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In this episode, Dr. Lottie talks about tetanus. How disease develops, why the clinical signs differ between species, what we can actually do to treat it and what the best prevention methods are.
Timeline:
00:00 Intro
00:43 Case
01:50 Aetiology & Pathogenesis
05:29 Clinical Signs
08:01 Diagnosis
11:54 Treatment
16:19 Prevention
19:13 Key Points
Recommended Reading
- ‘Chapter 14 - Diseases of the Nervous System’ – in Veterinary Medicine - A Textbook of the Diseases of Cattle, Horses, Sheep, Pigs and Goats
- ‘Tetanus’ – in Blackwell’s Five-Minute Veterinary Consult: Equine
References
- Popoff, M.R. (2020) ‘Tetanus in animals’, Journal of Veterinary Diagnostic Investigation, 32(2), pp. 184–191. Available at: https://doi.org/10.1177/1040638720906814.
- Linnenbrink, T. and McMichael, M. (2006) ‘Tetanus: pathophysiology, clinical signs, diagnosis, and update on new treatment modalities’, Journal of Veterinary Emergency and Critical Care, 16(3), pp. 199–207. Available at: https://doi.org/10.1111/j.1476-4431.2006.00192.x.
- Gohari, I.M. and Prescott, J.F. (2022) ‘Clostridium’, in Veterinary Microbiology. John Wiley & Sons, Ltd, pp. 309–334. Available at: https://doi.org/10.1002/9781119650836.ch34.
- Burkitt, J.M. et al. (2007) ‘Risk factors associated with outcome in dogs with tetanus: 38 cases (1987–2005)’, Journal of the American Veterinary Medical Association, 230(1), pp. 76–83. Available at: https://doi.org/10.2460/javma.230.1.76.
- Chase, C. et al. (2017) Blackwell’s Five-Minute Veterinary Consult: Ruminant. Newark, UNITED STATES: John Wiley & Sons, Incorporated.
- Lavoie, J.-P. (2020) Blackwell’s Five-Minute Veterinary Consult: Equine. Third. Hoboken, NJ: John Wiley & Sons, Inc.
- Tilley, L.P. and Smith, F.W.K. (2011) Blackwell’s Five-Minute Veterinary Consult: Canine and Feline. Hoboken, UNITED STATES: Wiley.
- Constable, P.D. et al. (2017) ‘Chapter 14 - Diseases of the Nervous System’, in Veterinary Medicine - A Textbook of the Diseases of Cattle, Horses, Sheep, Pigs and Goats. 11th edn. St. Louis, Missouri: Elsevier.
Current Vet is an educational podcast intended for veterinary students, veterinary professionals, and individuals with an interest in veterinary medicine.
All content provided in this podcast and its associated materials is for educational and informational purposes only. It is not intended as, and must not be considered a substitute for, professional veterinary advice, diagnosis, or treatment.
Any clinical cases discussed in this podcast are fictional, and are designed to reflect typical or likely clinical scenarios for educational purposes. They do not represent specific real-life cases, clients, or animals.
While every effort is made to ensure accuracy and alignment with current evidence at the time of publication, veterinary medicine is a rapidly evolving field, and recommendations may change over time
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In each episode, Dr. Lottie breaks down clinical conditions, cases, and concepts across species, focusing on pathophysiology, decision-making, diagnostics, and what actually matters in practice. It’s the kind of context that makes your knowledge finally click.
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Hello, hello and welcome back to Current Vet. If you're new here, this is the podcast that makes veterinary medicine simple. I'm Dr. Lottie, and today's topic is one that every vet needs to know about, no matter what species you work with, and that is tetanus. Tetanus is a condition where those affected go from being healthy and okay to critically unwell very quickly.
It's relevant across the board because it can affect pretty much any species. It's just that different species are more or less sensitive to the bacterial toxins. So let's get straight into it.
It is a late afternoon after a busy day of ambulatory visits, and you're called to see Ranger, a 12-year-old gelding who's been a bit stiff since yesterday.
When you arrive, the owner mentions he stepped on a loose nail in the paddock two weeks ago. There was a bit of bleeding, they cleaned it with saline, and the wound looked fine, so they forgot about it. You greet Ranger and immediately notice he's standing with a slightly sawhorse stance. His limbs are rigid and his tail is slightly elevated.
His ears are pointed upright, and when he tries to back away from you, his movements are jerky and stiff. You gently lift a lip to check his mucus membranes and note that the muscles around his mouth are quite tight. As you begin your exam, you clap your hands lightly to move a chicken out the way and ranger it startles dramatically triggering a whole body spasm.
The owner says he's been hypersensitive to noises all morning and has seemed really on edge.
So now that we've got the background with our case, let's break down what tetanus actually is.
Tetanus is caused by a Clostridium tetani, which is an obligate anaerobic gram-positive spore forming bacillus bacteria. So let's try and decode what all of those words mean. An obligate anaerobic means that the bacteria only survives in environments without oxygen.
Gram positive means that the bacteria retains gram stain, so therefore it has a thick peptidoglycan cell wall around it. Spore forming means that the bacteria produces spores, and bacillus means that it is rod shaped. The bacteria is ubiquitous in soil all over the world, and its spores can remain viable for years thanks to that incredible resistance to heat, desiccation and disinfectants.
But the clinical disease itself is not actually caused by the bacteria. It's caused by the neurotoxins that the bacteria produces, known as tetanospasmin and tetanolysin.
These Clostridium tetani spores in the environment enter the body through deep breaks in the skin. So things like puncture wounds like we saw in Ranger with that nail wound, deep lacerations, surgical sites, and in foals we can have things like umbilicus infections, and then we can also see infection through castration wounds.
So while infection can occur in most species, sensitivity to the neurotoxins vary. So for example, horses like Ranger are extremely sensitive, far more than dogs and cats, and this is why equine vaccination to tetanus is so essential. Now let's talk about the most important part, which is the toxin mechanism.
The reason these spores thrive in deep or penetrating wounds is because as the injured tissue becomes necrotic and starts breaking down, it creates the perfect anaerobic environment, which allows the bacterial spores to germinate into bacteria. So once inside these suitably anaerobic conditions, the spores germinate, and these bacteria begin producing neurotoxins. The specific role of the neurotoxin tetanolysin isn't really certain, but it's sought to contribute to tissue necrosis and breakdown.
Tetanospasmin, however, binds to nerve endings near the wound site and travels retrograde along these motor neurons towards the central nervous system.
When it reaches the spinal cord and brainstem, tetanospasmin blocks inhibitory interneurons. This prevents the release of GABA and glycine, which are major inhibitory neurotransmitters. It does this by cleaving a SNARE protein called synaptobrevin, which is required for neurotransmitter vesicle release. This then leads to uncontrolled excitation of motor neurons and continuous muscle stimulation, because they are not having that inhibitory input.
Because the toxin binds to neuronal endplates irreversibly, recovery from this infection requires new axonal growth, which takes weeks. So this is why early intervention is really key and why the clinical signs can actually worsen before they start to improve.
So what are these clinical signs gonna be? As we said before, sensitivity in different species varies, but as horses are most commonly and severely affected, let's discuss what you might see in Ranger our clinical case. So the top things are gonna be that stiff stilted gait known as the sore horse stance.
The third eyelids can prolapse, the head and neck are rigid, the tail head is elevated, erect immobile ears, hyperesthesia, which means that small stimuli can trigger really large spasms. Trismus, also known as lock jaw, and a sardonic grin known as risus sardonicus, which is caused when the muscles in the face tighten, giving a quite creepy smile almost.
And then we can also see sweating because of the constant muscle contraction. As the infection progresses, the horse can become recumbent. We see respiratory muscle paralysis, which causes dyspnea and potentially leads to aspiration, pneumonia, and then if there is no intervention and the disease is progressing, there will be death.
Just to highlight a couple of the comparisons that we see between different species, so in dogs , we usually see localized tetanus, so stiffness in one limb near the wound, and they can have more subtle, generalized signs, and the prognosis is much better than it is in horses. Cats are actually relatively resistant to tetanus. Cases can occur, but they require a much higher toxin load before you see severe clinical signs.
And then ruminants. So goats and sheep can develop classical generalized tetanus, often linked to castration or tail docking wounds.
But across all species, clinical progression is generally gradual at first and then rapid once the toxins reach the central nervous system.
Remember that a tiny wound or no visible wound at all does not mean that tetanus is ruled out or that the infection is gonna be mild. Toxin production in the wound is what matters, not the wound size.
So if we think back to Ranger, his trismus, third eyelid prolapse, stiff gait and dramatic startle response are very fitting for our clinical picture of tetanus.
Now, unlike a lot of conditions in vet med, tetanus diagnosis doesn't rely on lab tests. It's primarily a clinical diagnosis. So let's talk about what we can do and what's actually useful in theory versus in practice.
First up, those typical findings are gonna be what is most important for a diagnosis. We see stiffness, spasms, trismus, the third eyelid prolapse, hyperesthesia, and generalized rigidity. In practice, if you see these signs and you suspect tetanus, treat it immediately. Don't wait for confirmation.
The second thing we could do is find a wound. But remember that actually up to about 90% of horses we don't see a wound.
Or potentially it went unobserved or the owners forgot about it because they didn't think that it was important.
In horses though, a couple of common sites include hoof punctures, the castration wounds we were talking about, wire injuries or deep lacerations.
Thirdly, we could do a bacterial culture. However, this is rarely helpful because Clostridium tetani bacteria are anaerobic, so culturing the bacteria takes specialized equipment. Sample contamination is common, and as we said, because c tetani is ubiquitous in soil, it is a really common sample contaminant, which means that we don't actually know if we're growing tetanus bacteria in our sample because it's a true infection or because we have contamination from the soil. So that means that the presence of the organism in a culture or even in the wound, doesn't actually prove that toxin production has occurred, which is what's gonna be causing the disease.
And finally, a negative culture doesn't actually rule tetanus out because the bacteria may be present in the wound, but we weren't vigilant with our sample collection, or potentially the bacteria were collected and simply didn't grow because the environment wasn't right. We can also do PCRs from swabs of wound material, but similar to culture, they aren't entirely reliable and are really only available to labs, so aren't commonly done in practice.
The fourth thing we could do is testing for the toxins. So there are methods to detect tetanospasmin, through potentially a mouse bioassay or toxin serology, but these methods take days to come back with results, they aren't very reliable diagnostic methods, as with the culture, they require specialized labs and the use of mice for tetanus testing is ethically questionable and quite outdated.
Finally, we could do blood work. This is not diagnostic, but it helps to assess systemic health of the animal and see the extent of disease. A couple of things we might see on the blood work results are an increased creatinine kinase or AST levels due to the muscle damage and muscle rigidity, we might see dehydration and electrolyte derangement and secondary infection changes, so things like leukocytosis, neutrophilia, or changes concurrent with aspiration pneumonia. But basically these findings are non-specific and non-diagnostic, so aren't helpful for confirming tetanus as the cause of disease.
So I mean, we have plenty of suggestions of things to try, but the reality is none are very effective or widely available.
So the best thing we can do is start treatment based on what we see clinically. So if you suspect tetanus, you act.
Now let's talk about treatment. There are three main goals when it comes to treating tetanus. First is to neutralize the circulating toxins. Second to stop further toxin production, and thirdly, to control muscle spasms and provide supportive care. So how are we gonna firstly, neutralize that unbound toxin?
And we can do this with tetanus antitoxin. The tetanus antitoxin binds to circulating unbound tetanus spasm, but the key point is that it does not affect toxins that have already bound to neurons, so it won't reverse existing clinical signs. This antitoxin can be given intravenously, intramuscularly, subcutaneously, or injected locally around a wound or even intrathecally, which means into the spinal theca to target toxins around the central nervous system.
But actually the efficacy and safety of this procedure is a bit questionable. So recommended to go IV IM or sub cut. There is a risk of anaphylaxis after this injection, especially when the antitoxin is given to dogs and cats as the formulation is for horses. But we can give a small initial dose, monitor the animal's response, and then continue with the remainder of the dose if it is deemed safe.
Kind of like how you do with a blood transfusion. Tetanus antitoxin can also trigger a form of serum hepatitis in horses known as Theiler's disease, which very rapidly leads to liver failure.
The next step of treatment is to stop further toxin production, and this is done with antibiotics. So penicillin is the most commonly used antibiotic for tetanus, but other options include metronidazole and tetracyclines, like oxytet. Debridement, flushing and opening the wound to oxygenate are also really important to disrupt that anaerobic environment and inhibit bacterial growth.
And finally we have supportive care starting with controlling those muscle spasms. So to do this, we can use sedatives like Acepromazine, Xylazine, Detomidine, whatever is useful in that species and anti-convulsants like diazepam and phenobarbital.
These all help to prevent the animal from falling over sustaining fractures or injuries from falling. It reduces the risk of rhabdomyolysis from muscle spasms, and it can help ease respiratory distress, especially when the animal is incredibly sensitive and hyperresponsive to stimuli.
Some other aspects of supportive care can include placing the animal in a dark, quiet environment that isn't gonna cause that stimulation.
Minimal handling, deep bedding, again, to minimize that risk of injury. Turning the animal over every few hours if they're recumbent, to prevent sores and things like muscle ischemia. IV fluids, nutritional support, and remember that things like feeding tubes are likely to be necessary because the muscles of mastication and the esophageal muscles may be rigid and stiff so the animal won't be able to eat on their own.
And then we need to monitor for aspiration pneumonia as well. If respiration is severely compromised, we should be intubating and providing oxygen, or in extreme cases, we should be considering a tracheostomy. For Ranger, you begin aggressive treatment immediately. So IV tetanus, antitoxin, you give sedation to control spasms and calm him down, you give a toxoid booster, which we'll come on to talk about in a second. You give penicillin, you debride and clean the hoof wound, and you quietly isolate him in a box with minimal stimulation. Over the next three days, his signs worsened slightly, but by the end of week two, he had stabilized. He's less reactive to sound and is walking much more normally, although still slightly stiff.
So let's come on to prevention. The single most effective way to prevent tetanus across all species is vaccination with the tetanus toxoid. The toxoid is an inactivated form of the toxins that the Clostridium technique bacteria produce, and those safely stimulate the immune system to produce long-lasting protective antibodies.
Horses are, like we said before, the most sensitive and the most important species for vaccination. The way that we vaccinate horses is with an initial two doses, four to six weeks apart, then the first booster, which is given 12 months after the initial course, and then routine boosters every one to two years.
Pregnant mares also receive another booster around six weeks before foaling to ensure that the foals are receiving maternal derived antibodies in the colostrum.
Dogs and cats aren't routinely vaccinated in most countries because susceptibility is low, but vaccination is safe and effective when needed. For small ruminants like goats and sheep, vaccination is strongly advised due to the risk from castration, tail docking and outdoor lambing and kidding, because these environments are naturally gonna be contaminated with the Clostridium bacteria.
These species are often given a combined clostridial vaccine like the five in one or seven in one vaccines available.
So the next step of prevention is going to be wound management. Because Clostridium tetani thrives in deep anaerobic contaminated wounds, good wound care is a critical part of prevention. So the key principles are gonna be identifying these wounds early, especially things like puncture wounds or hoof abscesses.
Clip and thoroughly clean the area, debride any necrotic tissue, flush with sterile saline and avoid creating pockets that can trap debris or bacteria.
And then finally, we can actually use the tetanus antitoxin prophylactically. While the toxoid builds long-term immunity, the antitoxin provides immediate short-term protection by neutralizing those circulating toxins. But we can give this prophylactically in high risk situations. So for example, if an animal sustains a high risk wound, or you know that you're gonna be doing a high risk surgery, but it's also really important to note that, if you're giving the toxoid and antitoxin together, always inject them in different anatomical sites and use different syringes for both. This prevents the antitoxin from actually neutralizing the toxoid, and basically making your vaccination entirely ineffective.
So before we wrap up, here are the essential points to know. Tetanus is caused by Clostridium tetani bacteria, but it's the neurotoxins produced by the bacteria that cause clinical disease. These toxins irreversibly bind to neuron end plates and inhibit inhibitory interneurons, which basically means that the muscles are being continuously stimulated by nerves.
Horses are the most susceptible species, and the classic signs include trismus, third eyelid prolapse, that sawhorse stance erect is and hyperesthesia anesthesia leading to spasms. Dogs and less sensitive species may only be affected with a mild localized form of tetanus. Diagnosis is typically on clinical presentation based on these characteristic signs and potentially a history of a wound.
There are three key stages to treatment. First, the antitoxin to neutralize unbound toxins in the body, then antibiotics and wound care to stop further toxin production. And finally, sedation and intensive supportive care for a couple of weeks until those new end plates form. Vaccination with the tetanus Toxoid is very effective for prevention alongside good wound care and possibly prophylactic antitoxin use in high risk cases.
And that is tetanus. Thank you for listening to this episode of Current Vet. If you found it helpful, follow or subscribe wherever you get your podcasts and share it with a friend or colleague who will also find it really useful.
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