Chapter 17 of 61 · 6199 words · ~31 min read

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.

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.