Tetanus: Causes, Symptoms, and Prevention

TETANUS By. Dr. Hussein AlNaji

2 ETIOLOGY Tetanus is caused by C. tetani, a gram positive, spore-forming obligate anaerobe bacillus. It is a ubiquitous organism and a commensal of the gastrointestinal tract of domestic animals and humans. The organism forms highly resistant spores that can persist in soil for many years..

3 Occurrence Tetanus occurs in all parts of the world and is most common in closely settled areas under intensive cultivation. It occurs in all farm animals, mainly as individual. Case Fatality Rate In young ruminants the case fatality rate is over 80%, but the recovery rate is high in adult cattle. Source of Infection C. tetani organisms are commonly present in the feces of animals, especially horses, and in the soil contaminated by these feces.

4 Transmission 1. The portal of entry is usually through deep puncture wounds. 2. Introduction to the genital tract at the time of parturition is the usual portal of entry in cattle. A high incidence of tetanus may occur in lambs following castration, shearing, docking, vaccinations, or injections of pharmaceuticals, especially anthelmintics. 3. Neonatal tetanus occurs when there is infection in the umbilical cord associated with unsanitary conditions at parturition. 4. Outbreaks of idiopathic tetanus occur occasionally in young cattle without a wound

Pathogenesis 5 Spores germinate to their vegetative form to proliferate and produce tetanolysin, tetanospasmin and neurotoxin only if environmental conditions are attained, lowering of O2 tension. The tetanus spores remain localized at their site of introduction and do not invade surrounding tissue Of the three mentioned exotoxins, tetanospasmin is the most relevant for the pathophysiology of the condition. tetanolysin caused local tissue necrosis. neurotoxin, or nonspasmogenic toxin, which is a peripherally active for the pathophysiology of tetanus . Tetanospasmin diffuses to the systemic circulation, is bound to motor end plates, and travels up peripheral nerve trunks via retrograde intra axonal transport to the CNS

6 it blocks the release of neurotransmitters such as GABA and glycine, which are essential for the synaptic inhibition of gamma motor neurons in the spinal cord it leads to an unmodulated spread of neural impulses producedby normally innocuous stimuli, causing exaggerated responses and a state of constant muscular spasticity Death occurs by asphyxiation caused by fixation of the muscles of respiration.

CLINICAL FINDINGS 7 1- The incubation period varies between 3 days and 4 weeks. In sheep and lambs cases appear 3 to 10 days after shearing, docking, or castration. 2- Initially, there is an increase in muscle stiffness, accompanied by muscle tremor. 3- There is trismus with restriction of jaw movements. 4- Prolapse of the third eyelid. 5- Stiffness of the hindlimbs causing an unsteady, straddling gait; and the tail is held out stiffly, especially when backing or turning. 6- Retraction of the eye and prolapse of the third eyelid (a rapid movement of the third eyelid across the cornea followed by a slow retraction) is one of the earliest and consistent signs (with the exception of sheep) and can be exaggerated by sharp lifting of the muzzle or tapping the face below the eye.

8 7. The animal may continue to eat and drink in the early stages but mastication is soon prevented by tetany of the masseter muscles and saliva may drool from the mouth.. 8. Muscular tetany increases and the animal adopts a sawhorse posture. 9. The course of the disease and the prognosis vary both between and within species. The duration of a fatal illness in horses and cattle is usually 5 to 10 days, but sheep usually die on about the third or fourth day. NECROPSY FINDINGS There are no gross or histologic findings by which a diagnosis can be confirmed.

Differential Diagnosis 9 All species Ruminants Strychnine poisoning Meningitis Hypomagnesemia (cows, sheep and calves) Horses White muscle disease Hypocalcemic tetany (eclampsia) Polioencephalomalacia. Acute laminitis Enterotoxemia Hyperkalemic periodic paralysis Myositis, particularly after injection in the cervical region

10 TREATMENT These are the main principles in the treatment of tetanus: 1. Eliminate the causative bacteria bythe parenteral administration of penicillin in large doses (44,000 IU/kg IV) . Other antimicrobials that have been proposed include oxytetracycline (15 mg/kg), macrolides, and metronidazole. 2. Neutralize residual toxin administering tetanus antitoxin.

11 3. Control muscle spasms until the toxin is eliminated or destroyed by used relaxation of the muscle tetany can be attempted with various drugs. Chlorpromazine (0.4 0.8 mg/kg BW intravenously, or 1.0 mg/kg BW intramuscularly, three or four times daily) and acepromazine (0.05 mg/kg BW three to four times daily) administered until severe signs subside, are widely used in horses. A combination of diazepam (0.1 0.4 mg/kg) and xylazine (0.5 1.0 mg/kg intravenously or intramuscularly) 4. Maintain hydration and nutrition by by intravenous or stomach-tube feeding during the critical stages when the animal cannot eat or drink. 5. Provide supportive treatment

12 Control Regular vaccination if tetanus toxoid (R-1) Tetanus antitoxin (1500 IU per dose IM in unvaccinated animals with fresh wounds) (R-1) IM, intramuscularly, IV, intravenously.

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