tetanus

Identity

Preferred Scientific Name

• tetanus

International Common Names

• English: tetanus in large animals

Overview

Most domestic species are susceptible to tetanus, and as in human beings, the limiting factor on incidence is probably vaccination. Some species, such as horses, are particularly prone to develop tetanus, and special care must be taken in any medically related procedure to avoid it. The disease has been extensively reviewed in the context of clinical disease and pathogenesis, and case reports are commonly found in the literature (Ratcliffe, 1989; Gardner, 1990; Hatheway, 1990; Bizzini, 1993; Green, 1993; Merrett, 1993; Songer, 1997, 1998; Pages, 1999; Bagley, 2000; Greene, 2000).

Hosts/Species Affected

Disease occurs frequently in horses (Edwards et al., 1989; Cygan, 1996; Sedrish et al., 1996; Ramachandran and Harbola, 1997a,b; Sakdinun et al., 1997), less often in other herbivores, and occasionally in pigs and carnivores. In the dog, tetanus often follows operative or other injuries (Wurst, 1988; Toolan, 1989; Benzerrak, 1990; Dieringer and Wolf, 1991; Bagley et al., 1994; Engels et al., 1995; Utpal and Gupta, 1997; Kjellerstedt, 1997). In cats (Bieringer, 1994), the disease is often localized rather than generalized (Malik, 1989; Takano et al., 1989; Touffut et al., 1992; Seyrek-Intas, 1995; Habibah et al., 1998).

Cattle may develop tetanus as a result of growth of C. tetani in the rumen (Wallis, 1963; Herd and Riches, 1964; Whitehead and Ellicott, 1996; Preece and Bostelmann, 1996; Spiece, 1997; Finni et al., 1998). Tetanus also occurs in cattle under other circumstances (Beattie, 1988; Ellison, 1992; Bhikane and Kulkarni, 1998), including following elastic castration (O’Connor et al., 1993). Sheep are also commonly affected (Buxton, 1991; Coda et al., 1996; Lewis, 1998), including one outbreak in which 3% of a group of 600 lambs developed tetanus following ear tagging (Aslani et al., 1998).

Other hosts have also been reported, including camelids (Lopez and Snyder, 1995), a buzzard (Kummerfeld et al., 1996), a domestic monkey (Sharma et al., 1990) and a falcon (Oaks, 1989).

Distribution

Large blocks of territory are not represented by readily accessible reports in the published literature. However, given the wide geographical distribution of published reports, it is probably reasonable to assume that tetanus occurs in most areas where hosts are available.

Distribution Table

The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Pathology

Gross and microscopic pathology in cases of tetanus is negligible to non-existent.

Diagnosis

Diagnosis of tetanus is often based upon clinical signs (Crossman, 1989; Gray et al., 1991), and clinical presentation is certainly a good basis for initiation of treatment. Confirmation of a diagnosis is on the basis of toxin detection, by way of mouse inoculation. An enzyme immunoassay has been developed for diagnosis, particularly in waterfowl. The definition of the enzyme activity of tetanus toxin may provide the basis for a specific assay for toxin detection.

Isolation of C. tetani by bacteriological culture is supportive, but a diagnosis cannot be based upon this finding.

List of Symptoms/Signs

Disease Course

Spores of C. tetani are introduced to animal hosts, usually traumatically; infection can also occur via the umbilical stump, contamination of surgical wounds, injection sites, or docking, castration and ear tagging wounds, or following damage to the reproductive tract during labour and delivery (Char et al., 1993). The wound may be so trivial that it goes unnoticed, but at some level, necrosis, with reduced oxygen and lowered redox potential, are required.

Tetanus toxin is produced after germination of spores (Shoesmith and Holland, 1972; Wells and Balish, 1983). The incubation period ranges from 24 h to 2 weeks (Chapleo, 1991), depending on the toxinogenicity of the strain, rate of toxin transfer to target tissues and the relative host sensitivity (Kryzhanovsky, 1981; Wellhöner, 1982). Ascending tetanus results from retrograde intra-axonal transport of toxin, via the peripheral motor nerve endings, to the neurons of the CNS. After passing across the synapse, toxin binds to presynaptic axonal terminals. Hyperactivity of motor neurons causes sustained spasms in the innervated muscles. Travelling within the spinal cord, toxin can affect other muscle groups.

Descending tetanus follows vascular dissemination of toxin; manifestation of this form of tetanus may begin in sites distant from the nidus of infection.

Early signs are muscular tremor and increased stimulus response, followed by impaired head and neck muscle function, and difficulty in chewing and swallowing due to lockjaw. Affected horses may have flared nostrils and stiffly erect ears, and the third eyelid is retracted (Calil et al., 1989). Tetanic spasms are followed by permanent rigidity of the muscles of the back and tail, with orthotonus. In a few days to 2 weeks, in young animals and adults, respectively, respiration becomes increasingly difficult, with eventual failure resulting in death (Calil et al., 1989; Crossman, 1989; Katitch, 1990). Mortality is at least 50% and is highest in the young. Incubation and disease progression are often longer in carnivores (Timoney et al., 1988).

Epidemiology

Spores of C. tetani are commonly found in soil, especially soil rich in animal manure (Wilkins et al., 1988). Vegetative cells and spores are often detected in the digestive tract of cattle, horses, sheep, dogs, chickens, rats, guinea pigs and humans (TenBroeck and Bauer, 1922). Studies of the prevalence of C. tetani in the environment have revealed rates of isolation from 25 to 65%. C. tetani can also be recovered frequently from fomites (Mitra and Das, 1993), and more than 25% of nails, tins, broken glass and wooden sticks yielded toxigenic isolates. Higher prevalence rates in the environment do not necessarily correlate with increased incidence of disease (Wilkins et al., 1988). Experimental inoculation of horses does not give rise to a long-term carrier state (Wilkins et al., 1988).

Impact: Economic

There are apparently no estimates of the economic importance of tetanus in domestic animals.

Zoonoses and Food Safety

Tetanus is not considered to be a zoonosis, nor are there likely to be significant food safety issues. The organism was found in large numbers on the skin of animals at slaughter (Chandran and Masillamony, 1991) and has been isolated from meat products (Schocken-Iturrino et al., 1988), but given the route of exposure which results in disease, this seems an unlikely source of disease for humans.

Disease Treatment

The three important facets of therapy are neutralization of preformed toxin, elimination of toxin production and symptomatic treatment of the patient (Lebedev et al., 1991; Pearce, 1994; Kollias Baker, 1999). Tetanus antitoxin provides immediate passive protection, but is much more effective when used prophylactically than therapeutically (Chang and Weinstein, 1957). Attention to the wound, if any is apparent, and administration of large doses of penicillin (Step et al., 1991) can be effective in halting production of toxin. Penicillin therapy on its own is often insufficient and should be accompanied by the use of antitoxin (Svedberg, 1999). Muscle relaxants and sedatives are usually useful, and artificial feeding may be necessary (van Ham and van Bree, 1992).

Prevention and Control

Innate resistance to tetanus occurs in some species, usually in the absence of specific antitoxic antibodies (Metchnikov, 1898). Acquired resistance requires circulating antitoxin, and widespread vaccination has greatly decreased the impact of tetanus on animal production (Manzat and Herman, 1999; Brunner and Danner, 1999). Passive immunity protects neonates for 2-3 months, after which they can be actively immunized with toxoid. Boosters are recommended at 1-5 year intervals. Recombinant DNA technology promises even more effective means of protection against tetanus (Mesnage et al., 1999).

Vaccines comprise multiple toxoids and bacterin toxoids; domestic animals are immunized against tetanus alone or combined with immunizations for other clostridia or other bacteria. Adverse effects may include infection site reactions.

References

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Char NL; Rajeswari KR; Reddy BVR, 1993. An outbreak of tetanus in sheep. Indian Veterinary Journal, 70(4):297-300; 4 ref.

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Habermann E, 1989. Structure and function of tetanus toxin. Approaches by DNA and protein chemistry. Natural toxins. Proceedings 9th World Congress on Animal, Plant and Microbial Toxins, Stillwater, Oklahama, August 1988., 102-109; 11 ref.

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Lebedev AV; Rodionov NN; Cheredeev OG, 1991. Treatment of tetanus in horses. Veterinariya (Moskva), No.4:36-38; 10 ref.

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Mânzat RM; Herman V; Ciorba D; Zlibut Z, 1996. Research concerning the antagonistic action between tetanus and botulinum toxins. Revista Româna de Medicina Veterinara, 6(3):263-267; 4 ref.

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Distribution Maps