Systemic Pathology of the Respiratory System
Anatomy and Congenital Abnormalities of the Respiratory System
The respiratory system is composed of the following structures: the external nostrils or nasal fossae (associated with nasal cartilages), the nasal cavity (comprising the nasal meatus and conchae), the paranasal sinuses, the nasopharynx, the larynx, the trachea, the bronchi, the bronchioles, the alveolar ducts, and finally the alveoli. Congenital abnormalities in the nasal cavity are generally infrequent across all species and are often associated with more extensive craniofacial defects. Animals born with absent, underdeveloped, or severely distorted nasal regions are typically stillborn or die shortly after birth.
Atresia of the choanae is a specific congenital failure where the communication between the nasal cavity and the nasopharynx fails to form. This condition is particularly common in llamas, alpacas, and foals, though it can also occur in dogs, cats, and sheep. The obstruction may be membranous or osseous and can present as either unilateral or bilateral. Clinical signs of choanal atresia include partial or complete obstruction of airflow, exercise intolerance, aspiration pneumonia, and malnutrition. Other rare congenital findings include aplasia of the olfactory bulb and tract.
Non-Neoplastic Proliferative Disorders and Neoplasia
Progressive ethmoid hematoma is a hemorrhagic nasal polyp primarily affecting older equines. It originates in the submucosa of the ethmoidal concha as an aberrant vasoproliferative response to submucosal hemorrhage. Macroscopically, it appears as a mottled, hemorrhagic fibrovascular mass that can extend into the external nasal fossae. Endoscopically, it may appear yellow with superficial hemorrhage on the capsule. Clinical signs typically include low-volume, unilateral epistaxis. Microscopically, it is characterized by organized hemorrhages of varying ages with extensive hemosiderosis and mineralization of connective tissue fibers and vascular walls.
Nasopharyngeal polyps are non-neoplastic proliferations caused by chronic inflammation. These polyps typically arise from the middle ear or the auditory tube, although their exact etiology remains unknown. They represent a progressive expansion of the mucosa in response to localized chronic inflammation. Depending on their size and location, they can cause dyspnea, dysphagia, sneezing, nasal discharge, or ataxia. Microscopically, they feature a loose fibrovascular core covered by respiratory ciliated or squamous epithelium, with a mixed chronic inflammatory infiltrate consisting of lymphocytes, plasma cells, and macrophages.
Neoplasias of the nasal system are relatively infrequent but most common in dogs and cats, while equines more frequently develop them in the sinuses. Progression occurs through three stages: Stage 1 involves local, unilateral growth resulting in nasal discharge; Stage 2 involves bilateral growth causing dyspnea due to obstruction; and Stage 3 involves metastasis and invasion of adjacent tissues such as facial bones, leading to facial distortion, exophthalmos (if the retroorbital space is invaded), or seizures and depression (if the cribriform plate and brain are affected). Carcinomas are the most frequent nasal tumors, followed by chondrosarcomas, fibrosarcomas, and osteosarcomas. Carcinomas are further classified into adenocarcinoma (the most common, forming acini and tubules), adenoid cystic carcinoma, adenosquamous carcinoma, and squamous cell carcinoma. Olfactory neuroblastoma is a rare tumor derived from the olfactory epithelium of the ethmoidal and dorsal conchae.
Inflammatory Diseases: Sinusitis and Rhinitis
Sinusitis is the inflammation of the paranasal sinuses, often resulting in facial deformity, fistulas, and variable nasal discharge. It can manifest as mucocele (seromucous) or empyema (purulent exudate). Causes include fractures, iatrogenic injury, periodontitis, or perforating trauma. Rhinitis refers to the inflammation of the nasal tissue and can be a local or systemic manifestation. It results from viral, fungal, parasitic, or allergic agents, as well as irritant gases or dust. The discharge typically progresses from serous to catarrhal, suppurative, or hemorrhagic.
Fibrinonecrotic rhinitis is caused by the inhalation of toxic gases, Alphaherpesvirus (such as Bovine Herpesvirus 1, the cause of Infectious Bovine Rhinotracheitis), and Fusobacterium necrophorum. Acute microscopic changes include epithelial degeneration, loss of cilia, and the formation of pseudomembranes due to fibrin and inflammatory infiltrate in the lamina propria. Chronic rhinitis is classified by its infiltrate: Eosinophilic Rhinitis is associated with allergies, fungal plaques, and carcinomas; Lymphoplasmacytic Rhinitis is a chronic condition of diverse or idiopathic etiology featuring epithelial attenuation and lymphoid tissue hyperplasia; Suppurative Rhinitis is caused by bacteria, Aspergillus, or foreign bodies. Granulomatous rhinitis may be caused by fungal infections such as Rhinosporidium seeberi.
Allergic rhinitis is a sporadic Type I hypersensitivity reaction. Clinical signs include sneezing, oculonasal discharge, and variable epistaxis. Macroscopically, the mucosa is pale, edematous, and thickened. Microscopically, there is a presence of eosinophils in the exudate, epithelial and glandular hyperplasia, and fibrinoid necrosis. Suppurative rhinitis can be caused by Streptococcus canis and Streptococcus equi ssp. zooepidemicus, which can lead to meningitis if the cribriform plate is involved, or Aspergillus fumigatus in dogs and cats. Verminous rhinitis is caused by parasites like Oestrus ovis.
Disorders of the Guttural Pouches
The guttural pouches are unique equine respiratory structures that function as diverticula of the Eustachian tubes. They balance pressure between the ear and pharynx, assist in phonation, and help control the temperature of blood in the carotid arteries. The stylohyoid bone divides each pouch into medial and lateral compartments. The medial compartment contains the internal carotid artery and the hypoglossal and glossopharyngeal nerves, while the lateral compartment contains the external carotid and maxillary arteries. Empyema of the guttural pouches is a suppurative inflammation usually following a respiratory infection by Streptococcus equi.
Guttural pouch mycosis is primarily caused by Aspergillus spp. and leads to fibrinonecrotic inflammation. This can have severe complications, including vascular erosion causing epistaxis, or neuritis of the glossopharyngeal and facial nerves leading to dysphagia or facial paralysis. The infection can spread to adjacent structures, making it more dangerous than simple empyema.
Laryngeal and Tracheal Pathology
The larynx consists of unpaired cartilages (thyroid, cricoid, epiglottis) and paired cartilages (arytenoid, corniculate of Santorini, and cuneiform of Morgagni or Wrisberg). Subepiglottic cysts, associated with thyroglossal duct remnants, can cause respiratory noise and exercise intolerance. Epiglottic entrapment, often associated with epiglottic hypoplasia, involves the epiglottis becoming stuck in the aryepiglottic fold, predisposing the animal to dorsal displacement of the soft palate.
Laryngeal paralysis in equines is often subclinical but can cause "roaring" and low performance. It is characterized by left-sided hemiplegia due to idiopathic degeneration of the left recurrent laryngeal nerve, resulting in atrophy of the dorsal cricoarytenoid muscle. In canines, laryngeal paralysis tends to be bilateral and is associated with systemic neuromuscular disorders in large breeds. Microscopically, this involves the loss of myelin in nerve tracts. Laryngeal edema can result from trauma, anaphylaxis, or irritants. Laryngitis include Calf Diphtheria caused by Fusobacterium necrophorum, laryngeal erosion from anhydrous ammonia exposure, and infarcts caused by Histophilus somni. The parasite Mammonogamus laryngeus may also inhabit the bovine larynx.
Brachycephalic syndrome in dogs is characterized by stenotic nares, an elongated and thickened soft palate (due to insufficient pharyngeal space), and tracheal hypoplasia where the lumen diameter is reduced. Tracheal edema and hemorrhage syndrome, or "Honker Syndrome," occurs in feedlot cattle, typically during warm months. It involves partial obstruction of the distal third of the trachea due to edema and hemorrhage, often associated with negative intratracheal pressures during hyperpnea.
Developmental and Mechanical Lung Disorders
Congenital lung anomalies include pulmonary agenesis, which is incompatible with life, and pulmonary hypoplasia. Hypoplasia involves a reduced number of alveoli and is often caused by compressive effects from congenital diaphragmatic hernias, thoracic masses, or pleural effusion. Torsion of pulmonary lobes occurs in the right middle lobe for large breeds and the left cranial lobe for small breeds, presenting with dyspnea, coughing, and hemoptysis. Affected lobes appear deeply congested and may show coagulative necrosis (infarction) microscopically.
Atelectasis is the incomplete expansion of the lung. There are three types: Congenital (fetal appearance, lung does not float in formalin), Obstructive (complete airway blockage by exudate), and Compressive (due to pleural masses or fluid). Pulmonary emphysema is the abnormal expansion of tissue by air. Alveolar emphysema involves the destruction of alveolar septa, while interstitial emphysema involves air in the interlobular spaces. This often results from an imbalance between serine proteases (elastase from neutrophils) and antiproteases (). Genetic deficiencies or oxidative stress can reduce antiprotease function, weakening the septa. Rupture of emphysematous bullae can cause fatal pneumothorax.
Circulatory Disorders and Hypertension
Pulmonary edema is a common complication that reduces lung compliance and obstructs gas exchange. According to Starling's Law, it is caused by increased venous hydrostatic pressure (e.g., left-sided heart failure), increased permeability of the alveolar barrier (e.g., pneumonia, sepsis, anaphylaxis), or decreased oncotic pressure (hypoproteinemia). Macroscopically, edematous lungs are heavy, wet, and do not collapse, with frothy fluid present in the trachea and nostrils. Pulmonary thromboembolism involves thrombi or emboli (bacteria, parasites) originating from Virchow's Triad: hypercoagulability, endothelial damage, or blood stasis. Pulmonary infarction is rare due to the lung's dual blood supply.
Pulmonary hemorrhages can range from petechiae to extensive filling. Causes include thrombocytopenia, sepsis, trauma, and exercise-induced pulmonary hemorrhage (EIPH). EIPH affects of racehorses, occurring in the caudodorsal region due to extremely high vascular pressures during strenuous exercise, leading to capillary rupture and hemosiderosis. Pulmonary hypertension occurs when pressure exceeds . It is characterized by vascular remodeling, including intimal thickening (endothelial proliferation and fibrosis), medial hypertrophy (smooth muscle), and adventitial edema. Mineralization, or uremic lung, occurs in cases of acute or chronic renal failure, resulting in a gritty, porous lung texture.
Patterns of Pneumonia
Pneumonia is classified by morphological pattern, histological character, and etiology. Common types include:
Suppurative Bronchopneumonia: Aerogenous entry, cranioventral distribution, firm texture, and purulent exudate. Often caused by opportunistic bacteria under stress.
Fibrinous Bronchopneumonia: Aerogenous entry, cranioventral (lobar) distribution, hard texture with fibrin on the pleura. Example: Pneumonic mannheimiosis (Shipping fever).
Interstitial Pneumonia: Aerogenous or hematogenous entry, diffuse distribution, elastic texture with rib imprints. It involves damage to the alveolar septa. Diffuse Alveolar Damage (DAD) is a common form, featuring hyaline membranes and Type II pneumocyte proliferation.
Granulomatous Pneumonia: Aerogenous or hematogenous entry, multifocal nodular distribution with caseous necrosis. Examples include Tuberculosis and systemic mycoses.
Embolic Pneumonia: Hematogenous entry (septic emboli), multifocal purulent foci randomly distributed. Often results from vegetative endocarditis or ruptured liver abscesses.
Bronchointerstitial Pneumonia: manifest as a combination of bronchiolar and alveolar epithelial injury, often due to aerogenous viral infections or inhaled toxins.