Acute sinusitis is common following upper respiratory tract infection and is often due to infection by Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis. It is generally treated with antibiotics and is rarely sampled. If sampled, sinus tissue will show abundant edema and infiltration by a mixture of inflammatory cells, with the predominant cell type being neutrophils.

Chronic sinusitis, on the other hand, is often sampled, as debridement is sometimes the surgical treatment of choice. The pathogenesis of the disease is thought to be related to multiple factors, including infection, allergy, and the anatomy and physiology of the individual patient.

Microscopically, the respiratory tissue will show variable inflammation composed mostly of lymphocytes, plasma cells, and eosinophils, with the proportions of these cells relative to one another varying from case to case (Fig. 13.1, e-Fig. 13.1).⁵ Subepithelial and stromal fibrosis can be present, depending on the overall chronicity of the process, with epithelial hyperplasia and even polyp formation often seen. Goblet cells may be more numerous, as may seromucinous glands. Fragments of underlying bone can have sclerotic, reactive changes.

A specific cause of chronic sinusitis is primary ciliary dyskinesia, also known as Kartagener syndrome. This disease is associated with male sterility, chronic bronchitis, bronchiectasis, and situs inversus.^6,7 It is a genetically heterogeneous disease and typically inherited in an autosomal recessive pattern.

From the pathologic standpoint, assessment of this disease is usually twofold. Functional analysis of the cilia typically involves a wet preparation of scraped nasal epithelium with assessment of the ciliary motility. Normal function should be coordinated and should demonstrate both
intracellular and intercellular synchrony, with cilia typically beating at a frequency of 8 to 20 Hz. Normal function excludes a diagnosis of primary ciliary dyskinesia for all practical purposes. Anatomic analysis of the cilia is performed using electron microscopy. Normal motile cilia are composed of microtubules arranged in a 9 + 2 configuration (Fig. 13.2). Each of the nine outer doublets is attached to the adjacent doublets via nexin links, contains both inner and outer dynein arms, and has radial spokes. A description of all the variants of dysmotile cilia is beyond this book; however, the majority of dysfunction is associated with the absence of inner and/or outer dynein arms.

Fungi are the causative agents of a number of pathologic conditions involving the nasal cavities.^8,9 Commonly, they are related to allergic rhinitis and thus may play some role in the development of chronic sinusitis and secondary complications from such. They also play a role in a number of other pathologic conditions of the sinuses, in which they can be either noninvasive or invasive.

Involvement of the upper airway in tuberculosis is uncommon, and because of current chemotherapy, it is seldom considered in the differential diagnosis of nasal or pharyngeal disease.^19,20 Infection by Mycobacterium tuberculosis can be primary to the site or secondary to a more widespread infection. Infection creates chronic symptoms, with mucorrhea and epistaxis when the nasal cavity is involved and cervical adenopathy is often noted with involvement of the nasopharynx. A discrete mass or ulcer may be present and some ulcers may be deep enough to lead to perforation of the nasal septum. Microscopically, sections will show caseating granulomata with Langhans-type giant cells (Fig. 13.7). Acid-fast stains may reveal the characteristic minute organisms, and immunohistochemical studies with relatively specific antimycobacterial antibodies may also be of value. These techniques, especially the acid-fast stains, are notoriously insensitive, however, and culturing the lesion is essential for the specific diagnosis.

Leprosy is an infectious, granulomatous disease that involves the slightly cooler regions of the body and therefore typically favors the skin and peripheral nerves and may sometimes involve the mucous membranes and nose.^21,22 This is especially true with lepromatous leprosy. It most often involves the inferior turbinates and septum, and crusting, obstruction, and bleeding may be noted. The hallmark microscopic features of leprosy, epithelioid granulomata with foam cells, are often not seen in nasal biopsy specimens. Investigators have noted that sections predominantly show an inflammatory infiltrate rich in macrophages with admixed neutrophils, eosinophils, plasma cells, and mast cells (Fig. 13.8). Bacilli are typically numerous and easily identified with special stains. They tend to be located within macrophages, although nearly all cells may contain the organism (e-Fig. 13.6).

Rhinoscleroma is a chronic, granulomatous inflammatory condition caused by Klebsiella rhinoscleromatis.^23,24,25 and ²⁶ It is endemic to Africa, Central and South America, South Central and Eastern Europe, the Middle East, and China. Sporadic cases, however, have been seen elsewhere, including the United States.²⁶ The disease almost always involves the nasal cavity, although it may extend into the palate or pharynx. It is not very contagious and affects primarily immunocompetent individuals.

Affected individuals tend to be young, often in their second or third decade of life, and may present with a midfacial necrotizing lesion. They may also initially notice a fetid, purulent rhinorrhea with nasal obstruction. Crusting, epistaxis, and nasal deformity can occur as the disease progresses, which is frequent as early diagnosis is often missed.

The histologic features are characterized by the particular stage: exudative, proliferative, or fibrotic (cicatricial). The early exudative phase is characterized by abundant acute and chronic inflammation with suppurative necrosis or microabscess formation. Edema and granulation tissue may be present. The proliferative or granulomatous phase shows persistent chronic inflammation with groups or even sheets of foamy macrophages (Fig. 13.9, e-Fig. 13.7). Plasma cells may become prominent and Russell bodies are often seen. Special staining will reveal numerous Gramnegative coccobacilli consistent with K. rhinoscleromatis (e-Fig. 13.8). Overlying pseudoepitheliomatous hyperplasia is common. The sclerotic stage is characterized by dense sclerosis with diminished chronic inflammation. Macrophages with definitive organisms may be difficult or impossible to identify at this stage.

Rhinosporidiosis is endemic to South India and Sri Lanka and is caused by the fungus Rhinosporidium seeberi.^25,27 The disease usually involves the nasal cavity and is typically unilateral. Clinically, the nasal mucosa often appears polypoid, and the patient may complain of obstruction, epistaxis,

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