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 etiology of the disease is thought to be related to multiple factors including infection, allergy, and the individual patient’s anatomy and physiology.

Histologically, the respiratory tissue will show variable inflammation composed mostly of lymphocytes, plasma cells, and eosinophils with the relative proportions of these cells to one another varying from case to case (Fig. 13.1, eFig. 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. 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 also 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. Diagnosis requires clinical findings with anatomic and/or genetic findings, as neither anatomic nor genetic testing is entirely sensitive and specific.⁸

From the anatomic pathologic standpoint, assessment for this disease is usually twofold. Functional analysis of the cilia typically involves a wet preparation of scraped nasal epithelium with assessment of the cilia motility. Normal function should be coordinated and 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 by 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 etiologic agents of a number of pathologies of the nasal cavities.⁹,¹⁰ 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 sinus pathologies that 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.²⁰,²¹ Infection with 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. Histologically, sections will show caseating granulomata with Langhans-type giant cells (Fig. 13.7). Special staining for acid-fast bacilli may reveal organisms. Culturing the lesion is essential for the specific diagnosis.

Leprosy is an infectious, granulomatous disease that involves the skin and peripheral nerves and may sometimes involve the mucous membranes and nose.²²,²³ 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 typical histologic features of leprosy with epithelioid granulomata with foam cells are usually not seen with nasal samples. Investigators have noted that sections predominately show an inflammatory infiltrate rich in macrophages with admixed neutrophils, eosinophils, plasma cells, and mast cells (Fig. 13.8). Bacilli are easily identified with special stains and tend to be located within macrophages although nearly all cells may contain the organisms (eFig. 13.6).

Rhinoscleroma is a chronic, granulomatous inflammatory condition caused by infection with Klebsiella rhinoscleromatis.²⁴,²⁵,²⁶,²⁷ 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 in the United States.²⁷ 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.

Clinically, patients tend to be young, in their second or third decade of life, and may present with a midfacial necrotizing lesion. Patients may also initially notice a fetid, purulent rhinorrhea with nasal obstruction, and crusting, epistaxis, and nasal deformity can occur as the disease progresses (which can happen as early diagnosis is often missed).

The histology is 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, eFig. 13.7). Plasma cells may become prominent and Russell bodies are often seen. Special staining will reveal numerous gram-negative coccobacilli consistent with K. rhinoscheromatis (eFig. 13.8). Overlying pseudoepitheliomatous hyperplasia may also be present. 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.²⁶,²⁸ The disease usually involves the nasal cavity and is usually unilateral. Clinically, the nasal mucosa may appear polypoid, and the patient may present with obstruction, epistaxis, or rhinorrhea. The epithelium may show ulceration. Abundant acute and chronic inflammation is usually present with eosinophils and occasional giant cells. Sporangia are easily identified and are characterized by thick walls and measure from 10 to 200µm in diameter (Fig. 13.10, eFig. 13.9).

Nasal involvement is not uncommon in patients with cutaneous leishmaniasis, and it can sometimes be seen alone.²⁹,³⁰ Other portions of the upper respiratory tract may also be involved. Lesions can appear polypoid or simply as ulcers. Biopsy typically shows epithelial ulceration. Lymphoid aggregates, plasma cells, and granulomata are typically present with multinucleated giant cells. Histiocytes containing Leishman-Donovan bodies are often seen.²⁹