Author:
Dr B S Suvarna
B.A, D.I.Hom[Lond.], M.I.H, PhD, PGDPC (Psychotherapy & Counselling, USA)
HOMOEO PHYSICIAN
MAMTHA HOMOEO CLINIC
Jeevan Shanthi
Karnataka State, India
Dysentery is inflammation of the intestine, often resulting innecrosis and ulceration of the mucosa due to certain specific bacilli, protozoa or helminthes and characterized by pain, rectal tenesmus, intense diarrhoea with the frequent passage of small amounts of mucus and blood and symptoms of toxemia.
In general any irritation of colons as with the bacterial infection in enteritis leads to large secretions of water and electrolytes as also the mucus by the mucus membrane. This acts to dilute the irritating factors and to cause rapid movement of faces towards the anus, resulting in diarrhea and thereby an early recovery even through there is loss of water and electrolytes. As such dysentery is a physiological act of the organism to get rid of the noxious micro organisms from the colons and restore health in the living being.
Principal types:
Bacillary: Acute and Chronic Bacillary dysentery
Shigellosis: An infectious disease which primarily involves the colon caused by a species of the genus shiqella dysenteriae.
Sonne: One of the commonest forms of intestinal infection caused by shiqella sonnei.
Protozoal: Amebic [amebic colitis]
An infectious disease due to infestation of the colon with entamoeba histolytica.
Balantidial:
That due to infestation by balantisium coli characterized by diarrhea and dysentery also called balantidiasis.
Malignant tertian malaria: caused by Plasmodium falciparum.
Helminthic: Schistosomal: a type caused by schistosoma mansoni.
Non Specific: Chronic ulcerative colitis: An idiopathic, non specific, inflammatory disease of the colon, characterized by friability and ulceration of the mucosa. It is generally considered to be a psychophysiologic, autonomic and visceral disorder.
Clinical picture and treatment of these disorders are being taken up below.
SHIGELLOSIS – Acute bacillary dysentery
Self limited infection of the intestinal tract. Characterized by diarrhea, fever and abdominal pain, frequently called bacillary dysentery. Shigellosis is world wide in distribution. The convalescent or asymptomatic carrier is the only reservoir. The spread from person to person takes place when organisms on hands and other objects, contaminated with infected feces are ingested.
Eg: The contaminated food by careless handling, contaminated drinking water, swimming in contaminated rivers and pools. Flies that come in contact with human faces serve as important carries in the transmission of the disease. Poor sanitation, low standards of personal hygiene, crowded conditions and a high proportion of children in a population favour spread of the infection.
After ingestion the organisms first adhere to the mucosal surface and then penetrate the epithelial cell living within 12th ingested organisms proliferate in the small intestine to very high concentrations. This phase of the infection is associated with fever and watery diarrhea.
Later on penetration of the mucosal surface, they multiply within epithelial cells, cause shallow ulcer that bleed readily.
Clinical Picture:
The initial phase of infection beginning after an incubation period of 24th causes fever, infrequent, voluminous, watery stools and colicy abdominal pain. After 24-48 hours, the frequency of bowel movements increases 5 to 50 times daily, but the volume of stools and their water content decreases and mucus and blood appear in stools. Fever lowers down, but greater urgency for stool, tenesmus and painful defecation set in.
Nausea, vomiting, headache, muscular pains, respiratory symptoms and in children, convulsions may be associated with the complaints. Dehydration and circulatory collapse may take place as a result of severe diarrhoea and high fever. Lower abdominal tenderness and hyperactive bowel sounds are common.
Sigmoidoscopy reveals difuse mucosal inflammation with multiple ulcerations. Microscopic stool examination shows shreds of mucus and erythrocytes, stools culture usually are positive. Shigellosis is a self limited disease and patients become afebrile in about 4 days, most of the patient recover within a week.
Chronic bacillary dysentry:
Follows the acute attack and present itself with frequent defecation, tenesmus, muco-pus or blood in stools. During exacerbations, abdominal colic and fever may recur, emaciation, weakness, anemia and often oedema of limbs follow, descending colon becomes thickened, spastic and palpable.
Medicines: [only their indications in dysentry given]
Merc. cor: Incessant tenesmus not relieved by stool. Stools bloody, slimy with cutting pains and shreds of mucus membrane.
Mer. sol: Painful, greenish, bloody and slimy stools along with nausea, abdominal colic and chillness and an incomplete sensation persisting after stools.
Nux. Vomica: Constant uneasiness in rectum, stools relieving pains for a time.
Colchicum: Ineffectual pressing, feels feces in rectum but cannot expel them, painful, scanty, transparent, jelly like mucus.
Colocynthis: Abdominal colic bending double. Jelly like stools, renewed each time by the least food or drink.
Gambogia: Tenesmus after stools with burning at anus.
Collinsonia: Stools with tenesmus, sensation of sharp sticks in rectum.
Trombidium: Brown, thin, bloody stools with tenesmus.
Acetic acid: Anemia and oedema of limbs.
Achyranthes: Yellow watery stools mixed with flakes of mucus.
Aegle marmelos: Obstinate chronic dysentery.
Alstonia constricta: Violent purging and cramp in bowels, boldly stool.
Terminalia chebula: Small stool with mucus.
AMOEBIASIS:
It is an infection of the large intestine produced by entamoeba histolytica. It may be an a symptomatic state in carriers but diseases ranging from chronic, mild diarrhea to fulminant dysentery can occur. The commonest complication is hepatic abscess that may rupture into peritoneum, pleura, lung or pericardium.
E. histolytica exists in two forms:
The motile trophozoites are parasitic in nature requiring the presence of bacteria or tissue substance as nutrition in the lumen or wall of the colon where they dwell and multiply. In diarrhea, trophozoites are passed on unchanged in the liquid stools. In dysentery, however these are larger in size, often containing ingested erythrocytes.
In this absence of diarrhoea the trophozoites usually incest before leaving the gut and the cysts are highly resistant to environmental changes. Chlorine concentrations found in water purification systems and gastric acid and thus are primarily responsible for the transmission of the disease.
Infection is world wide is low. Humans are the principal host and reservoir of E.histolytica. symptomatic amebiasis is unusual below the age of 10 years in temperate climates and both intestinal and hepatic lesions predominate in adult males, because trophozoites die rapidly after leaving the intestine, asympotomatic cyst passers are the source of new infections. The cyst are usually spread directly from person to person under conditions of poor personal hygiene. Food and water borne transmission may also take the epidemic form.
After ingestion cysts undergo further nuclear division. In the small intestine, the cyst wall disintegrates and trophozoites are released. The immature amebas are carried to the large intestine, where they live in the lumen of the gut as commensals feeding on bacteria and debris.
In susceptible hosts or with virulent infecting organism, ameba may invade the mucosa causing ulcerations that are sufficient to produce symptoms. High iron and carbohydrate intake corticosteroids and pregnancy all render the host more susceptible. Amoebic ulceration of the intestinal wall is characteristic. There is little acute inflammatory response and in contrast to the picture in bacillary dysentery. The mucosa between ulcers is normal, the sites of involvement in order of frequency are cecum and ascending colon, rectum, sigmoid, appendix and terminal ileum. Amebas can enter the portal circulation and lodge in venules, liquefaction necrosis of liver tissue leads to the formation of an abscess cavity.
Clinical picture:
- Asymptomatic Cyst Passer: E.histolytica in these persons lives as a commensal in the bowel lumen. Besides the invasion of the mucosa in person living in temperate climates is much less. Even so the treatment of cyst passers is very essential.
- Symptomatic intestinal amoebiasis: In some patients there is intermittent diarrhea consisting of one to four foul smelling loose or watery stools daily at times containing mucus or blood, loose stools alternate with periods of relative normality and may persist for months or years. Flatulence and abnormal cramping are frequent. Liver is enlarged and tender, sight pain is felt by the patient when cecum and ascending colon are palpated. Sigmoidoscopy reveals typical bottle shaped ulcerative lesions with areas of normal mucosa interspersed. The diagnosis depends on finding the organism in the feces or in ulcers.
Fulminating attacks of amoebic dysentery are less common. This may occur in debilitating individuals precipitated by pregnancy or corticosteroids with abrupt high fever[104-105F], severe abdominal crumps and profuse bloody diarrhea with tenesmus. There is diffuse abdominal tenderness, hepatomegaly and extensive rectosigmoid ulceration visualized on sigmoidoscopy. Numerous trophozoite in stool and ulcers.
Repeated severe attacks of amoebic dysentery will lead to extensive destruction of the colonic mucosa/submucosa, massive hemorrhage or perforation of the bowel wall with resultant peritonitis. Differential diagnosis to be made with shgellosis, salmonellosis, ulcerative colitis and schistosomiasis. The invasive bacterial infections are more acute, severe and self limited than amoebic dysentery. Stool samples in these infections contain large number of polymorphonuclear leukocytes and not so in amoebic dysentery.
Balantidial dysentery:
It occurs in people who handle pigs. There are frequent muco-sanguinous stools, anaemia, ulcers from in colon and may perforate. Clinically indistinguishable from amoebic ulceration diagnosis to be by confirmation of balantidial colicysts in stool samples.
Prevention:
Avoidance of contaminated food and water, scalding of vegetables and the use of iodine releasins tablets in drinking water. Improvement in general sanitation and the detection of cyst passers and their removal from food handling duties.
Treatment:
Consists of relief of symptoms, replacement of fluid, electrolyte and blood losses, low residual diet and eradication of the organism by appropriate medicines as described below:
- Arsenicum album: Liver enlarged and painful, stool small, dark, bloody and offensive with much prostration.
- Carbo vegetabilis: Abdomen greatly distended passing wind flatulent colic, simplest food disagrees.
- Cornus circinate: Loose, windy, dark stool, immediately after dinner.
- Colocynthis: Abdominal distention, cramps, bending double. Intestines feel as if bruised.
- Elaterium: Profuse black, fetid stools with pain in umbilicus.
- Podophyllum: Morning painless diarrhea of long standing, constipation alternating with diarrhea.
- Trombidium: Urgent loose stools on raising.
- Phosphorus: Very fetid stools and flatus, painless, copious and debilitating diarrhea.
- Natrum sulphuricum: Liver enlarged and painful, large stools flatulency.
- Nux vomica: Alternate constipation and diarrhea.
- Gallicum acidum: Copious stools, anus feels constructed chronic mucus discharge per rectum.
Sachistosomal Dysentry:
In the early stages there are loose motions containing mucus and blood, later there are often solid stools coated with mucus containing the ova of smansoni. Tenesmus, loss of weight and secondary anemia may follow. There may be leukocytosis and usually eosinophilia.
Medicines: Colch, Merc-c, Alts, Coll, Chin.
Malarial Dysentery:
The plasmodium falciparum variety may manifest itself by severe diarrhea with blood and mucus, similar to bacillary dysentery, diagnosis by finding parasites in blood smears.
Medicines: Alst, Cina, Rhus tox.
Chronic Ulcerative Colitis:
Is usually insidious in onset but may follow the acute variety. It occurs most commonly in adults and has a tendency to relapses.
Clinical Picture: Initially,
- Diarrhea, watery stools containing bright red bold and mucus.
- Lower abdominal flatulence, colic before stools.
- Tenesmus, later with worsening of disease.
- 20-30 stools a day, blood and muco-pus with each stools leading to
- Extereme exhaustion, dehydration, marked weight loss and anaemia.
- Remittent temperature (103-104)
It is psychogenic in origin and occurs in hypersensitive subjects with its onset and relapses frequency following emotional trauma.
Treatment:
Is necessarily prolonged complete rest during the acuteness of complaints is very necessary. The diet must be ample and varied a high calorie, high protein, low vegetable residue diet should be given. The patient is to be treated with intercurrent constitutional remedies in the lucid phases to check further attacks of ulcerative colitis. Medicines helpful for the acute complaints are:
Sulph, Phos, Arg-n, Colch, Podo, Verat, Aloe, Ars, Coloc, Mag-c, Coll, Tromb, Elat, Gamb, Ferr-ar, Merc-d, Ferr-I, Lept, Corn.
