Tetanus, also known as lockjaw, is a neurological condition caused by infection with Clostridium tetani bacteria, which often presents with muscle stiffness and spasms. All animal species are susceptible to tetanus, but there is variability in species susceptibility. The most susceptible species are horses, guinea pigs, monkeys, sheep, mice, goats and humans. Carnivores such as cats and dogs are less vulnerable, which is why cats and dogs are not routinely vaccinated against tetanus. Birds are resistant, and cattle are also very resistant (Popoff, 2020).
This article will discuss the pathophysiology, clinical presentation, diagnosis and treatment of tetanus in cats and dogs.
Tetanus is caused by the neurotoxin tetanospasmin, which is formed by the Gram-positive obligate anaerobe Clostridium tetani. C. tetani spores are present in the environment, particularly in soil, faeces and dust. They can be found in the faeces and skin of domestic dogs and cats. Penetrating wounds, abscesses, injuries with a foreign body, contaminated body cavity surgery and dental infections can be a possible source of the infection; however, a wound cannot always be identified in all dogs with tetanus. In cats, who are more resistant to tetanus compared to dogs, tetanus is often associated with larger wounds producing greater amounts of toxin.
The binding of tetanospasmin to the inhibitory interneurons in the CNS results in irreversible damage to the interneurons. Recovery requires the generation of new nerve terminals
Spores enter the body through a wound, and under anaerobic conditions they convert into a vegetative form. The vegetative form of the C. tetani bacterium produces the neurotoxin tetanospasmin which binds to the telodendrion at the neuromuscular junction and is transported retrograde to the nerve cell body in the central nervous system (CNS). The tetanospasmin reaches the neuromuscular junction directly through the wound or indirectly through the bloodstream. Tetanospasmin can also be transported directly to the CNS through the bloodstream. Once in the CNS, the tetanospasmin prevents the release of inhibitory neurotransmitters (glycine and GABA) from the inhibitory interneurons. The binding of tetanospasmin to the inhibitory interneurons in the CNS results in irreversible damage to the interneurons. Recovery requires the generation of new nerve terminals, which explains why recovery from tetanus is slow.
Damage to the inhibitory interneurons results in uncontrolled and sustained skeletal muscle contraction. All muscles are affected, but the main clinical signs are extensor muscle rigidity and trismus (locked jaw). In a later stage, the autonomic nervous system can be affected as well. The exact mechanism is unknown; however, it is possible that the inhibitory circuits of the autonomic nervous system are affected by tetanospasmin.
In cases of tetanus, the time of onset of clinical signs after sustaining a wound or undergoing surgery is variable. In dogs, the range is between 3 and 18 days (with an average of 5 to 10 days). In cats, which are more resistant, it can take longer (up to three weeks) before signs of tetanus become apparent (Dewey and Talarico, 2016).
Tetanus can be localised or generalised. Localised tetanus means only a focal group of muscles, such as those in a limb or the head, is affected, whereas in animals with generalised tetanus, the entire body is affected.
The facial muscles are often some of the first muscles to be affected. The main reason for this is the relatively short cranial nerves compared to the longer nerves that innervate the limb muscles. This results in very typical signs such as trismus (“lockjaw” or the inability to open the mouth) and risus sardonicus (“rictus grin”), which comprises narrowed palpebral fissures, drawing back of the lip, wrinkling of the forehead and the tips of the ears being pulled towards each other (Figure 1). Due to the trismus, affected animals can have difficulty eating and drinking. Enophthalmos and protrusion of the third eyelids are a result of contraction of the third eyelid.
If the patient remains ambulatory, they develop a stiff and stilted gait with a wide-based stance and the tail curved dorsally. If the patient is recumbent, severe extensor muscle rigidity is present. This rigidity often gets worse with stimulation (tactile or auditory) and sometimes results in severe muscle tetany and opisthotonus. Muscle tetany is painful and can cause life-threatening hyperthermia. Increased urethral and anal sphincter tone can cause urine retention and constipation. Although rare, laryngeal spasm can occur and result in respiratory failure (Rochelle et al., 2006).
Autonomic dysfunction can result in bradycardia, tachycardia, other cardiac arrhythmias, hypotension and/or hypertension. In patients with tetanus, parasympathetic hyperactivity occurs more frequently than sympathetic signs. Signs of parasympathetic overactivity are bradycardia and hypotension, while signs of sympathetic overactivity are tachycardia and hypertension. Body temperature is often elevated in dogs and cats with tetanus. This can be due to sustained muscle contraction, persistent clostridial infection or both (Penderis, 2012; Dewey and Talarico, 2016).
Diagnosis of tetanus is based on the above typical clinical signs. The history of a wound supports the diagnosis, but a wound is not always present.
The aim of tetanus treatment is to avoid further toxin production, neutralise the circulating toxin and provide supportive care. The author advises following the steps below when treating a dog or cat with tetanus (Penderis, 2012; Dewey and Talarico, 2016).
The aim of tetanus treatment is to avoid further toxin production, neutralise the circulating toxin and provide supportive care
Step one: administration of tetanus antitoxin
In small animal practice, anti-tetanus equine serum is most often used as antitoxin. It is important to administer the antitoxin before wound debridement as more toxins will be released into the circulation during wound debridement. The recommended dose of anti-tetanus equine serum is 100 to 1,000 units/kg, with a maximum of 20,000 units. Preferably, the antitoxin should be given as a bolus intravenously over 30 minutes. As anaphylactic shock is a risk, it is recommended to give a small amount (0.1 to 0.2ml) subcutaneously first. If there is no reaction after 30 minutes, the full dose can be given intravenously.
Step two: administration of antibiotics
Metronidazole is the antibiotic of choice for tetanus patients. The recommended dose is 10 to 15mg/kg IV every eight hours for dogs and every 12 hours for cats. Antibiotics need to be given for at least 10 days. Possible alternative antibiotics are erythromycin, tetracyclines, chloramphenicol, clindamycin and amoxicillin-clavulanate.
Step three: wound debridement
If a wound has been identified, it should be thoroughly flushed; foreign bodies need to be removed and necrotic tissue debrided. Hydrogen peroxide is recommended to flush the wound.
Step four: supportive care
Supportive care is the most important aspect of treatment, but caring for a dog with severe tetanus can be very labour-intensive. Severely affected tetanus patients will need constant monitoring due to the risk of muscle tetany with secondary hyperthermia, respiratory failure due to laryngospasm, or aspiration pneumonia. Patients should be kept in a dark and quiet environment to reduce the risk of muscle tetany – earplugs can be used to reduce auditory stimuli. Severe cases can be recumbent for two to three weeks. Therefore, soft bedding and regular turning is necessary to avoid decubital ulcers. Patients should be kept dry and clean all the time.
Supportive care is the most important aspect of treatment, but caring for a dog with severe tetanus can be very labour-intensive
Nutritional support with tube feeding is necessary to support patients with trismus, and severely affected patients can benefit from the placement of a central venous line. Patients with urinary or faecal retention will need bladder catheterisation or an enema, respectively. Sedation is also necessary to reduce hyperexcitability in severely affected patients. Acepromazine is a good first-choice sedation. To reduce muscle stiffness or to treat more severe tetany, muscle relaxants such as midazolam or diazepam can be used.
Step five: further care and treatment
In severe cases which are refractory to the classic combination of acepromazine and benzodiazepines, a constant rate infusion of medetomidine, pentobarbital or propofol can be considered (Rochelle et al., 2006; Penderis, 2012). Supraphysiological magnesium therapy can be helpful for dogs with severe tetanus to reduce the muscle spasms (Simmonds et al., 2011; Royaux et al., 2020).
The recovery of tetanus patients depends on the formation of new nerve terminals, which is a slow process. It often takes a couple of weeks before any improvement is seen. The average hospitalisation time for a dog with tetanus is 13 to 17 days (Dewey and Talarico, 2016). Most dogs recover completely within a month (Bandt et al., 2007). In cats, however, it can take several months before they return to normal (Dewey and Talarico, 2016). The survival rate in dogs ranges between 50 and 92 percent (Adamantos and Boag, 2007; Burkitt et al., 2007; Bandt et al., 2007).
Younger dogs with tetanus might be more likely to develop severe clinical signs […] and dogs recovering from tetanus can suffer from an REM sleep disorder
Younger dogs with tetanus might be more likely to develop severe clinical signs (Burkitt et al., 2007), and dogs recovering from tetanus can suffer from an REM sleep disorder (Shea et al., 2018). It is important to warn owners about REM sleep disorders as they can easily be confused with epileptic seizures.