18-year-old, thoroughbred mare (Equus caballus).The mare had a several year history of a polyp in the nasal cavity. The mass was
surgically removed and submitted as an excisional biopsy.
The biopsy sample comprised a 2 x 1.5 x 1 cm smooth, pink-tan, spongy mass with multifocal
ulcers and a narrow stalk at one edge.
sections of the tissue comprise a polypoid proliferation of loose fibrovascular
tissue covered by a hyperplastic, acanthotic stratified squamous epithelium
with multifocal erosions and an eosinophilic exudate of mucin admixed with
necrotic neutrophils, debris and erythrocytes. Numerous protistan organisms at
varying stages of development are embedded within the surface exudate,
epithelium, and submucosa, which is infiltrated by moderate numbers of
lymphocytes, plasma cells, macrophages, fewer neutrophils, and variable amounts
of hemorrhage and edema. Immature sporangia (trophocytes) are round and 10-100
μm diameter, with a 2 μm thick eosinophilic wall, lacy amphophilic
cytoplasm, and a single, central, round karyosome (nucleus). Intermediate
sporangia lack a nucleus and contain innumerable immature sporangiospores
(endospores). Immature endospores are 1-4 μm diameter, with a thin wall,
scant to moderate amounts of lightly basophilic cytoplasm, and irregularly
round, para-central eosinophilic structures. Mature sporangia located
throughout the epithelium are spherical and 100-400 μm diameter, with a
2-5 μm thick, bilamellar, outer eosinophilic and inner amphophilic wall.
The mature sporangia contain mature endospores or a mixture of mature and
immature endospores. Mature endospores are 5-8 μm diameter spherical
structures with a thin unilamellar wall, scant clear cytoplasm, and multiple,
central, round eosinophilic bodies. Within mature sporangia, immature
endospores are often located peripherally or emerge unilaterally from the wall
of the sporangium. Mature sporangia are multifocally ruptured, releasing mature
endospores through an apical pore in the epithelium or into the adjacent
stroma, and surrounded by dense aggregates of neutrophils with fewer
lymphocytes, plasma cells, and macrophages.
Horse, nasal mass: Chronic polypoid and suppurative
rhinosinusitis with protistan sporangia and endospores (consistent with Rhinosporidium
Nasal rhinosporidiosis/Rhinosporidium seeberi
seeberi is an uncommon cause of rhinitis and nasal polyps in humans, dogs,
cats, horses, cattle and waterfowl.3, 4, 7, 9, 10, 11, 12 The
organism was originally identified in tissue extracted from nasal polyps of
people in Argentina, and has since most commonly been diagnosed in tropical
climates such as India and Sri Lanka.3 It has been reported
sporadically in horses from the Americas and Europe. 2, 9, 10, 11,
Patients with nasal rhinosporidiosis may be asymptomatic, or present with clinical signs that include respiratory noise, sneezing, nasal discharge, and epistaxis.2, 3, 4 If masses become large, obstruction of the nasal passage can occur.1, 3 Examination of the nasal cavity reveals a unilateral polypoid mass protruding from the nasal mucosa, though laryngeal masses in association with R. seeberi have been reported in horses.2, 11 Close inspection of the surface of the mass may reveal small, white foci. In humans, there are reports of nasal, ocular, laryngeal and genital rhinosporidiosis.3
Histologic examination reveals a fibro-vascular polyp covered by stratified squamous to pseudostratified ciliated columnar epithelium. Sporangia in varying stages of development are observed throughout the fibrovascular and epithelial components of the polyp. Identification of sporangia with endospores in a polypoid nasal mass is diagnostic for R. seeberi.7 Organisms are readily observed in H&E-stained sections; however, histochemical stains, such as GMS and PAS, can be used to highlight the walls of the sporangia.5 Polymerase chain reaction (PCR) and DNA sequence analysis of tissue samples can be used to confirm the etiologic agent.2
The classification of R. seeberi has long been controversial. The organism was once considered to be protozoan, fungus, or a cyanobacterium. More recently, phylo-genetic analysis categorized R. seeberi as a eukaryote within the class Mesomycetozoa, a group of aquatic protistan parasites.5, 6
The pathogenesis of rhinosporidiosis is poorly understood, though stagnant water appears to be the reservoir for R. seeberi. The proposed mechanism of infection involves pre-existing defects in the epithelial barrier of the nasal passage, allowing mature endospores to enter the nasal mucosa from contaminated water.3 Once within host tissues, endospores localize to the sub-epithelial connective tissues and mature into immature sporangia (trophocytes). Immature sporangia have thick, unilamellar eosinophilic walls, a central nucleus, and fine cytoplasm. As immature sporangia become intermediate sporangia, a bilamellar wall develops, the nucleus is lost, and the cytoplasm condenses to form immature sporangiospores (endospores). Intermediate sporangia eventually become larger, contain both immature and mature endospores, and are localized within the superficial epithelium. At this stage, the sporangia are considered mature and will continue to house developing endospores until release. Mature endospores contain multiple, central eosinophilic bodies, and are released from sporangia through apical pores in the epithelium into the nasal passage. Infective, mature endospores released into the nasal passage are then excreted into the environment along with nasal secretions.
Surgical removal of any visible polyps is the treatment of choice for nasal rhino-sporidiosis. Excision is typically curative; however, recurrence is reported.2, 3, 7 A diagnosis of concurrent nasal adeno-carcinoma and rhinosporidiosis was reported in a cat housed on a horse farm.1
In this horse, infectious organisms were embedded within a polypoid proliferation, grossly and histologically resembling a nasal polyp. Because rhinosporidiosis in humans is associated with polypoid proliferations, the authors speculate the proliferative (polypoid) response in this horse may be secondary to chronic infection and inflammation, rather than represent a primary nasal polyp. Free endospores within the submucosa often elicit a pyo-granulomatous to granulomatous response; however, in this case, the predominant inflammatory infiltrates were neutrophils admixed with lymphocytes, plasma cells, and macrophages.
For this horse, travel history, clinical signs, laboratory findings and post-operative follow-up were not provided by the submitting veterinarians.
Rhinitis, polypoid, chronic-active, diffuse, severe, with numerous protistan
sprorangia and endospores, thoroughbred, Equus caballus
The contributor provides an exceptional review of the epidemiology, clinical
presentation, gross lesions, histopathologic findings, and differential
diagnosis for Rhinosporidium seeberi in horses. Conference participants
were impressed by the tremendous numbers of protistan endospores and striking
variation in the size of the sporangia in the section. Despite slight slide
variability, conference participants noted chronic mixed inflammation with
hemorrhage, edema, and granulation tissue in the subepithelial connective
tissue and stalk of the nasal polyp.
Rhinosporidium seeberi is one of the few pathogens which reproduce by endo-sporulation.3 The endospore is implanted in tissues and grows into much larger and variably sized sporangia. As sporangia grow and mature, endospores are produced and released into the surrounding tissue generating marked pyogranulomatous inflammation and effectively reinitiating the pathogens lifecycle.3 Conference participants discussed other endosporulators of veterinary significance including: Prototheca wickerhamii, Chlorella sp., Coccidioides sp., and Batrachochytrium dendrobatidis. Based on the size of the sporangia and observation of endo-sporulation, the differential diagnosis in this case includes Coccidioides sp. (see 2016-2017 WSC 4 Case 4). The endospores of Rhinosporidum seeberi contain inner granules, while Coccidioides sp. endospores do not. Also, R. seeberi endospores completely stain with Periodic acid-Schiff (PAS), while only the walls of the endospores stain in Coccidioides sp.8 However, finding large sporangia in a polypoid nasal mass of a horse is typically considered diagnostic for rhinosporidiosis.1,3
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