Nasal rhinosporidiosis in a mule

A mass was removed from the nostril of a mule that exhibited unilateral epistaxis and nasal discharge. Impression smears revealed oval structures consistent with spores of Rhinosporidium seeberi. Microscopically, the mass was composed of fibrovascular granulomatous tissue containing sporangia R. seeberi. Surgical excision and antifungal treatment proved curative.     

Cytologic identification of immature endospores in a dog with rhinosporidiosis

An 8-year-old, intact, male Labrador Retriever was presented to the Boren Veterinary Medical Teaching Hospital at Oklahoma State University with a 2-month history of severe sneezing episodes that resulted in epistaxis and bilateral sanguineous discharge. Rhinoscopy revealed a small polypoid mass, and specimens were obtained for histopathology. Microscopic examination of formalin-fixed tissue specimens revealed organisms consistent with Rhinosporidium seeberi. The mass was surgically excised and impression smears were made for cytology examination. Smears revealed high numbers of endospores, typical of those previously described for R seeberi. In addition, numerous smaller structures, presumed to be immature endospores, were noted. The immature endospores were morphologically distinct from mature endospores and have not been described previously. Recognition of immature forms of Rhinosporidium may help prevent misidentification of the organism or misdiagnosis of a dual infection.     

Rhinosporidiosis in a cat.

A polypoid nasal mass from an adult cat was submitted for routine biopsy examination and was found to contain sporangia and sporangiospores consistent with Rhinosporidium seeberi. Inflammatory infiltrates were moderate and pyogranulomatous to lymphohistiocytic and were associated with hyperplasia of the transitional nasal epithelium. Apparently, this is the first reported case of rhinosporidiosis in a cat.     

Rhinosporidiosis in a dog

Rhinosporidiosis was diagnosed in a black and tan coonhound. Clinical signs were characterized by 6 to 8 months of intermittent sneezing. Numerous polypoid nodules were removed from the nasal cavity. Histologic examination of the nodules revealed chronic pyogranulomatous inflammation caused by infection with Rhinosporidium seeberi. Rhinosporidiosis has been reported in human beings, dogs, and several other domestic species. It is an uncommon disease in the United States.     

Nasal rhinosporidiosis in the dog

Rhinosporidiosis was diagnosed in six dogs from the southeastern United States. All six dogs had unilateral nasal polyps with multiple small white sporangia visible beneath the surface. Microscopically, the polyps consisted of organisms and fibrovascular tissue with a surface of columnar or squamous epithelium. Juvenile sporangia were unilamellar, 15-75 microns in diameter, nucleated, and accounted for about 65% of sporangia seen. Approximately 5% of the sporangia were in intermediate stages of maturation, were bilamellar, 100-150 microns in diameter, and contained immature endospores. Mature sporangia comprised about 30% of the total, were usually unilamellar, 100-400 microns in diameter, and contained a mixture of immature and mature endospores. The inner layer of the wall of the intermediate sporangia and the single wall of the mature sporangia were argyrophilic and carminophilic. Ultrastructurally, the earliest stage contained a nucleus and many ribosomes, lipid droplets, and phagolysosomes. Maturing sporangia contained discrete membrane-bound, round clevage products. These structures subsequently matured to spores, each of which had a wall and contained a nucleus and many lipid droplets. The organism from one dog was cultured and grown in vitro for 7 months and is the first successful cultivation of Rhinosporidium seeberi.     

Rhinosporidiosis in a dog

A dog with a nasal papilloma due to Rhinosporidium seeberi is presented. The causative organism was found using cytopathology and histopathology. The young Doberman dog had never travelled out of the province of Ontario and is the first case of rhinosporidiosis reported in Canada.     

DIAGNOSTIC SENSITIVITY OF SUBJECTIVE AND QUANTITATIVE LARYNGEAL ULTRASONOGRAPHY FOR RECURRENT LARYNGEAL NEUROPATHY IN HORSES

Recurrent laryngeal neuropathy (RLN) is the most common cause of laryngeal hemiplegia in horses and causes neurogenic atrophy of the intrinsic laryngeal muscles, including the cricoarytenoideus lateralis muscle. Recurrent laryngeal neuropathy results in paresis to paralysis of the vocal fold and arytenoid cartilage, which limits performance through respiratory compromise. Ultrasound has previously been reported to be a useful diagnostic technique in horses with RLN. In this report, the diagnostic sensitivity of subjective and quantitative laryngeal ultrasonography was evaluated in 154 horses presented for poor performance due to suspected upper airway disease. Ultrasonographic parameters recorded were: cricoarytenoideus lateralis echogenicity (subjective and quantitative), cricoarytenoideus lateralis thickness, vocal fold movement, and arytenoid cartilage movement. Ultrasonographic parameters were then compared with laryngeal grades based on resting and exercising upper airway endoscopy. Subjectively increased left cricoarytenoideus lateralis echogenicity yielded a sensitivity of 94.59% and specificity of 94.54% for detecting RLN, based on the reference standard of exercising laryngeal endoscopy. Quantitative left cricoarytenoideus lateralis echogenicity values differed among resting laryngeal grades I–IV. Findings from this study support previously published findings and the utility of subjective and quantitative laryngeal ultrasound as diagnostic tools for horses with poor performance.     

Experimental crush of the equine recurrent laryngeal nerve: a study of normal and aberrant reinnervation

Experimental reinnervation of the equine larynx in healthy ponies was studied after the recurrent laryngeal nerve was crushed, using endoscopic, electromyographic, and microscopic techniques. In 12 ponies, the recurrent laryngeal nerve was crushed unilaterally in the midcervical area. All showed postoperative paralysis of the larynx on the operated side. In 8 ponies, recovery of movement of the vocal folds occurred at different times (2.5 to 8 months) after surgical operation was done. These movements, which were often abnormal, included trembling and asynchronism. In 2 of these ponies, complete return of normal vocal fold function occurred. Return of function was due to reinnervation, as determined by electromyographic examination of the laryngeal muscles and microscopic evaluation of these muscles and the recurrent laryngeal nerves. In the muscles, there was evidence of fiber-type grouping, and the nerves showed regenerative activity. In 3 ponies, there was evidence of aberrant reinnervation, with adductor or abductor muscles discharging during an inappropriate phase of the respiratory cycle. Further evidence that reinnervation occurred in the larynges of these ponies was determined in microscopic sections of the recurrent laryngeal nerves and muscles, which showed regenerative activity and muscle fiber-type grouping, respectively. The endoscopic abnormalities in these ponies were compared with those seen in horses with spontaneous subclinical laryngeal paralysis. However, the possibility that the abnormal endoscopic findings in this latter group of horses are due to aberrant reinnervation is thought to be unlikely.     

Surgical relief of severe laryngeal malformation in an English Bulldog

A 22 month old English Bulldog was presented with progressive upper airway obstruction associated with an elongated soft palate, tonsillitis, everted laryngeal saccules and laryngeal malformation. Surgical management of the case consisted of resection of the elongated soft palate and everted laryngeal saccules, unilateral tonsillectomy and correction of the laryngeal stenosis. The latter was achieved by using a castellated incision through the laryngeal cartilages and first tracheal ring. From this case, it is postulated that, at least in some cases, the common upper airway obstruction syndrome in Bulldogs may not be due to laryngeal collapse as previously thought but rather to congenital malformation of the laryngeal cartilages.     

The pathogenesis of equine laryngeal hemiplegia--a review

Recent research on the muscular and nervous changes which occur in idiopathic equine laryngeal hemiplegia has indicated that many of the traditional concepts of the aetiology of this disease are erroneous. In light of the new knowledge gained, the various predispositions and possible causes of laryngeal hemiplegia are discussed, and it is suggested that the underlying mechanism of axonal damage in this neuropathy of horses may be related to abnormal energy metabolism in the axon.     

Correlation of the Havemeyer endoscopic laryngeal grading system with histopathological changes in equine Cricoarytenoideus dorsalismuscles

The establishment of a single validated endoscopic laryngeal grading system for assessing recurrent laryngeal neuropathy (RLN) is desirable to facilitate direct comparisons between the findings of different clinical and research groups worldwide. The objective of this study was to assess the relationship between the Havemeyer endoscopic laryngeal grading system and histopathological changes consistent with RLN in the left cricoarytenoideus dorsalis (CAD) muscle of horses of different breeds with a full range of clinical severities of RLN, i.e., from normal endoscopic laryngeal function to complete laryngeal hemiplegia. Endoscopic grading of laryngeal function of 22 horses was performed using the Havemeyer endoscopic laryngeal grading system. A biopsy sample of the left CAD muscle was obtained from each horse, either at post mortem examination (n = 16), or during routine laryngoplasty surgery (n = 6). A semi-quantitative histopathological scoring system was used to grade the severity of histopathological lesions consistent with RLN in the left CAD muscle of each horse. A significant positive correlation (rs = 0.705, p < 0.001) was found between the Havemeyer grades and sub-grades of laryngeal function and the semi-quantitative assessment of histopathological lesions consistent with RLN in the left CAD muscle. However, a wide spread of muscle histopathological scores was obtained, particularly from horses with Havemeyer sub-grades II.1, III.1 and III.2. In conclusion, the Havemeyer endoscopic laryngeal grading system was found to broadly correlate with histopathological changes consistent with RLN in equine cricoarytenoideus dorsalis muscle.     

Surgical relief of severe laryngeal malformation in an English Bulldog

A 22 month old English Bulldog was presented with progressive upper airway obstruction associated with an elongated soft palate, tonsillitis, everted laryngeal saccules and laryngeal malformation. Surgical management of the case consisted of resection of the elongated soft palate and everted laryngeal saccules, unilateral tonsillectomy and correction of the laryngeal stenosis. The latter was achieved by using a castellated incision through the laryngeal cartilages and first tracheal ring. From this case, it is postulated that, at least in some cases, the common upper airway obstruction syndrome in Bulldogs may not be due to laryngeal collapse as previously thought but rather to congenital malformation of the laryngeal cartilages.     

Temporary right recurrent laryngeal neuropathy in a horse associated with a left prosthetic laryngoplasty procedure

Right recurrent laryngeal neuropathy (RLN) is an uncommon, acquired disease for which the aetiology can frequently be diagnosed. Numerous aetiologies have been proposed for right‐sided RLN which comprises 2% of all cases of RLN. In this report we discuss the clinical course, treatment and outcome following right‐sided laryngeal paralysis as a complication of left‐sided prosthetic laryngoplasty in a horse. To the authors' knowledge, this is the first report of such a surgical complication.     

Acquired bilateral laryngeal paralysis associated with systemic lupus erythematosus in a dog

A 4 yr old spayed female Labrador retriever was referred for acute respiratory distress and was found to have bilateral laryngeal paralysis. Physical examination and biochemical testing were consistent with systemic lupus erythematosus (SLE) and did not reveal a likely alternative cause for the laryngeal paralysis. Following immunosuppressive and supportive treatment, the dog regained normal laryngeal function. At a scheduled follow-up examination 6 wk later, normal laryngeal function was confirmed via sedated laryngeal examination. Laryngeal paralysis associated with SLE has been reported in humans, but this is the first known report of acquired laryngeal paralysis associated with SLE in the dog.     

Pathological classification of equine recurrent laryngeal neuropathy

Recurrent Laryngeal Neuropathy (RLN) is a highly prevalent and predominantly left‐sided, degenerative disorder of the recurrent laryngeal nerves (RLn) of tall horses, that causes inspiratory stridor at exercise because of intrinsic laryngeal muscle paresis. The associated laryngeal dysfunction and exercise intolerance in athletic horses commonly leads to surgical intervention, retirement or euthanasia with associated financial and welfare implications. Despite speculation, there is a lack of consensus and conflicting evidence supporting the primary classification of RLN, as either a distal (“dying back”) axonopathy or as a primary myelinopathy and as either a (bilateral) mononeuropathy or a polyneuropathy; this uncertainty hinders etiological and pathophysiological research. In this review, we discuss the neuropathological changes and electrophysiological deficits reported in the RLn of affected horses, and the evidence for correct classification of the disorder. In so doing, we summarize and reveal the limitations of much historical research on RLN and propose future directions that might best help identify the etiology and pathophysiology of this enigmatic disorder.     

Equine laryngeal hemiplegia. Part IV. Muscle pathology

This study confirmed that neurogenic muscle pathology exists in intrinsic laryngeal muscles supplied by the recurrent laryngeal nerves in horses subclinically and clinically affected with laryngeal hemiplegia. An important additional observation was the occurrence in three out of four laryngeal hemiplegic horses of neurogenic muscle changes in a hindlimb muscle, the extensor digitorum longus, a muscle supplied by another long peripheral nerve. This finding suggests that a polynenropathy exists in laryngeal hemiplegic horses, and supports the classification of this disease as a distal axonopathy. Comparison of the degree of pathology in the intrinsic laryngeal muscles and that of the recurrent laryngeal nerves innervating them, demonstrated a strong correlation between the extent of damage in the distal left recurrent laryngeal nerve and the overall degree of muscle pathology. The muscle damage in clinically affected horses is a reflection of the nerve damage present in the most distal portion of the recurrent laryngeal nerve. The more variable pathological changes found in proximal levels of the left and right recurrent laryngeal nerves probably reflects the ongoing nature of the pathological process affecting nerve fibres. The existence of a subclinically affected group of horses, the earliest involvement of an adductor, the left cricoarytenoideus lateralis muscle, and the presence of changes in the right intrinsic laryngeal muscles all confirmed the findings of previous workers.     

Equine laryngeal hemiplegia. Part II. An electron microscopic study of peripheral nerves

The recurrent laryngeal nerves were examined by electron microscopy in five control, four subclinical and four clinical laryngeal hemiplegic horses. In addition, the peroneal nerve was examined in two horses in the latter group. The distally distributed loss of large myelinated fibres in the left recurrent laryngeal nerve seen by light microscopy was confirmed. In addition, active axonal pathology was found to be more evident than indicated by light microscopic investigations. The onion bulb formations observed indicated the repetitive nature of the damaging influence to nerve fibres. Although the pathological changes were most obvious in the distal left recurrent laryngeal nerve, alterations similar in type and distribution were present in other areas of the left and right nerves, and in the distal hindlimb nerves. The observation of fibres with inappropriately thick myelin sheaths relative to their axonal calibre, was confirmed statistically by determining the regressions of axis cylinder perimeter against the number of myelin lamellae. In conclusion, the peripheral nerve pathology of equine laryngeal hemiplegia was demonstrated to be a distally distributed loss of myelinated fibres, with considerable active axonal damage, in conjunction with axonal atrophy. These features suggest that this disease may be classified as a distal axonopathy.