Morphology and cultural characteristics
Salmonella species are small to medium Gram-negative rods (ranging from 0.7×1.5 to 2–5 µm in size). They are motile via peritrichous flagella and generally do not form a capsule.
These bacteria are unfastidious in cultivation: they grow well on simple nutrient media and bile-containing media. When grown on solid media, they form smooth (S-forms) and rough (R-forms) colonies. S. Paratyphi B exhibits a specific feature—it forms characteristic "mucus ridges".
For isolation and identification, elective enrichment media (bile and selenite broths) and differential diagnostic media are used:
- Lactose-containing media (Endo, Ploskirev agar): colonies remain colorless because the pathogen does not ferment lactose.
- Bismuth sulfite agar: black colonies grow due to the ability of Salmonella to produce hydrogen sulfide.
Biochemically, the genus is highly active: bacteria ferment glucose to acid and gas, but there is an important exception—the typhoid fever pathogen (S. Typhi) ferments glucose to acid only (without gas production). Salmonella do not produce indole.
Antigenic structure and the Kauffmann-White scheme
Due to the similarity of biochemical properties within the genus, the antigenic structure plays the main role in differentiation. Modern taxonomy distinguishes only two species: S. enterica (infects humans and warm-blooded animals) and S. bongori (infects cold-blooded animals). Within subspecies, microorganisms are divided into thousands of serovars according to the Kauffmann-White scheme, which takes into account:
- O-antigen (somatic): thermostable lipopolysaccharide of the cell wall. Specificity is determined by the terminal sugar of the side S-chain. Based on O-antigen structure, Salmonella are grouped into serogroups (A, B, C, D, E).
- H-antigen (flagellar): thermolabile protein. Encoded by two genes, thus exhibiting diphasic nature (1st phase is specific, designated by letters; 2nd is nonspecific, designated by numbers). Based on the H-antigen, serogroups are divided into serovars.
- K-antigen (capsular): presented in S. Typhi by a special Vi-antigen. It shields the O-antigen (causing the O-inagglutinability phenomenon) and serves as a receptor for phages, which is used for phage typing to trace the source of infection.
Genetics and pathogenicity factors
A distinguishing feature of the species S. enterica is the presence of specific genomic regions called pathogenicity islands (SPI). The first two play a key role in the development of the disease:
- SPI-1: encodes the type 3 secretion system (TTCC-1). Its effector proteins rearrange the cytoskeleton of intestinal cells, ensuring bacterial penetration into the epithelium and the development of diarrhea.
- SPI-2: encodes the TTCC-2 system, which blocks the fusion of the phagosome with the lysosome. This protects the bacterium from destruction inside the macrophage, allowing it to multiply and spread through the bloodstream across the body (generalization).
In addition, Salmonella secrete two types of toxins. Endotoxin causes severe fever upon cell destruction and activates the arachidonic acid cascade. Protein enterotoxin (similar to cholera toxin) increases cAMP levels in enterocytes, leading to a massive efflux of water and ions into the intestinal lumen.
Typhoid fever and salmonellosis
Diseases caused by Salmonella are divided into anthroponotic and zoonotic:
Typhoid fever and paratyphoid fevers: Strict anthroponoses (the source is exclusively humans). The pathogen (S. Typhi, S. Paratyphi A/B) enters the small intestine, passes through M-cells, and is captured by macrophages. Within them, it is transported to Peyer's patches, where the primary focus is formed. Then the bacteria break into the bloodstream (bacteremia) and settle in internal organs (liver, spleen). Next, they accumulate in the gallbladder, from where they re-enter the intestine via bile flow. This secondary invasion causes hyperergic inflammation of sensitized Peyer's patches, which can lead to necrosis, ulcers, and intestinal perforation. The disease proceeds cyclically with high fever, rash, and intoxication.
Salmonellosis (foodborne toxicoinfections): Acute zoonotic infections reservoir-hosted by animals and birds (especially chickens, in which transovarial transmission is possible). The infectious dose is very high. The disease most frequently occurs in a localized form—as gastroenteritis with pronounced diarrheal syndrome. Diarrhea occurs due to massive macrophage death, inflammation, prostaglandin release, and enterotoxin action.
Briefly: answers to topical questions
What clinical forms of salmonellosis are distinguished in humans?
Localized and generalized clinical forms of salmonellosis, as well as bacterial carriage, are distinguished in humans.
- Localized forms — include the gastrointestinal form, which presents as gastritis, gastroenteritis, and gastroenterocolitis variants.
- Generalized forms — are subdivided into typhoid-like and septic variants.
- Bacterial carriage — asymptomatic shedding of the pathogen.
Additionally, depending on the source of infection and pathogenesis, three main groups of diseases are distinguished: typhoid and paratyphoid fevers, zoonotic salmonellosis, and hospital-acquired (nosocomial) salmonellosis.
What laboratory diagnostic methods are used in typhoid fever during the first, second, and third weeks of the disease?
Laboratory diagnosis of typhoid fever depends on the stage of the infectious process.
- First week — bacteriological method is used: isolation of the pathogen from blood (blood culture).
- Second week — serological methods are used: antibodies against Salmonella Typhi are determined in the blood using the Widal test.
Diagnostic methods specific to the third week are not detailed in the sources, yet at various stages of the disease, stool, urine, and bile cultures, indirect hemagglutination assays (IHA) with erythrocytic O-, Vi-, and H-diagnosticums, ELISA, and co-agglutination reactions are also employed.
Which antibiotic groups and drugs are used for etiotropic treatment of typhoid fever?
Antibacterial drugs, taking into account the susceptibility of the isolated Salmonella Typhi strain, are used for the etiotropic treatment of typhoid fever.
- Chloramphenicol — a nosologically specific antibiotic, used systemically as a reserve drug (in case of resistance to safe alternatives or dangerous allergies).
- Aminopenicillins (ampicillin) — used as second-line drugs.
The duration of antibiotic therapy is determined individually based on the strain's susceptibility phenotype, the type of drug used, and the severity of the disease.
What type of immunity is formed after recovering from typhoid fever, and which antibody classes are produced?
A robust, long-lasting (usually lifelong) immunity is formed after recovering from typhoid fever. Cell-mediated immunity, implemented via activated macrophages, plays the leading protective role. Humoral immunity serves as a marker of the infectious process. Specific immunoglobulin classes are not specified in the sources, but the production of antibodies to specific antigens is described:
- Antibodies to the O-antigen — appear by the end of the first week, serving as a marker of the acute phase.
- Antibodies to the H-antigen — appear during the convalescence period and persist for a long time.
- Antibodies to the Vi-antigen — serve as a marker of bacterial carriage.
To remember the exception regarding sugar fermentation: "The typhoid pathogen (S. Typhi) was too tired to pass gas" — it ferments glucose only to acid, without gas production.
Class and exam questions
Why do Salmonella colonies turn black on bismuth sulfite agar?
Salmonella species possess high biochemical activity and produce hydrogen sulfide (H2S). It reacts with bismuth sulfite in the medium, causing the colonies to turn black.
What is the essence of the O-inagglutinability phenomenon?
In some Salmonella species (e.g., the typhoid fever pathogen), the surface Vi-antigen physically blocks the somatic O-antigen. Consequently, the bacterium stops reacting with diagnostic O-sera.
What causes bacterial carriage after a past infection?
Bacterial carriage occurs due to the functional insufficiency of the patient's macrophages — they are unable to completely digest and eliminate the pathogen. Antibodies to the Vi-antigen serve as a marker of this condition.
What else to study on this topic
- Mechanisms of formation and antibody dynamics (against O, H, and Vi antigens) in diagnostics.
- Principles of Salmonella phage typing for epidemiological investigation.
- Specific prevention of typhoid fever (types of vaccines used).
- Features of generalized forms of salmonellosis (septicopyemic form).
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