Pathogenesis of Salmonellosis
Salmonella, having overcome the factors of nonspecific protection of the oral cavity and stomach, enter the lumen of the small intestine, where they attach to the membranes of enterocytes and secrete thermostable and / or thermolabile exotoxins. With the help of permeability factors (hyaluronidase), pathogens penetrate into the enterocytes through the brush border. The interaction of bacteria with epithelial cells leads to degenerative changes in microvilli. Intervention of pathogens in the submucosal layer of the intestinal wall is counteracted by phagocytes, which is accompanied by the development of an inflammatory reaction.
When the bacteria are destroyed, the lipolysaccharide complex (endotoxin) is released, which plays a major role in the development of intoxication syndrome. The lipopolysaccharide complex activates the arachidonic cascade through the lipoxygenase and cyclooxygenase pathways. The lipooxygenase pathway leads to the formation of leukotrienes, stimulating chemotaxis and degranulation, enhancing vascular permeability, and, indirectly, reducing cardiac output. The cyclooxygenase pathway leads to the formation of prostanoids (thromboxanes, prostaglandin E, PGF2aa, etc.). The enhanced synthesis of prostanoids induces platelet aggregation, leading to thrombosis in small capillaries. The DIC-syndrome with disturbances of microcirculation develops. The latter cause changes in metabolism with the accumulation of acidic products in organs and tissues (metabolic acidosis). Prostaglandins stimulate the secretion of electrolytes and fluid in the lumen of the intestine, reduce smooth muscle and increase peristalsis, which ultimately leads to the development of diarrhea and dehydration of the body. Moreover, the action of bacterial enterotoxins, which activate the adenylate cyclase system and the production of cyclic nucleotides, promotes dehydration. The consequence of dehydration and intoxication is a violation of the cardiovascular system due to extracardiac mechanisms, which is manifested by tachycardia and a tendency to lower blood pressure. With the maximum severity of exsicosis, the development of cellular hyperhydration is possible due to the difference in osmotic potentials between cells and the intercellular space. Clinically, the condition is manifested by acute swelling and edema of the brain. Disturbances of microcirculation and dehydration lead to dystrophic processes in the tubules of the kidneys. Develops acute renal failure, the first clinical sign of which is oliguria with the further accumulation of nitrogenous slag in the blood.
Usually (95-99% of cases), salmonella does not spread beyond the sub-mucosal layer of the intestine, causing the development of the gastrointestinal form of the disease. Only in some cases penetration of pathogens into the blood is possible, while a generalized form of salmonella with a typhoid-like or septic course is observed. The infection is facilitated by the inadequacy of cellular and humoral immune responses.
At a microscopic examination, the intestinal walls reveal changes in the vessels in the form of hemorrhages in the mucous and submucous layers of the intestinal wall. In the submucosal layer, in addition to microcirculatory disorders, leukocyte reaction and edema develop.
Clinical Picture of Salmonellosis
The following forms and variants of the current are distinguished:
1. Gastrointestinal (localized) form:
- gastritis variant,
- a gastroenteric variant,
- gastroenterocolitis variant.
2. Generalized form:
- typhoid-like variant,
- septic variant.