Equine Health Update EHU Vol 21 Issue 01 | Page 37

CPD Article | EQUINE Clinical signs There is usually a history of a wound or surgery in the preceding 1-4 weeks 10 . At first, clinical signs may be vague with a mild lameness or stiffness and this may be particularly localised to the contaminated wound area 8 ; colic may also be noted. The clinical signs will progress over the next 24 hours with a more generalized stiff or spastic gait exhibited and the tonic spasms of the striated muscles 8 can be seen. The progression of the disease depends on a poor vaccination status, the extent of infection and the size and age of the horse 5 . Older and larger animals seem to be less severely affected 8 . There is no confirmed incubation period 10 as clinical signs are dependent on the amount of tetanospasmin toxin that is produced within the favourable anaerobic environment; however signs are often evident 10 days after a deep penetrating wound 2 12 . Common signs seen are 5,9,10 : • Trembling, sweating and mild pyrexia, • Flared nostrils and erect ears, • “Sawhorse” stance with raised and rigid tail, • Extensor muscle rigidity that is exacerbated with external stimulus, • Enophthalmos and prolapse of the third eyelid especially after a stimulus, • “Lockjaw” from the spasm of master muscles resulting in the inability to prehend or to masticate, • Dysphagia, ptyalism and laryngeal spasm, • Recumbency due to marked extensor rigidity making voluntary movement impossible, • Respiratory failure due to the spasm of respiratory muscles and death, Further complications include: decubital ulcers from prolonged recumbency, regurgitation or aspiration pneumonia due to the laryngeal spasm, dysuria due to hypertonic urethral sphincter and constipation with gaseous distension as a result of the hypertonia of the anal sphincter and lack of exercise 8 . Involvement of the autonomic nervous system results in cardiac arrhythmias, tachycardia and hypertension. Diagnostic approach A detailed clinical examination coupled with the history of a recent wound and an unvaccinated horse allows for a presumptive diagnosis 2,9 of tetanus which is important as an early diagnosis is a significant factor in improving the treatment outcome 2 . Occasionally horses may still develop tetanus despite being vaccinated 5 but this is unusual. Confirmation of the infection by anaerobic culture or gram staining is not usually attempted as C.tetani is often found in low concentrations within the wound and strict anaerobic culture is required, therefore there is no reasonable or easy diagnostic confirmation 4 or testing readily available. Radiographs or thoracic ultrasonography of horses suspected to have developed aspiration pneumonia may be of use 5 in case prognosis and management. Haematology, serum biochemistry and CSF analysis are usually unremarkable8. There are no characteristic post mortal lesions that can be ascribed to the tetanus toxin. Treatment Tetanospasmin binding is extremely difficult to combat and new interneuronal synapses need to develop to replace those inactivated by the bound toxin8, therefore recovery from an infection is slow. Treatment success is based on the following goals 8 : interruption of toxin production, neutralization of unbound toxin, muscular spasm control and supportive care. To stop further tetanospasmin production, the use a parenteral antibiotic is imperative. The following systemic antimicrobials can be administered: penicillin, • Volume 21 Issue 1 | March 2019 • 37