83 Rhinosporidiosis

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Infectious Diseases of the Dog and Cat, 3rd Edition

CHAPTER 83 Rhinosporidiosis

M. Cecilia Castellano

Edward B. Breitschwerdt

ETIOLOGY

Rhinosporidiosis, a chronic granulomatous disease caused byRhinosporidium seeberi, induces tumorlike growths

of epithelial tissues in domestic animals, birds, and people.6,13,15

The taxonomy ofR. seeberihas long been controversial. Based on its morphologic characteristics, it has been

classified in the past few years as a fungus by most microbiologists. Phylogenetic analysis indicatesR. seeberito

be a member of a newly recognized group of human and animal pathogens that form a branch in the evolutionary

tree near the animal-fungal divergence.8,10

It has been proposed that this new phylogenetic group be referred to as

the class Mesomycetozoea (between fungi and animals) andR. seeberibe considered a monotypic genus within

this class.10,19

Genetic analysis of isolates suggests that host-specific strains of the organism may exist.22a

Like

other mesomycetozoeans,R. seeberiis associated with aquatic environments. AlthoughR. seeberiis generally

believed to be the causative agent of rhinosporidiosis, a few challenge this accepted premise. In one study, a

cyanobacteriumMicrocystis aeruginosawas isolated from water in which human patients with the disease were

bathing.2,3

The organism was also identified in clinical specimens; however, additional confirmation is needed for

this hypothesis. Microscopic findings of lesions indicate thatR. seeberi, and not a bacterium, is the cause of this

disease.

Although a few successful attempts to propagateR. seeberiin tissue culture have been described,6,14

the results

have been questioned.18

Most microbiologists considerR. seeberito be intractable to culture.8,10,19

The infective

unit is a small (7- to 15-m), round spore that once implanted in tissues progressively develops into large (100- to

450-m), spherical bodies known as sporangia. Sporangia undergo a maturation process, resulting in the

production of 16,000 to 20,000 endospores that are then discharged through an apical pore, and the cycle is

reinitiated.6

EPIDEMIOLOGY

Rhinosporidiosis is endemic in India, Sri Lanka, and Argentina and is reported sporadically from other parts of the

world. In the United States, canine rhinosporidiosis has been reported only in the southern states; however,

occurrence of the disease in a dog native to Ontario and in a cat from a suburb of Washington, DC, suggests the

possibility of a more widespread distribution in North America. In Europe, canine rhinosporidiosis has been

recognized only in northern Italy.7

Feline rhinosporidiosis has been reported in two outdoor cats, both in the United States.20,23

R. seeberiis stimulated to develop mature endospores that are released from its sporangia after exposure to water,

thus the disease is associated with wet environments and the host's moist mucous membranes. Most affected

animals are exposed to flowing or impounded water. Infection frequently involves the mucous membranes of the

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nasal cavity, but it may occasionally affect the ear, pharynx, larynx, trachea, esophagus, urogenital mucosae, and

skin. Reported cases of canine and feline rhinosporidiosis have involved only the nasal cavity.

The disease is more common in large-breed dogs with a mean age of 5 years (and a range of 1.5 to 13 years) and

seems to be more common in males, as it is in people and horses. Behavioral and biologic factors may be

responsible for this apparent predisposition. Because of the few reported cases, it is not known whether the same

tendencies are found in cats.

PATHOGENESIS

The pathogenesis of rhinosporidiosis has not been completely characterized because of the difficulties associated

with in vitro propagation of the organism.

R. seeberihas not been detected in the environment, and its natural host remains unknown. Reports from endemic

areas suggest that infection is acquired by mucosal contact with stagnant water. Mucous membrane trauma may be

a predisposing factor. In arid countries, most human infections are ocular, and dust is postulated to be a fomite. In

vitro studies suggest that endospore release from mature sporangia is stimulated by mucous secretions.

18

Onceimplanted in tissues, endospores elicit a severe, focal pyogranulomatous reaction.

Little is known about the immune response toR. seeberi. A mucoidlike layer with immunogenic properties has

been recognized beneath the sporangium's cell wall.11,18

It has been suggested that it may play a role in the

immunology of the disease.

CLINICAL FINDINGS

Clinical findings include wheezing, sneezing, unilateral seropurulent nasal discharge, and epistaxis. Polypoid

lesions may be visible in the nares (Fig. 83-1) and may also be visualized by rhinoscopy in the rostral nasal cavity

(Fig. 83-2). Single or multiple polyps ranging in size from a few millimeters up to 3 cm are pink, red, or pale gray

and covered by numerous pinpoint white-yellowish granules (sporangia). Polyps may be sessile or pedunculated,

and the superficial surface is irregular, glistening, and possibly ulcerated. Duration of clinical signs in reported

canine cases ranges between 2 weeks and 8 months.

DIAGNOSIS

The organism can be demonstrated by several stains: hematoxylin-eosin, Wright, Gridley's, toluidine blue,

periodic acidSchiff, and Grocott's. Cytologic examination of nasal exudate and of scrape or brush samples

obtained from the surface of the polyp usually allows diagnosis through identification of single or clusters ofR.

seeberispores. Although less common, sporangia may be observed (Fig. 83-3). Sporangia and spores should be

easily recognized by histologic examination.

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Fig 83-1 Two-year-old male dog of mixed German shepherd breeding from

Argentina, with a bright red sessile growth in the right nostril.

Rhinosporidiosis was diagnosed after histologic examination.

Fig 83-2 Rostral rhinoscopy in dog with rhinosporidiosis. Polyp is attached to nasal

mucosa. (Courtesy University of Georgia, Athens, Ga.)



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Fig 83-3 Scrape smear of nasal polyp. A, Numerous single endospores of R.

seeberidispersed in epithelial-cell background (PAS stain, 200). B,

Juvenile sporangium of R. seeberi. Note transparent capsules andnumerous endospores with internal globular bodies (Wright stain, 200).

A polymerase chain reaction assay specific forR. seeberihas been developed.8

PATHOLOGIC FINDINGS

Microscopic examination reveals that polyps are composed of fibrovascular tissue lined by squamous or columnar

epithelium that is frequently ulcerated.6Sporangia at different stages of maturation can be seen (Fig. 83-4) and

may be releasing spores through the epithelium to the superficial surface. A superficial exudate most prominent inareas of spore extrusion is composed of spores, neutrophils, epithelia, and erythrocytes. A mixed inflammatory

response consisting predominantly of plasma cells and lymphocytes and to a lesser extent, macrophages, is

scattered throughout the tissue.

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Fig 83-4 Nasal polyp. Note larger mature sporangium (arrow)and smaller trophic

stages throughout stroma (H and E stain, 160). (From Gardiner CH,

Fayer R, Dubey JP. 1988.An atlas of protozoan parasites in animal tissues,Beltsville, Md, USDA, Agriculture Handbook No 651.)

THERAPY

Surgical excision remains the treatment of choice and may be curative when a single polyp is excised. Because of

the frequent rostral location of the polyps, surgical excision through the nares or by anterolateral approach to the

nares generally is possible, negating the necessity for the more invasive dorsonasal flap procedure. In four dogs

treated with surgery alone, no recurrence was noted after 1 to 2 years.7Recurrence has been reported 2 to 12

months after surgery in dogs with single or multiple lesions. Dapsone has been used to treat human

rhinosporidiosis with variable success12,6

and might be considered as an adjunct to surgical removal of lesions in

dogs or cats. Light and electron microscopic studies have demonstrated that dapsone induces degenerative changes

inR. seeberiby inhibiting division of the organism.22

Treatment with dapsone (1 mg/kg every 8 hours for 2

weeks, followed by 1 mg/kg every 12 hours for 4 months) likely cured a dog that developed polyps after surgical

extirpation.6,17

Ketoconazole (8.7 mg/kg every 8 hours for 21 days) eliminated nasal discharge in a dog after 4

days, and visual and cytologic resolution of the polyps occurred after 21 days of therapy.6Although treatment

continued for an additional 21 days, the disease recurred 6 months later, necessitating surgical excision of a large

polyp. Medical therapy of rhinosporidiosis may be improved by screening antiparasitic drugs that have an effect

on other members of the Mesomycetozoea class.

PUBLIC HEALTH CONSIDERATIONS

Although people are also affected with this disease, no evidence supports the possibility of transmission ofR.

seeberifrom animals to people. Dogs and people appear to become infected from common environmental sources.

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Suggested Readings*

* See the CD-ROM for a complete list of references.

7. Caniatti, M, Roccabianca, P, Scanziani, E, et al.: Nasal rhinosporidiosis in dogs: four cases from Europe

and a review of literature. Vet Rec. 142, 1998, 334338.

19. Mendoza, L, Taylor, JW, Ajello, L: The class Mesomycetozoea: a heterogeneous group of

microorganisms at the animal-fungal boundary.Annu Rev Microbiol. 56, 2002, 315344.

20. Moisan, PG, Baker, SV: Rhinosporidiosis in a cat.J Vet Diagn Invest. 13, 2001, 352354.

23. Wallin, LL, Coleman, GD, Froeling, J, et al.: Rhinosporidiosis in a domestic cat.Med Mycol. 39, 2001,

139141.

Uncited references

9. Fredricks, DN, Jolley, JA, Lepp, PW, et al.:Rhinosporidium seeberi: a human pathogen from a novel

group of aquatic protistan parasites.Emerg Infect Dis. 6, 2000, 273282.

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