Tetanus

Chapter 102 Tetanus



Simon R. Platt, BVM&S, DACVIM (Neurology), DECVN, MRCVS



KEY POINTS



• Tetanus is the result of a bacterial infection by Clostridium tetani following a skin wound, surgery, or even parturition.

• The clinical signs are due to the effects of an exotoxin produced by the bacillus that prevents neurotransmitter release.

• Common signs include spasms of the masticatory, pharyngeal, and facial muscles, but the whole body can be involved.

• Definitive diagnosis is difficult in many cases unless serum antibodies can be associated with the bacterial toxin.

• Treatment is initiated immediately on suspicion of the disease based on clinical signs.

• Tetanus antitoxin can prevent further deterioration of the patient from unbound toxin at time of treatment, but improvement relies on regrowth of axons and nerve terminals.

• Broad-spectrum anaerobic antibiotics, wound cleansing, muscle relaxants, and sedatives are the important constituents of medical management.

• A quiet environment and intensive nursing care are essential for the success of treatment regimens.


ETIOLOGY


Tetanus is caused by the neurotoxins released by Clostridium tetani, a motile, gram-positive, nonencapsulated, anaerobic, spore-forming bacterium. The toxin is produced during vegetative growth of the organism in a suitable environment.1 The deoxyribonucleic acid for this toxin is contained in a plasmid and is antigenically homogenous. The organism’s resistant spores are ubiquitous, with a natural habitat in moist fertile soil; however, they can survive indefinitely in dusty indoor environments. Resistance of the spores has been proven to boiling water and an autoclave temperature of 120°C for up to 20 minutes.2 However, the vegetative phase of this bacterium is susceptible to chemical and physical inactivation. Organisms can be isolated from the feces of dogs, cats, and humans, but presence of the organism does not indicate infection because not all strains possess the plasmid.1


Cats and dogs are considered to be relatively resistant to infection by the bacterium, especially when compared with horses and humans. In part the resistance in these species is due to the inability of the toxin to penetrate and bind to nervous tissue.2



PATHOGENESIS


Tetanus develops when spores are introduced into wounds or penetrating injuries. Most cases develop after skin wounds, but infection can follow parturition or ovariohysterectomy.3-5


Under anaerobic conditions found in necrotic or infected tissue, the tetanus bacillus secretes two exotoxins: tetanospasmin and tetanolysin. Tetanolysin is capable of locally damaging otherwise viable tissue surrounding the infection and optimizing the conditions for bacterial multiplication.1


Tetanospasmin leads to the clinical syndrome of tetanus. This toxin may constitute more than 5% of the weight of the organism.1 It is a two-chain polypeptide of 150,000 daltons that is initially inactive, made up of a light and a heavy chain. The light chain acts presynpatically to prevent neurotransmitter release from affected neurons. Tetanospasmin binds to the membranes of the local motor nerve terminals. If toxin load is high, some may enter the bloodstream from where it diffuses to bind to nerve terminals throughout the body, and may even enter the central nervous system (CNS) through an intact blood-brain barrier. The toxin is then internalized and transported intraaxonally and in a retrograde fashion to the cell body at a speed of 75 to 250 mm per day.1,2 Transport occurs first in motor and later in sensory and autonomic nerves. Further retrograde intraneural transport occurs with toxin spreading to the brain stem in a bilateral fashion, up the spinal cord. This passage includes retrograde transfer across synaptic clefts by a mechanism that is unclear.


It is after internalization in inhibitory neurons that the light chain becomes activated; at this stage the toxin is no longer accessible for neutralization by antitoxin.6,7 It prevents neurotransmitter release by cleaving and inactivating synaptobrevin, a membrane or “docking” protein necessary for the export of intracellular vesicles containing the neurotransmitter.8 In addition to disrupting docking proteins, the toxin may lead to cross-linking of synaptic vesicles to the cytoskeleton, further preventing neurotransmitter release.9


The toxin predominantly affects inhibitory interneurons, inhibiting release of glycine and γ-aminobutyric acid (GABA).1,7 Interneurons inhibiting α-motor neurons are first affected, and the motor neurons lose inhibitory control. The disinhibitory effect on the motor neuron may cause diminution of function at the neuromuscular junction, so the clinical effect is dissimilar to that of the related botulinum toxin. Medullary and hypothalamic centers may also be affected. Disinhibited autonomic discharge leads to disturbances in autonomic control, with sympathetic overactivity and excessive plasma catecholamine levels.


Neuronal binding of toxin is thought to be irreversible. Recovery requires the growth of new nerve terminals, which explains the long duration of tetanus.10



CLINICAL PRESENTATION


Clinical signs can take up to 3 weeks from the onset of infection to be apparent, although most cases exhibitsymptoms within 5 to 12 days.11 The clinical signs initially can be localized or generalized, with the former possibly being more common in dogs and cats. A study of 38 dogs with tetanus revealed that ocular and facial changes were the most common initial signs. Localized signs begin proximal to the site of introduction of the infection and can include single muscle rigidity, entire limb rigidity, and facial muscle spasms. The clinical signs may progress with more extensive muscle involvement.12 Generalized signs include a stiff gait affecting all limbs, increased muscle tone, dyspnea, an elevated tail and a “sawhorse stance,” although the animal may become uncomfortable standing with such excessive muscle activity. At least 50% of dogs will progress within a median of 4 days (range 0 to 14 days) to recumbency with severe muscle spasms.


Involvement of the head can lead to spasms of the masticatory and pharyngeal muscles, causing trismus (lockjaw) and dysphagia. This can be functionally exacerbated by increased salivation, increased bronchial secretions, and increased respiratory rate resulting from involvement of the parasympathetic and somatic cranial nerve nuclei. Regurgitation and gastroesophageal reflux can result rarely from esophageal hiatal hernia and megaesophagus, which may lead to aspiration pneumonia when combined with the problems described earlier.13 Excessive contraction of the facial muscles causes erect ears and a wrinkled forehead (Color Plate 102-1), and gives the animal a characteristic sneering of the lips known as risus sardonicus, or the sardonic grin (Color Plate 102-2).7 Additionally, the patient can exhibit protrusion of the third eyelid and enophthalmos, resulting from retraction of the globe from hypertonus of the extraocular muscles.12 Reflex muscle spasms can occur in animals with generalized tetanus or intracranial involvement; these may be painful and resemble seizure activity, affecting agonist and antagonist muscle groups together.12 Severe progression of signs can cause recumbency, opisthotonus, seizure-like activity, respiratory paralysis, and central respiratory arrest, potentially causing death if not rapidly recognized and managed.7 Death was reported in 18% of dogs (7 of 38) in one retrospective study, and 6 of these dogs demonstrated concurrent autonomic signs.


It is possible to see an effect on the autonomic system evidenced by episodes of bradycardia and tachycardia, hypertension, marked vasoconstriction, and pyrexia.12,14,15 A study of 38 dogs with tetanus revealed that 37% demonstrated abnormalities of blood pressure or rectal temperature, or both, consistent with autonomic disturbance. In the mild generalized cases, autonomic involvement may be manifested by dysuria and urinary retention, constipation, and gaseous distention. In humans, “autonomic storms” occur, causing marked cardiovascular instability, severe hypertension alternating with profound hypotension, and even recurrent cardiac arrest.1 During these “storms,” plasma catecholamine levels are raised up to 10-fold, similar to levels seen in animals with a pheochromocytoma.1


A neurologic examination of these patients can reveal normal initiation of a response to postural reaction testing but a stiff and reduced motor response.2 Myotatic reflexes are generally accentuated and flexor reflexes depressed, but both may be difficult to assess because of the extreme rigidity of the limbs. Although a complete neurologic examination is always ideal, it should be emphasized that animals can become very sensitive to tactile, visual, or auditory stimulation that can exacerbate clinical signs, occasionally causing a mild, generalized form of the disease to progress to a crisis situation.

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Tetanus

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