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Tetanus in Steers Following Failed Ring Castration

Katelyn Braine, District Veterinarian, Murray Local Land Services, Deniliquin NSW and Andrew Lean, Veterinarian, Finley Veterinary Clinic, Finley NSW

Posted Flock & Herd February 2022


This case report describes a disease investigation of neurological signs and death in steers due to tetanus following failed ring castration. Tetanus is a highly fatal disease characterised by hyperaesthesia, tetany, and convulsions. It is caused by a neurotoxin produced by Clostridium tetani bacteria from a localised wound.1 Tetanus can affect all domestic animals with horses being the most susceptible.2 Although tetanus is endemic in Australia, it is not commonly seen in cattle.1 This is likely due to lower disease susceptibility of cattle and the widespread use of clostridial disease vaccination.


In October 2021, a cattle producer called their Murray Local Land Services District Veterinarian regarding recumbency and death in a mob of 39 weaner cattle. The producer had one deceased steer and another steer down on the point of death. The weaners were 6-7 months of age and had been weaned around 10 days prior. The mob consisted of around 19 steers and 20 heifers. Castration rings were used at weaning to mark all the steers. Both the steers and heifers were unvaccinated and undrenched. The cattle were grazing a mostly ryegrass pasture over the previous week. There was no supplementary feeding at the time of the disease investigation, but the cattle had been supplementary fed with silage up until August.

Clinical Findings

One steer showing clinical signs was examined at the initial visit. The steer was alive and presented in lateral recumbency (figure 1) with extended stiff legs, opisthotonos, severe dyspnoea, tachycardia, and a temperature of 42.5°C. On examination of the cranial nerves, the menace, palpebral and corneal reflexes were normal, there did not appear to be any blindness and the jaw was hard to open but not locked. The castrating ring had caused an infected wound around the neck of the scrotum (figure 2). The ring had lost its pressure and was no longer effective. The steer was euthanised with a captive bolt and a necropsy was conducted.

Image of moribund steer lateral recumbency
Figure 1: Affected steer presenting in lateral recumbency with extended stiff legs and opisthotonos
Image of bovine scrotal strangulation wound
Figure 2: Scrotal wound caused by the ring castration

A revisit was conducted four days later as a further two steers had died during this time, and another four steers were now recumbent. At the revisit, all four steers presented in lateral recumbency with signs of extended stiff legs, opisthotonos, severe dyspnoea and tachycardia. Menace, palpebral and corneal reflexes were again normal, and no blindness was observed. Lockjaw was present in all recumbent steers and the ears appeared erect. There was no evidence of paddling marks on the ground around the steers. All four steers also had scrotal wounds caused by the castration rings. The temperatures of these steers ranged from 39.8 to 40.0°C.

Another 11 steers were examined in the yards from a distance. These steers were able to walk around the yards but most of them were observed to have a stiff gait. There was no evidence of blindness as all steers were able to navigate the yards. Flicking or protrusion of the third eyelid (video 1) was observed in at least three of the steers. Scrotal swelling and scrotal wounds due to the castration rings was observed to varying degrees.

Video 1: Steer showing clinical sign of a protruding third eyelid

The producer reported that the deaths were occurring within 48 hours of the steers becoming recumbent.

No clinical signs or deaths had been observed in the heifers that had been running with the steers.

Necropsy Findings

The necropsy conducted at the initial visit was relatively nonspecific with the most significant findings being enlarged mesenteric lymph nodes and sparse thick, creamy intestinal contents. Plastic silage rap was also observed in the rumen.

Urinalysis was performed using a Combur 9 urine dipstick (Table 1).

Table 1: Urine dipstick results conducted at post-mortem

Urine dipstick Result
Leukocytes Negative
Nitrite Negative
pH 6
Protein 2+
Glucose 1+
Ketones Negative
Urobilinogen Normal
Bilirubin Negative
Blood 4+

Laboratory Findings

Samples from the post-mortem were collected from the initial visit and sent to Laboratory Services at Elizabeth Macarthur Agriculture Institute (EMAI).

Blood biochemistry revealed marked elevations in Creatinine Kinase (CK) and Aspartate aminotransferase (AST) consistent with either a primary or secondary myopathy, marked haemoconcentration and hyperalbuminemia suggestive of dehydration, and moderate to marked azotemia (Table 2).

Table 2: Blood biochemistry results

Sample result Normal reference values
GGT (u/L) 18 0 - 35
GLDH (u/L) 2 0 - 30
AST (u/L) 763 0 - 120
BIL (umol/L) 15.0 0 – 24.0
CK (u/L) 37713 0 - 300
UREA (mmol/L) 13.6 2.1 – 10.7
CREAT (umol/L) 415 0 - 186
PHOS (mmol/L) 4.02 0.80 – 2.80
UREA/CREA 0.03 0 - 0.07
PROTEIN (g/L) Assay interference by haemolysis 60 - 85
ALBUMIN (g/L) 43.2 25 - 38
GLOB (g/L) Assay interference by haemolysis 30 - 45
ALB/GLOB Assay interference by haemolysis 0.7 - 1.1
BHB (mmol/L) 0.99 0 - 0.8
Ca (mmol/L) 1.95 2.0 – 2.75
Mg (mmol/L) 1.06 0.74 - 1.44
Hapto (g/L) 1.03 0 - 0.3
Serum HB (g/dL) 1.25 0 - 0.2

Blood haematology revealed a marked leucocytosis characterised by a marked neutrophilia, lymphocytosis and a mild monocytosis. The blood lead level was not elevated (Table 3).

Table 3: Blood hematology and lead results.

Sample result Normal reference values
PCV (%) 54 23 - 44
RBC (1012/L) 12.22 5 – 8
HB (g/dL) 18.6 8 - 16
MCV (fL) 44 44 - 62
MCHC (g/dL) 34 30 - 35
MCH (pg) 15 14 - 20
WBC (109/L) 28.5 4 - 12
Band N. (109/L) 0.0 0 - 0.12
Neutro. (109/L) 18.53 0.6 – 4.0
Lympho. (109/L) 9.12 2.5 – 7.5
Mono. (109/L) 0.86 0.03 - 0.84
Eosino. (109/L) 0.0 0 – 2.4
Baso. (109/L) 0.0 0 – 0.2
Platelet (109/L) 319 100 – 800
Blood lead (umol/L) < 0.10 < 0.24

Epsilon toxin bacteriology assay conducted on small intestinal contents was negative.

Histology was conducted on the liver, kidney and intestinal samples, revealing a hepatic sinusoidal neutrophilia.


A diagnosis of tetanus was made at the second visit based on the unvaccinated status of the weaner cattle, the presence of deep wounds caused by the castration ring, and the clinical signs observed in the steers.

Diagnosis was unable to be made at the lab due to the lack of a Clostridium tetani specific assay.


Following the initial visit all cattle in the mob were vaccinated with 7-in-1 vaccine and a booster shot was given four weeks later.

Twice daily systemic penicillin treatment was initiated by the producer in all steers, three days after the initial visit, when more steers started to show clinical signs. A dose rate of around 23,000 IU/kg was administered IM. The producer discontinued the penicillin treatment after all steers had received three doses.

To prevent further disease progression and deaths, a private veterinarian was engaged to assess and treat the remaining nine steers. All remaining steers had severe necrotic wounds to the neck of the scrotum due to the castration rings. Following this assessment all steers were castrated using emasculators. Any remaining necrotic tissue was debrided with gauze and irrigated to clean the wound. The producer declined any further treatment with penicillin and/or tetanus antitoxin.


Cl. tetani is a gram-positive anaerobe that can be found in the soil and the gastrointestinal tract of herbivores. Under aerobic conditions Cl. tetani produce large spores that can remain viable in the soil for years.1,3

The bacteria will multiply in an anaerobic environment, usually a wound or necrotic tissue, producing the neurotoxin tetanospasmin that spreads from the infection site to the spinal cord. Here the toxin stops the release of glycine and gamma-aminobutyric acid (GABA) from presynaptic nerve endings, thus inhibiting the inhibitory neurons of the spinal cord.1,2,3 Cl. tetani also produces the exotoxin, tetanolysin, which has a necrotising effect on tissues. This may further decrease tissue oxygenation and encourage proliferation of the bacteria.1,3

The effects of the neurotoxin results in the characteristic clinical signs of tetanus including a stiff, stilted gait particularly of the hindlimbs, muscle spasm or tremors, protrusion of the third eyelid, and lockjaw. Signs of a mild degree of bloat can also be seen in the early stages of the disease.1,3 As in this case, producers may report sudden death as the first sign if clinical signs have not been observed.1

The incubation period of tetanus depends on the time taken for colonisation of the bacteria and production of the toxin to occur after the initial infection, and on the distance between the site of infection and the spinal cord.1 On average clinical signs are usually seen around 10-14 days after infection, as was seen in this case, but may be seen up to 60 days post infection.1,3

There are no specific pathological lesions on necropsy or reliable laboratory tests to confirm a diagnosis of tetanus.1,3 Diagnosis is, therefore, generally made on the distinctive clinical signs of the disease and history.

Cases of tetanus in livestock mainly occur as individual, sporadic cases, however outbreaks can occasionally be observed.2 In cattle, most cases of tetanus are associated with castration, tail docking and calving.1

In this case the producer lost a total of 11 of 19 steers with the mortalities occurring between 10 – 26 days post application of the castration rings. These steers were vulnerable to tetanus infection as they were not vaccinated against clostridial disease,and the castration rings were not used on the calves when they were small enough to work properly. This timing of application resulted in failure of the rings to apply enough pressure through the large amount of scrotal tissue of a six-month-old weaner to cut off blood supply to the scrotum and testicle. The result was an area of ischaemic necrosis around the neck of the scrotum, an ideal environment for the proliferation of Cl. tetani. The producer in this case also utilises strip grazing, which had the potential to increase the density of faeces in the area being grazed, thus increasing the risk of exposure to Cl. tetani.

Differential diagnoses associated with similar neurological signs include lead toxicity and polioencephalomalacia (PEM). Lead toxicity was ruled out based on a blood lead level <0.24 umol/L. PEM was considered unlikely because there was nothing in the dietary history suggestive of PEM, and the fact that the clinical signs and deaths were isolated to only the steers and not seen in the co-grazing heifers. In addition, the clinical signs of the protruding third eyelid and the lockjaw are characteristic of tetanus and are not seen with either lead toxicity or PEM. Furthermore, signs of blindness and absence of menace or palpebral responses as associated with lead toxicity or PEM were not seen in this case. PEM can be excluded at the laboratory through histology of the brain; however, a brain was not submitted in this case.

The effectiveness of treatment of tetanus cases depends on the stage of the disease. The earlier the treatment is administered, the more likely it is to be effective.1 Cases showing advanced clinical signs are unlikely to respond to treatment.3 The principles for treatment and management focus on the following: (i) neutralisation of the toxin; (ii) prevention of further toxin production; and (iii) relaxation of tetany and supportive treatment.

Tetanus antitoxin can be used to neutralise the tetanus toxin, but only if the toxin has not become bound to the nerve.1,3 Generally tetanus antitoxin is of little value once clinical signs have appeared.2 Preventing further toxin production may be achieved by eliminating the organism producing the toxin through debridement and irrigation of the wound, and high dose penicillin treatment. Dose rates of 22,000 - 44,000 IU/kg IM penicillin every 12 hours have been reported for cases of tetanus in cattle and treatment is generally required over several days.3 However, if clinical signs are advanced, treatment using penicillin may also be of little value.

While cattle are reported to be less susceptible to tetanus compared to other livestock,1,3 vaccination of cattle with clostridial vaccines (5-in-1 or 7-in-1) is extremely effective at reducing the risk of tetanus.1 Dams should be given an annual clostridial vaccination booster before calving to maximise maternal antibody protection and provide protection in the first few weeks of life. As this maternal antibody protection diminishes over time, calves will then need to receive two clostridial vaccinations, 4-6 weeks apart. To achieve a high level of protection against tetanus at marking, it is recommended that calves should receive their first dose 4-6 weeks prior to marking and then their second dose at marking.4 While some immunity develops after the first vaccination, this protection is generally temporary, and a second vaccination is needed to achieve long lasting immunity.1

Ideally, castration of calves should be performed before they are six months of age, and generally the younger the calf at the time of castration the better it is for the calf. Early castration has been shown to reduce pain to the calf, decrease the risk of bleeding and infection, and result in a shorter recovery time after castration. Castration using rubber rings is recommended in calves from two days to two weeks old. Other methods of castration such as using a knife should be used in calves older than two weeks of age. It is also important to note that castration of calves older than six months of age is illegal under some state and territory legislation, unless completed under veterinary supervision with the use of local anaesthesia or analgesia.4

Utilising good hygiene at calf marking is also an effective at preventing tetanus. Parkinson, Vermunt & Malmo (2010) also report that the administration of tetanus antitoxin prior to high-risk periods may also be used as a preventative measure.

Not only was this case an interesting case to investigate given tetanus is not commonly seen in cattle, but it also highlighted the importance of continual education of producers around the use of clostridial vaccination programs and castration practices of livestock, as discussed above.


Thank you to District Veterinarian, Linda Searle for her help with talking through this case, the staff at EMAI for their assistance with laboratory testing, and to the veterinarians at the Finley Vet Clinic for their assistance with treatment of this case.


  1. Parkinson TJ, Vermunt JJ, Malmo J. Diseases of Cattle in Australasia. Vet Learn, Wellington, 2010
  2. Radostits O, Gay C, Hinchcliff K, Constable P. Veterinary Medicine; a textbook of the disease of cattle, horses, sheep, pigs, and goats. Saunders, U.S.A, 2006
  3. Garber JRO, Smith BI. Tetanus in Cattle: review and case description of clinical tetanus in a Holstein heifer. The Bovine Practitioner. 2011; 45:2:110-117
  4. Newman R. A guide to best practice husbandry in beef cattle: branding, castration and dehorning. Meat and Livestock Australia, 2012


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