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Salmonella

For medical students3 min readUpdated 2026-10-10

Salmonella is a genus of motile, Gram-negative bacilli that cause intestinal infections, paratyphoid fever, and typhoid fever in humans and animals. They exhibit high environmental resistance, a complex antigenic structure, and the ability to parasitize immune system cells intracellularly.

MorphologyGram-negative bacilli, motile via peritrichous flagella.

AntigensPossess O- and H-antigens, less commonly K-antigen (as Vi-antigen).

SurvivalRemain viable for up to 1 year in frozen meat and eggs, and up to 3 months in soil.

Parasitism TypeFacultative intracellular parasites (replicate within macrophages).

Morphology and Cultural Properties

Salmonellae are small to medium Gram-negative bacilli (measuring 0.7×1.5 to 2–5 µm). They are motile due to peritrichous flagella and typically do not form capsules.

These bacteria are not fastidious in culture: they grow exceptionally well on standard nutrient media and bile-containing media. When grown on solid media, they form smooth (S-forms) and rough (R-forms) colonies. S. Paratyphi B possesses a specific trait, forming characteristic "mucous ridges".

Elective enrichment media (bile and selenite broths) and differential diagnostic media are used for isolation and identification:

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 salmonellae to produce hydrogen sulfide.

Biochemically, the genus is very active: the bacteria ferment glucose to acid and gas, with one important exception—the typhoid fever agent (S. Typhi) ferments glucose to acid only (without gas production). Salmonellae do not produce indole.

Antigenic Structure and the Kauffmann-White Scheme

Due to biochemical similarities within the genus, the antigenic structure plays the primary 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 accounts for:

O-antigen (somatic): a thermostable lipopolysaccharide of the cell wall. Specificity is determined by the terminal sugar of the lateral S-chain. Based on O-antigen structure, salmonellae are grouped into serogroups (A, B, C, D, E).
H-antigen (flagellar): a thermolabile protein. Encoded by two genes, it exhibits biphasic expression (phase 1 is specific, denoted by letters; phase 2 is non-specific, denoted by numbers). Serogroups are subdivided into serovars based on the H-antigen.
K-antigen (capsular): represented in S. Typhi by a specialized Vi-antigen. It shields the O-antigen (causing O-inagglutinability) and serves as a receptor for bacteriophages, which is utilized in phage typing to trace infection sources.

Genetics and Virulence Factors

A distinctive feature of S. enterica is the presence of specialized genomic regions called pathogenicity islands (SPI). The first two play a key role in disease development:

SPI-1: encodes the type III secretion system (T3SS-1). Its effector proteins rearrange the cytoskeleton of intestinal cells, ensuring bacterial entry into the epithelium and the development of diarrhea.
SPI-2: encodes the T3SS-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 via the bloodstream throughout the body (systemic dissemination).

Additionally, salmonellae produce two types of toxins. Endotoxin, upon cell lysis, causes high fever and activates the arachidonic acid cascade. Protein enterotoxin (similar to cholera toxin) increases intracellular cAMP levels in enterocytes, leading to massive fluid and electrolyte secretion into the intestinal lumen.

Typhoid Fever and Salmonellosis

Diseases caused by salmonellae are divided into anthroponoses and zoonoses:

Typhoid Fever and Paratyphoid Fevers: Strict anthroponoses (the source is exclusively human). The pathogen (S. Typhi, S. Paratyphi A/B) enters the small intestine, crosses M cells, and is engulfed by macrophages. Inside them, it is transported to Peyer's patches, where the primary lesion forms. The bacteria then enter the bloodstream (bacteremia) and seed internal organs (liver, spleen). Subsequently, they accumulate in the gallbladder and are reintroduced into the intestine via bile flow. This secondary invasion triggers a hyperergic inflammation of sensitized Peyer's patches, which can lead to necrosis, ulceration, and intestinal perforation. The disease follows a cyclic course with high fever, rash, and intoxication.

Salmonellosis (Foodborne Toxic Infections): Acute zoonotic infections with animals and birds serving as reservoirs (especially chickens, in which transovarial transmission is possible). The infectious dose is very high. The disease most commonly presents in a localized form—as gastroenteritis with prominent diarrheal syndrome. Diarrhea results from massive macrophage destruction, inflammation, prostaglandin release, and enterotoxin activity.

Mnemonic

To remember the sugar fermentation exception: "The typhoid agent (S. Typhi) is too tired to pass gas" — it ferments glucose to acid only, without gas production.

Frequently asked 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, presenting 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 infection source and pathogenesis, three main disease groups are recognized: typhoid and paratyphoid fevers, zoonotic salmonelloses, and hospital-acquired (nosocomial) salmonellosis.

What laboratory diagnostic methods are used for typhoid fever during the first, second, and third weeks of illness?

Laboratory diagnostics of typhoid fever depend 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: detection of antibodies against Salmonella Typhi in the blood using the Widal test.

Diagnostics for the third week involve isolating stool, urine, and bile cultures, indirect hemagglutination assays (IHA) with erythrocyte O-, Vi-, and H-diagnostic reagents, ELISA, and co-agglutination assays.

Which antibiotic groups and drugs are used for etiotropic treatment of typhoid fever?

Antibacterial agents selected based on the susceptibility profile 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 safer alternatives or dangerous allergies).
Aminopenicillins (ampicillin) — used as second-line agents.

The duration of antibiotic therapy is determined individually depending on the susceptibility phenotype, the drug used, and disease severity.

What type of immunity develops after recovering from typhoid fever, and which antibody classes are produced?

A robust, long-lasting (usually lifelong) immunity develops after recovering from typhoid fever. Cellular immunity, mediated by activated macrophages, plays the leading protective role. Humoral immunity serves as a marker of the infectious process. Specific antibody responses include:

Anti-O antibodies — appear by the end of the first week, serving as a marker of the acute phase.
Anti-H antibodies — appear during convalescence and persist long-term.
Anti-Vi antibodies — serve as a marker of bacterial carriage.

Why do Salmonella colonies turn black on bismuth sulfite agar?

Salmonellae possess high biochemical activity and produce hydrogen sulfide (H2S). It reacts with bismuth sulfite in the medium, turning the colonies black.

What is the basis of the O-inagglutinability phenomenon?

In some salmonellae (e.g., the typhoid fever agent), the surface Vi-antigen physically masks the somatic O-antigen, preventing the bacterium from reacting with diagnostic O-antisera.

What causes bacterial carriage after a resolved infection?

Bacterial carriage results from 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 for this state.

Go deeper

Mechanisms of antibody formation and dynamics (anti-O, anti-H, and anti-Vi antibodies) in diagnostics.
Principles of Salmonella phage typing for epidemiological investigation.
Specific prophylaxis of typhoid fever (types of vaccines used).
Features of generalized forms of salmonellosis (septicemic-pyemic form).