Differential Diagnoses

Rhinosporidiosis

Background

Rhinosporidiosis is a chronic granulomatous infection of the mucous membranes that usually

manifests as vascular friable polyps that arise from the nasal mucosa or external structures of
the eye. Initially described by Seeber in 1900 in an individual from Argentina,
rhinosporidiosis is endemic in India, Sri Lanka, South America, and Africa. Many cases from
the United States and Southeast Asia, as well as scattered occurrences throughout the world,
have been reported. Most cases of rhinosporidiosis occur in persons from or residing in the
Indian subcontinent or Sri Lanka.

The etiologic agent, Rhinosporidium seeberi, has never been successfully propagated in vitro.
Initially thought to be a parasite for more than 50 years, R seeberi had been considered a
water mold. Molecular biological techniques have recently demonstrated that this organism is
an aquatic protistan parasite. It is currently included in a new class, the Mesomycetozoea,
along with organisms that cause similar infections in amphibians and fish.

Pathophysiology

Rhinosporidiosis is an infection that is typically limited to the mucosal epithelium. Infection

usually results from a local traumatic inoculation with the organism. The disease progresses
with the local replication of R seeberi and associated hyperplastic growth of host tissue and a
localized immune response.

Infection of the nose and nasopharynx is observed in 70% of persons with rhinosporidiosis;
infection of the palpebral conjunctivae or associated structures (including the lacrimal
apparatus) is observed in 15%.

Other structures of the mouth and upper airway may be sites of disease. Disease of the skin,
ear, genitals, and rectum has also been described. Genital disease has been described in the
vagina, penile urethra or meatus, and scrotum. Dissemination of infection has been described
in only 3 individuals.

Frequency

United States

Cases in the United States are rare but are more common in Texas and the Southeast.

International

Rhinosporidiosis usually affects persons in or from southern India and Sri Lanka. Cases have
been reported worldwide, with an increased incidence in South America and Africa.

Mortality/Morbidity
Rhinosporidiosis can cause prolonged painless disease with limited morbidity.
Disease of up to 30 years' duration has been reported. Secondary bacterial
infection can cause morbidity. Death has been reported in only the few rare
reports of disseminated disease.

Race

Rhinosporidiosis has no known racial predilection.

Sex

Men are affected more commonly than women, with a male-to-female ratio of 4:1.

Age

The disease most commonly occurs in children and in individuals aged 15-40 years.

Clinical
History

• Nasal disease may present with unilateral nasal obstruction or epistaxis.

Other symptoms may include local pruritus, coryza with sneezing,
rhinorrhea, and postnasal discharge with cough. Patients often report a
sensation that a foreign body is present in their nasal canal.
• Eye involvement is initially asymptomatic. Increased tearing may be
reported as the disease progresses. Photophobia, redness, and secondary
infection may occur.
• Skin lesions begin as papillomas that gradually become verrucous.

Physical

• Soft polyps may develop on the nose or eye. These polyps are pink to
deep red, are sessile or pedunculated, and are often described as
strawberrylike in appearance. Because the polyps of rhinosporidiosis are
vascular and friable, they bleed easily upon manipulation.
• This appearance results from sporangia, which is visible as gray or yellow
spots in the vascular polypoid masses.

Causes

• The etiologic agent of rhinosporidiosis, R seeberi, has traditionally been

considered a fungus. Recent 18S ribosomal ribonucleic acid (rRNA) gene
analysis has placed R seeberi into a novel group of aquatic parasites of the
class Mesomycetozoea, some of which cause similar diseases in
amphibians and fish.
• Most persons with rhinosporidiosis have had bathing or working exposure
to stagnant water.
• No immune deficiency has been associated with infection.
Other Problems to Be Considered

Osteoarthritis (OA) can usually be diagnosed on clinical grounds. The history and physical
examination findings are sufficient. Radiographic findings confirm the initial impression (see
Imaging Studies), and laboratory values are typically within the reference range. The initial
goal is to differentiate osteoarthritis from other arthritides (eg, rheumatoid arthritis).

Rheumatoid arthritis predominately affects the wrists and the metacarpophalangeal (MCP)
and PIP joints. Rheumatoid arthritis rarely, if ever, involves the DIP joints or lumbosacral
spine. Rheumatoid arthritis is associated with prominent prolonged (>1 h) morning stiffness.
Radiographic findings of rheumatoid arthritis include bone erosion (eg, periarticular
osteopenia, marginal erosions of bone) rather than formation. Laboratory findings that further
differentiate rheumatoid arthritis include systemic inflammation, positive rheumatoid factor
results, joint fluid with polymorphonuclear cell predominance, and a substantially elevated
WBC count.

Clinical history and characteristic radiographic findings can be used to differentiate

spondyloarthropathy from sacroiliac and lumbosacral spine involvement.

Secondary osteoarthritis must be considered in individuals with chondrocalcinosis, joint

trauma, metabolic bone disorders, hypermobility syndromes, and neuropathic diseases.

Reactive arthritis is another problem that may be considered.

Workup
Laboratory Studies

• No specific laboratory abnormalities are associated with osteoarthritis (OA).

o Levels of acute-phase reactants and erythrocyte sedimentation rate are within
the reference range.
o Synovial fluid analysis usually indicates a WBC count below 2000/µL with a
mononuclear predominance.

Imaging Studies

• Radiography
o Conduct imaging studies of the affected joint.
o The presence of osteophytes (ie, spurs at the joint margins) is the most
characteristic findings.
o Other findings in osteoarthritis include asymmetric joint-space narrowing,
subchondral sclerosis, and subchondral cyst formation.
o Roentgenographic findings are often poor predictors of the degree of
symptomatology in a particular patient.

Procedures
Arthrocentesis of the affected joint can help exclude inflammatory arthritis, infection, and/or
crystal arthropathy.

Histologic Findings

Histologically, the earliest changes occur in the cartilage. Proteoglycan staining is

diminished, and, eventually, irregularity of the articular surface with clefts and erosions
occurs.