Strangles in horses: what is known about silent carriers and the duration of shedding

What a silent carrier is

Strangles is a bacterial infection of the horse's upper airways, caused by Streptococcus equi subspecies equi. The acute picture, with fever, nasal discharge and swollen lymph nodes, is well known. What happens afterwards is far less so. In some horses the organism does not disappear along with the signs: it withdraws into the guttural pouches, two air-filled outpouchings of the Eustachian tube inside the horse's head. There it can persist for months without anything being visible on the animal. Such horses are called silent carriers, or long-term carriers.

The figure that circulates most often on this point runs as follows: around one tenth of recovered horses develops a persistent infection of the guttural pouches. It is an order of magnitude settled within the discipline, not a measurement. It appears as an opening sentence, among other places in a genomic study of 670 isolates from 19 countries, without that study having established it itself. The values actually measured lie far apart, and that is precisely where the heart of the subject lies.

Why the guttural pouches of all places?

The guttural pouches communicate with the pharynx only through a narrow opening and drain poorly by themselves. Pus can thicken there and form firm lumps, known as chondroids. In a series of 14 carriers without symptoms from three outbreaks, the infection sat in the guttural pouches in 13 of them. It is reachable there, but only with an endoscope.

A revised consensus statement published in 2018 by a panel of specialists gives particular prominence to the importance of these carrier states for transmission, and at the same time redefines what should count as the reference method for detection. It is an ordering text produced by an expert panel, not a measurement of its own, and it can therefore support none of the figures in this article.

How many horses remain carriers after an outbreak

The most robust figures come from outbreaks that were followed for months. In three protracted British outbreaks on holdings of differing kinds, 29 to 52 per cent of the horses sampled were infected depending on the yard, and between 9 and 44 per cent of the infected animals still carried the organism after the clinical signs had gone. The guttural pouch was the dominant site.

Two outbreaks followed later show how strongly these proportions depend on the detection method. In a herd of 98 yearlings, in which around half the animals had been ill, the proportion of carriers stood at 3 per cent on culture and at 15 per cent on PCR. In a second herd of 38 adult Icelandic horses, in which every animal had been ill, it reached 13 against 37 per cent. Every horse positive on culture was also positive on PCR; the reverse does not hold. A horse negative on culture and positive on PCR must therefore, in the authors' view, be treated as carrying live bacteria until the contrary is established.

Carriers also come to light outside documented outbreaks. In an American clinical review of 108 strangles cases, 12 of 25 horses infected for longer than forty days showed no clinical signs at all. The comparison limps, however: carriage is defined here by the duration recorded in the case file, not by an endoscopically confirmed guttural pouch finding.

How long shedding continues

The longest documented courses come from a 1997 study on a holding with around 1,500 horses. Long-term carriage was demonstrated there in four clinically healthy convalescents and in two of 350 newly introduced ponies, and it lasted between seven and thirty-nine months. In the three British outbreaks of the following years, prolonged shedding lasted up to eight months.

One finding of the same work is rarely quoted and is nonetheless the most uncomfortable: in these horses, prolonged shedding did not stop of its own accord before treatment was begun. What would have happened without intervention the data do not say, because every affected animal was treated. In an accompanying series, 14 of 15 carriers were cleared under veterinary treatment without surgery, a third of them only at the second attempt. That series has no comparison group: it shows that clearance is possible, not which approach would be the best.

Does a carrier shed all the time?

No. In an Icelandic outbreak, ten persistent carriers were sampled eleven times over thirteen months. Of 115 samples, 61 were positive on PCR and only 32 of those were positive on culture as well. A carrier can therefore appear unremarkable for weeks and then release live bacteria again.

The same work also showed that the organism changes within the carrier. Three months after the first sample, variants appeared carrying a single substitution in the surface gene; after six months, in two horses, shortened forms of the same gene. One of these forms persisted and turned up later in two further horses. A carrier is accordingly not a reservoir at rest but an inhabited place, in which the organism goes on evolving and from which it is evidently passed on.

Why detection so often misses

What decides the matter is not the refinement of the test but the place where the search is made. In a study of 44 convalescents, every horse was sampled in three ways: with a swab from the nasopharynx, with a lavage of the same region and with a lavage of the guttural pouches. Positive were 1 of 41 swabs, 6 of 38 nasopharyngeal lavages and 24 of 44 guttural pouch lavages. The authors put the difference in favour of the guttural pouch sample at a factor of 51. It is a ratio of odds, as they themselves report it, not a probability in the strict sense.

The 1997 work already pointed in the same direction: a single culture from the swab found 45 per cent of the carriers, a single culture from the endoscopically obtained guttural pouch lavage 88 per cent. Repeated swabbing over two to three months eventually found the organism in all but one of the carriers, but with runs of negative results lasting weeks in between.

Even in the acute phase detection is not certain. In a Swedish series of 57 horses from eight confirmed outbreaks, PCR run directly on the nasopharyngeal lavage found the most infected animals, 48 of 57, against at most 22 of 57 for biochemical identification after culture. Three horses stayed negative on every sample.

Does a blood test give the carrier away?

No, and this has been checked several times. Among 287 horses at a quarantine facility, nine were guttural pouch carriers, and no recognisable link existed between serology and carrier status: only one of the nine stood out on the stricter criterion. A second study covering three outbreaks reached the same conclusion.

That second study followed 235 horses from three outbreaks for six months to two years. Neither clinical examination, nor the white blood cells, nor serum amyloid A, an acute phase protein, nor serology distinguished carriers from non-carriers in the same group. Three of the twelve horses positive on culture were even negative on serology. The authors record that in a yard where exposed and unexposed horses live together, carriers cannot be found by serology alone.

The question of when a horse may be regarded as free has also been studied. In an outbreak involving 41 Icelandic horses, of 24 animals later spared, only 4 had been negative on three consecutive weekly lavage samples. Of 11 horses with at least three negative samples spread over several months, by contrast, 10 were genuinely free. The authors put it cautiously: repeated samples at several separate time points can help with this judgement, they prove nothing.

Carriers with no outbreak history: the background level

All the figures cited so far come from yards with a known outbreak. How high the background level lies in an unremarkable population has been studied more rarely. A Dutch survey sampled 166 apparently healthy adult horses and ponies from 86 holdings three times at weekly intervals by nasopharyngeal lavage. The estimated true carrier prevalence averaged 2.0 per cent, with an uncertainty range running from 0.1 to 5.9 per cent.

This figure is more of a lower estimate, since the guttural pouches were not lavaged. Nor does it stand for every part of the world. In a Colombian survey of 137 horses from 15 holdings, in which the guttural pouch was sampled endoscopically, streptococci could be cultured in 15 per cent of the animals, of which 13.5 per cent were the strangles organism itself. A change of location in the history was associated with detection, and the probability of a positive finding fell with each year of life. The authors consider the organism endemic in this population.

A British review of a rescue centre describes the intake. Of 626 equids admitted, 34 were flagged at entry screening, among them 24 positive on PCR for the strangles organism, that is 3.8 per cent. Two further animals carried chondroids although PCR and culture came out negative. Such populations are not comparable with well-run private yards, and without a comparison yard it is impossible to say what the screening achieved.

How strongly do carriers drive the spread?

That an organism persists does not yet mean that it starts outbreaks from there. On the infectious power of strangles as a whole there is a quantitative synthesis of ten outbreak reports. It estimates the basic reproduction number, that is the number of horses a single infected animal infects on average in a fully susceptible herd, at 2.2 with an uncertainty range of 1.9 to 2.5; in a less conservative calculation, at 2.7. The authors expressly describe this value as a computational quantity for models, not as a field measurement, and consider it rather too low given the thin data.

How strongly carriers contribute to that figure is open. A modelling study named exactly this gap: the infectious power of a carrier relative to a horse in the acute phase, and the duration of carriage, are the two decisive unknowns. From simulations and antibody data the study estimates the relative infectious power at 0.05 to 0.5 and the duration of protection after an infection that has been overcome at probably four to six years. The model suggests that the mere presence of carriers can be enough to hold the organism in a population indefinitely. It remains a calculation, not an observation: its most important inputs are precisely those the authors describe as unknown.

A British genomic study supplies the counter-argument. From 511 isolates from the years 2015 to 2022 a rapidly shifting picture emerged: nine groups were distinguished, two of them covering 82 per cent of the strains, one increasing markedly over the study period, the other declining. Such rapid turnover indicates, in the authors' view, that acutely ill and freshly recovered horses with a short shedding period matter more for transmission than long-term carriers. The sample comes from positive laboratory results, however, and silent carriers are systematically under-represented in it.

What does not give the carrier away

The obvious supposition would be that a particular variant of the organism causes carriage. It has been examined and has not been confirmed. One study compared isolates from acutely ill horses with isolates from silent carriers in Sweden and Pennsylvania, in part from the same animal at different times, on three levels: the accessory genetic material, the chemical marking of the hereditary substance and gene activity. On none of these levels could the groups be separated, and not a single gene was read differently between them.

The authors' conclusion shifts the question: if it is not the bacterium that makes the difference, then it is probably the horse. Which property of the host favours carriage remains unanswered to this day. An absent difference is moreover no proof of sameness, and the number of isolates examined was limited.

That leaves an uncomfortable position. A silent carrier can be recognised by nothing visible on the horse or measurable in the blood, and the organism inside it cannot be told apart from the one in an acutely ill animal. It can be found only where it sits, and only if the search there is made more than once.

What follows from this body of evidence and what does not

The secure core is narrow and load-bearing all the same: some of the recovered horses remain infected for months, usually in the guttural pouch, usually without any sign, and shedding runs irregularly. This finding has been established by independent groups in Great Britain, Sweden, the Netherlands, Colombia and the United States, with different methods and over almost three decades.

Almost everything quantitative stays blurred. How many carriers there are depends on where, with what and how often the search is made. How infectious a carrier is compared with an acutely ill horse is estimated, not measured. Whether long-term carriers or freshly recovered animals carried the outbreaks of recent years is answered in opposite ways by two research groups.

For everyday life in the yard, one thing above all follows: the moment at which a strangles episode is over cannot be read from the appearance or the behaviour of the horses. That is why the usual recommendations on isolation and follow-up checks extend beyond the fading of the signs. How a particular yard proceeds belongs in the hands of the attending veterinary practice; this text places the evidence in context and replaces neither examination nor advice.

The same organism, a different figure: sampling site and method in direct comparison

Original analysis

Limitations and uncertainty

• Only one of the works used here reaches the level of a systematic review with meta-analysis, and it concerns the infectious power of strangles as a whole, not carriage. The editorial requirement to rest at least half the sources on that level cannot be met here: carriage is studied through outbreak cohorts, cross-sectional surveys and genomic analyses, not through randomised trials.
• Almost all the carrier cohorts come from single outbreaks with very small carrier numbers, in part from a single breed on a single holding. The range from 3 to 44 per cent describes convenience samples, not a distribution across horse populations.
• There is no independent yardstick for carriage: every study determines carrier status with the same imperfect methods that it is testing. Statements about the detection rate and about the meaning of negative findings are therefore systematically uncertain.
• The work with the longest documented shedding times dates from 1997 and remains the basis for the range of seven to thirty-nine months. Management, trade and detection methods have changed since then.
• Population figures without an outbreak history are available from the Netherlands, from Colombia and from a British rescue centre. For Switzerland, this search found no comparable prevalence data.
• Whether long-term carriers or briefly shedding horses dominate transmission is answered in opposite ways by two research groups, and both answers rest on samples in which silent carriers are under-represented.

Open questions

• Which property of the horse decides whether the organism stays after recovery, given that it demonstrably does not come down to the bacterial variant?
• How infectious is a silent carrier really, compared with an acutely ill horse? So far this quantity has only been estimated, not measured.
• Do long-term carriers or freshly recovered horses account for the larger share of transmissions, and can the contradiction between genomic data and model calculations be resolved?
• How high is the proportion of carriers in Swiss yards with no known outbreak history?

Frequently asked questions

My horse had strangles and has been perfectly well for a long time. Can it still infect others?

It is possible, and it cannot be seen on the horse. In three outbreaks followed for months, between 9 and 44 per cent of the infected horses still carried the organism after the clinical signs had gone, usually in the guttural pouches. In an American clinical review, 12 of 25 horses infected for longer than forty days no longer showed any signs at all. None of these figures says what the risk is in an individual case: they describe groups, not your horse. Judging a particular yard is a matter for the attending veterinary practice.

How long does a horse stay infectious after strangles?

There is no fixed period, and that is the most important point. Shedding times of seven to thirty-nine months are documented in a study from 1997, and up to eight months in three later British outbreaks. Shedding does not run continuously: in ten persistent carriers, of 115 samples taken over thirteen months, 61 were positive on PCR and only 32 of those on culture as well. A negative sample therefore describes the day of sampling, not the state of the horse over the following weeks.

Is a nasal swab enough to find a carrier?

No, a single swab is not enough. In a study of 44 convalescents in which every horse was sampled at three sites, 1 of 41 nasopharyngeal swabs was positive, against 24 of 44 guttural pouch lavages. Back in 1997, a single swab culture found 45 per cent of the carriers, against 88 per cent for a single culture from the endoscopically obtained guttural pouch lavage. Repeated swabbing over two to three months eventually found almost all the carriers, but with runs of negative results lasting weeks in between. Which sample makes sense is for the vet to decide.

Can a blood test show whether my horse is a carrier?

No, and this has been checked twice independently. Among 287 horses at a quarantine facility, nine were carriers, and no recognisable link existed between serology and carrier status: only one of the nine stood out on the stricter criterion. In a second study of 235 horses from three outbreaks, neither clinical examination, nor the white blood cells, nor serum amyloid A, nor serology distinguished carriers from non-carriers in the same group; three of the twelve horses positive on culture were even negative on serology. During an outbreak, blood tests serve other purposes.

How many horses in a perfectly ordinary yard carry the organism?

In yards with no known outbreak history the proportion is low, but not zero. A Dutch survey of 166 apparently healthy horses from 86 holdings estimated the true carrier prevalence at around 2 per cent, with an uncertainty range of 0.1 to 5.9 per cent. At a British rescue centre, 24 of 626 equids admitted were positive, that is 3.8 per cent. In a Colombian population with endoscopic sampling, by contrast, the value reached 15 per cent. The background level therefore depends heavily on region, trade and management conditions, and does not transfer to Switzerland.

Does the organism eventually disappear by itself?

In some of the horses apparently yes, in others not. In three British outbreaks, prolonged carriage stopped of its own accord in none of the affected horses before treatment was begun; since all of them were treated, the data say nothing about a course without intervention. In an accompanying series, 14 of 15 carriers were cleared under veterinary treatment without surgery, a third of them only at the second attempt. That series has no comparison group: it shows that clearance is possible, not which approach is the best.

Sources

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   From ten pooled outbreak reports, eight of them from peer-reviewed publications, the basic reproduction number is estimated conservatively at 2.2 and less conservatively at 2.7, expressly as a computational quantity for models and probably too low for want of follow-up data.
2. Houben RMAC, Broens EM, Broekhuizen-Stins MJ, Sloet van Oldruitenborgh-Oosterbaan MM. The prevalence of Streptococcus equi subsp. equi carriers in the Netherlands. Equine Veterinary Journal, 2026 (Cross-sectional study | Horse)DOI 10.1002/evj.70177
   In 166 apparently healthy adult horses and ponies from 86 holdings, examined three times at weekly intervals by nasopharyngeal lavage, the true carrier prevalence was estimated at 2.0 per cent on average, with an uncertainty range from 0.1 to 5.9 per cent.
3. McGlennon AA, Verheyen KL, Newton JR, van Tonder A. Unwelcome neighbours: Tracking the transmission of Streptococcus equi in the United Kingdom horse population. Equine Veterinary Journal, 2026 (Cross-sectional study | Horse)DOI 10.1111/evj.14558
   From 511 British isolates from the years 2015 to 2022 a rapidly shifting population structure emerged, with nine groups of which two covered 82 per cent of the strains; the authors conclude from this that acutely ill and freshly recovered horses are likely to matter more for transmission than long-term carriers.
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   Typing of 670 isolates from 19 countries documents national and international transmission events that keep the organism in circulation worldwide; the often quoted figure of around 10 per cent persistently infected guttural pouches comes from the introductory literature reference, not from a measurement in this work.
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   In 235 horses from three outbreaks, examined six months to two years afterwards, neither clinical examination, nor the white blood cells, nor serum amyloid A, nor serology distinguished the carriers from non-carriers in the same group; three of the twelve horses positive on culture were negative on serology.
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   In two natural outbreaks the proportion of carriers stood at 3 per cent on culture against 15 per cent on PCR, and at 13 against 37 per cent in the second herd; a carrier negative on culture became culture-positive again eight months later, which is why the authors class horses positive on PCR as carrying live bacteria.
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   Among 41 Icelandic horses all positive at the outset, of 24 animals later spared only 4 were negative on three consecutive weekly samples, against 10 of 11 horses with at least three negative samples spread over several months; repeated samples at several time points can support freedom from carriage, but cannot prove it.
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   In ten persistent carriers from an Icelandic outbreak, of 115 samples taken at eleven time points over thirteen months 61 were positive on PCR and 32 of those on culture as well; sequencing of the surface gene showed that the strain changes within the carrier and that changed forms pass on to further horses.
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   Among 287 horses at a quarantine facility, 9 were guttural pouch carriers, with no recognisable link between serology and carrier status: only one of the nine was seropositive on the stricter criterion and three on the more permissive one, which is why the authors warn against ruling out carriage by serology.
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    In the same 44 convalescents, 1 of 41 nasopharyngeal swabs, 6 of 38 nasopharyngeal lavages and 24 of 44 guttural pouch lavages were positive; the authors put the advantage of the guttural pouch lavage at a ratio of odds of 51 and recommend it as the sample of choice for the search for carriers.
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    On a holding with around 1,500 horses, carriage lasted seven to thirty-nine months in four clinically healthy convalescents and in two of 350 purchased ponies; a single sample found 45 per cent of the carriers on the swab against 88 per cent on the endoscopic guttural pouch lavage. Founding work of the field, and cited for that reason despite its age.
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    In three protracted outbreaks, 29 to 52 per cent of the horses sampled were infected, and 9 to 44 per cent of the infected animals still carried the organism after the signs had faded, predominantly in the guttural pouch and for up to eight months; prolonged carriage ended of its own accord in no animal before treatment.
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    Of 14 carriers without symptoms from three outbreaks, 13 carried the organism in the guttural pouch, and 14 of 15 carriers under care were cleared without surgery, a third only after a second attempt; without a comparison group the series shows feasibility alone, not the superiority of any approach.
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    Neither accessory genetic material, nor chemical marking of the hereditary substance, nor gene activity separated isolates from acutely ill horses from isolates of silent carriers, not even in the same animal over time; the authors conclude from this that properties of the host rather than of the bacterium are likely to explain carriage.
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    Updated consensus statement from an expert panel: it redefines the reference method for detecting the organism, places PCR and serology within outbreak management and highlights the role of carrier states in transmission, without collecting data of its own.
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    In 108 strangles cases set against 215 febrile comparison horses, 12 of the 25 horses classed as carriers, that is animals infected for longer than forty days, showed no clinical signs whatever; the definition of carriage rests here on the duration recorded in the case file, not on an endoscopically confirmed guttural pouch finding.
17. Lindahl S, Båverud V, Egenvall A, Aspán A. Comparison of sampling sites and laboratory diagnostic tests for S. equi subsp. equi in horses from confirmed strangles outbreaks. Journal of Veterinary Internal Medicine, 2013 (Cross-sectional study | Horse)DOI 10.1111/jvim.12063
    In 57 horses from eight confirmed outbreaks, PCR run directly on the nasopharyngeal lavage found the most infected animals, 48 of 57, against at most 22 of 57 for biochemical identification after culture; three horses stayed negative on every sample, and the combination of lavage and swab captured over 90 per cent of the acute cases.
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    In a Colombian population of 137 horses from 15 holdings, not selected on disease history, streptococci could be cultured from the endoscopically sampled guttural pouch in 15 per cent of the animals, of which 13.5 per cent were the strangles organism; a change of location in the history was associated with detection, age negatively so.
19. McLinden LA, Kemp-Symonds JG, Daly JM, Blanchard AM. Effectiveness of a screening protocol employed at a UK rescue centre to prevent introduction of strangles. Equine Veterinary Journal, 2026 (Cross-sectional study | Horse)DOI 10.1111/evj.70080
    Of 626 equids admitted between 2017 and 2021, 34 were flagged at entry screening, among them 24 positive on PCR for the strangles organism and two carrying chondroids despite negative PCR and culture; without a comparison yard the retrospective analysis permits no causal conclusion about the effect of the screening.
20. Houben RMAC, Newton JR, van Maanen C, Waller AS. Untangling the stranglehold through mathematical modelling of Streptococcus equi subspecies equi transmission. Preventive Veterinary Medicine, 2024 (Other | Horse)DOI 10.1016/j.prevetmed.2024.106230
    The model calculation names the relative infectious power of carriers and the duration of carriage as the decisive gaps in knowledge, estimates the former at 0.05 to 0.5 and the duration of protection after an infection that has been overcome at four to six years, and suggests that the mere presence of carriers can keep the organism endemic.