Etiology and Pathogenesis
The causative agents of yersiniosis are the bacteria Yersinia enterocolitica and Yersinia pseudotuberculosis, which are genetically related to the plague pathogen and act as intracellular parasites that destroy cells using specific enzymes. The primary natural reservoirs and sources of infection are rodents and cats, with transmission occurring via the fecal-oral route; children are affected most frequently. While certain endemic regions exist, sporadic cases are reported worldwide.
The portal of entry and primary site of infection are frequently the tonsils, which can initially manifest clinically as tonsillitis or pharyngitis. Subsequently, the pathogen spreads through the digestive tract, targeting the terminal ileum and cecum as the primary organs.
Clinical and Morphological Forms
In the pathologic anatomy of yersiniosis, three main clinical and morphological forms are distinguished:
- Abdominal form — characterized by catarrhal or catarrhal-ulcerative gastroenteritis, gastroenterocolitis, and terminal ileitis. The intestinal wall is infiltrated by neutrophils, lymphocytes, plasma cells, and a small number of eosinophils. Hyperplasia and ulceration of Peyer's patches are observed in the lymphoid tissue.
- Appendicular form — presents as a combination of acute appendicitis, terminal ileitis, and mesenteric lymphadenitis.
- Generalized form — develops against the background of immunodeficiencies, anemias (especially iron deficiency anemia), and renal pathology. It is characterized by vasculitis, thrombovasculitis, and rash, with a mortality rate reaching 50%.
Morphology of Lymph Nodes and Granulomas
Regional lymph nodes are involved in the inflammatory process during yersiniosis (mesenteric lymphadenitis): they become infiltrated by leukocytes, matted together into conglomerate packs, and may develop microabscesses, while the spleen undergoes hyperplasia.
Occasionally, specific yersinial granulomas (pseudotuberculosis) form within the intestinal mucosa against a background of catarrhal or catarrhal-erosive inflammation with diffuse eosinophilic infiltration. Structurally, they resemble tuberculous granulomas—containing epithelioid cells, macrophages, and sometimes Langhans giant cells, with a necrotic center exhibiting karyorrhexis. The main difference from tuberculosis is that yersinial granulomas undergo suppuration with abscess formation, resolving via scar formation.
Complications and Prognosis
The pathologic process may be accompanied by various complications, among which are:
- Intestinal hemorrhage and bowel wall perforation;
- Bacterial infections of the respiratory tract and middle ear;
- Dysbiosis.
In most cases, the prognosis for yersiniosis is favorable, ending in recovery, although relapses and progression to a chronic course are possible. The generalized form of the infection carries an unfavorable prognosis.