Sixty Cases of Amœbic Dysentery Illustrating the Treatment ... · Nov., 1912.] DYSENTERY: ROGERS...


Transcript of Sixty Cases of Amœbic Dysentery Illustrating the Treatment ... · Nov., 1912.] DYSENTERY: ROGERS...

Page 1: Sixty Cases of Amœbic Dysentery Illustrating the Treatment ... · Nov., 1912.] DYSENTERY: ROGERS 421 ?riginal ^rliclfs. SIXTY CASES OF AMCEBTC DYSENTERY ILLUSTRATING THE TREATMENT

Nov., 1912.] DYSENTERY: ROGERS 421

?riginal ^rliclfs.




C By LEONARD ROGERS, m D., f r.c p. i.m s.t

Professor of Pathology, Calcutta.

X have already published details of several cases of amoebic dysentery, hepatitis and liver abscess successfully treated by hypodermic injec- tions of soluble salts of emetine (1 and 2) in which the rapidity of recovery from both very acute and very chronic attacks was 1 emavkable. Wrhat is wanted, however, to enable the merits of the new method to be estimated, is a consecutive ser- ies of cases of amoebic colitis compared with a

similar series in which the well established treat- ment with ipecacuanha has been used. This desideratum I propose to supply in the present paper, which will deal with thirty consecutive cases under my care in the Isolation Ward of the Medical College Hospital in which ipecacuanha was used, and twenty-six in which emetine was administered. Before dealing with this material it will be well first briefly to discuss the preval- ence and differential diagnosis of amoebic colitis as I have found the new treatment to have little or no effect on bacillary dysentery, so that unless the nature of the disease is first ascertained the

druo- is liable to be unjustly condemned owing to being ignorantly used in the wrong class of case ; which would be equivalent to saying that quinine is no use in malarial fever because it failed to control the pyrexia of a case of typhoid wrong- ly diagnosed as malaria. That this warning is by no means superfluous I already have


The Prevalence of Amcebic Dysentery in India.

As I am dealing with the prevalence of amoebic disease in India at greater length in another com- munication, the somewhat scanty evidence at

hand will be only briefly summarised here. An

analysis of nearly 150 dysentery post mortems performed by me at the Medical College Hospital shows that the majority of deaths due primarily to dysentery were of the amoebic variety, while

if terminal bacillary cases and amoebic colitis com-

plicated by liver abscess are included, then the

mortality produced by the amoebic disease m

Calcutta is almost twice that due to bacillary in-

fection. Grreig and Wells (3) have shown that the protozoal kind is also the more frequent in Bom- bay, while I am informed that during the Abor Expedition ipecacuanha treatment proved much

more efficient than salines, so that it is clear that the amoebic disease is the common type in the

damp hot parts of India. In Jails Forster(4) found a preponderance of bacillary disease, but also

some amcebic cases, while I have met with the

latter variety in a Calcutta jail during the pre- sent year, so more work is required in these

institutions before the true relative prevalence will be known.

Once more, as I demonstrated as early as 1902, tropical or amcebic liver abscess is solely related

to the protozoal disease and never originates from bacillary dysentery, so that wherever large liver abscesses frequently occur there we may

safely conclude that amoebic dysentery is also

prevalent. Utilising this test I have worked out the proportion of liver abscess cases to dysentery admissions in the British Army for the ten years 1901-10, and find that the rate for the whole of

India is one liver abscess admission to seven dy- sentery ones: a very high ratio which can only be explained on the supposition that amcebic

dysentery is widely prevalent over India, and is probably the preponderating form. Moreover

the same figure for the previous decade was only 1 to 14i. due to the dysentery admissions having recently fallen by one half, while the liver abscess ones have slightly risen. This may be due to

sanitary advances having reduced the incidence of bacillary dysentery, just as typhoid due to the

same class of bacilli has fallen, while but little

affecting that of the amoibic form. If this is

the case&it is still more likely that the amoebic

disease is now the commoner form in the British

Army in India. Once more, the proportion of

liver abscess to dysentery admissions from 1901-10 was very similar all over India. Indeed from

steamy Bengal to the very dry Punjab and also

all over Central India the figure only varied

between 1 to 6 and 1 to 7, strongly indicating that amoebic dysentery is a common disease in

the dry as well as in the moist parts of the

country. During the last nine months I have been care-

fully investigating the dysentery cases under

my care, and find that over two-thirds of them

were undoubtedly amcebic, while there was a

marked increase in the proportion of this variety with the onset of the monsoon rains, so that the

proportion may be still higher when a full year's records are available.

Enough has been said to prove that now as

rapidly effective specific treatment is available

for amcebic dysentery, it has become a matter of urgent practical importance to all medical

men working in tropical and sub-tropical coun- tries to familiarise themselves with the clinical

and microscopical methods of differentiating between the two great classes of dysenteries, with- out a knowledge of which they will not be able to do justice to their patients.

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Some Points in the Clinical Differentiation

of Amosbic Colitis.

The term dysentery as applied to amoebic

disease of the large bowel is not infrequently dangerously misleading, as dysenteric symptoms are by no means always result, and such cases

are very liable to be overlooked and allowed to

drift on until serious hepatic or other complica- tions ensue. This fact is forcibly brought out

by the simple statement that out of 45 cases of

primary death from amoebic dysentery among one thousand post-mortems at the Medical College Hospital, in no less than 18, or 40 per cent., the clinical diagnosis was not even dysentery at all, although all but four of these cases were

over two days in hospital. The most frequent erroneous designations were


diarrhoea", tubercular diarrhoea " and "

peritonitis," the latter in the very severe cases with spread of the inflammatory condition to the serous coat of the bowel. In considering the clinical differentiation of dysenteries, it is therefore necessary to

emphasize the important fact that, although certain signs may suggest the presence of the amoebic form of the disease, it cannot be

recognised with certainty without microscopical confirmation, while this insidious and frequently deadly disease can never be excluded without

proof by repeated examinations of the stools of

the continued absence of pathogenic amoebas. The following remarks on the clinical differentia-

tion of the dysenteries must be read in the light of the foregoing statement, and it must constantly be borne in mind that there is no pathognomonic s}^mptom of amoebic disease, and none which

may not mislead if trusted to alone. I hope before very long to deal at length with this

difficult subject in a work on dysenteries I have for some time been engaged on, but hope the

following data, based on a series of 56 cases

with careful notes and microscopical examinations of the evacuations, may meanwhile be of some

help to others practising in India and elsewhere in the Tropics.

Fever and Constitutional Symptoms.?Even in first attacks of amoebic dysentery fever is about as often absent as present, and is seldom more than a slight intermittent rise to from 100

to 102?F. for a day or two. In a few very severe

cases remittent fever may occur, the prognosis is in such cases being much more grave. On the other hand, in acute bacillary dysentery fever of several days duration, with considerable constitu- tional disturbance, is the rule at the onset of the disease, although the pyrexia has often

passed off before a patient comes to hospital. In chronic dysentery slight intermittent fever is only occasionally seen in the amoebic disease, and is also frequently absent in the bacillary variety, although in the latter an evening rise

to between 99 to 101?F. is often an indica-

tion that the morbid process is still active, an exacerbation of the bowel symptoms accom-

panying even such slight febrile paroxysms. In

chronic amoebic disease the appearance of an

intermittent type of fever should always excite

suspicion of some complication, usually hepatic in nature. If the spleen is much enlarged complication with malaria or kala-azar may be

the cause of fever. Abdominal Symptoms.?Pain in the region

of the navel, griping in the abdomen and

tenesmus?that is, severe straining during the passage of the stools?are frequent in both forms of dysentery, but in my experience the last is

more common in the bacillary form, as the

rectum not infrequently escapes attack by the

amoebic disease for some time at any rate. Very numerous stools without tenesmus is, therefore, often a point in favour of the protozoal disease.

Of more importance is localised abdominal ten-

derness and distinct thickening of the bowel

detected by palpation. The sigmoid flexure is

commonly tender and slightly thickened in both

forms, especially in chronic cases, but if there is

also marked pain on gentle pressure in the right iliac fossa, and still more if the ccecum can be

felt as a tender thickened mass, the disease is much

more likely to be amoebic in origin. In the most

serious type of this disease sausage-like very tender masses of greatly thickened bowel may be felt anywhere in the coarse of the large in- testine and is a sign of extensive involvement of

all the coats of the great bowel, including its

peritoneal covering, and unless the true nature of such cases is early detected and very full doses of the specific drug administered without delay, such cases are likely to prove fatal within two or three days. When the caecum is'chiefly involved these cases are very likely to be mistaken for appendi- citis, with disastrous results. It should also be

remembered that such acute attack may occur as

acute exacerbations in a chronic amoebic dysen- tery. After death in such a case the wall of the

large bowel may be half an inch in thickness in

places and so much softened as to resemble damp blotting paper and be often impossible to remove without rupturing the tube. Yet during life no

actual perforation may have taken place, although the presence of patches of lymph on the surface of the bowel shows the presence of local peritonitis.

The Diagnostic and Prognostic value of the blood changes.?The great value of the leucocyte changes in dysenteries has not yet been ade-

quately recognised. Space will not allow of my

dealing fully with the large amount of material

I have accumulated on this point, but I may briefly summarise the more important conclu-

sions I have arrived at. In the first place, in

amoebic dysentery either an actual or a relative

leucocytosis is rarely absent, Thus out of sixty

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Nov., 1912.1 DYSENTERY: ROGERS 423

consecutive cases in my ward (including foui still

in hospital and not therefore shown in the tables) an actual leucocytosis was found in three-

fourths of the cases, while a relative one

(that is one in which owing to the presence of

anaemia, reducing the number of the red cor-

puscles, although the total leucocytes do not

exceed 10,000 per c. cm., yet the ratio of the

white to the red corpuscles is greater than the

normal maximum of 1 to 500) was present in 8 more leaving only seven, or 11 '4 per cent, with- out even a relative leucocytosis, and one of these also suffered from kala-azar, while two more had

enlarged spleens probably due to that disease, which accounts for their few leucocytes. On the other hand, among 21 recent cases of

dysentery in which I could find no amoeba3, most of which yielded other evidence of being bacil-

lary in nature, in only three was any actual leu-

cocytosis found, two of these being very severe cases and all of them recent acute ones, while in

two more a relative increase of the leucocytes was present; leaving 76 per cent, with no increase in the leucocytes. The presence, then, of leu-

cocytosis is a point in favour of a diagnosis of

amoebic dysentery, while its absence is very much against that type being present unless some leu- cocyte reducing disease such as kala-azar is also

present. The degree of the increase of the leucocytes is

also of great prognostic as well as diagnostic sig- nificance. In the first place, four out of the

seven cases without any leucocyte increase proved fatal, usually with gangrene of the bowel, al- though over three-fourths of the total series re-

covered, so that an absence of leucocytosis in a

severe case is of very bad prognostic import, being a sign of feeble resisting powers. Secondly, the very high degree of leucocytosis commonly met with in amoebic disease is very striking, for in no less than ten cases out of sixty over 30,000 white corpuscles were present per c. cm., and in seven more between 20,000 and 30,000. Yet

in 21 non-amoebic cases in no single case

were 20,000 found, and in only one over 15,000, although higher counts have been occasionally recorded in bacillary dysentery by others, but

as a rule only in recent acute cases with well

marked fever, which are not likely to be mistaken for amoebic disease.

Once more, a count of 25,000 leucocytes and

upwards is of very serious prognostic significance, tor only one out of nine such shown in the table of cases treated with ipecacuanha was cured, while

of four discharged " otherwise" only one had

improved under it while in hospital. On the other

hand, out of five cases treated with emetine

injections four recovered, the fatal case giving a

count of G 1,750 and succumbing in less than

twenty-four hours after admission before ^


drug had a chance. These results.are a striking

testimony to the value of the new method in these terribly acute cases, which I had previously come to look on as almost inevitably fatal. Such decrees of leucocytosis can be detected by a

o-lance at a blood film, so it only takes a few minutes to detect them, while when found it furnishes a clear indication for immediate and full doses of emetine hydrochloride hypodermi- cally, one grain being given immediately and repeated once or twice in the twenty-four hours. In fact I look on such liigli leucocyte counts in amoebic colitis as of equal prognostic significance as finding very numerous malignant tertian parasites in every field of the microscope in malaria; for like the latter it enables the danger- ous nature of the infection, and the necessity of especially vigorous specific treatment being at once adopted if tlie patient's life is to be saved, being recognised early even when the clinical signs are deceptive.

Lastly. the percentage of polynuclear leucocytes is shown in the tables, but is of less importance than the other points. Except in some chronic cases they are increased, the pro- portion being usually highest in very acute infections, but very rarely exceeds 90 per cent.

Characters of the Stools.?It is not safe to

rely on the appearance of the stools for the differentiation of the two kinds of dysentery, ̂

for there are no constant and characteristic differences. Nevertheless, as a general rule if there are separate large rosy blood-stained masses of mucus constituting all or most of the evacua- tion amoebae will very probably be found, while when large white masses of mucus or small translucent raw white-of-egg-like pieces alone are present, intimately mixed with loose fecal matter the case is more likely to be bacillary in nature, although there are many exceptions to these statements. It should not be forgotten, however, that in amoebic disease diarrhceal stools, without either blood or mucus may show numerous pathogenic amceba3, so that the foregoing observations afford only very rough indications to be confirmed or otherwise by microscopical tests.

Examination of the Stools for Amcebcv.?It will be gathered from what has already been said that the only way in which amoebic colitis can be recognised with certainty is by finding the pathogenic amoeba3 in the evacuations. In fact, the microscopical examination of the stools in tropical and sub-tropical regions in diseases of the bowels is an even more urgent necessity than that of the blood in fevers, for in the latter class of diseases four-hour temperature charts will often allow of a correct diagnosis being made with a very fair degree of certainty, while an inspection of the evacuations in the former class will rarely furnish absolutely reliable indica- tions, and may be very misleading. Fortunately

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the hunt for amoebae is a much simpler and more rapid process than an examination of the

blood for malarial parasites, and with the follow-

ing precautions reliable results can nearly always be obtained with very little trouble.

The stool should be examined as fresh as

possible, preferably within an hour or so of being passed, as putrefactive changes may rapidly destroy the activity of the amoeba?, which should be seen in an active condition to enable them to

be identified with certainty in an unstained

specimen, for large mucous cells, frequently seen

in bacillary dysentery, and which may otherwise be easily mistaken for quiescent parasites by the inex- perienced. Further, full doses of ipecacuanha or emetine should not be given before the amoebae are sought for, except in urgent cases, as the amoebae rapidly disappear under such treatment

just as malarial parasites do with quinine. A

single examination is not sufficient, as T have several times failed to find the protozoa one day, when they were numerous on the following day. In 42 per cent, of my cases the amoebae were so

numerous in the blood-stained mucus thinly spread out under a cover-glass that they were seen in nearly every field of the microscope, while in 90 per cent, they were present in sufficient numbers to permit them to be found within two or three minutes. In the few cases in which they are scanty the search is much facili- tated by mixing a small drop of one per cent, watrry solution of mythelene blue with the mucus and examining immediately, when the pus and epithelial cells will be found to have taken the

stain, while for a time the amoebae resist it, and thus stand out as clear active organisms amid their blue surroundings. I have recently dis- covered that by his method they can with a little practice be detected with a half inch lens, a

higher power being turned on to confirm the find. I have also spotted them in a fresh specimen with the ̂ inch power and a fully-lowered condenser as glistening particles, and proved their presence with a greater magnification. The advantage of this plan is that a considerable piece of mucus under a full-sized cover-glass can be completely searched in two or three minutes, and the

organisms readily discovered when quite scanty in numbers. A second piece of mucus should be examined before a negative result is recorded.

It may be objected that non-pathogenic amoeba coli may be easily confused with the active causal amoeba of dysentery and lead to an erroneous

diagnosis of amoebic colitis. Little or no harm would result from the use of emetine in such a

case, as the failure to get great improvement within two or three days would lead to the detec- tion of the mistake. In my experience it is very rare to find anything resembling the amoeba coli in dysentery cases, and if fairly numerous, or

even scanty, large active amoebic, with clear

pseudopodia, faintly marked eccentric nucleus, and containing red corpuscles are met with, the emetine treatment has always proved rapidly effective.

Results of Treatment with Ipecacuanha.

As Docker showed in 1858 sixty grain doses of powdered ipecacuanha are remarkably efficient in curing early acute cases of amoebic dysentery in

good subjects, such as the British soldiers, he had to treat in Mauritius. Unfortunately his suc- cessors have commonly been satisfied with very much smaller doses, and partly owing to this and partly to it's failure in bacillary cases the

drug temporarily lost much of its repute. More

recently it has been recognised as the specific treatment for the amoebic disease, but is still too often given in insufficient quantities to obtain

rapidly its full effects. Personally I venture to differ from Sir Patrick Manson's advice to begin with a full dose and decrease it by five grains each day, as in many severe or chronic cases met with in India this plan does not administer

enough of the drug to get a complete cure with a single course of the powder. I prefer to begin with not less than thirty grains, and in bad cases to give that amount twice in the twenty-four hours, and if improvement does not take place within

two or three days to increase the amount by ten

grains at a time until it does, the precaution of proving the case to be an amoebic one having of course been taken 011 the patient's admission. Even with such a radical treatment many of the

patients admitted to civil hospitals in India

present either too acute and fulminant a type, or too chronic and advanced disease to allow of a very large proportion of cures. The data entered in Table I will serve to illustrate these and other points. They have been arranged in three series in accordance with the ultimate

result, those who died in hospital being shown first, then those who were discharged

" other-

wise" uncured, at the request of themselves or

their friends, and lastly those discharged cured. In each set the acute cases, namely, those

in which the duration of the disease on

admission was less than one month, are entered first and are followed by the more chronic

cases. In the right hand part of the table the

number of days in hospital is shown, after

which comes the number of days under ipeca- cuanha treatment, which in the case of the cured

patients is only calculated up to the first day on

which the stools became finally free from blood

and mucus, many of them having had consider-

able amounts subsequently to this. It must be

remembered that a large proportion of the

patients are admitted in a very debilitated and

emaciated condition, and some of them practic- ally moribund.

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Nov., 1912.J DYSENTERY: ROGERS. 425

Table I.

Amcebic Dysentery Cases treated with Ipecacuanha.


5 6 7 S 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26

1 N 2 H 3 M 4 M 5 H

6 M 7 M

8 H 9 H 10 M 11 N 12 H

<= I ? i: o.2 a-n

Hem. Int. Nil Nil Kem.

3 weeks 8 days 1 month 2 months 7 days 8 days Int. 20 days Rem 15 days Nil. 8 months Nil. 3 months j Int. Chronic Nil.

18 days Nil. 6 days Nil. 10 days Int. 2 month* ; Int.

H M 30 I 7 months ; Nil. 38 ; 2 months i Nil. 35 10 days Nil. 40 | 11 days Nil. 36 15 days ! Int.

M i 40 14 d;i'ys Nil. F 4't 9 days Nil. M : 55 1 month Int.

1 month | Chronic i Int. 5 months 1J months

years 1 year 3 months

M i 20 M 21 M i 29 Yl j 32 M 25 M 15 M 36


Int. Int. Int.


3 O

?5 4,750,000 29 ; 6,1'0,000 20 j 3,2(10,010 15 2,940 000 IS ; 6,010,0011 25 i 4.690,000 20 : 5,29D,000 25 3,650.000 '2 | 2.30'i,0<'0 12 4,-150.000 31 ! 4.340.000 15 j 5 500,000 11 3,220.000 27 i 3.960.000 11 4.700.000 7 i 4.870,000 7 4.090,0110

25 ! 5 580,' On 11 5.730.000 7 j 5.800.000

: 4 230.000

7 ! 4.270,000 29 3.440.000

3.840,000 2.730 000 3,860,000 3.280.000 2 610.000 4,330.00'> 3,280,000


"S O t.

8.750 I 11.000 1

30,2." 0 35,750 13,000 31,000 26,(100 4,250

14,('00 8,000 11.750 32.500 8.500

25.000 35.750 33,750 12,5"0 37,v50 13.250 7,500 11.750 12,000 15,500 9,750 7.25"

21,500 1(1.00(1 12.500 13.000 14,750

-541 ?5 .2 -1(6 -82 -?4ol -151 ?2(?3 ?859

164 ?5 6 -347 ?164 -379 ?118 ?124 ?144 -327 -150 ?433 -507 ?360 ?356 -222 -394 -.376 -181 -328 -209 -333 -239

72-0 86 4 75 6 76-0 71 6 78 8 81-6

724 82-4 81 6 58-4 79 6

87 6

85-0 82-4

74-4 72-8 74-4

53-6 44-8 81-6

_ .g


120 '/(V) 90 410 25(1 160 180 90

1,000 350 30 30 180 420 480 360 300 180 460 360 270 220 400

1,320 140 370



Otherwise better. >, no better. >, very bad. ,, no better.

Cured. very bad.

Table II.

Anicebic dysentery cases treated with emetine salts hypodermically.

12 days 1 day

30 '

7 months

M. j 30 ! 2

F. 40 ! 5 days F. 38 ! 1 day M. j |ft 15 days M. 38 14 ?

F. ! 20 ; 6 1Y1. 52 ^ 20 M. 17 10 F. 29 ! 3 ?

M. 24 | 1 day M. 32 I 15 days M. i 30 ; 5 M. M. F. M. M. M. M. M. 24 M. 22 M. ! 36

30 1A months 25 i 6" ?

52 I 1 month 32 3 months 20 : 4 32 j 1 year 20 6 months

F. | 34

4 years 1^ months 14 ?

Int. Int. Item.


Int. Nil Int. Int. Int. Nil Nil Nil Rem. Nil Int. Int. Nil 4

Nil Nil Nil Nil Nil Nil Nil Nil Nil

5.960.000 5,660,000


5,340.000 5.320,000 3,340.000 5.560,001) 1,9:0,000 5.240.000 3,890,000

5,560,000 5,550,0(0 2,490 000 6,270,000 4,930,000 3.600.000 5,140.0)0 5 670.000 4,030,000 5.210,000 4.010.000 3.460,000 3,040.000 3,550,000

22,250 I 1?2^8

61,750 | 1- 92


1J.000 14,000 10,500 28,000 2.750 12,250 10,250

32! 500 13.750 5.500

30.500 12.000 26,250 12.2.r0 21.250 13.750 13.500 7,500

11,000 9.500 8,250


1?381 1-380 1?318 1-198 1?72' 1 428 1-380

1?171 1-404 1-4S3 1-206 1-411 1-137 1?348 1?261 1-366 1-385 1-535 1-314 1-320 1-430

884 84-8



70-4 66 0

85-2 78-4

89-8 79 6 760 90 8

88 8 86 8 68 8 90-0 56 6 73-2 67 6 72*4 80-4



Died gangrene.

,, heat- stroke.

,, cancrum- oris.


Races.?M. = Mahomedan. H. = Hindu. E.=European. N.=Native. J. Japanese. C. - Chinese.

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Deaths.?No less than 11 out of the 30 cases

died in hospital, while six were discharged otherwise, two of whom were very bad and nearly certain to die, and one only was better. Of the

eleven fatal cases four died within less than three days of admission, and were hopeless when brought. As the mortality in any given series of cases will largely depend on the accidental factor of the proportion of such moribund

patients, they should rightly be excluded in

comparing the results of different forms of

treatment, for no method can be expected to avail once gangrene of the large bowel and

peritonitis have set in. After deducting these four cases in three of which death took place before ipecacuanha was begun, and adding the two removed in a dying condition after failure of treatment of more than three days duration, we have nine deaths among twenty-six cases, or

34'6 per cent, a very high figure, and one which clearly shows the difficulty of getting ipecacuanha into the system quickly enough by oral adminis- tration to save many of these grave cases. On the other hand, thirteen patients were cured out

of the twenty-six non-moribund admissions, while if we include the patient who left much

improved but not quite cured, this would give a

percentage of good results of 53'85 per cent., leaving three cases discharged at their own request with no change in their condition after only a

short time in hospital.

Results of the Treatment with Soluble

Emetine Salts.

Table II shows twenty-six consecutive cases

treated in the same ward by my new plan of

administering soluble salts of emetine hypoder- mically, or in a few of them by the mouth. They are classified in the same way as those in

Table I so as to be readily comparable. The first two patients were admitted in a hopeless condi- tion and died under three days, gangrene of the ctecum being found in the first case post unortem, although an extraordinary improvement in the stools had taken place within forty-eight hours and no amcebte could be found remaining in the bowel wall after death, having apparently all been killed by the 3| grains of emetine

hydrochloride he had received during life. In the cases of the next two patients the dysenteric symptoms cleared up completely within two days under emetine, but one European female died of heat-stroke some days after being convalescent of her dysentery, and the other, a very anaemic and dropsical subject, developed cancrum oris and died ten days after his

dysentery was cured. These two cases, then, are

both remarkable examples of the rapid cure of

dysentery by emetine in subjects who were so

debilitated as to succumb shortly after to other diseases, and cannot fairly be treated as failures

of the emetine treatment. All the remaining twenty-two cases have recovered: a remarkable

testimony to the value of the new treatment, as

they included a number of very severe and advanced cases, while no less than four of them showed the very high degree of leucocytosis, which has already been pointed out as being of most fatal import under the old methods of treatment. The only failures, therefore, have been in the two patients who were moribund on admission, while no case has been discharged " otherwise" at his own request while still uncured. As the emetine series also include a

fair number of chronic cases with dysentery of from one month to one year's duration, they are

good samples of all types and stages of amoebic colitis.

The Duration of the Treatment and

Doses required.

If we take the cases in which a cure was

effected as judged by the final disappearance of blood and mucus from the stools we find that the duration of the treatment with ipecacuanha varied between 5 and 44 days, and averaged 11 '4 days, during which periods from 140 to 1,320 grains of the drug were taken, the average quan- tity being 40G grains. On the other hand, with the emetine treatment the stools finally became healthy in from 1 to 4 days, the average time

being 2*3 days, while the quantity of emetine taken up to that time averaged 2 grains, and the total amount given while the patient remained in hospital averaged 5'03 grains. The stay in

hospital of the ipecacuanha cases varied from 7 to 60 days, the average being 16*4 days, while under emetine it lasted from 5 to 11 days and averaged 7*2 days, which included one day during which they were kept under observation before the specific treatment was begun, unless the con- dition was an urgent one. I should prefer to

keep the patients in longer, but when the dysen- teric symptoms regularly disappear completely in two to four days and solid diet then begun causes no relapse, it is very difficult to persuade them to stay. I have got a number of them to

return to see me after an interval, and so far no true relapse of amoebic disease has come to my notice. One patient of the above series did return and die of dysenter}?', but after death the upper part of the large bowel showed extensive

scars of healed amoebic ulcers, while the lower

half revealed an acute bacillary dysentery from which Shiga bacilli were cultivated. In a second similar case in another ward pneumonia was found

post mortem, together with paralytic dilatation

of the caecum and ascending colon, due to the extensive destruction of the muscular as well as

the mucous coats, but only scars and no recent

ulcers were present. Yet this man had only re-

ceived three grains of emetine five weeks before

Page 7: Sixty Cases of Amœbic Dysentery Illustrating the Treatment ... · Nov., 1912.] DYSENTERY: ROGERS 421 ?riginal ^rliclfs. SIXTY CASES OF AMCEBTC DYSENTERY ILLUSTRATING THE TREATMENT


his death, and he also had a small encysted liver

abscess, free from both bacteria and amoeba:1, and evidently beginning to dry up. These two cases

of apparent relapse only proved that the former amoebic disease had been completely eradicated, and indicate that about three grains of emetine had really completely sterilised all the tissues of the body as far as the amoeba is concerned. If further experience confirms these results the emetine salts will constitute the most remarkable

therapeutic remedy yet discovered.

The Intravenous Injection of Emetine.

The occasional failure of hypodermic injections of emetine salts in the case of very acute slouch- ing amoebic dysentery dying within less than three daj^s of admission led me to consider the

possibility of giving the salt intravenously. In a recent very severe case with great thickening of the cEECiim anol local peritonitis, I oave a dose of half a grain of the hydrochloride dissolved in five c.c. of normal saline injected very slowly into an arm vein, watching the pulse carefully, and found it did not depress it at in the least. In the evening I gave two-thirds of a grain in the same way, and on the following day a full grain, in addition to subcutaneous injections, and at the time of writing the local symptoms have much improved, the passage of sloughs has ceased, while the amoebre disappeared from thp d-nnk within

twenty-four hours of the a?d there is fair hope of his recovery. Whatever the ultimate result may be, it is at least clear that very full doses of the drug may safely be injected intravenously, which is clearly the best plan in these desperate cases. There was no sickness or

nausea after the last two large intravenous doses, but bilious vomiting both before and after the hist one, so it is clear that the vomiting after ipecacuanha by the mouth is due to a local action on the stomach.

References. 1. British Medical Journal, June 22nd. 1912. 2. British Medical Journal. August 24th, 1912. 3 Scientific Memoirs, No. 47. 4. Transactions of the Bombay Medical Congress. /