BACILLARY DYSENTERY While sharing with the amoebic the clinical dysenteric syndrome above described, it differs therefrom by the shortness of the incubation period, generally 24 to 72 hours, its acute onset with fever that may persist several days or more, and other symptoms of toxaemia; extreme contagiousness; seasonal prevalence (mid summer and autumn) ; epidemic character and incidence in tem perate regions, where the amoebic type is practically limited to sporadic cases ; higher death-rate. It also differs in the complica tions that may follow infection more especially with B. dys. Shiga, namely : arthritis, fibrositis, conjunctivitis, muscular paralysis and myocarditis. Clinically it may vary from mild to severe, and occasionally be hypertoxic, typhoidal or ulcero-gangrenous. Out breaks of dysentery in asylums, prisons, concentration camps and ships are generally bacillary in type.
The bacillary dysentery group comprises : I. B. dys. Shiga, containing endotoxins pathogenic to man and experimental animals.
2. B. dys. Schmitz, containing endotoxins acting severely on rabbits but much less pathogenic to man. Its incidence is rare.
3. B. dys. Flexner-Hiss, heterogeneous group fermenting man nite and producing indol from peptone. It contains many species recently distinguished by agglutination and absorption reactions.
4. A further group rarely found and having specific agglutina tion and absorption properties and power to ferment certain sugars; e.g., Bacillus of Strong, Castellani, Gay, d'Herelle and others, each capable of producing a mild, clinically dysenteric syndrome in man.
Clinical symptoms vary, as do the degree of the intestinal lesions and the toxicity of the causal bacillus. Infec tions with B. dys. Shiga are the most severe. The ulcerative lesions are not confined to the large bowel but extend one to two feet up into the small intestine. The bacilli pass through the stomach, multiply in the small intestine and produce at least two toxins which are absorbed into the blood, one acting on the nervous system and the other excreted into the large bowel, causing in flammation with coagulation of lymph, thrombosis of vessels and necrosis of the submucous layer and superimposed mucous mem brane. The bacilli proliferate on the bowel wall, diphtheritic-like membrane, forms and separates off, leaving superficial ulcers with raised, red, oedematous edges. These may deepen by continued microbic action and even perforate, leading to peritonitis, or gan grene may set up in the damaged necrosed tissue, and in either case death follows unless surgical intervention is early. Repair proceeds along the same lines as in amoebic cases, but, the ulcers being generally more superficial, the permanent damage is not so great.
The stools have a characteristic microscopic appearance, as numerous pus and epithelial cells and large, macrophage cells are present in the mucus. Microscopically the stool most often con sists of mucus, like cloudy-grey jelly streaked or stained by bright red blood, or the mucus may be bile-stained in a diarrhoea-like stool, or, in very severe cases, there are shreds of necrosed mucosa.
In bacillary dysentery the patient is much more ill than in amoebic, and treatment is directed to neutralizing the toxins which act strongly on the heart and other vital organs, and elimination of the micro-organism from the intestines. Infections with B. dys. Shiga are outstandingly the most severe, and it is the anti-Shiga serum which is the most efficacious. It has also been used in severe cases due to B. dys. Flexner-Hiss with some success. A serum prepared by inoculating strains of both these groups of micro-organisms has been extensively used in cases of either in fection. The injections should be given as early in the disease as possible and in large doses, e.g., 6oc.c., 4oc.c., 20c.c., on successive days in a severe case; saline aperients until the stools become faecal should be given frequently. Heart stimulants may be needed. Diet as above. Thereby amelioration is rapid, sequelae rare, the bacillus early eliminated and convalescent carriers much more rare than after amoebic dysentery, and the bowel wall is not so often permanently damaged. After an attack careful diet ing is needed.
The general prophylactic measures are the same as those against infections with E. histolytica. Dependent on several factors, bacillary is more contagious than amoebic dysen tery. Inoculations with a vaccine of B. dys. Shiga were made in epidemic areas in the World War. Its contained toxins give rise to acute local reactions unless modified prior to inoculation by special methods. These series of inoculations made by various workers gave encouraging results. Vaccine-therapy employed to rid the convalescent carrier of B. dys. Shiga has not been suc cessful. In striking contrast with B. dys. Shiga the killed and un treated emulsions of the B. dys. Flexner-Hiss group give rise to no reaction, even in high doses.
This is due to Spirochaeta eury gyrata (Le Dantec 1900, Werner 1910). Evidence is increasing that this spirochaeta is capable of giving rise to an acute con dition with passage of blood and mucus or, more frequently, of maintaining a chronic or intermittent mild form of dysentery. It is never found free in faecal matter but only in mucous shreds excreted, in the detached crypts and occasionally within the lining epithelial cells of the mucous membrane. Many observers consider that it proliferates and gains a footing on a bowel dam aged by the entamoeba. It is a rare form of dysentery but has a wide endemic distribution in tropical and subtropical countries. Treatment of the very rare acute condition is by frequent saline aperients. In its chronic form best results have followed enemata containing oil of eucalyptus, or by calomel followed by a saline aperient or by Slovarsol.
The chief helminths which give rise to dysentery are the bilharzia worms, Schistosoma mansoni, in Africa, South America, West Indies and Schistosoma japonicum in the Far East. Another trematode which may cause dysenteric symptoms is Fasciolopsis buski, found in China, Assam and India. Thymol or beta-naphthol are used in treatment of this latter.
Infections with hookworm (see HOOKWORM), Ankylostoma duodenale, are widely distributed in tropical lands and extend to subtropical regions. In such infections blood and mucus are some times passed in large quantities and these cases may be mistaken for true dysentery.
Ciliar dysentery due to Balantidium coli is a form of dysentery that has been found in Europe, Japan and the Philippine Is., but rarely elsewhere. An investigation of a number of habitants of Utuado, Porto Rico, led to the detection of many carriers with out symptoms. The ciliar form of dysentery is rarely seen out side endemic regions.
A certain number of cases of dysentery become convalescent carriers, harbouring the parasite in the intestine with or without obvious activities on the host. The contact or healthy carrier may have no signs past or present. Neither type of carrier is common in the bacillary form, but both are not very uncommon in amoebic dysentery.
Dysentery is markedly more frequent in hotter countries and tends to arise in subjects of lowered body resistance. The disease appears in its most devastating epidemic form in armies, fugitives, refugees and pioneers, and vanishes before the comfort and prosperity of a well-fed and settled people, especially when living under favoured climatic and sanitary con ditions. During the World War, its incidence was great in all armies, especially those fighting in tropical countries where the conditions favoured it, and in parts of eastern Europe where san itary control was not scrupulously exercised. On the Gallipoli Peninsula, nearly every soldier who landed suffered from dysentery or diarrhoea, and few escaped the former disease. Severity of the climatic conditions, difficulties of obtaining adequate food and sterilized water, fly pests, fatigue, hastily improvised resting places and sanitary arrangements, prolonged periods in trenches, were the important factors conducive to infection. The com paratively small death roll was due to the knowledge that dysen tery may be due to diverse organisms, each having a specific line of treatment. Most deaths were due to B. dys. Shiga infections.
In most temperate zones the incidence of dysen tery is practically limited to occasional small outbreaks of the bacillary form, to sporadic cases of this or of the amoebic form due to infection from a patient or carrier, and to cases that have been infected in tropical or subtropical lands or under war and such like conditions of life; but in hot climates these forms of dysentery normally claim a very high incidence and death rate, approximating to that of malaria.
To show the benefit arising from applied research it suffices to mention that amoebic dysentery, once so prevalent in the Panama Canal Zone, is now uncommon there, while in the Malay States, where bacillary dysentery is the more frequent form, there has been an increasing fall in the number of cases and death rate.
BIBLIOGRAPHY.-Medical Research Council, Special Reports Nos. 15 Bibliography.-Medical Research Council, Special Reports Nos. 15 and 40 (1918 and 1919) ; Ministry of Health, Report on Public Health and Medical Subjects, No. 14 (1920) ; L. P. Phillips, Amoebiasis and the Dysenteries (1915) ; H. Vincent and L. M. Muratet, Les dysen teries; le cholera asiatique; le typhus exanthematique (1917) ; A. Cas tellani and A. J. Chalmers, Manual of Trop. Medicine, p. 1824 (3rd ed. 1919) ; Sir Leonard Rogers, Bowel Diseases in the Tropics (1921) ; W. Bryan and R. G. Archibald, The Practice of Medicine in the Tropics, vol. ii., pp. 'Jos, 1,342 (1922).
