Page 1100 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Nervous system 1075

VetBooks.ir introduced C. tetani may have healed by the time Clinical presentation
Clinical signs of tetanus occur within days to weeks
clinical signs are observed, which may compli-
cate diagnosis. Clinical cases of tetanus tend to be
unvaccinated. (2–21 days) of a wound becoming infected and
relate to muscle hypertonia, with superimposed
In an anaerobic environment, such as devitalised clonic paroxysmal muscular spasms (summarised in
tissue, C. tetani spores germinate and produce exo- Table 10.5). Mild and early signs include hyperaes-
toxins. These proteases include tetanospasmin, teta- thesia and a protruding nictitans membrane. The
nolysin and non-spasmogenic toxin. The action of patient may be reluctant to walk forward and have a
the latter two toxins has not been fully elucidated, stiff gait and a raised tail head. Contraction of the
but tetanolysin is thought to cause tissue necrosis. muscles of facial expression results in flared nos-
Like botulinum neurotoxin (BoNT), tetanospasmin trils, trismus (lockjaw), erect ears and an elevated
(TeNT) binds to the motor neuron nerve terminal. upper lip.
However, in contrast to BoNT, which acts locally at More severely affected animals are unable to walk
the neuromuscular junction, TeNT is transported in and may become recumbent with extensor rigidity,
a retrograde fashion up the motor neuron axon to the opisthotonus and severe trismus. Some patients may
spinal cord, where it accumulates in the ventral horn have seizures. Advanced and severe cases of tetanus
of the grey matter. Within the spinal cord, TeNT are unable to stand or eat, and die from respiratory
migrates trans-synaptically from the dendrites of failure due to spasm of the diaphragmatic and inter-
peripheral motor neurons into the inhibitory inter- costal muscles. Complications of severely affected
neurons, which are responsible for coordinated animals include: decubital ulceration from increased
voluntary muscle contraction. TeNT cleaves syn- recumbency, ileus, gastrointestinal (GI) impactions,
aptobrevin, a cell membrane protein responsible for pneumonia, myopathies, urine retention and cysti-
the release of inhibitory neurotransmitters (glycine tis. Dysphagia may lead to aspiration pneumonia.
in the spinal cord and gamma- aminobutyric acid Muscle hyperactivity and sweating cause dehydra-
[GABA] in the brainstem), leading to decreased tion and electrolyte abnormalities. Hyperaesthesia
suppression of muscular activity. combined with extensor muscle rigidity may cause

Table 10.5 Clinical signs of tetanus in the horse

SEVERITY
OF DISEASE CLINICAL SIGNS
Mild • Mild hyperaesthesia that may be exacerbated by performing a menacing gesture/slapping the neck and assessing
response (muscular spasm or a flashing nictitans membrane) (Fig. 10.26)
• Rigid posture: ‘saw-horse’ stance and stiff gait, but still able to walk (Fig. 10.27)
• Elevated tail head
• Altered facial expression and dysphagia: retracted lips; flared nostrils; caudal-pointing/erect ears; flicking/
prolapsing nictitans membrane
Moderate • Hyperaesthesia
• Limbs stiff, with generalised clonic muscular spasms
• Walks with difficulty
• Trismus present (‘lockjaw’), but can still eat and drink slowly
Severe • Severe hyperaesthesia, whereby mild external stimuli may lead to extreme extensor muscle rigidity/clonic muscle
spasm. In some cases, this clonic paroxysmal muscular spasm may cause a horse to fall down, or to fracture long
bones/pelvis
• Unable to walk, may be capable of standing
• Opisthotonus may be seen in recumbent cases (or standing foals)
• Severe trismus and reduced ability to prehend, masticate and swallow, or unable to ingest water or food