Tetanus is a neurological disorder caused by the action of a powerful neurotoxin produced and released by Clostridium tetani. This disorder is very rare in dogs and cats since they are naturally resistant to the effects of the toxin. Horses and humans are the species most sensitive to the toxin.
CAUSATIVE AGENT
Clostridium tetani is a Gram-positive, anaerobic, mobile, non-encapsulated, spore-forming bacterium. The vegetative forms produce two different toxins: tetanolysin, not responsible for significant clinical forms, and tetanospasmin, which instead causes serious neuromuscular signs.
MODE OF TRANSMISSION
Tetanus is manifested clinically when spores enter the body through puncture wounds. The anaerobic environment and the presence of foreign bodies, other micro-organisms, and the formation of abscesses in the entry wound contribute to the germination of the spores and to the production of the toxins. The clinical signs that subsequently develop are caused by the action of tetanospasmin on the nervous system.
Other routes of transmission: tetanus toxins have a high molecular weight which prevents them from crossing the placental barrier. They are not absorbed from the gastrointestinal tract because they are destroyed by gastric juices.
PATHOGENESIS
The tetanus toxin is a dimer composed of one protein that binds to the nerve cells and to carrier proteins and another protein that blocks the release of neurotransmitters. The toxin penetrates into the axons of the nearest motor nerve at the neuromuscular junction and travels, by means of retrograde transport, up to the central nervous system. In the brain and spinal cord tetanus toxin inhibits the release of glycine and gamma-amino butyric acid (GABA), inhibitory neurotransmitters, causing prolonged muscle spasm. The fact that facial muscles are affected first could be attributed to the fact that the facial nerve is shorter than the nerves in the limbs.
The toxin also has pathogenic effects at the neuromuscular junctions and the ganglia of the autonomic nervous system. In addition, it shows a special affinity for the gangliosides found in the grey matter of the central nervous system. This would appear to justify the greater presence of cerebral clinical signs in some patients and the absence of spinal signs. The bond between the tetanus toxin and the presynaptic sites is irreversible and thus recovery depends on the formation of new axonal endings.
CLINICAL SIGNS
The incubation period may vary from around 5 days up to 3 weeks from the penetration of the spores into the wound. This period varies according to the wound’s nearness to the central nervous system. Often, especially in dogs, wounds may not be noticed because of their smallness; this can delay the assessment of the clinical picture. On the other hand, in cats, given their greater and innate resistance to the tetanus toxin, the wound generally has to be large enough to be noticeable in order to cause the disease. When the wound is near the central nervous system the signs develop more quickly and are more widespread than when the wound is located on a limb. Tetanus can also be a serious complication of surgical operations such as ovariohysterectomy, pregnancy and births associated with foetal death.
There are two forms of tetanus, localised and generalised. The localised form is more common in dogs and cats because of the resistance of these species to the toxin. The localised form is characterized by extensor rigidity of only one limb or of both hind or front limbs. Generally speaking, the rigidity develops near the wound and subsequently spreads to the entire limb and possibly to the contralateral limb.
The generalised form is characterized by extensor rigidity involving all four limbs; the postural reactions are normally preserved but spinal reflexes cannot be evoked because of the extensor rigidity. In this phase the animal often stands with limbs spread apart, in a “sawhorse” stance (Fig. 1). Subsequently the intracranial signs appear, which lead to a progressive increase in muscle tone, obliging the patient to lie down. Further and progressive signs may include protrusion of the third eyelid and enophthalmos due to hypertonia of the extra-ocular muscles, wrinkled forehead and erect ears with contraction of the facial muscles (Fig. 2), leading to a “sardonic smile”, lockjaw, tachycardia, drooling, laryngeal spasm and dysphagia.
Auditory or tactile stimuli, even slight ones, can trigger generalised muscle spasms and convulsions, often associated with urinary retention and constipation due to contraction of the bladder and anal sphincter. Hyperthermia is a frequent complication related to persistent muscle contraction. The disease may even lead to death through respiratory failure due to respiratory muscle spasm, laryngeal spasm and central respiratory paralysis. Patients usually remain conscious until convulsions develop; reflex muscle spasms are very painful so they are often accompanied by vocal lamentation by the animal.
LABORATORY TESTS
The main clinicopathological alterations are non-specific and include marked neutrophilia with a left shift and a moderate increase in muscle enzymes.
DIAGNOSIS
The diagnosis of tetanus is based on the assessment of recent wounds associated with the symptoms and signs.
Diagnostic tests
- Serology may be used to identify the presence of anti-toxin antibodies. The antibody titres should be compared to those of healthy control subjects.
- It can be difficult to isolate C. tetani from wounds and often it is not even useful since the organism is usually present in very low concentrations and appears morphologically identical to many other Gram-positive bacteria.
DIFFERENTIAL DIAGNOSIS
- Localised form: post-traumatic contractures, Neospora.
- Generalised form: encephalitis, neoplasms, vitamin B12 deficiency, poisoning (strychnine, lead), metabolic disorders (hypocalcaemia, hypoglycaemia), diffuse brain disorders, congenital disorders.
TREATMENT
Treatment may take a very long time and often requires hospitalisation of the patient. The prognosis always remains guarded. Untreated subjects may die. Generally speaking, dogs and cats respond well to treatment since they are resistant to the tetanus toxin and the most frequent clinical forms are of medium severity.
Treatment includes administration of the tetanus antitoxin, derived from equine hyperimmune serum or human globulins (100-1000 IU/kg i.v., in 15-30 minutes). This acts by binding the circulating toxins and thus controlling the progression of the signs, especially when administered early. It does not act on the toxins already bound to the nerve cells. Anaphylactic shock is a potential serious side effect; since tetanus antitoxins are heterologous proteins, we recommend first an intradermal test, with the administration of 0.1-0.2 ml. Repetition of the intravenous administration considerably increases the risk of anaphylactic shock. After a single dose the therapeutic effects persist for approximately 14 days. In the case of obvious wounds, peri-lesional administration of doses of less than 100 IU is possible.
Both local and parenteral antimicrobial therapy should always be given, in order to kill vegetative forms of C. tetani in the wound. Antibiotics that can be used include penicillin G and metronidazole, for at least 10 days. In some cases it may be necessary to control muscle spasms and convulsions using phenothiazines, benzodiazepines and barbiturates.
It is a good rule to clean the wound carefully, removing necrotic tissue, so as to facilitate eradication of the infection.
Healing occurs approximately 3 weeks after the beginning of treatment.
A recent retrospective study conducted in England on 13 cases of tetanus in dogs showed healing and return to complete normality in 12/13 subjects. This confirms that the prognosis of subject with tetanus is good, even though continuous monitoring during critical care are necessary for recovery.
PROPHYLAXIS
Given their natural resistance to the tetanus toxin, dogs and cats, unlike other susceptible species such as horses and humans, are not vaccinated.
Cleaning infected wounds and correct antibiotic therapy can reduce the risk of tetanus. It is also important to sterilise surgical instruments properly; cold sterilisation is not recommended.
RISKS FOR HUMANS
Dogs and cats with tetanus do not represent a risk of direct transmission for humans. Clostridium tetani is a commensal of the gastrointestinal tract of many herbivorous mammals, especially horses and sheep. The elimination of spores with the faeces of these animals means that the risk of infection is highest in “tetanigenous fields”, fertilised damp and clayey areas or where these animals are raised. Puncture wounds, especially from barbed wire, or lacerated and contused wounds (from falls, glass, stones and farm tools) are the most responsible for tetanus toxin infection in industrialised countries. For this reason, dog and cat bites and scratches could be potentially dangerous, since they can passively transmit contaminated material from spores of the bacterium.