Review of Streptococcus equi Infections in Horses: Guidelines for Treatment, Control, and Prevention of Strangles

This manuscript reflects the contents of the American College of Veterinary Internal Medicine consensus statement [1] on Streptococcus equi. The foundation of the consensus statement is evidence-based medicine, but if such evidence is conflicting or lacking, the authors provide interpretive recommendations based on their collective expertise. The statement is intended to be a guide, not a standard of care or a substitute for clinical judgment.

1. Introduction

Disease caused by Streptococcus equi infection in horses, commonly referred to as strangles, was described in early veterinary science literature and first reported by Jordanus Ruffus in 1251. Although its official name is S. equi ssp. equi, there is compelling evidence that it is derived from an ancestral S. zooepidemicus as a genovar or biovar of the latter. We have decided to use the descriptive term S. equi throughout the manuscript based on its widespread usage in the scientific literature over the past century. This manuscript reflects our current knowledge and opinion of epidemiology, treatment, and control of strangles. The information should aid veterinarians in devising control procedures and in the managing strangles outbreaks.

2. Epidemiology

Transmission

Purulent discharges from horses with active and recovering strangles are an important and easily recognizable source of new S. equi infections among susceptible horses. Transmission of infection occurs when there is either direct or indirect transfer of S. equi within these purulent discharges between affected and susceptible horses. Direct transmission refers to horse-to-horse contact, particularly through normal equine social behavior involving mutual head contact. Indirect transmission occurs through the sharing of contaminated housing, water sources, feed or feeding utensils, twitches, tack, and other less obvious fomites such as the clothing andequipment of handlers, caretakers, farriers, and veterinarians; however, barrier precautions can be taken to prevent the spread of S. equi.

It is increasingly recognized that transmission may originate from outwardly healthy animals. In this situation, the source of infection may not be readily recognized, and clinical signs may appear unexpectedly in in-contact animals. S. equi may originate from outwardly healthy horses that are incubating the disease and go on to develop the disease. It is assumed that normal nasal secretions are the source of infection in these animals.

Horses that appear healthy and are recovering from recent disease may continue to harbor the organism after full clinical recovery. There is evidence that a moderate proportion of horses continue to harbor S. equi for several weeks after clinical signs have disappeared, even though the organism is no longer detectable in the majority of horses 4 - 6 wk after total recovery. A recovered horse may be a potential source of infection for at least 6 wk after its clinical signs of strangles have resolved.

Other fully recovered horses may continue to be infectious for prolonged periods through shedding of S. equi. These horses are referred to as long-term, subclinical S. equi carriers and can be a source of infection for susceptible animals. Their introduction to herds may be a source of new outbreaks, even in well-managed groups of horses. The efficacy of control for strangles must include recognition of this category of animal and adoption of appropriate methods for detection and treatment. The best recognized site of prolonged carriage of S. equi among subclinical long-term carriers is the guttural pouch, which is known to become infected in the early phases of infection and after the rupture of the adjacent retropharyngeal lymph nodes through the floor of the pouch. It is likely that short-lived guttural pouch empyema is the most frequent outcome of uncomplicated drainage of retropharyngeal lymph node abscessation. The carrier state develops in up to 10% of affected animals, which results in chronic empyema of the pouches. If the purulent material persists in the guttural pouch, it can become inspissated and eventually form into discrete masses known as "chondroids". Chondroids may occur singly or as multiples, sometimes in very large numbers. Chondroids formed after strangles can harbor S. equi; this has been shown in the cultures of chondroids removed from these animals and observed histologically on the surface and lining fissures within their structure. In some animals, guttural pouch empyema with S. equi infection may persist asymptomatically for many months or even years. About 50% of horses with guttural pouch empyema cough sporadically, and some may have an intermittent unilateral nasal discharge.

Environmental Persistence of S. equi

Currently, there is a lack of field-based proof for prolonged environmental persistence of S. equi. One laboratory-based study [2] documented that the organism in the form of a smeared laboratory-grown bacterial suspension survived for 63 days on wood at 2°C and for 48 days on glass or wood at 20°C. This study did not include coinfection with other normal environmental bacterial flora. S. equi is sensitive to bacteriocins from environmental bacteria and does not readily survive in the presence of other soil-borne flora. Thus, the authors suggest that the results of the study by Jorm [2], as they apply to field conditions, should be interpreted with caution. Further studies to evaluate the environmental persistence of S. equi in clinical samples (e.g. , purulent discharges from cases of strangles) under field rather than laboratory conditions are warranted.

3. Diagnosis

Culture

Cultures of nasal swabs, nasal washes, or aspirated pus from abscesses remain the gold standard for detection of S. equi. Specimens should be plated on Columbia CNA (colistin and nalidixic acid) agar with 5% sheep or horse blood added. The presence of other beta hemolytic streptococci, especially S. zooepidemicus may complicate the interpretation of cultures. Colonies of virulent S. equi are always mucoid, whereas those of the attenuated live vaccine available in North America are small and dry. Colonies of commensal S. zooepidemicus are also typically non-mucoid, whereas fresh isolates from invasive infections are often mucoid. Unlike S. equi, S. zooepidemicus ferments sorbitol and lactose.

Nasal washes are more effective than swabs in detection of small numbers of S. equi, because a greater surface area within the internal nares is sampled. The technique involves instilling ~50 ml of warm normal saline through a 15-cm length of soft rubber tubing (5 - 6 mm in diameter), inserting the tubing to the level of the nasal canthus, and collecting the washings [3,4]. These washings are centrifuged, and the pellet is cultured. Culture may, however, be unsuccessful during the incubation and early clinical phases. S. equi is normally not present on the mucosa until 24 - 48 h after the onset of fever, and therefore, horses monitored by the daily measuring of rectal temperatures during an outbreak may be recognized early and isolated to limit transmission of S. equi.

Polymerase Chain Reaction

The polymerase chain reaction (PCR) is designed to detect DNA sequence of SeM, the gene for the antiphagocytic M protein of S. equi. Although an allele of this gene is found in some strains of S. zooepidemicus, much of the sequence is of low homology, and primer sequences designed from SeM will not prime synthesis of an amplicon from S. zooepidemicus. There is also no evidence that a SeM-like protein is expressed by S. zooepidemicus. Therefore, the PCR based on SeM offers an adjunct to culture for detection of S. equi [5]. Because the test can be completed in a few hours, results may be available on the same day that samples are taken. However, PCR does not distinguish between dead and live organisms, and therefore, a positive test result must be confirmed by culture. In addition, clinical samples that contain polymerase inhibitors or abundant S. equi may give negative PCR results when cultures of the same samples confirm the presence of S. equi. PCR is approximately three times more sensitive than culture [4,6].

PCR accompanying a culture of a nasal swab or wash may be used in a control program to select animals for guttural pouch endoscopy [6]. PCR is capable of detecting SeM DNA of S. equi in guttural pouch lavages for weeks after the disappearance of live organisms. This is not the case for the nasopharynx, where the efficient mucociliary apparatus removes organisms and DNA at the same time.

PCR is useful to

1. detect asymptomatic carriers;
2. establish S. equi infection status before transport;
3. establish S. equi infection status between transport and commingling; and
4. determine the success of the elimination of S. equi from the guttural pouch.

Serology

Fifteen or more surface-exposed or secreted proteins of S. equi elicit strong serum antibody responses during infection and convalescence. The most reactive and best studied of these is SeM, a major virulence factor and protective immunogen [7]. A proprietary enzyme-linked immunosorbent assay (ELISA) for measuring the SeM-specific antibody is commercially available [a]. It is useful for diagnosing recent (but not necessarily current) S. equi infection, determining the need for booster vaccination, and aiding in the diagnosis of purpura hemorrhagica and metastatic abscesses. It does not distinguish between vaccine and infection response. Comparison of titers obtained from sequential samples may provide an indication of exposure and infection status. Serum titers peak ~5 wk after exposure and remain high for at least 6 mo [8]. Responses to commercial extract vaccines peak at ~2 wk and remain high for 6 mo [8].

Considerable variation in the responses of individual horses should be kept in mind when interpreting results of measurement of the SeM-specific antibody. Horses at risk for development of purpura are hyper-responders and make very strong antibody responses. Such animals, with titers in excess of 1:3200, should never be vaccinated.

The SeM-specific ELISA is useful to

1. detect recent infection;
2. determine need for vaccination;
3. identify animals with existing high levels of the antibody that may pre-dispose them to purpura hemorrhagica;
4. support a diagnosis of existing S. equi-associated purpura hemorrhagica; and
5. support diagnosis of bastard strangles.

4. Vaccination

During recovery from strangles, most horses develop a solid immunity that persists in >75% of animals for 5 yr or more [9,10]. This indicates that stimulation of a high level of immunity is biologically feasible, given appropriate presentation of protective immunogen(s). S. zooepidemicus, although closely related to the clonal S. equi, does not stimulate immunity that is cross protective [11], and so, recent and current research on protective immunity is heavily focused on identifying immunogens expressed by S. equi but absent from S. zooepidemicus. The basis of acquired resistance to strangles is not completely understood, but it is believed to reside in part in antibodies to SeM and other immunogens unique to S. equi. Early studies in Australia suggested that the protective immunogen(s) is sensitive to temperature in excess of 56°C [12]. There is evidence that immunity in horses resistant to reinfection is mediated at the mucosal level and functions to block entry of S. equi. However, systemic immunity after parenteral inoculation of avirulent live S. equi is also protective. Together, these findings indicate that optimum immunity may require both systemic and mucosal responses.

Earlier bacterin-type vaccines have been superseded (North America and Australia) by adjuvanted extracts of S. equi prepared by hot acid or by mutanolysin plus detergent extraction. Hot acid cleaves and removes acid-resistant proteins, and carbohydrate mutanolysin (muramidase) hydrolyses the bacterial cell wall, releasing intact surface proteins in the presence of detergent. Both types of vaccine are potent and contain the immunogenic SeM. However, the efficacy of extract vaccines has been disappointing with little published data to support significant protection. One study suggested a reduction in the clinical attack rate of 50% in vaccinates a few weeks after the final booster [13]. Adverse reactions include soreness or abscesses at injection sites and occasional cases of purpura hemorrhagica.

Use of an attenuated non-encapsulated strain of S. equi, with defects in carbohydrate use and a design that mimics the immunity caused by natural infection, stimulated a high level of immunity against experimental challenge [4].

The inductive sites are the pharyngeal and lingual tonsils, and therefore, vaccine organisms must reach these sites in sufficient numbers to trigger protective responses. Safety issues include residual virulence with formation of slowly developing mandibular abscesses in a small percentage of vaccinates, nasal discharge, and occasional cases of immune-mediated vasculitis (purpura). Because the vaccine contains live S. equi, accidental contamination of remote injection sites will result in abscess formation at these locations. For that reason, no other vaccinations should be given concurrently or administered before the intranasal vaccine. No data is available on the effect of concurrently administering a different intranasal vaccine. The genetic stability of the vaccine has recently been improved by the deletion of portions of two genes (HasA and B) required for capsule synthesis. The deletion has also provided a reliable means of identifying the vaccine from wild strains using colony characteristics and PCR.

It is likely that more effective and safer vaccines will eventually be developed based on genomic sequence information from S. equi and S. zooepidemicus. However, the magnitude of this task is considerable. Protective immunogens must be identified for systemic and mucosal responses, and the appropriate modes of presentation must be proven through experiment. Because it is likely that different immunogens function at the tonsillar and lymphatic levels, the appropriate combination of these components will also have to be identified in multiple experiments with ponies and horses.

Extract Vaccines

Extract vaccines are given intramuscularly or subcutaneously and elicit serum antibody responses 7 - 10 days later. Naïve horses and foals require a schedule of two or three doses at an interval of 2 wk. Booster doses are given once annually. Pregnant mares may receive boosters a month before the expected date of foaling. Horses known to have had strangles within the previous year should not be vaccinated. Horses with signs of strangles should not be vaccinated. During an outbreak, only horses with no known direct contact with strangles cases or the exudates from these cases should be promptly vaccinated. However, published data does not show that vaccination with the avirulent, non-encapsulated strain Pinnacle® I.N. [b] would be detrimental to horses exposed to strangles. However, development of immunity after vaccination takes ~2 wk. Additionally, there is a real risk of transmitting the virulent, wild S. equi to other horses when they are being vaccinated.

S. equi-specific serum antibody levels of valuable horses could be assayed before decision to vaccinate. Animals with titers of 1:1600 or greater in the SeM ELISA should not be vaccinated.

Attenuated Live Intranasal Vaccine

Live vaccine should be administered only to healthy non-febrile animals free of nasal discharges. Vaccine is given in a schedule of two doses at 2 - 3 wk intervals. Annual booster doses are recommended. Live vaccine should not be used during an outbreak except in horses with no known contact with infected or exposed animals. The mode of application should be such that an adequate amount of vaccine reaches the pharyngeal and lingual tonsils.

Transfer of passive immunity to the foal mainly involves antibodies of the IgGb isotype that are distributed to the serum and nasal secretions. Pre-partum vaccination of the mare significantly increases colostral levels of these antibodies. Foals from vaccinated mares have significantly higher titers of SeM-specific IgGb but not IgA in mucosal washes during the first 2 mo of life; additionally, colostral levels of SeM-specific IgA are significantly increased by vaccination. Resistance of the foal to strangles during the first months of life seems to be mediated by IgGb in mucosal secretions and milk and not by IgA. There is no data available about colostral antibody levels after administration of the intranasal vaccine to broodmares.

5. Control of Outbreaks

Outbreak Investigations

Investigation of strangles outbreaks should begin by an interview with horse owners to obtain a detailed history and to evaluate the potential extent of the disease problem. The review should identify affected groups of horses and allow the geography of the premises and the management practices to be assessed for further risks and future opportunities for disease control.

A practical disease control strategy should then be agreed on and implemented. This outlined strategy may need to be adapted to the individual circumstances of specific premises and outbreaks. To summarize:

• All movements of horses on and off the affected premises should be stopped, and segregation and hygiene measures should be implemented immediately.
• Cases of strangles and their contacts should be maintained in well-demarcated "dirty" (i. e. , S. equi positive) quarantine areas.
• Rectal temperatures should be taken at least once daily during an outbreak to detect, promptly segregate, and possibly treat new cases.
• The aim of the control strategy after bacteriological screening is to move horses from the "dirty" to the "clean" areas, where non-affected and non-infectious horses are kept.
• Every care should be taken to ensure very high hygiene standards throughout the premises and for the duration of the outbreaks.
• Screening of all convalescing cases after clinical recovery and their healthy contacts should be conducted using swab or lavage of the nasopharynx, with special care taken to maintain good hygiene to avoid inadvertent transmission between horses during sampling.
• After recovery, swabs or lavage fluid should be collected at weekly intervals for several weeks and tested for S. equi by conventional culture and PCR.
• Because PCR can detect dead as well as live bacteria, positive PCR results are regarded as provisional and subject to further investigation.
• Because the vast majority of subclinical long-term carriage of S. equi seems to occur in the guttural pouches of recovered horses, endoscopy of the upper respiratory tract and guttural pouches should be performed in all outwardly healthy horses in which S. equi is detected; culture or PCR should be used.
• Lavage samples from guttural pouches should then be tested for S. equi by culture and PCR.
• Sites such as the cranial nasal sinuses or tonsils should be considered in horses that continue to harbor S. equi in the absence of pathology or that have a S. equi infection of the guttural pouches.

Detection of Carriers with S. equi Infection of the Guttural Pouches

Diagnosis of S. equi infection associated with guttural pouch empyema with or without chondroids after strangles is best achieved by direct visual assessment of both pouches using endoscopy. Cytological assessment, cytological culture, and PCR for detection of S. equi in lavage samples collected through a sterile disposable catheter passed through the biopsy channel of the endoscope are recommended to accompany visual examination, because infection and inflammation may be present in the absence of obvious and visible pathology. Diagnosis of guttural pouch empyema with or without chondroids may also be made by radiography of the guttural pouch area, although changes may not be visible in all cases.

S. equi may be cultured from lavages collected by direct percutaneous sampling of the pouch, although this is not recommended because of the high risk of injury to important anatomical structures in the region.

Treatment of Carriers with S. equi Infection of the Guttural Pouches

Appropriate methods of treatment of guttural pouch empyema in individual horses depend on the consistency and volume of the material within the pouches. Repeated lavages of pus-filled pouches, using rigid or indwelling catheters with isotonic saline or polyionic fluid and with subsequent lowering of the head to allow drainage or use of a suction pump attached to the endoscope, aid the elimination of empyema. Sedation aids in implementation of the endoscopy and facilitates drainage of flush material from the guttural pouches by lowering the horse's head.

Administration of both topical and systemic benzylpenicillin seems to improve the treatment success rate. Verheyen et al. [14] reported on the method of delivering a gelatin and penicillin mix. To make 50 ml of the gelatin/penicillin solution:

1. weigh out 2 g of gelatin (Sigma G-6650 or household grade) and add 40 ml of sterile water;
2. heat or microwave to dissolve the gelatin;
3. cool gelatin to ~45 - 50°C;
4. meanwhile, add 10 ml of sterile water to 1,000,0000 units (10 Mega) of sodium benzylpenicillin G;
5. mix penicillin solution with the cooled gelatin to make a total volume of 50 ml; and
6. dispense the solution into syringes and allow to set overnight at 4°C.

The gelatin/penicillin mix is more effective in remaining in the pouches than a straight aqueous solution, and it is a useful way of delivering a large dose of penicillin where it is needed. Installation is easiest through a catheter inserted up the nose and endoscopically guided into the pouch opening. The catheter works best with the last 1 inch bent at an angle to aid entry under pouch flap. Other recommendations include elevating the horse's head after infusion.

Topical installation of 20% weight by volume acetylcysteine solution has also been used to aid the treatment of empyema. Acetylcysteine has a denaturing and solubilizing activity by disrupting disulphide bonds in mucoprotein molecules, thus reducing mucus viscosity and theoretically, facilitating natural drainage. Erythema of the mucus membranes lining the guttural pouch has been observed after installation of the 20% acetylcysteine solution. More long-standing cases, in which there is inspissation of the purulent material that does not readily drain into the pharynx, are more difficult to treat topically, because they can be refractory to large-volume irrigation. Use of a memory-helical polyp retrieval basket through the biopsy channel of the endoscope does allow non-surgical removal of chondroids, even when present in very large numbers and in conjunction with empyema. When combined with topical and systemic antimicrobial treatment, this is usually sufficient for curing severe guttural pouch lesions. Surgical hyovertebrotomy and ventral drainage through Viborg's triangle carries the inherent risks of general anesthesia and surgical dissection around major blood vessels and nerves; S. equi contamination of the hospital environment is also a concern. Scarring of the pharyngeal openings of the guttural pouch may preclude both natural drainage of purulent material and endoscopic access to the guttural pouches. Such cases may require conventional surgical or endoscopically guided laser treatments to break down scar tissue and allow access to the pouches.

Hygiene Measures

Particular care should be taken with hygiene measures during strangles outbreaks to prevent indirect transfer of S. equi from infectious horses (including potential subclinical carriers) to susceptible animals. Personnel should use dedicated protective clothing when dealing with infectious animals and should not deal simultaneously with susceptible animals. If this is unavoidable, infectious horses should be dealt with after susceptible animals. Specific equipment should be used only for infectious horses, and it should be thoroughly disinfected between animals. When cost is not a factor, consideration should be given to the destruction of equipment after eradication of the infection. In disinfecting stables used by infectious horses, care should be taken to ensure thorough cleaning to remove all organic material. Particular care must be taken with feed and water troughs as well as wooden fencing or other wooden surfaces. Manure and waste feed from infectious animals should be composted in an isolated location. Personnel dealing with susceptible animals should avoid contact with waste from infectious horses. After removal of organic material from stables, all surfaces should be thoroughly soaked in an appropriate liquid disinfectant or steam treated and allowed to dry. This should be repeated, if possible. Care should be taken with wooden surfaces. After a thorough cleaning and soaking in liquid disinfectant, wooden surfaces should be treated with suitable wood preservative or sealed with epoxy paint. Pastures used to hold infectious animals should be rested for 4 wk. There is no evidence for prolonged survival of S. equi in pastures. Care should be taken to disinfect water troughs at least once daily during an outbreak. Horse vans should be hosed clean and disinfected after each use.

S. equi does not present any more problems with disinfection of equipment than other bacterial species; normal common sense approaches should be adopted at all times. This should include physical removal of visible organic material and use of an appropriate disinfectant (following appropriate manufacturers' guidelines on dilution) that is proven to act against S. equi.

Cases of S. equi infection in debilitated humans have been reported. Animal handlers, caretakers, veterinary practitioners, pathologists, and equine post-mortem attendants should take particular care to avoid unnecessary contamination from infectious horses, especially avoiding respiratory and oral contamination by purulent material. However, it should be remembered that S. equi is highly host adapted, and infections of humans have rarely been confirmed.

Prevention Using Quarantine and Bacteriological Screening

• Prevention of strangles through quarantining and screening is difficult to achieve, especially without specific measures to reduce the risk of inadvertent introduction of S. equi infection through subclinical carriers. The owner/farm manager/trainer should always be questioned as to the possible exposure of the animal to strangles.
• Prevention through quarantining and screening is particularly difficult at farms where there is frequent moving and mixing of horses during the breeding season, at racetracks, and at other places where strangles outbreaks have not been appropriately investigated and controlled.
• Wherever possible, animals being introduced to a new population of horses should be isolated for 3 wk and screened for S. equi by repeated nasopharyngeal swabs or lavages. This should be done according to the protocol outlined for controlling outbreaks (i. e. , three samples taken at weekly intervals). Samples should be tested for S. equi by culture and PCR, and animals testing positive should be retained in isolation for further investigation and treatment.
• High standards of hygiene should also always be maintained to avoid indirect transmission between quarantined and resident horses.

The Horserace Betting Levy Board in the United Kingdom has established guidelines on strangles included in its Codes of Practice. The Codes of Practice can be viewed at the following web address: http://www.hblb.org.uk/hblbweb.nsf/Codes%20of%20Practice%202004.pdf.

6. Treatment

Appropriate treatment of horses with strangles usually depends on the stage and severity of the disease. Veterinary opinion on the use of antibiotic treatment remains markedly divided. However, the majority of strangles cases require no treatment other than proper rest, a dry, warm stall, and soft, moist, and palatable food of good quality for the duration of the disease. Food and water should be easily accessible to the horse.

Horses with Early Clinical Signs

During an outbreak, immediate antibiotic therapy of new cases in the early acute phase with fever and depression may be curative and may prevent focal abscessation. Antibiotics should be given for 3 - 5 days. However, treated animals are likely to remain susceptible to reinfection. Experimentally infected ponies treated with antibiotics at onset of fever usually do not develop lymph node abscessation if protected from further exposure. Because abscesses have not developed at this early stage, the antibiotics have adequate access to the bacteria.

Unfortunately, antibiotic treatment will also inhibit the synthesis of protective antigens, and the development of protective immunity will not be stimulated from strangles [15] ; therefore, if the horse remains exposed to infected horses, it will be highly susceptible to reinfection when treatment is discontinued.

It has been argued on theoretical grounds that treatment of strangles with antibiotics is contraindicated, because killing the organisms is indirectly affecting the development of immunity and thereby increasing the risk of bacteremia, septicemia, and metastatic abscessation. There is no experimental or clinical data to support such a phenomenon.

Immediate treatment of horses that show the earliest clinical sign of fever could be an effective way of controlling strangles outbreaks in racing stables or riding barns; however, the disadvantages of treatment should be weighed.

Horses with Lymph Node Abscessation

After an external lymphadenopathy is detected in an otherwise alert and healthy horse, antibiotic therapy is probably contraindicated. Although it provides temporary clinical improvement in fever and lethargy, it only prolongs the inevitable enlargement and eventual rupture of lymph node abscess. Antibiotics may suppress the bacteria within the lymph nodes sufficiently for a time, only to have a simmering infection flare and abscessation return when the antibiotics are discontinued.

Therapy should be directed toward enhancing maturation and drainage of the abscesses. Topical treatments such as ichthammol or a hot pack may be applied to promote maturation of the lymph node abscess, although objective-controlled data supporting the use of these techniques are lacking. Surgical drainage of lymphadenopathies is sometimes indicated if abscesses do not rupture spontaneously; however, it is critical to wait until the abscess has matured and thinned out ventrally. Earlier than this, surgical intervention may only result in minimal exudate drainage and continued lymph node swelling, because the abscess has enough internal structure (honeycomb loculations) to block drainage through a single surgical incision. Daily flushing of the open abscess with a 3 - 5% providone iodine solution should be continued until the discharge ceases.

The use of non-steroidal anti-inflammatory medications such as phenylbutazone or flunixin meglamine may improve the horse's demeanor by reducing fever, pain, and inflammatory swelling at the site of the abscesses. This may, in turn, encourage eating and drinking. Consideration must be given to the complications seen after the use of non-steroidal anti-inflammatory medications in dehydrated and anorectic horses.

Even in the face of detectable lymphadenopathy, if the horse is febrile, depressed, anorexic, and especially manifesting dyspnea as a result of partial upper airway obstruction, antibiotic therapy is indicated to decrease abscess size and prevent complete airway obstruction. Rarely, affected horses may require intensive supportive therapy, including IV fluids, naso-gastric tube feeding, and tracheostomy. An animal requiring a tracheostomy should be given systemic antimicrobial drugs to prevent secondary bacterial infections of the lower respiratory tract.

Some clinicians believe that antibiotic therapy started after the abscesses have ruptured is indicated, because it may hasten recovery, improve appetite, and reduce loss of body condition.

Horses with Complications

Horses that develop complications from strangles should receive symptomatic therapy.

Drugs of Choice for Therapy

Penicillin is generally considered the drug of choice for the treatment of non-pneumococcal streptococcal disease, with alternative drugs used depending on ease of administration or the site of infection. Other agents for therapy include cephalosporins and macrolides. Based on in vitro antimicrobial susceptibility testing where testing methods follow the Clinical and Laboratory Standards Institute's guidelines, the majority of S. equi isolates are susceptible to trimethoprim-sulfadiazine (TMS). However, this may or may not translate into in vivo efficacy. Many veterinarians have anecdotally indicated that horses with strangles have improved with TMS treatment. Although there is evidence that TMS did not eliminate S. zooepidemicus infection in tissue chambers implanted subcutaneously in ponies, the study did not determine its effectiveness against S. equi. [16]

S. equi is consistently sensitive to penicillin; thus, it is considered the antibiotic of choice. Laboratories [c] handling hundreds of S. equi strains have noted no emerging antibiotic resistance to penicillin by S. equi or S. zooepidemicus. The incidence of resistance to most other drugs is low with the exception of aminoglycoside resistance, including gentamicin, which is consistently observed.

The authors thank the American College of Veterinary Internal Medicine (ACVIM) Board of Regents for determining the need for a consensus statement on the topic of S. equi infections and the ACVIM membership for their input on the consensus statement.

Footnotes

[a] EBI, IDEXX, Lexington, KY 40511.
[b] Fort Dodge Animal Health, Fort Dodge, IA 50501.
[c] Timoney JF and Newton JR. Personal communication. 2004.