Tetanus

Etiology and morphology of the pathogen

The causative agent of the disease is Clostridium tetani, belonging to the family Bacillaceae and the genus Clostridium. It is a motile, anaerobic, spore-forming, Gram-positive rod, 4 to 12 µm long and 0.3–1 µm wide.

• Flagellar apparatus: the bacterium has up to 20 flagella (peritrichous), ensuring motility and active participation in metabolic processes with the external environment.
• Sporulation: under adverse conditions, a single oval colorless spore is formed, located terminally. This makes the microbe look like a «racket» or «drumstick». Spores have high resistance to physical and chemical factors.
• Antigenic structure: includes a heat-labile flagellar H-antigen (10 serotypes) and a heat-stable somatic O-antigen, common to all variants.
• Cultivation: the optimal growth temperature is +37°C. The microbe thrives in the presence of oxygen-consuming microorganisms, such as Bacillus subtilis or coccal flora.

Ecology and conditions of infection

In the form of vegetative cells, the bacterium saprophytes in the intestines of humans and animals, from where it enters the soil with feces.

The microorganism itself lacks invasive properties and penetrates inside exclusively through damage to the skin, mucous membranes, and soft tissues contaminated with spores.

For the bacillus to multiply, a low oxidation-reduction potential (low oxygen concentration) is required in the inoculation zone. Deep puncture wounds, crushed tissues, and «pockets» serve as ideal conditions where the microbe acts as a «necroparasite». The biochemical activity of the bacterium is weak; it lacks pronounced proteolytic properties, therefore standard signs of inflammation are absent at the site of bacillary multiplication in the absence of pyogenic microorganisms.

Pathogenesis and action of the exotoxin

Multiplying in the primary focus, vegetative forms do not leave its boundaries, but actively produce an exotoxin (tetanospasmin). This is one of the most powerful neurotropic poisons in nature, second in potency only to botulinum toxin (the lethal dose is less than 2.5 ng/kg).

• Molecular domains of the toxin bind to gangliosides, penetrate peripheral nerves, and reach neurons.
• The poison selectively affects interneurons of polysynaptic reflex arcs, blocking inhibitory neurotransmitters responsible for central inhibition.
• As a result of the blockage of inhibitory mechanisms, convulsive contractions of skeletal muscles and severe attacks of tonic and tetanic spasms occur against the background of pronounced muscle hypertonia.

Clinical features and diagnostics

The main manifestation of the pathology is attacks of generalized tonic and tetanic spasms against the background of pronounced skeletal muscle hypertonia. During the course of the disease, various degrees of severity, possible complications, and specific features in newborns are distinguished.

Diagnosis is based on two main pillars:

1. Epidemiological data: the fact of previous wounds and injuries with violation of the integrity of integuments during the incubation period.
2. Clinical picture: identification of the main symptoms of muscle hypertonia and convulsive seizures.

Class and exam questions

What else to study on this topic

• Severity degrees and complications of tetanus
• Features of the course of tetanus in newborns
• Principles of complex treatment (etiotropic, pathogenetic, and symptomatic therapy)
• Injury prevention and specific tetanus prophylaxis
• Pathogenic action of Clostridium perfringens toxins and gas gangrene
• Clostridial phlegmon and infections caused by non-spore-forming anaerobes

Other topics in the "Additional Topics" section

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