Key issues

1. Arytenoid cartilage infection thought to be secondary to trauma and extension of mucosal bacterial or viral infection.
2. Can progress to deformation of cartilage and granuloma formation, requiring surgical resection.
3. Mixed bacterial infections common.

Arytenoid chondritis is a performance limiting upper airway disease most commonly reported in young thoroughbred horses (1). The aetiology is thought to be secondary to trauma to the arytenoid cartilage, with subsequent extension of mucosal bacterial or viral infection into the cartilage. The cartilage infection often progresses, to result in permanent enlargement or deformation of the arytenoid cartilage, requiring arytenoidectomy or resection of a granuloma. Clinical signs include insidious and progressive onset of respiratory noise, exercise intolerance and/or coughing. Bacterial cultures from the infected cartilages and granulomas have revealed mixed infections, with 58% growing Gram-positive bacteria, 54% Gram negative bacteria and 33% anaerobic bacteria (Johnston and Lumsden, 2020). Streptococcus spp. were the most common (32%), followed by members of the Enterobacteriaceae (13%). In this report, bacterial isolates were susceptible to ceftiofur (83%), ampicillin (64%), tetracycline (48%), enrofloxacin (45%), trimethoprim-sulphadiazine (41%) and gentamicin (18%). Susceptibility of bacteria often varies substantially by geographic area, so local data should drive decision making. Ceftiofur and enrofloxacin are high importance antimicrobials and should not be used as first line therapy.

Diagnostics

Endoscopy of the larynx is the most widely used diagnostic tool, but ultrasonography of the larynx is useful to determine the extent of the chondropathy.

Culture of the cartilage resected during arytenoidectomy or removal of the granuloma is important, but culture of the surface of these lesions during upper airway endoscopy is not considered useful.

Treatment

Broad spectrum antimicrobial therapy is indicated. Penetration into the infected cartilage is an issue, as vascularisation is poor. Penicillin and gentamicin are recommended, but oral therapy is often used as longer courses of intramuscular antimicrobials can be poorly tolerated by yearlings. Antimicrobial therapy is usually required for at least five to seven days, when some improvement of the endoscopic appearance is expected. If there is no improvement apparent on repeat endoscopic examination, arytenoidectomy or resection of the granuloma should be considered if there is an impediment to the airway and a future athletic career is anticipated. Culture and susceptibility testing should be performed on the resected infected cartilage and granuloma. The total course of treatment can be weeks, depending on rate of resolution of these lesions.

Anti-inflammatory therapy with phenylbutazone (2 g IV or PO q 24 h for the first five days of treatment) is a useful adjunctive therapy.

Antimicrobials used

• Procaine penicillin G (22 000 IU/kg IM q 12 h) and gentamicin (6.6 mg/kg IV q 24 h)
• OR oxytetracycline (6.6 mg/kg IV q 12 h)
• OR trimethoprim-sulphadiazine (30 mg/kg IV or PO q 12 h)

Prognosis

Reduction in the lesion size and improvement in arytenoid movement after antimicrobial therapy is encouraging. The prognosis for performance following arytenoidectomy is considered guarded due to the propensity of recovered horses to aspirate.

Key issues

1. Mucosal lesions can resolve with rest and anti-inflammatory therapy.
2. Cartilage involvement necessitates broad-spectrum antimicrobial therapy.
3. Epiglottic entrapment requires surgical intervention.

Epiglottitis can occur with ulceration of the epiglottis and in severe cases can lead to exposure of the epiglottic cartilage (Figure 3.2. Image A). Mucosal lesions most result from trauma and this allows extension of mucosal bacterial and viral infection into the cartilage. Epiglottic entrapment is a cause of exercise intolerance and inspiratory and expiratory noise. The epiglottis becomes enveloped by the aryepiglottic fold (Figure 3.2 Image B).

Figure 3.2: A. Epiglottic entrapment in a horse. B. Epiglottitis in a horse. (Images courtesy of Leanne Begg.)

Diagnostics

Both conditions are diagnosed by endoscopy. With epiglottic entrapment, the distinct serrated margins of the epiglottis and the dorsal epiglottic vascular pattern are obscured by a fold of aryepiglottic mucosa. Cartilage involvement is diagnosed when there is thickening and disfigurement of the cartilage of the epiglottis.

Treatment

Mucosal lesions are best treated with rest and anti-inflammatory drugs. If the epiglottic cartilage is exposed, broad spectrum antimicrobial therapy is indicated.

Epiglottic entrapment requires surgical division of the aryepiglottic fold, which is usually performed standing if it is permanently entrapped but needs to be done under general anaesthesia if it is only intermittently entrapped.

Antimicrobials used

• In cases with exposed epiglottic cartilage, procaine penicillin (22 000 IU/kg IM q 12 h) and gentamicin (6.6 mg/kg IV q 24 h) for a minimum of 7 days or until clinical resolution is apparent on repeat endoscopic examination.
• OR trimethoprim-sulphadiazine (30mg/kg PO q 12 h) for a minimum of 7 days or until clinical resolution is apparent on repeat endoscopic examination.

Prognosis

Epiglottitis generally has a good prognosis after antimicrobial therapy unless infection of cartilage leads to disfigurement and compromise of epiglottic function.

Epiglottic entrapment has a good prognosis for future athletic performance following surgery.

Key issues

1. Pharyngeal cysts are congenital cysts that are usually identified when investigating respiratory noise.

Subepiglottic cysts are an uncommon cause of respiratory noise in young horses. They are usually present from birth but are diagnosed as horses begin to exercise, when they may cause exercise intolerance or respiratory noise. Large cysts are diagnosed earlier in foals, as they lead to coughing, dysphagia and food aspiration.

Diagnostics

Subepiglottic cysts are diagnosed by endoscopy.

Treatment

Pharyngeal cysts are removed by surgical resection.

Antimicrobials used

• Pharyngeal cysts do not require antimicrobial therapy other than peri-operative therapy. There is no evidence for duration of therapy but some surgeons advocate for  3 days post-operatively due to the proximity to the epiglottal cartilage. Upper airway surgery in other species (dogs, humans) are generally performed with perioperative (<24h therapy) surgical prophylaxis alone or without surgical prophylaxis.

Prognosis

Subepiglottic cysts have a good prognosis following surgical resection.

Key issues

1. Pharyngeal lymphoid hyperplasia is not considered a cause of poor performance.

Pharyngeal lymphoid hyperplasia (PLH) usually occurs in young horses. These follicles are lymphoid tissue that spreads over the larynx. Hyperplasia occurs with lymphoid stimulation. They are usually considered of little significance and not a cause of poor performance.

Diagnostics

PLH is diagnosed by endoscopy (Figure 3.3).

Figure 3.3. Pharyngeal lymphoid hyperplasia in a young thoroughbred. (Image courtesy of Leanne Begg.)

Treatment

No treatment is recommended for pharyngeal lymphoid hyperplasia. Rest and anti-inflammatory drugs may be indicated if it is severe.

Antimicrobials used

• Antimicrobial therapy not indicated for pharyngeal lymphoid hyperplasia.

Prognosis

Pharyngeal lymphoid hyperplasia has excellent prognosis for future athletic performance.

Key issues

1. Sinonasal and guttural pouch mycoses are both uncommon in Australia.
2. Aspergillus species are the most frequent cause of guttural pouch mycosis.
3. Histopathological examination and culture are required for diagnosis, although care should be taken with guttural pouch mycosis as exsanguination is possible.

Fungal infections of the upper respiratory tract are more commonly seen in warm and humid climates, but they do occur rarely in Australia. Aspergillus species are the fungi most commonly isolated  from sinonasal mycotic infections in cold climates (1), but three cases of cryptococcal infection have been described in Australia (2-4) and Conidiobolomycocosis is also seen. Clinical signs include dyspnoea, abnormal respiratory noise and decreased airflow through the nares, a unilateral or bilateral nasal discharge that may be malodorous, and bony swelling over the sinuses.

Clinical signs of guttural pouch mycosis include unilateral or bilateral epistaxis, nasal discharge and dysphagia. Epistaxis occurs because of the erosion of the guttural pouch mucosa by the fungal plaque, resulting in haemorrhage from the internal carotid, occipital or maxillary arteries. Severe haemorrhage can result in exsanguination and death (5). Aspergillus species are the fungi most commonly isolated from cases of guttural pouch mycosis (6).

Diagnostics

Upper airway endoscopy, including into the guttural pouch, is usually diagnostic for both sinonasal and guttural pouch mycosis. Superficial fungal plaques, as most often seen with Aspergillosis, can be sampled using a cytology brush. For granulomatous masses in the nasopharynx, deep biopsy samples are required. These samples need to be collected with a uterine biopsy instrument as the small endoscopic biopsy instruments are usually too superficial to be diagnostic.

In cases of guttural pouch mycosis, the diagnosis is generally made by endoscopy alone, in conjunction with the clinical history, because of the risk of haemorrhage from disturbance of fungal plaques on arteries.

Serological testing using latex agglutination to identify cryptococcal capsular antigen (LCAT) may be useful if Cryptococcus spp are suspected based on cytological examination.

Where samples can be safely collected, fungal culture should be pursued to confirm the diagnosis and allow for susceptibility testing. This includes cases of sinonasal mycotic infections, which also require imaging studies and are discussed further in Chapter 5.2 Sinusitis (see Section 5 - Dentistry).

Treatment

Surgical treatment of guttural pouch mycosis is traditionally aimed at obstructing blood flow through at-risk vessels by ligation, balloon-tipped catheter placement or transarterial coil embolism, which also results in inhibition of fungal growth, probably because of the reduction in the availability of oxygen (7). Antifungal medical therapy (systemic or topical) is not required. Laser salpingopharyngostomy into the guttural pouch has been used more recently as an adjunct to treatment of guttural pouch mycosis to alter the guttural pouch environment. This has been shown to specifically alter the oxygen and carbon dioxide concentrations, but not the temperature and humidity, within the guttural pouch (8) and is an alternative option for treatment when the fungal plaque is not associated with haemorrhage. When lesions are located over major arteries then there is always the risk of sudden fatal haemorrhage.  If surgical intervention is not available, and the lesions are not over major arteries then repeated topical therapy with nilconazole or nystatin has been used successfully. When lesions affect cranial nerves and dysphagia results, then horses may need prolonged feeding of gruel via a nasogastric tube and possibly treatment for aspiration pneumonia.

Sinonasal mycotic infections caused by Conidiobolomycosis coronatus and Cryptococcus spp are usually successfully treated with 1-3 months of oral fluconazole. Antifungal susceptibility testing is warranted for other organisms, including Aspergillis spp. Not all laboratories offer this service, so it is worth discussing this with laboratories prior to sample submission. Extensive infiltration can be surgically debulked prior to lavage and oral antifungal therapy. One case of cryptococcal rhinitis in Australia was successfully treated with sinonasal bathing with fluconazole under general anaesthesia (4).

Antimicrobials used

Guttural pouch mycosis

Surgical therapy alone is generally successful for guttural pouch mycosis and reduces the risk of exsanguination.

For superficial lesions:

• Topical enilconazole q 12h (volume chosen according to size of the lesion to ensure that it is completely covered by the drug solution) can be diluted 1:4 to facilitate passage of the solution through the biopsy channel of the endoscope.
• Final concentrations of 0.2- 3% have been reported in the literature without complications (9).
• Treatment is until endoscopic resolution which can take 1.5-5 weeks.

Nystatin or amphotericin B have also been administered via inhalation through a nebuliser twice daily most commonly for 2 weeks. The efficacy and effectiveness of this therapy is unknown as all cases have also been treated with topical therapy (1).

Sinonasal mycosis

Superficial plaques due to Aspergillus fumigatus should be treated based on results of culture and susceptibility

Extensive cryptococcal granulomas, lesions probably benefit from surgical debulking followed by:

• Fluconazole: loading dose 14 mg/kg PO followed by 5 mg/kg q 24h for 1-3 months.
• Duration of therapy is likely dependent on severity of the lesion, but long-term treatment is typically required (several months).
• Lesions should be monitored endoscopically and by reduction in cryptococcal antigen titres (LCAT) (10)
• Conidiobolmycosis coronatus granulomas respond well to 1-3 months of oral fluconazole(11).

Prognosis

Good for guttural pouch mycosis. Reasonable with prolonged treatment, with reports of one to five months needed to see resolution of fungal plaques when medical therapy is used. Recurrence, sometimes years later, is frequently reported.

Further reading

• Stewart AJ. Diagnosis and treatment of cryptococcal infections in horses. Equine Veterinary Education. 2020;32(11):576-9.(10).

Key issues

1. Persistent infection and shedding continue for 3-6 weeks following clinical recovery
2. Guttural pouches may serve as S. equi reservoirs (empyema/chondroids or colonisation)
3. Sequelae may be fatal and include metastatic abscessation of internal organs, purpura haemorrhagica (see Chapter 2), and immune-mediated myositis (see Chapter 11)
4. Cross-reactivity of serological tests and PCR/culture contamination may reduce specificity of tests for S. equi. It is important to interpret results in the full context of the clinical disease and outbreak epidemiology.

Streptococcus equi subspecies equi (S. equi) are beta haemolytic Gram-positive cocci.Considered a pathogen of the upper equine respiratory tract, S. equi is closely related to Streptococcus equi subspecies zooepidemicus (S. zooepidemicus). Unlike S.equi, S. zooepidemicus is considered a commensal organism of equine mucosa and an opportunistic pathogen. The genetic similarity between these two bacterial subspecies has clinical relevance, as it may complicate serological testing and agent identification in many assays.

Stranglesis a highly contagious upper respiratory tract disease of horses. A proportion of affected horses will establish an infection in the guttural pouch and remain persistent carriers of S. equi. Most carriers clear their infection after several weeks, but some remain infectious for months to years. Outbreaks in training yards, agistment facilities and on farms are not uncommon and can be difficult to control. Identification of carriers is challenging, so detection of horses in the early stages is critical, as effective isolation of large groups of animals can be logistically difficult. Unidentified carriers, nose-to-nose contact, fomite transfer on personnel and equipment and in shared water or feeding troughs may perpetuate the outbreak. Strangles is a notifiable disease in some Australian jurisdictions and practitioners are encouraged to inform and seek advice from their local veterinary authorities.

Infection with S. equi in horses generally produces a pyretic episode that precedes clinical signs of upper respiratory tract disease, such as muco-purulent / purulent nasal discharge, pharyngitis and subsequent abscessation of the draining lymph nodes. The severity of the clinical disease may be affected by the age and immune status of the horse. Fever typically occurs 3-14 days after exposure and generally persists until the lymph node abscesses rupture. The substantial pharyngitis results in reluctance to eat and drink. Lymphadenopathy is a typical clinical sign – classically affecting the submandibular and retropharyngeal lymph nodes, although the parotid and cranial cervical lymph nodes are also occasionally involved. Abscesses generally rupture between one and four weeks after infection. Guttural pouch infection and empyema results from abscessation of the retropharyngeal lymph node and subsequent rupture of the abscess into the guttural pouch. Some of these carrier horses develop aggregations of inspissated pus and debris, known as chondroids, which play a role in shielding the bacteria from the immune response and prolonging persistent infection.

Inflammation associated with pharyngitis and formation of lymph node abscesses may cause obstruction of the upper respiratory tract (hence “Strangles”) necessitating temporary tracheotomy.

Although rare, metastatic abscesses can also occur in multiple sites, including the abdomen, and these cases are commonly referred to as “bastard strangles.” There is a clinical impression that the rate of bastard strangles is higher in horses treated with antimicrobials but there is no evidence one way or the other in the literature. Other complications following strangles infection are also well recognised and include purpura haemorrhagica (see Section 2, Chapter 3), and immune mediated myositis (Section 11, Chapter 2). Myocarditis is a less commonly reported sequela of strangles infection.

The overall complication rate increases with the duration and intensity of exposure and may be as high as 20%. Overall case fatality rates can be as high as 8.1% to 9.7% in large farm outbreaks.

Diagnostics

Although the clinical signs of strangles are highly indicative, collection of an appropriate sample and identification of the organism is critical, as infection with S. zooepidemicus can mimic the clinical signs of strangles. In the early stages of disease an aspirated sample of pus from an abscessed lymph node provides the ideal, least contaminated sample. Swab samples from burst lymph node abscesses may be of some value if samples are collected carefully to minimise contamination with skin commensals. PCR methods have greater sensitivity for detection of S. equi than traditional culture methods, as have newer molecular methods, such as isothermal assays such as loop-mediated isothermal amplification (LAMP).

In horses with evidence of clinical disease due to S. equi, a complete blood count is non-specific with leukocytosis characterized by a neutrophilia and often hyperfibrinogenaemia. These changes are indicative of a non-specific inflammatory response.

Serial nasopharyngeal swabs and/or guttural pouch washes are often used to detect S. equi following resolution of clinical disease. This sampling is important, as shedding of S. equi after infection may be a source of infection of new horses and thus prolong the outbreak. A minority of horses may continue to shed the organism, maintaining a carrier state via colonization of guttural pouches (with or without chondroid formation). It is important to allow horses to recover from the acute disease before sampling to identify persistent carriers (Figure 3.4).

Several commercial ELISAs are available targeting IgG antibodies against surface proteins of S. equi. These tests have differing sensitivities and specificities, depending upon the type used and stage of disease. The duplex iELISA is useful to manage an outbreak of strangles, as recent infection can be detected by an increase in antibody levels in paired sera taken 10-14 days apart). Other antibody assays, such as the SeM ELISA assay, may detect antibodies directed against SeM of S. zooepidemicus and this cross-reaction leads to reduced specificity of the assay (and false positive results). Microbiological testing of guttural pouch lavages by qPCR or culture can be used to identify sub-clinically infected persistent carriers at the end of an outbreak (Tables 3.1 and 3.2). Sampling for persistent S. equi shedding should commence no sooner than 3-4 weeks after the resolution of clinical signs.

The SeM antibody response can be used to detect horses at risk for development of purpura haemorrhagica, with the recommendation from the USA that horses with strong antibody responses are not vaccinated against S. equi until the antibody levels have subsided.

Treatment

Fever without clinical signs in a strangles outbreak may be an indication for antimicrobial therapy if there is certainty that other clinical signs have not commenced. For this condition to be met, horses must be able to be kept isolated and body temperature monitored twice daily to ensure that treatment is commenced immediately following development of fever. Early treatment may reduce formation of abscesses and therefore shedding. However, if abscesses have already started to form, antimicrobial therapy is highly unlikely to result in bacteriological cure and will only delay abscess rupture thereby prolonging the clinical course and that of the outbreak. Procaine penicillin is the drug of choice.

Uncomplicated strangles infection can usually be managed using supportive treatments. Lancing abscesses to establish drainage will hasten recovery, but most abscesses burst and drain, either externally or internally, within one to four weeks. Non-steroidal anti-inflammatories can reduce fever and improve appetite until drainage is established. Bathing and lavage of burst abscesses and non-steroidal anti-inflammatory medications generally results in rapid healing. Despite a perceived indication by many practitioners and lay personnel, the use of antimicrobials is not indicated in uncomplicated cases of strangles and may delay recovery, especially when there is lymphadenopathy (abscess formation) and drainage has not been established.

Antimicrobials are indicated in infected horses with respiratory distress where abscess drainage is not possible or does not resolve airway obstruction. The antimicrobial drug of choice is penicillin given the predictable sensitivity of S. equi to this antimicrobial.

Oral antimicrobials are sometimes preferred for logistical reasons and trimethoprim-sulfadiazine (TMS) [30 mg/kg PO q 12 h] has in vitro efficacy against S. equi, however anecdotal reports of clinical efficacy vary. In emergency situations, penicillin should be used as streptococci are highly susceptible.

Guttural pouch empyema may require repeated lavage with isotonic saline or polyionic fluids. Both topical and prolonged systemic penicillin administration (10 days) have been used successfully to treat these cases. Endoscopic basket removal of any chondroids is preferred over surgery, as complications with surgery are common.

Metastatic abscessation is considered a complication of a small proportion of strangles cases and is commonly referred to as “bastard strangles”. Sites of infection include internal abdominal organs, lungs and brain. These cases remain difficult to diagnose and need to be treated on a case-by-case basis. As with all abscesses, drainage is the key to clinical resolution. Considerations influencing antimicrobial selection administration include efficacy against S. equi but also include formulation suitable for long-term administration and ability to penetrate tissue (high lipid solubility). Procedures to assist local drainage are indicated, if practical.

Antimicrobials used

• No indication for antimicrobials in uncomplicated infections – effective drainage is sufficient
• For cases with respiratory distress: penicillin at 22,000–44,000 IU/kg IM q 12 h or IV q 6 h for 5-7 days

Metastatic strangles: penicillin 22,000 IU/kg IM q 12 h (if tolerated long term) or trimethoprim-sulphadiazine at 30 mg/kg PO q 12 h – treatment should continue until the abscesses are no longer visible on ultrasound (which may be several weeks to months). Consideration should be given to attempt surgical drainage if possible.

Prognosis

In uncomplicated cases, the prognosis for clinical recovery is good. However, complications, including death, metastatic abscessation and immune-mediated sequelae, are reported in up to 20% of cases following an outbreak.

It is important to recognise that many horses that recover from clinical infection may become latent carriers of S. equi,serving as a transmission risk for in-contact horses.

Further reading

Equine Infectious Diseases second ed. Sellon, D.  Long, M(12).

Figure 3.4. Biosecurity approach to Strangles outbreaks on farms (reproduced with permission from J. Gilkerson).

Tables

Table 3.1. Tests available for strangles

(Reproduced with permission from J. Slater)

Table 3.2. Role of S. equi tests in the control of strangles outbreaks

(Reproduced with permission from J. Slater)

*qPCR and newer molecular techniques, including LAMP, are preferred over PCR. Culture and susceptibility are not recommended as sensitivity and specificity are poor.

** the duplex iELISA is preferred for serial serological testing, as SeM ELISA cross reactivity with S. zooepidemicus can lead to false positive results. The SeM ELISA is useful in identifying individuals at higher risk of developing purpura haemorrhagica in response to S. equi vaccination, so may be used to assess vaccination risk after outbreak resolution.

Key issues

1. Equine herpesviruses and equine picornaviruses usually cause mild and self-limiting upper respiratory tract disease.
2. Abortion and neurological disease can be sequelae of vasculitis associated with systemic EHV-1 infection.
3. Management is key to limiting spread of infection.
4. Vaccination for EHV1 and 4 is useful for increasing herd immunity.

Upper respiratory tract viruses are common, especially in young horses after weaning or when horses are run together in large open groups. As equine influenza is not present in Australia,  the equine herpesviruses (EHV 1 and 4) and equine picornaviruses (ERAV and ERBV) are the most common known causes of equine upper respiratory disease (13). Infections can be mild or subclinical, but intermittent fever, mucoid to purulent nasal discharge, and coughing may be present (14). The lungs usually sound normal on auscultation. Unfortunately, laboratory confirmation of the cause of outbreaks of viral respiratory disease is not commonly undertaken in Australia, with practitioners opting to wait and see if the horses recover.

The equine herpesviruses are the major viral respiratory pathogens affecting horses in Australia. All herpesviruses establish lifelong latent infections, with reactivation occurring during times of stress. The two endemic alphaherpesviruses, EHV-1 and EHV-4, are both transmitted via the respiratory route, with primary replication in the epithelium of the upper respiratory tract. Replication in the epithelium is associated with the observable clinical signs of rhinitis, such as serous nasal discharge, mandibular lymphadenopathy and occasionally ocular discharge. Infected horses are febrile at this stage. The nasal discharge often becomes mucopurulent, but this is usually self-limiting. Clinical signs last for a variable length of time, with clinical resolution between 2 to 10 days after experimental infection (15). Both EHV-1 and EHV-4 are contagious when horses come into contact with nasal discharge or droplets from the respiratory tract, but transmission requires relatively close contact between affected and susceptible horses. The virus can persist in the environment for several days, especially after abortion where virus loads are high. EHV 1 infections can progress from a local respiratory tract infection to a systemic viraemia, with virus in the bloodstream associated with circulating leukocytes. Systemic EHV-1 infections can cause a vasculitis as a result of infection of the endothelial cells of the arterioles supplying the endometrium, which can lead to abortion in pregnant mares; or the arterioles supplying the central nervous system, causing neurological disease in adults. EHV-1 neurological disease is infrequently diagnosed in Australia. EHV-1 abortions were first reported in Australia in the 1970s and are still a common infectious cause of abortion in Australia. EHV 4 is primarily a respiratory tract pathogen and is the most common cause of upper respiratory disease in weaned foals and yearlings throughout Australia (16). The equine gammaherpesviruses, EHV-2 and EHV-5, are commonly detected in secretions and samples from the respiratory tract, but their role in acute respiratory disease is unclear. Care should be taken when ascribing clinical significance to the detection of these viruses.

Other viruses endemic in Australia that are associated with self-limiting respiratory disease are the equine picornaviruses (equine rhinitis A virus, or ERAV and equine rhinitis B virus, or ERBV). ERAV has been identified as a common cause of, sometimes severe, respiratory disease of performance horses in Canada (17). The equine picornaviruses have been detected in horses with and without clinical signs of respiratory disease, but this is consistent with the serological evidence that horses are exposed to these viruses by aerosol or direct contact early in life (18). ERAV is associated with more severe respiratory signs, characterized by nasal discharge, pyrexia, and a viraemia that lasts 4 to 5 days.

Diagnostics

PCR testing of respiratory secretions on nasopharyngeal swabs is the diagnostic test of choice. Viral culture and isolation can be performed on swab material but is rarely done. Serology can be undertaken to demonstrate seroconversion, but antibodies to EHV1 and EHV4 will cross-react in neutralisation tests. PCR can be performed on buffy coat cells from blood samples collected in EDTA tubes, or whole blood, to demonstrate viraemia.

Treatment

1. Antibiotics are not indicated unless there is secondary bacterial infection.
2. Non-steroidal anti-inflammatory drugs may be used to control fever (flunixin meglumine 1.1 mg/kg IV or PO q 24 h; phenylbutazone 2 g IV or PO q 24 h; meloxicam 0.6 mg/kg IV or PO q 24 h).
3. Management is important in horses with EHV1 infections to reduce sequelae (abortion in pregnant mares; neurological disease in adult horses). Recommendations include subdividing horses into smaller groups, minimizing stress, barrier nursing of infected horses and vaccination against EHV 1 and 4 to maximise herd immunity.

Antimicrobials used

• Not Indicated.

Prognosis

Good, as viral respiratory infections are usually self-limiting.

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