other dysentery cases was approximately 12. More particularly in Gallipoli combined infections were not uncommon and there were cases suffering from dysentery and enterica at the same time.
During 1920, of 6,193 returned troops claiming State aid for disability from war dysenteries, 446 were still harbouring the E. histolytica and over 80 % of these were intermittently or constantly passing blood or mucus ; two acquired a liver abscess when in England as a complication: eight were still infected with the B. dys. Shiga and four with B. dys. Flexner-Hiss; one case had mixed amoebic and bacillary (Shiga) infection, and three mixed amoebic and spirochaetic, and six spirochaetic dysentery.
By reason of the variety of the causal organisms, the clinical symptoms and pathological characters to which each gives rise and the specific treatment directed against it, each type of dysen- tery had best be considered separately, and the commoner types, amoebic and bacillary, discussed in greater detail.
Amoebic Dysentery (also called Amoebiasis, Loeschfasis or Tropical Dysentery, the latter because of its early endemicity and greater incidence there). The causal organism, E. histolytica (Loesch 1871), a species of the genus Entamoeba, affects man alone in nature, though the dog and cat and recently the guinea-pig have been infected experimentally. The E. histolytica in its life-cycle in man passes through three stages a large vegetative stage when living within the tissues, giving rise to ulceration and passage of blood and mucus ; a pre-cystic or minuta stage found in convalescents and in carriers when the amoebae are much smaller, live on the mucous membrane within the bowel, but which may pass through the membrane and assume the larger vegetative form, with ulceration and its symptoms following; and a cystic stage. The amoebae increase in numbers by division of the parent into two, but it is only the pre-cystic or minuta stage in which many of the amoebae contract into a smaller rounded or ovoid form, develop a firm outer wall and are trans- formed into cysts with the characteristic one to four nuclei and con- taining chromatoid rods which possibly act as food stores. Since it is only by swallowing these cysts that man is infected, the continu- ance of the entamoeba in nature is thus provided for. These cysts do not resist drying, but retain their vitality for two weeks if kept moist in the faeces or in water. They can therefore be transmitted by direct contamination with faeces through handling soiled linen, by flies carrying them on to food, by soil or by drinking contami- nated water; and prophylaxis must be directed accordingly.
Clinically the disease is characterized, as are all protozoal infec- tions, by its chronicity with tendency to recrudescence of symptoms. The onset is insidious, the sufferer first noticing a feeling of debility and lassitude with an increase of stools, soft in character, for several days. These may clear up and be the only signs noticed or may light up again and assume true dysenteric characters months later. Most often the initial stage is followed on by an acute exacerbation of symptoms, dependent in their degree upon the extent of the ul- ceration in the large bowel, the most markedly affected sites being the caecum and flexures. Stools become still more frequent, up to 40 or 50 in 24 hours, and the ulceration gives rise to abdominal pain and, if at the rectum, to severe tenesmus. The patient takes to his bed exhausted. In uncomplicated cases there is but slight rise of temperature or other symptoms of toxaemia as the entamoeba pro- duces no toxin. The entamoeba gains entrance to the body by the swallowing of its cysts, which pass through the stomach unchanged. In the small intestines they germinate and young amoebulae are set free in the lumen of the intestine. They increase in size, multiply by a process of division, and by means of their lytic or dissolving power penetrate through the mucous membrane lining the large bowel, rarely the appendix save at its base, into the sub- mucous layer, where they continue to proliferate, destroy the tissue, including the blood-vessels, thus leading to the haemorrhage that accompanies the mucus produced by the irritation of the membrane, and impede the circulation of blood and lymph at the site. A typical flask-shaped ulcer is formed, with roughened undermined edges at the orifice. When ulcers are situated approximately they are fre- quently joined by submucous tunnels, and, the ulcers being me- chanically produced, there is little accompanying inflammatory reaction. Occasionally super-added infection with other bowel organisms supervenes and gangrene may follow, or the amoebae may penetrate through the outer muscular walls of the large bowel, giving rise to perforation and accompanying peritonitis, or, by penetrating a blood-vessel, they may be carried off in the blood stream and give rise to an abscess in the liver, to which the blood first takes them, or, as most exceptionally happens, an abscess in the brain or elsewhere. Healing is brought about by the develop- ment of fibrous tissue at the sites of the ulcers, and this contracts and leads to a thickening of the walls and constriction of the lumen which, if extensive, produces subsequent chronic constipation; or, what is rare, to stenosis and blockage. Diagnosis is quickly made by examination of the stools. In the acute condition they may consist entirely of blood and mucus or contain also a little faecal matter. The mucus is stained a brownish colour by degenerated blood cells and the blood is usually in the form of clots, not evenly mixed through it. Microscopically the E. histolytica is readily found and is dis- tinguished by ils rapid movement, ill-defined nucleus and greenish-
tinted ectoplasm and ingested red cells. White blood cells apart from a relative increase of eosinophils are not seen in great numbers. Charcot-leyden crystals, as yet only seen in dysentery of the amoebic type, may be found.
The acute symptoms readily subside under appropriate treatment. The patient should be put to bed. The specific treatment is ipe- cacuanha or an alkaloid extracted from it, emetine. Combined hypo- dermic injections of emetine hydrochloride with oral administration of ipecacuanha (Brazilian), to attack the amoebae from within and without, have given striking results in allaying symptoms. More recently emetine alone or in combination as bismuth-emetine-iodine in a'salol capsuled pill has been widely employed and good results are claimed, especially in the treatment of chronic cases. The toxic action of emetine on the heart must be watched. Added to the specific treatment inacute cases there is the general and symptomatic, which should include a free flushing of the bowel by a dose of castor oil with tinct. opii. added; later followed by magnesium (or sodium) sulphate in hourly or two-hourly half or drachm doses for 12 or 2A hours. Morphia may be necessary to relieve the abdominal pain and straining. The diet must be light and easily assimilated. Milk and raw foods should be withheld.
The symptoms subside in one to three weeks and no further trouble may supervene. However, the patient not infrequently is left with symptoms, generally slight, from cicatrization of the bowel ; or, from persistence of the entamoeba, becomes a convalescent carrier as distinguished from a contact carrier, one who has never developed acute symptoms. The treatment of these carriers is one of considerable importance not only for the individual, who may re- develop acute symptoms or a liver abscess, but for the community, since these carriers pass in their stools the cysts of the entamoeba which can infect others. Treatment apart from symptomatic is directed to eliminate the amoeba in chronic cases and consists in giving orally ipecacuanha or emetine alone or combined with other drugs as a pill, capsule or paste in courses over a number of days. Emetine hydrochloride subcutaneously, or neosalvarsan intraven- ously, have been employed to supplement oral treatment. At the same time the large bowel is washed out by enemata per rectum, the use of appendicostomy wounds not having given sufficiently encouraging results, with solutions of quinine, tannin or, as recom- mended by the French, of neosalvarsan. Indiscretions in diet should at all times be avoided and it appears advisable for the carrier to reside in a temperate region. Amoebic hepatitis and a small abscess of the liver are cured by injections of emetine hydro- chloride or neosalvarsan, but a large abscess needs surgical inter- vention.
Bacillary Dysentery. While sharing with the amoebic the clinical dysenteric syndrome above described, it differs therefrom in the shortness of the inoculation period, generally 24 to 72 hours, by its sudden acute onset with elevation of temperature, which may per- sist several days or more, and other symptoms of toxaemia ; extreme contagiousness; seasonal incidence (midsummer and autumn); epidemic character and predilection for temperate regions; higher death-rate and in the complications that may follow infection with Bacillus dys. Shiga, namely: arthritis, conjunctivitis, muscular par- alysis and myocarditis. Clinically it may assume forms varying in symptomology from mild to severe, and occasionally be hypertoxic, typhoidal or ulcero-gangrenous in character. Outbreaks of dysen- tery in asylums, prisons, concentration camps and ships are gener- ally bacillary in type. In tropical regions the amoebic type also occurs, but in terrperate regions this latter form is practically lim- ited to sporadic cases.
The bacillary dysentery group comprises species of bacilli genet- ically related: I. The B. dys. Shiga (Chantmesse and Widal 1888, Shiga 1898, Kruse 1900), a well-defined homogeneous species, known as the true dysentery bacillus since it alone contains endo- toxins which are pathogenic to man and experimental animals.
2. B. dys. Schmilz (Schmitz 1916, Andrewes 1918, Broughton-Al- cock 1918), another homologous species and one which contains endotoxins acting severely on rabbits but less pathogenic to man.
3. B. dys. Flexner-Hiss, a very mildly toxic group of bacilli charac- terized by their power to ferment mannite, produce indol from pep- tone and containing many species as recently distinguished by the agglutination and absorption reactions. 4. A further group which embraces bacilli characterized by specific agglutination and ab- sorption properties and power to ferment certain sugars, e.g. Bacil- lus of Strong, Ca'stellani, Gay, d'Herelle and others, each capable of producing a mild clinically dysenteric syndrome in man.
Clinical symptoms vary, as does the degree of the intestinal le- sions and the toxicityof the causal bacillus. Infections with B. dys. Shiga are characteristically the most severe. The ulcerative lesions are not confined to the large bowel but extend one to two feet into the small intestine. Recent researches have proved that 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 inflammation with coagulation of lymph, thrombosis of vessels and necrosis of the submucous layer and superimposed mucous membrane. An exudative fibrinous diphtheritic-like membrane forms on the bowel wall and separates off, leaving superficial ulcers with raised red oedematous edges. These may
