Morphology of ulcer defect healing
The recovery stage begins from the moment ulcers form and continues even after clinical recovery occurs. Granulation tissue proliferates at the site of the intestinal wall defects, which eventually transforms into dense connective tissue. If the ulcers were deep or extensive, their healing leads to the formation of scars capable of significantly narrowing the intestinal lumen, causing cicatricial stenosis. Pronounced lymphadenitis and phenomena of myeloid metaplasia are observed in regional lymph nodes.
Systemic and general changes
The pathological process in dysentery affects not only the intestines but also other internal organs, causing characteristic non-specific changes:
- Moderate hyperplasia of the splenic pulp.
- Development of fatty degeneration of the myocardium and liver.
- In severe disease courses — the appearance of microfocal necroses in the liver and necrosis of the renal tubular epithelium.
Complications of the disease
The pathology may be complicated by pathological processes both within the gastrointestinal tract and beyond it.
Intestinal complications:
- Intestinal hemorrhage, intestinal wall perforation, peri- and paraproctitis.
- Rare conditions: peritonitis, intestinal phlegmon, or gangrene.
- Addition of a secondary purulent or putrefactive infection can cause toxic megacolon, rectal prolapse, intussusception, dysbiosis, and cicatricial stenosis.
Extraintestinal complications:
- Pylephlebitic liver abscesses and cerebral edema in neurotoxicosis in children.
- Development of infectious-toxic (ITSH) and hypovolemic shock.
- Bronchopneumonia, urinary tract infections (pyelitis, pyelonephritis).
- Toxic arthritis, amyloidosis, and general cachexia.
Prognosis
As a rule, the prognosis for this disease is favorable. The acute course of the infectious process usually ends in complete recovery of the patient.
Briefly: answers to topical questions
What stages of the local pathological process (colitis) are distinguished in dysentery?
In the classical course of dysentery, the following stages of development of the local pathological process (colitis) are distinguished:
- Stage of catarrhal colitis — 2–3 days: the intestinal lumen is narrowed, the mucosa is hyperemic and swollen, pinprick hemorrhages and areas of epithelial necrosis are visible.
- Stage of fibrinous (diphtheritic) colitis — 5–10 days: the intestinal lumen is sharply narrowed, the wall is thickened, brownish-green films appear on the necrotic mucosa; microscopically, areas of deep wall necrosis permeated with fibrin threads are noted.
- Stage of ulcer healing — begins from the moment ulcers form and continues after clinical recovery: defects of the wall are filled with granulation tissue, which matures into mature connective tissue; the outcome of deep or extensive ulcers may be cicatricial stenosis.
What type of exudative inflammation is typical for the peak of dysentery in the intestine?
The development of fibrinous (diphtheritic) inflammation is typical for the peak of dysentery in the intestine. This type of exudative inflammation is characterized by deep necrosis of the mucosa and submucosa of the large intestine. Dead tissues are soaked (imbibed) with fibrinous exudate, resulting in the formation of characteristic dense brownish-green films permeated with fibrin threads on the mucosal surface. As the process progresses, these films may be replaced by coarse dirty-green crusts.
Which parts of the gastrointestinal tract are predominantly affected in dysentery?
In dysentery, the distal large intestine is predominantly affected. The main morphological changes and inflammatory processes (colitis) are localized in the rectum and sigmoid colon. Towards the proximal parts of the intestine, the severity of pathological changes gradually decreases. In children, the lymphoid apparatus of the intestine is primarily involved in the pathological process with the development of follicular or follicular-ulcerative colitis (enlargement and ulceration of solitary follicles).
Which causative agent causes dysentery?
Dysentery (shigellosis) is caused by bacteria of the genus Shigella. Four main species (serogroups) of the pathogen are distinguished:
- Group A (Shigella dysenteriae) — possesses the most potent enterotoxic effect and causes a severe staged course of colitis.
- Group B (Shigella flexneri).
- Group C (Shigella boydii).
- Group D (Shigella sonnei).
In addition, a disease with the clinical presentation of dysentery syndrome can be caused by enteroinvasive Escherichia coli (Escherichia coli O-type), the pathogenesis of which is essentially identical to shigellosis.
Class and exam questions
What is the outcome of deep and extensive ulcers in dysentery?
Deep and extensive defects heal with the formation of connective tissue scars, which can cause cicatricial stenosis and narrowing of the intestinal lumen.
What general non-specific changes are observed in internal organs?
Moderate hyperplasia of the splenic pulp is noted, as well as fatty degeneration of the myocardium and liver. In severe cases, microfocal necroses in the liver and necrosis of the renal tubular epithelium may form.
What is the standard prognosis for the acute course of dysentery?
The prognosis is favorable, the acute course of the disease usually ends in complete recovery.
What else to study on this topic
- Yersiniosis enteritis and its forms
- Anaerobic infections and clostridiosis
- Pathogenesis of syphilis and its periods
- Morphology of congenital and acquired syphilis
- Features of gonococcal infection
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