Dysentery

Q: What pathogen causes dysentery?

Dysentery (shigellosis) is caused by bacteria of the genus Shigella. There are four main species (serogroups) of the pathogen: 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). Additionally, enteroinvasive Escherichia coli (O-type) can cause a clinical picture of dysentery syndrome, with a pathogenesis practically identical to shigellosis.

Dysenteria

For medical students2 min readUpdated 2026-10-10

Dysentery is an infectious gastrointestinal disease where the pathological process in the bowel is accompanied by mucosal defects, their subsequent healing, and a risk of severe complications.

Ulcer healingGranulation tissue fills the defects of the intestinal wall

Main riskCicatricial stenosis narrowing the intestinal lumen

Systemic shiftsFatty change of the myocardium and liver

Lymph nodesLymphadenitis and myeloid metaplasia develop

Morphology of Ulcer Healing

The recovery phase begins from the moment ulcers form and continues even after clinical recovery. Granulation tissue proliferates at the site of the intestinal wall defects, eventually transforming into dense connective tissue. If the ulcers were deep or extensive, their healing leads to scar formation, which can significantly narrow the intestinal lumen, causing cicatricial stenosis. Pronounced lymphadenitis and myeloid metaplasia are observed in regional lymph nodes.

Systemic and General Changes

The pathological process in dysentery affects not only the intestine but also other internal organs, causing characteristic nonspecific changes:

Moderate pulp hyperplasia of the spleen.
Development of fatty change in the myocardium and liver.
In severe cases, microfocal hepatic necrosis and necrosis of the renal tubular epithelium.

Complications

The pathology may be complicated by processes both within the GI tract and beyond.

Intestinal complications:

Intestinal hemorrhage, bowel perforation, peri- and paraproctitis.
Rare conditions: peritonitis, phlegmon, or gangrene of the intestine.
Secondary purulent or putrid infection can cause toxic megacolon, rectal prolapse, intussusception, dysbiosis, and cicatricial stenosis.

Extraintestinal complications:

Pilephlebitic liver abscesses and cerebral edema in children with neurotoxicosis.
Development of septic/toxic (STSH) 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. An acute course of the infectious process typically ends with complete recovery of the patient.

Frequently asked questions

What are the stages of the local pathological process (colitis) in dysentery?

In a classic course of dysentery, the following stages of the local pathological process (colitis) are distinguished:

Stage of catarrhal colitis — days 2–3: the intestinal lumen is narrowed, the mucosa is hyperemic and edematous, with petechial hemorrhages and areas of epithelial necrosis.
Stage of fibrinous (diphtheritic) colitis — days 5–10: the intestinal lumen is sharply narrowed, the wall is thickened, and brownish-green pseudomembranes appear on the necrotic mucosa; microscopy reveals areas of deep wall necrosis permeated with fibrin strands.
Stage of ulcer healing — begins when ulcers form and continues past clinical recovery: defects are filled with granulation tissue maturing into fibrous connective tissue; deep or extensive ulcers may result in cicatricial stenosis.

What type of exudative inflammation is typical for the peak of dysentery in the intestine?

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. The necrotic tissues are imbibed with fibrinous exudate, forming characteristic dense brownish-green pseudomembranes on the mucosal surface permeated with fibrin threads. 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?

The distal large intestine is predominantly affected in dysentery. The main morphological changes and inflammatory processes (colitis) are localized in the rectum and sigmoid colon. The severity of pathological changes gradually decreases proximally. In children, the lymphoid apparatus of the intestine is initially involved, leading to follicular or follicular-ulcerative colitis (enlargement and ulceration of solitary follicles).

What pathogen causes dysentery?

Dysentery (shigellosis) is caused by bacteria of the genus Shigella. There are four main species (serogroups) of the pathogen:

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).

Additionally, enteroinvasive Escherichia coli (O-type) can cause a clinical picture of dysentery syndrome, with a pathogenesis practically identical to shigellosis.

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 nonspecific changes are observed in internal organs?

There is moderate splenic pulp hyperplasia, as well as fatty change of the myocardium and liver. Severe cases may feature microfocal necrosis in the liver and necrosis of the renal tubular epithelium.

What is the standard prognosis for acute dysentery?

The prognosis is favorable; the acute course of the disease usually ends in complete recovery.

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