Morphological and tintorial features
The tetanus pathogen is a large, straight bacillus with rounded ends. The microorganism is motile due to flagella located all around the perimeter of the cell (peritrichous). In smears, the bacteria lie chaotically or form chains. When Gram stained, they show a positive reaction (Gram+).
The hallmark of Clostridium tetani is its ability to form terminal spores whose diameter significantly exceeds the width of the vegetative cell, giving the bacterium its characteristic "drumstick" appearance. Spores exhibit extreme resistance to environmental factors: they withstand low temperatures down to -60 °C, survive boiling for up to 6 hours, and are resistant to phenol and formalin. They can only be reliably destroyed by autoclaving at 130 °C for 20 minutes, whereas vegetative forms are killed by boiling within just 5 minutes.
Cultural and biochemical properties
The bacterium is an obligate anaerobe, meaning it grows and multiplies exclusively in oxygen-free conditions at a temperature of 37 °C.
On solid nutrient media (nutrient agar, gelatin), the pathogen can form two types of colonies:
- S-forms: smooth, transparent, lenticular.
- R-forms: rough, grayish-yellow, resembling "fluffs" with a dense center in the agar stab.
When inoculated on blood agar, growth is accompanied by a zone of hemolysis. In liquid Kitt-Tarozzi medium, the microorganism grows slowly, causing uniform turbidity and releasing a specific unpleasant odor.
The biochemical activity of C. tetani is extremely low. The bacterium is inert to most carbohydrates, and its proteolytic properties are limited to the slow breakdown of proteins with the formation of ammonia, indole, and volatile fatty acids. The pathogen produces gelatinase and a renin-like enzyme.
Pathogenicity factors
The pathogen's main weapon is the tetanus exotoxin. It is identical in all 10 serovars of the bacterium and is released upon lysis of the microbial cell. The toxin consists of two fractions:
- Tetanospasmin (neurotoxin): the primary pathogenic factor. It binds to the neuromuscular junction and reaches the motor neurons of the spinal cord and medulla oblongata via retrograde axonal transport. There, it blocks the release of inhibitory neurotransmitters, leading to uncontrolled clonic and tonic muscle contractions.
- Tetanolysin: destroys red blood cells and exerts a membrane-toxic effect on the tissues of the heart, lungs, liver, and kidneys, significantly worsening the patient's general condition.
Epidemiology and Clinical Presentation
Tetanus is a universally distributed sapronosis. The natural reservoir of infection is soil, where spores enter with human and animal feces (the pathogen is a normal intestinal inhabitant). Transmission occurs via contact (through wounds) when infected soil enters damaged tissues where anaerobic conditions are established. A sick person is not contagious to others.
The incubation period lasts from 1 day to several weeks (averaging 6–14 days). An important prognostic rule: the shorter the incubation, the more severe the infection. The disease begins acutely with the classical triad:
- Trismus: spasm of the masticatory muscles (the first symptom).
- "Sardonic smile" (risus sardonicus): uncontrolled spasm of the facial muscles.
- Opisthotonos: severe spasm of the back and limb muscles, causing the body to arch.
Diagnostics and prevention
Post-infectious immunity is not formed after tetanus because the lethal dose of the toxin is well below the threshold for activating the immune response.
Diagnostics include bacterioscopy (looking for "drumsticks") and bacteriological inoculation into Kitt-Tarozzi medium. The gold standard for detecting the exotoxin is the biological assay in white mice using a neutralization test.
The basis of protection against infection is routine immunization. It begins at 3 months of age with vaccines containing tetanus toxoid (DTP, DT), followed by revaccination every 10 years. For injuries, emergency specific prophylaxis is performed: administration of toxoid combined with specific human immunoglobulin or heterologous horse serum (administered using Besredka's method).
Briefly: answers to topical questions
What antibiotics are used for etiotropic therapy of tetanus?
For etiotropic therapy of tetanus, sources indicate:
- Metronidazole and tinidazole.
- Benzylpenicillin as the drug of choice for infection caused by Clostridium tetani.
Lincomycin and clindamycin belong to lincosamides, whose activity spectrum includes the tetanus pathogen.
Specifically, which inhibitory neurotransmitters does tetanospasmin block?
Tetanospasmin blocks the secretion of glycine and $\gamma$-aminobutyric acid (GABA). This neurotoxin cleaves synaptobrevin and vesicle-associated membrane protein, halting the release of these inhibitory neurotransmitters from spinal interneurons. As a result, a deficit of inhibitory influences occurs, leading to disinhibition of motor neurons and their overexcitation, which clinically manifests as sustained muscle contractions and spasms.
What is the antigenic structure of Clostridium tetani?
The antigenic structure of Clostridium tetani is represented by two main antigens:
- O-antigen — a somatic, thermostable antigen common to all variants of the pathogen.
- H-antigen — a flagellar, thermolabile antigen. Based on differences in its structure, 10 serological variants (serovars) of the bacterium are distinguished.
Regardless of the serovar, all strains of the microorganism produce an exotoxin that is absolutely identical in its antigenic properties.
How exactly is the biological assay in white mice performed to detect tetanus exotoxin?
The biological assay in white mice is performed in the format of a neutralization test using anti-tetanus serum.
- Part of the filtrate of the test material is mixed with anti-tetanus serum, incubated for 40 minutes, and administered to the first group of animals.
- The filtrate without serum is administered to the second group of animals.
- If Clostridium tetani is present, the animals in the second group develop symptoms of tetanus.
The classical clinical triad of tetanus is remembered by the descending direction of spasm development: J-F-B (Jaw — Face — Back), i.e., trismus, "sardonic smile", and opisthotonos.
Class and exam questions
Does immunity develop after recovering from tetanus?
No, it does not form. The lethal dose of tetanus exotoxin is infinitesimally small, and its quantity is insufficient to trigger a full-fledged immune response.
Why is the bacterium called a "drumstick"?
The microorganism acquires this appearance due to the presence of a terminal (at the end) spore. Its diameter is larger than the width of the vegetative cell itself.
How does the incubation period affect the prognosis of the disease?
There is a direct prognostic rule: the shorter the incubation period, the more severe and aggressive the infection.
What else to study on this topic
- The mechanism of retrograde axonal transport of tetanospasmin to CNS neurons.
- Schemes of emergency specific prophylaxis for vaccinated and unvaccinated patients.
- Principles of performing the neutralization test in white mice (biological method).
- Differences between DTP, DT, DT-M, and T vaccines.
- Rules for administering heterologous serum using Besredka's method to prevent anaphylaxis.
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