Abstract
Tetanus is rare in cats owing to their innate resistance. Clinical diagnosis may not be obvious in the early stages of the disease when characteristic signs of generalised tetanus are absent. However, the history of a penetrating/neglected wound and the presence of persistent involuntary muscle rigidity in a mentally alert animal should always lead to the suspicion of tetanus. Prompt diagnosis and treatment are the keys to a successful outcome.
Tetanus is a bacterial disease caused by Clostridium tetani that can affect all the domestic animals and humans. Resistant spores are found in the environment, especially in the soil. Disease occurs as a result of localisation of tetanus spores in an anaerobic environment, such as a necrotic wound, with conversion to a vegetative, toxin-producing form (Braund 1994). The toxin (tetanospasmin) binds to gangliosides in nerves, and travels to the spinal cord by retrograde axonal transport. Dogs and cats are much less susceptible to tetanus toxin than other species. It has been reported that the cat is 7200 times more resistant to tetanospasmin compared to the horse (Greene 1998). This innate resistance is related to the difficulty tetanospasmin has in penetrating and binding to nervous tissue. Tetanospasmin is a dimer composed of a heavy chain that binds to neuronal cells and transport proteins, and a light chain that blocks the release of glycine and gamma-aminobutyric acid (GABA) from CNS inhibitory interneurons (Sanford 1995). The binding of tetanus toxin to presynaptic sites of inhibitory neurons is irreversible, and recovery depends on sprouting of new axonal terminals (Sanford 1995).
The present report describes a cat with focal tetanus progressing to moderate generalised tetanus, and reviews diagnosis and treatment of this disease.
A 14-month-old, 5-kg, female spayed domestic short hair cat presented in lateral recumbency with profound rigidity in all four limbs. The owner reported that the cat was slightly hit by a car 2 weeks earlier. Thereafter, the cat did not show any signs. Ten days later, she started limping with the left thoracic limb. The owner noticed that this lameness worsened progressively until the cat was unable to get up and walk. On general physical examination, the cat was alert and showed marked rigidity of all four limbs (Fig 1). Rectal temperature, heart rate, and respiratory rate were within normal limits. Abdominal palpation revealed gas-filled bowel loops and distended urinary bladder probably secondary to anal and urethral sphincter spasms. A careful inspection of the integumentary system showed abrasions of the digital pad and periungual region of the III and IV digits of the left thoracic limb (Fig 2). It was hypothesised that these lesions occurred when the digital pads were dragged on the concrete 2 weeks earlier. Neurological examination showed normal mental status and spastic non-ambulatory tetraparesis. Muscle rigidity was more pronounced in the left thoracic limb. The head and the tail muscles had normal tone. Cranial nerve reflexes were normal. Postural reaction testing revealed normal initiation, but stiff performance of the motor response in both pelvic limbs and in the right thoracic limb. No response was observed in left thoracic limb. Flexor reflexes and patellar reflexes could not be elicited due to extensor rigidity. Sensation was normal in all four limbs.
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The appendicular muscles of the presented cat showing persistent tonic spasm, with the stronger muscles overpowering the weaker ones. Note the extensor rigidity of the hind limbs, shoulders, and elbows. The carpal joints are in partial flexion.
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Wounds on the foot of the left thoracic limb.
Complete blood count and chemistry panel were within reference range, except for a marked increase in creatine kinase (CK) 2300 U/l (reference range 0–314 U/l). Increased CK activity was probably related to muscle trauma secondary to constant hypertonicity and prolonged recumbency. Based on onset and progression of clinical signs and the presence of a recent wound, a presumptive diagnosis of moderate generalised tetanus was made.
The wounds on the III and IV digits of the left thoracic limb were debrided and irrigated with hydrogen peroxide (3% concentration). A single dose (100 IU/kg) of human tetanus antitoxin (Tetabulin, Baxter) was administered intramuscularly. A combination of amoxicillin and clavulanate (Synulox, Pfizer) was administered subcutaneously and then orally at a dose of 12 mg/kg every 12 h. In addition, metronidazole (Flagyl, Pharmacia and Upjohn, Zambon Italia s.r.l.) was given orally at a dose of 15 mg/kg once a day. The cat was hospitalised and maintained on padded bedding in a quiet dark environment with minimal stimulation. Diazepam (0.2 mg/kg intravenously (IV)) was administered every 8 h to control muscle spasm with little improvement in appendicular muscle rigidity. The cat was not able to move on her own, therefore she was gently turned every 4 h. For the first few days, thebladder was manually expressed every 8 h, as the cat could not empty it completely as a result of external urethral sphincter hypertonus. The cat was able to prehend and swallow canned food. She was fed a high-fibre diet (w/d, Hill's) in order to prevent constipation. Lactated Ringer's (Lactated Ringer's, Acme) was administered IV at a rate of 2 ml/kg/h to maintain hydration and electrolyte balance.
Since the day 6 of treatment, the cat's status progressively improved, and voluntary movement gradually returned to the pelvic limbs, right thoracic limb, and lastly to the left thoracic limb. Three weeks after presentation, the cat had fully recovered.
In the present case, the most likely portal of entry for clostridial organisms was the neglected wound on the extremity of the left thoracic limb, a hypothesis supported by skeletal muscle rigidity, becoming evident first in the left thoracic limb and subsequently involving the other limbs. This phenomenon reflects the typical course of tetanus, as the majority of toxin is absorbed by the peripheral nerve terminals near the contaminated wound and transported intraaxonally to the spinal cord. The incubation period was 10 days in our case. Cats have been reported to develop clinical signs 3 to 21 days following the organism's entrance into the body (Lee and Jones 1996, Greene 1998). The incubation period depends on proximity of the injury to the CNS, degree to which local oxidation–reduction potential favours toxin production, and number oforganisms present (Baker et al 1988).
Thoracic limb rigidity with elbow extension and carpal flexion has been previously described in cats with tetanus, and seems to be a feature of cats, as dogs with tetanus present with carpal extension (Baker et al 1988, Malik et al 1989).
Diagnosis of tetanus is usually based on history and clinical signs (Sanford 1995). However, clinical diagnosis may be particularly difficult in cats, as they are more likely to develop mild forms of the disease due to their innate resistance to tetanospasmin. The present case first developed localised tetanus to the left thoracic limb that subsequently progressed to moderate generalised tetanus. Intracranial signs were absent upon presentation. Diagnosis was based on the presence of a neglected wound, and on onset and progression of persistent involuntary muscle rigidity in a mentally alert animal. Prompt diagnosis and treatment of tetanus are the keys to a successful outcome. Untreated cases can prove fatal due to respiratory failure (Greene 1998). The clinical diagnosis of tetanus can be confirmed by electromyography, measurement of serum antibody titres to tetanus toxin, and isolation of C tetani from the wound. This latter procedure is unrewarding in the majority of cases (Greene 1998). Measurement of serum antibody titres to tetanus toxin has been used to substantiate the diagnosis of generalised tetanus (Baker et al 1988). Values must be compared with those of control animals (Baker et al 1988). The main limitation of these two laboratory procedures is that results are not available for days to weeks. On the contrary, electromyography provides fast and useful diagnostic information in cats with either localised or generalised tetanus. Changes in muscle electrical activity are characteristic and consistent with a continuous pattern of motor unit activity during rest and general anaesthesia (Jain et al 1982, Lee and Jones 1996). Unfortunately, electromyography was not readily available in our case.
Management of tetanus included the use of human antitoxin to neutralise any toxin unbound to the CNS or yet to be formed, wound debridement and irrigation with peroxide along with antimicrobical therapy to kill any vegetativeC tetani organisms present in the wound, and supportive care. Human antitoxin was administered intramuscularly with no complications. The product we used is approved for intramuscular use only. Alternatively, antitoxin of equine origin can be used IV, intramuscularly, or subcutaneously. Intravenous administration of antitoxin has been reported to be superior to intramuscular or subcutaneous administration (Greene 1998). However, intravenous antitoxin is associated with a high prevalence of anaphylaxis (Godwin 1985). To prevent this complication, an initial test dose (0.1–0.2 ml) of equine antitoxin can be given subcutaneously or intradermally 15–30 min before the administration of the intravenous dose (Greene 1998). Antitoxin administration should not be repeated owing to increased risk ofanaphylaxis.
Localisation and debridement of the wound site increase the chances of recovery. Hydrogen peroxide should be used to flush the wound, as it increases oxygen tension, which inhibits obligate anaerobes (Greene 1998).
For years, Penicillin G has been considered the antibiotic of choice for both humans and animals. However, recent studies in humans showed that metronidazole was more effective than penicillin G procaine in reducing hospitalisation time and mortality rate (Ahmadsyah and Salim 1985, Ernst et al 1997). Metronidazole is bactericidal against most anaerobes and achieves effective therapeutic concentrations even in anaerobic tissues (Greene 1998). Furthermore, penicillin is a GABA antagonist, just like tetanus toxin.
Supportive care is imperative for the successful management of tetanus. With appropriate treatment, generalised tetanus usually resolves in a few weeks. Localised tetanus may take up to 4 months to resolve (Malik et al 1989, Braund 1994). Cases of localised tetanus may progress to the more generalised form, and if there is improvement in these cases, the signs that were present first take longer to resolve. This phenomenon was observed in our case, as voluntary muscle function was recovered first in the pelvic limbs, then in the right thoracic limb, and lastly in the left thoracic limb. We felt it was worth reporting this case of ‘moderate generalised’ tetanus to help readers in the diagnosis of similar cases, as the early diagnosis of animals with an unusual presentation of a relatively rare disease is always difficult. Furthermore, to our knowledge, a case of feline tetanus with no intracranial signs and severe spastic tetraparesis has not been reported previously.