than on
agglutination because it was found that agglutinins for an acid
strain were not always more specific for such strains than for
nonacid ones.
At the same time it is the rule for a Flexner type bacillus to
show specificity for its serum and the Shiga type for the serum of
the more toxic, nonacid-fast Shiga strain cases. The statement of
Willmore and Savage that the differentiation of bacillary dysentery
infections is a refinement of technique seems a proper view because
with a polyvalent serum for treatment one only needs to know that
the case is one of bacillary dysentery for proper treatment. Of
course with a monovalent serum, effective only for the Shiga
bacillus, one would have to determine whether the organism
producing the dysentery was of that strain.
As a matter of fact it takes considerable time and laboratory skill
to carry out reliable cultural and serological tests.
From a practical standpoint we can use the therapeutic polyvalent
serum for agglutination and any organism recovered on the plate
made from the faeces which agglutinates in 1 to 50 or 1 to 100
may be considered as diagnostic of bacillary as against amoebic
dysentery. Often one does not see a case of dysentery until late
in the disease and then, provided the condition is serious and the
diagnosis points to a bacillary infection it would be better to
inject the curative serum rather than await laboratory confirmation.
PROPHYLAXIS AND TREATMENT
=Prophylaxis.=—The ease with which water-closet seats may be
contaminated should make us pay great attention to their disinfection
during an outbreak of bacillary dysentery. The same applies to the
bedclothes of such patients sent out for laundering.
Great care should be given to the washing of one’s hands prior to
eating. The greatest care must be taken with rectal tubes when
used for treatment. It is better to make an invariable rule to
confine the use of a single tube to a single patient, as the rubber
tubes are difficult to disinfect other than by boiling and such
treatment, especially in the tropics, soon ruins the tube. For
disinfecting tubes a 5% solution of liquor cresolis compositus is
good. The tubes should be thoroughly washed of the disinfectant
before using again. For disinfection of faeces one can use an
equal portion of the above disinfectant to a similar amount of
stool leaving the disinfectant to act on the stool at least one
hour before emptying the receptacle. Soiled clothes should be
disinfected in a 2½% solution of the compound cresol solution.
Flies must be kept in mind and water and milk supplies boiled. The
carrier is of as great importance here as in typhoid or cholera,
especially when assisting in preparing food.
=Vaccination.=—Vaccination against dysentery does not seem to have
made much headway owing to the very severe reactions following
injections of killed cultures of the Shiga bacillus. By injecting
such bacilli treated with an immune serum (sensitized) the reaction
is less severe.
Dean reports the value of treating the emulsion of organisms with
an equal amount of 1 to 1000 eusol. Gibson treated a suspension of
dead organisms with an equal amount of serum, mixing in the syringe
at the time of injection. Although this method was used during the
war its immunizing value was not settled.
The question of the best method of preparing vaccines for
prophylactic use is still unsettled. The greatest difficulty has
been experienced in making vaccines of the Shiga bacillus on
account of the great toxicity of such preparations.
The serum alone is used almost exclusively for curative rather than
prophylactic purposes.
=Treatment.=—In the treatment of bacillary dysentery absolute rest
in bed is important to keep up the strength of the patient and also
to protect the heart which tends to be more or less damaged by the
toxic action of the Shiga bacillus. Some prefer to prop up the
patient in bed, considering a strict dorsal decubitus as undesirable.
It is important to use sufficient covering on the patient to avoid
chilling. A light wool blanket spread over the abdomen is often all
that is needed in the tropics.
Some authorities deal with the subject of treatment without
referring to any other means than the administration of serum.
This probably is the proper attitude when the very fatal Shiga
type infections are encountered. It must be remembered that
certain epidemics, which as a rule are associated with the Shiga
type bacillus, give a very high mortality (20 to 40%) while other
epidemics seem associated with a less virulent strain of this
bacillus.
At any rate when a case is seen early it would seem advisable
to give about 2 grains of calomel in divided doses of ¼ grain
every half hour and then follow it up with saline treatment. Most
authorities recommend a preliminary dose of castor oil. During
the first day or two enemata of normal saline, boric acid or 1½%
sodium bicarbonate solution in 2 pint amounts would seem indicated
as assisting the salines in the elimination of toxic material.
After that time the tenesmus and rectal irritation make the use of
the rectal tube too trying to the patient. I have used the Murphy
protoclysis method with a certain degree of success, but this
procedure cannot be kept up long. Hot fomentations to the belly
relieve the griping pains.
The saline treatment is highly recommended by Buchanan who gives
60 grains of sodium sulphate every two or three hours until the
dysenteric character of the stool disappears.
Bahr in the Fiji islands treated 53 consecutive cases, of which
41% had marked constitutional symptoms, with a mortality of 13.2%.
He gave 1 dram of sodium sulphate every hour for the first day and
subsequently the same dose every four hours.
In a second series of 106 cases, of which 42% had marked
constitutional symptoms, he treated 34 with salines plus the
administration of capsules of cyllin. The remaining 72 cases
received in addition to this treatment injections of a polyvalent
serum obtained from the Lister Institute. The mortality in this
series was 1.8%. He notes that 5 of the cases in this second series
were of the severest type as evidenced by the gangrenous stools
and toxic condition and yet not one of these five serum-treated
cases died. He notes that the stools of those who received serum
injections became normal in five days for an average while for
those treated with saline alone the average period was eight days.
Bahr strongly recommends the combined treatment of salines and
serum. In very severe cases Bahr used 50 to 70 cc. of the serum but
ordinarily 20 cc. for adults and 10 cc. or less for children.
Willmore and Savage think one obtains the best results by injecting
from 80 to 120 cc. of a polyvalent serum into the subcutaneous
tissues of the flank or abdomen or intravenously. They think that
anaphylaxis is less liable to follow a massive initial dose of serum.
In the use of serum Shiga recommends a dose of 10 cc. for a mild
case or two injections of 10 cc. at intervals of ten hours for
cases of medium severity, while in very toxic cases he uses 60 cc.
in 3 daily doses of 20 cc. each. It is important to use serum early
as it has little or no effect if used after the 7th day (Klein).
The best known sera are those of Shiga, Dopter and that prepared by
the Lister Institute.
Animal charcoal and bolus alba are considered of value by some
physicians. Opium should be avoided. Intravenous saline injections
are of value in cases showing collapse signs. Again, such cases,
from the standpoint of possible adrenal insufficiency, may be
helped by adrenalin. Where there is a very small rapid pulse with
marked cardiac weakness injections of camphor in oil may be of
value.
Subcutaneous injections of ordinary or hypertonic saline containing
about 10 drops of 1 to 1000 adrenalin solution is of value in
collapse.
Ross considers opium as of value in dysentery and states that he
regards ipecac as of value not only in amoebic but in bacillary
dysentery as well. I have often given salol-coated pills containing
1 grain of ipecac and ⅙ grain of calomel every two hours to cases
of bacillary dysentery with apparent benefit.
For the diet of cases of acute bacillary dysentery albumin water
or barley water sweetened with lactose is to be preferred to milk,
which is usually not well borne by such patients. Kendall has noted
the value of sugar of milk in lessening the toxicity of various
organisms. Tea sweetened with lactose is usually well borne. Meat
juice expressed from a piece of lightly broiled steak is good.
Various jellies or sago pudding are of value. Willmore and Savage
praise yoghurt.
Unless given in small amounts liquid diet is apt to increase
evacuations and some cases seem to do better on ordinary diet.
In the tropics there are many brands of sterilized natural milk and
these can be inoculated with a culture of _B. bulgaricus_.
In chronic bacillary dysentery Rogers recommends 1 to 1½ pint
enemata of albargin in strength of 1 to 500. Protargol seems to
be equally efficient in the same strength. Owing to the effect
of organic material on silver nitrate this salt does not seem
so reliable as the organic silver compounds. It has also been
recommended to flush the colon with warm boric acid solution.
Another recommendation is to use milk for this purpose. Vaccine
treatment has been employed, in cases of chronic bacillary
dysentery. Either eusol-treated organisms or those sterilized by
0.25% trikresol are to be preferred.
CHAPTER XIII
PLAGUE
DEFINITION AND SYNONYMS
=Definition.=—Plague is primarily a disease of rats or other
rodents and is caused by a bacterium of the haemorrhagic septicaemia
group, _Bacillus pestis_. The disease exists in the rodent in both
an acute and chronic form. Acute plague of the rat is apt to be
septicaemic, so that when certain species of fleas which infest the
rat feed on the blood of their host they ingest plague bacilli.
These seem to multiply in the region of the proventriculus and cause
thereby an obstruction to the stomach. As a result the flea makes
vigorous and repeated but ineffectual efforts to feed. Regurgitation
of the contents of the oesophagus occurs, thereby inoculating
plague bacilli. When the rats die these fleas will attack man and
cause human plague. The ordinary type in man is bubonic plague,
characterized by extremely tender glandular enlargements. This form
of the disease is thought to be exclusively transmitted from man to
man by fleas or possibly bedbugs. A second type is pneumonic plague
which is a surely fatal pneumonia which is transmitted from man to
man by droplets of sputum expelled in coughing. Either the bubonic or
pneumonic types may become septicaemic or this form may exist from
the start.
Plague shows a marked clouding of the consciousness from the onset
and is characterized by toxic action on the heart and endothelial
lining of capillaries.
=Synonyms.=—Oriental Plague, Black Death, Pestis. French: La Peste.
German: Die Peste.
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—Ancient writers were accustomed to apply the
designation “plague” to any disease which was epidemic in character
and attended with great mortality. This explains why the plague of
Athens and that of Marcus Aurelius, which epidemics did not possess
the characteristics of oriental plague, were so designated. There
exist however writings which show that fatal epidemic diseases
attended with buboes and prostration were noted prior to the
Christian era.
It is probable that the biblical description of a disease among the
Philistines which was attended with buboes and killed the mice of
the field referred to plague.
In the 6th century, during the reign of Justinian, a disease
which was unmistakably plague started from Egypt and reaching
Constantinople caused the death of 10,000 persons in one day. It
spread throughout the entire Roman empire.
_The “Black Death.”_—The most noted epidemic of plague was that of
the “Black Death” of the 14th century. The disease seems to have
originated in the East, possibly in China, and eventually invaded
Asia Minor, Egypt and Europe. The disease was called “Black Death”
in Germany, on account of the petechial spots or “tokens” and in
Italy, the “Great Mortality.”
In the records of the epidemic we note that it was attended with
great stupefaction, the sick losing their speech from palsy of the
tongue. Others noted buboes of groins and arms while some noted a
putrid inflammation of the lungs with the expectoration of blood.
In the plague at Avignon it was noted that at first, for six or
eight weeks, the sick expectorated blood and that to come near them
was certain death. Afterwards buboes appeared in groin and axilla
and some of the sick recovered.
_Quarantine._—It was during this epidemic that quarantine became
a recognized procedure in Europe. The adoption of a period of
detention of forty days probably originated in the medical idea
that the 40th day was the last day of ardent diseases, this being
one of the critical days. The lazarettos, where strangers were held
in quarantine, appear to have first been established on some island
near Venice, in 1485.
It has been estimated that one-fourth of the population of Europe
succumbed to the “Black Death,” but estimates in certain parts
of Europe would indicate a mortality approaching 70% of the
inhabitants.
In 1665 occurred the Great Plague of London, during which year it
was estimated that approximately 60,000 out of a population of
450,000 died. It was thought that this epidemic was introduced from
the Levant by way of Holland.
There was much plague in Europe in the 18th century but it would
seem to have completely disappeared by 1841 and only to have
returned with the present pandemic.
_The Present Pandemic._—The plague epidemic with which all parts
of the world are now so concerned is supposed to have originated
in China, in the province of Yunnan, and from that center to have
reached Canton, in 1894, causing the death of 60,000 people in a
population of 1,500,000. In the same year it extended to Hong Kong
and from that great seaport has spread over the entire world. India
has suffered more than any other country, there having been years
when the plague deaths exceeded 1,000,000.
In a recent article by Low it is noted that the highest death rate
was reached in 1907 when 1,315,892 persons died. From the time of
the introduction of plague into India to the end of 1917 there were
9,841,396 deaths from this disease.
In its spread it has invaded Europe, Egypt, South Africa,
Australia, Japan, Philippine Islands, California and parts of
Central and South America. It has recently made its appearance in
New Orleans.
=Geographical Distribution.=—At present there are only two
important foci of endemicity, one Mesopotamia and another in the
region of the Himalayas (India, Thibet and Yunnan). There also
seem to be less important centers in Uganda, in Africa, and in the
trans-Baikal region of Siberia. In view of the rather widespread
infection of the California ground squirrels, from which rodents
the disease has from time to time spread to man, it would seem
probable that California might be considered another focus of
plague.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—The bacillus of plague was first isolated by Yersin
from a plague bubo, in 1894, at Hong Kong. It is true that Kitasato
reported a bacillus which he had isolated from the blood of a plague
patient, on July 7, 1894 (Yersin’s report was made July 30, 1894).
Kitasato’s bacillus was motile, Gram-positive, coagulated milk and
gave a turbidity in bouillon, characteristics which were just the
opposite of those of the organism reported by Yersin.
[Illustration: FIG. 63.—Pest bacilli from spleen of rat. (Kolle and
Wassermann.)]
As now recognized the plague bacillus, when in smears from
pathological material, shows the form of an oval bacillus, the ends
of which stain more intensely than the central portion (bipolar
staining). When cultured on ordinary agar, the morphology is more
rod-shaped with a tendency to pleomorphism.
These agar cultures are very sticky and mucilaginous. If 3% of
NaCl is added to the agar, this pleomorphism is exaggerated, there
occurring coccoid, root-shaped and various bizarre involution forms.
For obtaining the involution-form appearance on 3% salt agar one
should transfer liberally from the ordinary agar growth to the salt
agar rather than planting direct from the pathological material.
A bouillon culture, upon the surface of which there has been
deposited drops of oil or melted butter, shows a string-like
downward growth from the under surface of the oil globules. This
“stalactite” growth is very fragile and is difficult to obtain.
Ordinary bouillon cultures show a rather powdery deposit at the
bottom and a hanging-drop preparation from such a culture shows
chains of plague organisms resembling streptococci. Gelatine is not
liquefied. _Bacillus pestis_ grows readily at room temperature as
well as at 37°C, and one may be struck with the fact that colonies
on agar plates may show variations in degree of development so
that the suspicion of a contaminated culture may arise. Human
plague material for cultures or smears is best obtained from the
bubo prior to suppuration in bubonic plague, from the blood in
septicaemic plague and from the watery sputum in pneumonic plague.
_Plague in the Rat._—With acute plague in the rat one finds marked
injection of the subcuticular surface of an exposed abdominal flap;
certain glands, especially the neck ones, show marked congestion,
haemorrhagic necrosis and periglandular infiltration; the pleural
cavity contains much fluid; the liver has a yellow mottled appearance
liberally sprinkled with discrete, yellowish-white granules about
the size of a pin’s head, while the spleen is enlarged. Smears from
the spleen or affected glands, as a rule, show the bacilli in great
numbers. The San Francisco findings in plague rat autopsies varied
somewhat from those noted above, which held for Indian plague rats.
_Confusing Organisms._—Other organisms which may be obtained
from plague-suspected material are those of the proteus or colon
group, which may show bipolar staining, but culturally are quite
different. Klein has noted that a nonmotile rod, which gives a
striking bipolar staining and named _Bacillus bristolensis_, may be
mistaken for the plague bacillus. Its growth in bouillon is similar
to that of _B. coli_ and it coagulates milk.
An organism, _B. pseudotuberculosis rodentium_, resembles the
plague bacillus in a striking manner but is without virulence for
rats. It is virulent however for guinea pigs and these animals can
be immunized against plague with this closely related organism.
Litmus milk cultures of plague show a very slight acidity while
with _B. pseudotuberculosis rodentium_ there is a high degree of
alkalinity produced.
Wherry has reported two cases of ulcerative conjunctivitis with
lymphadenitis of cervical glands, fever and marked prostration,
due to infection with _B. tularense_, occurring in persons who had
handled rabbits which had died of this plague-like infection. The
organism was first noted by McCoy in squirrels in California. The
symptoms and lesions in these animals are those of plague. Guinea
pigs succumb after the cutaneous inoculation of material and show
lesions markedly resembling plague. The organism, however, will
not grow on ordinary simple media as does the plague bacillus. As
will be noted in the chapter on Tularaemia the disease has a very
limited geographical distribution.
The _crucial test_ for any plague material is the power of the plague
bacillus to infect a rat or guinea pig, when the material is rubbed
on the shaven skin of the animal. _B. tularense_ will also pass
through intact shaven skin and it produces lesions in the guinea
pig similar to those of plague. Other organisms, however which might
infect through intact skin produce lesions unlike those of plague. As
a practical point it may be stated that cases showing a profusion of
oval, bipolarly staining bacilli, in smears from glands or sputum,
and with clinical manifestations of plague, are not likely to be
other than plague; still, to be conservative, one should always
inoculate animals cutaneously or subcutaneously.
[Illustration: FIG. 64.—Plague bacillus involution forms produced by
growing on 3% salt agar. (Kolle and Wasserman.)]
=Epidemiology.=—Plague is primarily a disease of rodents, usually
rats, and man contracts his infection from these animals. With the
exception of pneumonic plague which, under certain circumstances, is
transmitted directly from man to man, plague infections originate
from the bite of fleas which have become infected from feeding on the
blood of plague rats. Infected fleas act as intermediaries in plague
epizootics among rats. It is true that a rat might become infected
from bites received in a fight with an infected rat, or man might be
infected through a cut on a finger while handling plague material,
but such methods play but a small part in plague epidemiology.
_Fleas and Plague._—In 1897, Ogata infected mice by inoculating
them with an emulsion of crushed fleas taken from plague rats. In
1898 Simond showed that if a rat, dead of plague, were placed in a
large bottle and a healthy rat confined in a small cage introduced
into the bottle and suspended above the dead rat, so that there
could be no contact between the dead and the living animal, the
well rat would contract the disease. If however the fleas were
removed from the dead rat, before the introduction of the caged
rat, no infection took place.
By reason of claims that the rat flea would not bite man these
convincing experiments were in a measure disregarded. The complete
confirmation of the correctness of this view, as to transmission of
bubonic plague, was brought about by the Indian Plague Commission.
In a large number of experiments it was shown that when healthy and
plague-infected guinea pigs were confined together in spaces where
there were no fleas, there were no plague infections of any of these
well animals.
[Illustration: FIG. 65.—1 and 2, male and female _Xenopsylla
cheopis_. 3, Head of _Ceratophyllus_. 4 and 5, male and egg-distended
female of _Sarcopsylla penetrans_.
_Xenopsylla cheopis_ is the most important plague transmitter of the
flea family as it is the common rat flea of India where there is so
much plague.
_Sarcopsylla_ or _Dermatophilus penetrans_ is an important factor in
a disabling skin disease, especially of the feet, in many parts of
the tropics.]
On the other hand in 35 experiments, when fleas had access to
the spaces, plague infections were the rule. Again, guinea pigs
in cages which were suspended only two inches above a plague
flea infected floor, became infected, but other animals, which
were suspended so high that the fleas could not jump up to them,
remained well. Two cages, each containing a monkey, were placed in
a plague flea infected room. One was surrounded with a protecting
zone of 6 inches of “tanglefoot” fly paper, this being the limit
of the distance a flea can jump, while the other cage was not
so protected. The monkey in the cage without the sticky paper
contracted plague while the second monkey remained well. It is
only when there is a great incidence of plague among rats that
we have outbreaks of bubonic plague in man, and it has been noted
that the greater the epizootic, the more heavily infected was the
blood of the sick rats with the plague bacilli. A flea with a
stomach capacity of about ½ c.mm. could take in several thousand
plague bacilli in a feeding on a rat whose blood was teeming with
bacilli. The blood of a rat dying with plague may contain as many
as fifty million bacilli to the cc. Human blood rarely contains
more than a million to the cc. There is a multiplication of the
organisms in the flea, so that when it defecates, thousands of
plague bacilli are deposited near the puncture wound made by the
flea when subsequently feeding on a man. The infected faeces are
rubbed into the wound by the man in scratching the site of the
bite, so that we have here an instance of a contaminative method of
infection as contrasted with the inoculative method by the mosquito
in malaria.
[Illustration: FIG. 66.—1, _Ctenocephalus felis_. 2, _Ceratophyllus
fasciatus_. 3, _Hoplopsyllus anomalus_. 4, _Ctenopsylla musculi_.
5, _Xenopsylla cheopis_. 6, _Pulex irritans_. 7, Internal anatomy
of flea. (After Fox.) (_a_) Maxillary palpus; (_a_-1) epipharynx;
(_a_-2) mandible; (_a_-3) labial palpi; (_a_-4) maxillae; (_a_-5)
basal elements of rostrum and mandibles; (_b_) salivary pump;
(_c_) hypopharynx; (_d_) aspiratory pharynx; (_e_) muscles of the
aspiratory pharynx; (_f_) eye; (_g_) oesophageal ganglia (brain);
(_h_) thoracic ganglia; (_i_) oesophagus; (_j_) salivary duct;
(_k_) gizzard; (_l_) salivary gland; (_m_) stomach; (_n_) aorta;
(_o_) ovaries; (_p_) malpighian tubules; (_q_) pygidium; (_r_)
rectum showing rectal glands; (_s_) anus; (_t_) intestines; (_u_)
bursa copulatrix; (_u_-1) ductus obturatorius (blind duct); (_v_)
receptaculi seminis or spermatheca; (_w_) ducts of spermatheca; (_x_)
vagina; (_y_) uterus; (_z_) abdominal ganglia.]
Bacot and Martin have shown that while infection may take place as
the result of the faeces being rubbed into the wound made at the time
of feeding yet the ordinary way is probably by regurgitation from the
oesophagus of the flea at the time of feeding.
Upon taking in plague septicaemia blood the bacilli multiply
about the site of the proventriculus as well as distending the
oesophagus. This makes an obstruction to the entrance of the
stomach resulting in starvation of the flea. This naturally makes
the flea more voracious and in the ineffectual muscular efforts
to take in blood, regurgitation of the contents of the oesophagus
occurs, thereby infecting the person upon whom the flea is trying
to feed. This obstruction apparently may be overcome in some way as
the plague-infected flea does not necessarily die. Still from lack
of sufficient fluid such fleas are liable to be killed off if the
relative humidity is low, as in dry weather. Further investigations
have shown that the proventricular plug may be channeled, but in
such case valve action is lost and the contents of the stomach are
regurgitated, thus making such a flea more dangerous than one with
an obstructed proventriculus. Such fleas may continue infectious
for 67 days.
Very interesting in this connection is the fact that Heiser found
plague-infected fleas in the desk of a European at Manila who died
of plague. A mummified rat was found in one of the drawers of
this desk, from which successful animal inoculations for plague
were made. Heiser notes that data would indicate that these fleas
probably remained alive 2 weeks after the death of the rat which
brought about their infection. Another very striking finding during
the same Manila plague outbreak (1912-1913) was that bedbugs found
on the sleeping mat of a human victim of plague showed bipolarly
staining bacilli.
Bacot has carried on experiments in which fleas infected two months
previously and kept in a cool place could transmit plague. This
would indicate the danger from plague-infected fleas which had been
held in material packed away in boxes.
_Method of Spread._—The spread of plague epizootics among rats seems
to be rather by the fierce brown sewer rat, _Mus norvegicus_. The
more delicate black house rat, _Mus rattus_, usually receives its
infection from the sewer rat. When the rat dies the fleas leave the
dead body and seek a new host, preferably one similar to the one just
abandoned. The sewer rat reaching the basement of houses and dying
of plague is deserted by his fleas. These will attach themselves to
the house rats which go from basement to roof of the house and later
these dying are abandoned by the fleas which, in the absence of a
rodent host, will feed on man and infect him.
The house rat is rarely found in Europe while in many parts of the
tropics it is common and in close association with man. The fact
that the sewer rat avoids the upper portions of houses probably
explains the greater infrequency of plague epidemics in Europe
where this rodent is common. In former ages when the house rat was
prevalent in Europe we had great epidemics there. _Mus (Rattus)
norvegicus_ is of stout build with a blunt nose and small opaque
ears which barely reach the eyes when laid forward. The tail is
shorter than the length of the head and body together (89% of such
length). With _Mus rattus_ we have a delicately built rat with a
slender head and sharp nose. The ears are translucent and large
and reach beyond the middle of the eye when extended. The rather
delicate tail is about 25% longer than the length of the head and
body taken together.
Recently it has been found that a guinea pig set free in a house
suspected of having plague fleas becomes infected if such fleas are
present. The fleas would probably prefer the guinea pig to man and
such a measure would in some degree be protective to man. It is
however for the detection of plague infection that the measure is
employed and the guinea pig is termed the “Plague barometer.” In
Madras there is practically an absence of _Mus norvegicus_ although
_Mus rattus_ is present in numbers and the comparative freedom of
the city from plague is striking.
The principal rat flea of the Orient is _Xenopsylla cheopis_. This
flea is without combs like _Pulex irritans_, the human flea, but
is of a lighter color and has an ocular bristle near the upper
margin of eye and two bristles posterior to the antennae. In Europe
and the United States _Ceratophyllus fasciatus_ is the common rat
flea. Many other species of fleas transmit plague and it is also
possible that the bedbug may play a part in spreading infections
from man to man. Vergbitski has transmitted plague from man to the
rat by infected bedbugs. In Siberia, a marmot, the tarabagan, is
supposed to play the part of the rat in plague transmission. In
California, the ground squirrel, _Citellus beecheyi_, has become
infected and may transmit the disease by its flea, _Ceratophyllus
acutus_. In the Tropics plague tends to prevail only at times when
the temperature is between 10° and 30°C. It is the effect on the
flea of cold weather which causes the disappearance of bubonic
plague at such times. The bacillus of plague can withstand freezing
temperatures. Sunlight and drying are the especially inimical
factors for _B. pestis_. Dry seasons are inimical to the spread of
plague and it is especially in very rainy seasons that epidemics
rage.
_Chronic Plague in Rats._—The Indian investigators have called
attention to the existence of a chronic plague in rats. In this we
have chronic buboes, areas of necrosis in spleen and abscesses of
the spleen. It is chiefly in the spleen that the lesions occur, thus
differing from the acute plague in rats above described. Of 27,699
_M. norvegicus_, examined in Bombay, O.57% showed signs of chronic
plague.
In the necrotic material plague bacilli can be found in
approximately one-half of these rats although frequently the
bacilli are nonvirulent. It is possible that this chronic plague
in rats may serve as the reservoir of infection which keeps up
plague epizootics from year to year. Plague in India, according to
White is less virulent now than formerly and this is attributed to
a greater immunity of the rats.