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The importance of respiratory diseases in the overall perspective of pathology and clinical medicine cannot be overemphasized. Primary respiratory infections such as rhinitis, tracheitis, bronchitis, and bronchopneumonia occur with frequency. Also, the respiratory apparatus, especially the lungs, is secondarily involved in the terminal states of most diseases. Thus, regardless of the primary disease, the immediate cause of death is often pulmonary embolism, pulmonary edema or bronchopneumonia. Actually, it is quite rare to find the lung uninvolved at postmortem examination.
In this section, the respiratory apparatus is discussed from an anatomic approach beginning with the nasal cavity and ending with the lungs and pleura. Those diseases and conditions encountered with reasonable frequency in veterinary medical practice are discussed in some detail. Less common disease entities are given brief consideration.
At the conclusion of this section, each student should be able to perform the following tasks:
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Linguatula
serrata-- Terminal bronchioles Empyemia--
Terminal respiratory unit Pyothorax--
Respiratory bronchiole Mucocele-Alveolar
ducts -- Cytomegalovirus disease Pulmonary
acinus -- Purpura hemorrhagica Pulmonary
lobule -- Extravasations-- Membraneous
pneumocytes Necrobacillosis--
Granular pneumocytes "Roaring" in
horses Surfactant --
Elementary bodies Surface
tension -- Bronchial stenosis Alveolar
macrophage -- "Heaves of horses" Giant cells
-- Brown induration of the lungs Monocytes --
Hypostatic congestion Pulmonary
arterial system -- Heart-failure cells Sinusitis --
Pneumonia/pneumonitis Epistaxis --
Arelectasis/emphysema Nasal polyps
-- Red hepatization Gray
hepatization -- Hydrothorax Immunodeficiency
-- Pneumothorax "Hog Flu" --
Chylothorax "Pearly
disease" -- Mesothelioma Lipid
Pneumonia -- Otitis Pneumonomycosis
-- Epithelioid cells Mycotic
pneumonia -- Cells of Tripier "Glycogen
stains" -- Fetalization of the lungs Hyphae --
Carnification of the lungs Mycelia --
Pneumoconiosis "Spherules"
-- Pulmonary adenomatosis Verminous
pneumonia -- Pleuropneumonia--Bronchiolar
carcinoma
Please attempt to define,
describe, spell, and use the following terms before and
after embarking on a study of the respiratory
system.
Bronchus
-- Oestrus ovis-- Bronchiole
The respiratory apparatus of mammals consist of the airways (nasal cavities, pharynx, larynx, trachea, bronchi), lungs, thorax, diaphragm, and muscles of the thorax. The exchange of oxygen and carbon dioxide between body tissues and the environment is the primary function of this apparatus.
The nasal mucosa is moist, highly vascular, and contains numerous glands, thus adding warmth, and moisture to inspired air. The pharynx is a common passageway for the respiratory and digestive tubes. The larynx is a musculocartilaginous vascular structure that serves as the principal organ of phonation. The tracheal mucosa has numerous glands and the epithelium is ciliated. The secretion of the glands and the motion of the cilia help to clear this structure of foreign material. Progressive branching of the major bronchi forms bronchioles. Further branching of bronchioles lead to the terminal bronchioles called the acinus or the terminal respiratory unit. Acini contain alveoli and are thus the site of gaseous exchange. An acinus is composed of
From blood to air, the alveolar walls consist of
Capillary endothelium is the first component of the alveolar wall to exhibit alterations when the lungs are injured. The alveolar epithelium is a continuous layer made up of two principal cell types (type I or membranous pneumocytes and type II or granular pneumocytes). Type I or membranous pneumocytes are flattened and cover 95% of the alveolar surface. These cells are highly susceptible to hypoxia and their regenerative capacity following injury is unknown. Hyperplasia or hypertrophy is seldom observed. Type II or granular pneumocytes are rounded and exhibit surface microvilli; they are the source of pulmonary surfactant (a substance that stabilizes the alveolar walls by lowering surface tension).
Also, type II pneumocytes are the main cell type involved in the repair of alveolar epithelium after destruction of type I cells. Alveolar macrophages are loosely attached to the epithelial cells or they are found free within the alveolar spaces. These cells originate from blood monocytes and they differ from monocytes found elsewhere in the body in being more dependent on aerobic metabolism.
The lungs are supplied by two rather efficient arterial systems (pulmonary and bronchial arteries). In the absence of significant cardiac failure the bronchial arteries of aortic origin can sustain the vitality of the pulmonary parenchyma when the pulmonary blood supply is obstructed.
Most antibody activity in the respiratory apparatus is associated with IgA. IgA is synthesized by plasma cells located in the lamina propria of bronchioles.
The respiratory system of birds is the most complicated and efficient in the animal kingdom. In birds, the main bronchus does not ramify as in mammals but passes through the entire lung giving off groups of secondary bronchi. However, the most striking difference of the avian respiratory tract is the elaborate system of air sacs and air spaces within the central areas of the bones. All of these sacs and spaces connect to the lungs and on inhalation, air passes completely through the lungs into the air sacs. On exhalation, air passes back again and more completely fills the air channels in the lungs. Actually, a bird with a blocked trachea can still breathe if a connection is made between one of its pneumatized bones and the outside air.
The lungs of reptiles and amphibia are relatively simple paired sacs; each contains one major respiratory bronchus. Fish and larval amphibia utilize gills for respiration and for excretion of salt and nitrogenous waste.
Inflammatory diseases are the most common disorders affecting the nose and paranasal sinuses. Most of these inflammations are not serious. However, persistent bacterial infections may give rise to clinically significant disease and, in these instances, spread of the infection may lead to dangerous sequelae. The mucous membranes of the nasal cavity and paranasal sinuses may be injured by infectious agents or chemicals brought to it in the inspired air. Injury by infectious microorganisms, including viruses, is most frequent. Neoplasms that may be encountered in the nasal cavity and sinuses include fibrosarcomas, squamous cell carcinomas, osteogenic sarcomas and chondrosarcomas; however, such neoplasms are infrequent.
Rhinitis is the designation given to inflammation of the nasal cavities. The condition may be acute or chronic, and the exudate may be serous, catarrhal, purulent,pseudome membranous. The cause of rhinitis is based on the interplay of viruses, bacteria, and allergens. Acute rhinitis is usually initiated by viruses which commonly evoke a profuse catarrhal discharge. Also, allergens may initiate an acute rhinitis, but they are important only in cattle. Bacterial infections become superimposed upon either the viral or allergic phase. However, it is not clear whether such bacterial infection is initiated by the common microorganisms that normally inhabit the nasal cavities, or whether such infection is due to the introduction of more pathogenic fresh contamination. Regardless, staphylococci, streptococci and pneumococci are commonly isolated.
During the initial acute stage of rhinitis, the nasal mucosa is swollen, edematous, and pale grey to red (depending on the degree of hyperemia). The mucosal surfaces are covered by a thin watery to mucoid discharge which is relatively clear. When such acute reactions persist for a few days, bacterial infection modifies the character of the discharge and produces a mucopurulent or suppurative exudate. Microscopically, edema is the most prominent feature; the lamina propria is sparsely infiltrated by inflammatory cells. Swelling of the mucous membrane may cause mild respiratory discomfort. Chronic rhinitis is characterized by the presence of fibrous connective tissue scarring; the epithelium becomes atrophic, foci of squamous metaplasia may develop and there is progressive atrophy of the mucous secreting glands.
In general, rhinitis is not in itself of much importance (being in most cases part of generalized widespread infections). However, localized infections may have unfortunate sequelae. For example, swelling of the nasal mucosa may obstruct the orifices of air sinuses and lead to sinusitis; aspiration of nasal exudate may lead to bronchopneumonia, etc. These complications, in light of the great frequency of nasal inflammations, are not common.
Amyloid is sometimes deposited in the nasal submucosa of horses. The deposition is not part of a generalized amyloidosis and the cause is unknown. The amyloid is deposited in the anterior portion of the nasal cavity and stenosis can be severe enough to cause clinical signs of nasal obstruction.
The term epistaxis refers to nasal hemorrhage. Hemorrhage from the nose may be traumatic, occur in the course of acute inflammation or occur spontaneously in any of the hemorrhagic diatheses. Remember, blood which is extravasated in the lungs may also be discharged from the nose; however, pulmonary hemorrhage of this degree is uncommon. Also, blood-stained foam is frequently emitted from the nose of carcasses, especially sheep. Such blood-stained foamy fluid is indicative of severe pulmonary congestion and edema with seepage of blood from the congested alveolar walls.
Nasal polyps are inflammatory new growths which resemble true neoplasms. They represent focal accumulations of edematous fluid accompanied by hyperplasia of submucosa connective tissue and inflammatory cells (neutrophils, lymphocytes, plasma cells). Older polyps may contain considerable fibrous connective tissue.
The larvae of a number of flies of the family Oestridae are parasites of the nasal cavities of domestic animals. However, Oestrus ovis (nasal bot of sheep) is most commonly encountered. The adult flies are relatively harmless from a pathologic point of view; however, they do cause considerable annoyance to their host. The first-stage larvae are deposited on the nares and moult twice as they migrate to the region of the turbinates and into the dorsal sinuses. These larvae are responsible for a catarrhal rhinitis with a discharge that may become copious. Also, larvae may penetrate the cranial cavity. Linguatula serrata is a tongue-shaped arthropod of the nasal cavities which utilizes carnivores as its definitive host.
In general, neoplasms of the nasal cavity are uncommon; however, a wide histogenic variety may be found (benign and malignant). Fibrosarcomas are the most common of the mesenchymal neoplasms and squamous cell carcinomas are the predominate neoplasm of epithelial cell origin.
Nasal granulomas can be caused by a variety of agents; only a few will be considered at this time. CRYPTOCOCCOSIS should be suspected in older cats with chronic nasal or ocular discharges, blindness, incoordination, and swellings in the nasal cavity and/or pharynx. In dogs, the organisms usually invade the brain, meninges and paranasal sinuses. However, the organisms may affect any species and invade a variety of organs and tissues. Microscopically, early lesions are characterized by a "soap bubble" appearance; cellular infiltration is usually minimal. ASPERGILLOSIS of the respiratory tract is usually a complication of some other debilitating disease. The condition may be localized or generalized. On mucous membranes, the usual type of reaction is caseous necrosis surrounded by a zone of hemorrhage. In the lungs, the lesions occur as one or more discrete nodules.
Congenital anomalies of the nasal structures are numerous. Many are of minor importance and will not be discussed. The most common congenital anomalies of the nose and pharynx are cleft lip and palate (these are discussed under the digestive system).
Inflammation of the paranasal sinuses is referred to as sinusitis. Almost invariably, rhinitis precedes and leads to infections and inflammations of the paranasal sinuses by obstructing the drainage orifices of the sinuses. Sinusitis is common in sheep as a response to the larvae of Oestrus ovis. Also, it follows penetration of infection in dehorning wounds (frontal sinusitis in cattle), periodontitis (maxillary sinusitis in horses) and fractures. The accumulation of seromucinous secretion in sinuses is referred to as Mucocele, and the accumulation of purulent exudate is referred to as empyemia of the sinuses. Remember, suppurative infection of the sinuses are of more significance than those in the nose because of the close relationship of these structures to the cranial vault.
In addition to the specific diseases discussed in this section, rhinitis is a lesion in a number of other diseases, including canine distemper, feline, pneumonitis, listeriosis, oral necrobacillosis, etc.
Inclusion body rhinitis of swine is a cytomegalovirus disease characterized by a mild catarrhal to purulent rhinitis and by the presence of intranuclear inclusion bodies within glandular epithelial cells. The cytomegaloviruses are classified within the herpesvirus group. The disease occurs in suckling pigs of approximately 2 to 3 weeks of age. Morbidity is high but the mortality is low in the absence of complicating secondary infections. Microscopically, there is a non-suppurative rhinitis with large, basophilic intranuclear inclusion bodies in epithelial cells of glands and ducts. As the inclusions develop, the nucleus and cytoplasm of affected cells increase in size. Ultimately, the inclusions completely fill the nuclei. In addition to rhinitis, foci of necrosis or inflammation associated with cytomegalic inclusions have been reported in the adrenals, liver, kidneys, as well as in the central nervous system.
Affects a variety of animal species, including man. The cytomegalic viruses (classified with the herpesvirus group) are rather host-specific. Most of these viruses have a particular affinity for salivary glands and the infection is usually latent or subclinical. However, under proper circumstances, overwhelming, generalized, and often fatal infection can develop. Specific cytomegaloviruses have been isolated from guinea pigs, mice, rats, ground squirrels, horses, swine (inclusion body rhinitis), and man.
Atrophic rhinitis of swine is an insidious disease characterized by sneezing which is followed by atrophy of the turbinate and nasal bones. These changes may be followed by twisting or shortening of the upper jaw. The etiologic mechanism has not been completely elucidated. However, Bordetella bronchiseptica is considered to be an important primary etiologic agent. There is a high incidence of atrophic rhinitis in most of the major pig-raising areas of the world. The initial clinical signs are those of rhinitis with sneezing dyspnea and a serous to mucinous nasal discharge which may become purulent as the course advances. The disease is not fatal unless complicated and its importance is related to the retarded growth rate in affected pigs. Grossly, typical lesions are confined to the nasal cavities. In the early stages, there is an acute inflammatory reaction (pus may accumulate), but in later stages, there is evidence only of atrophy of the mucosa and decalcification and atrophy of the turbinate and ethmoid bones. At necropsy, the degree of turbinate symmetry, volume of atrophy and medial septum deviation should be assessed by inspection of a transverse section made with a saw at the level of the 2nd premolar tooth (or the first cheek tooth in pigs up to 7-9 months of age.). There are no inclusion bodies associated with this disease.
("Bull Nose," Rhinohyperplasia) is characterized by irregular proliferation of fibrous connective tissue and bone over the snout region. Apparently, a variety of infectious agents can initiate the condition. Such agents usually enter through defects in the gums.
Strangles is an acute contagious disease of horses caused by Streptococcus equi and characterized by inflammation of the upper respiratory tract and abscessation in the regional lymph nodes. After an incubation period of 3 to 4 days, onset of the disease is indicated by fever, a slight cough, and bilateral nasal discharge (which changes from serous to catarrhal and then purulent). At the same time, there is swelling of the regional lymph nodes (especially the submaxillary and pharyngeal nodes). Subsequently, abscessation of the lymph nodes occurs. In the nasal cavities, a purulent rhinitis develops and large amounts of creamy yellow pus collect in the folds of turbinates. The nasal mucosa is edematous and hyperemic and occasionally small ulcers may develop. Hematogenous metastatic abscesses occasionally form in internal organs (liver, kidneys, brain, etc.). After an attack of strangles has subsided, purpura hemorrhagica may occur due to the development of sensitivity to streptococcal protein. Vaccines are effective in controlling strangles.
Is an afebrile syndrome characterized by numerous petechial and ecchymotic size hemorrhages in the skin and mucous membranes. The condition is most frequently reported in horses apparently recovering from some infectious or necrotizing disease such as strangles or other upper respiratory infection. Streptococcal organisms are the usual cause.
The pharynx is common to both the respiratory and digestive systems and shares the misfortunes of both. Guttural pouches are diverticula of the eustachian tubes and they are found only in the horse. Occasionally, the guttural pouches become infected by extension of infections from the eustachian tubes. Such infections are entirely comparable with those of the paranasal sinuses.
Inflammation is the most common and important disorder affecting the larynx and trachea. Because of their location, these structures frequently become inflamed as a part of inflammatory diseases of either the upper or lower parts of the respiratory tract. Thus, laryngitis and, to a lesser extent, tracheitis is expected to accompany rhinitis; whereas tracheitis and, to a lesser extent, laryngitis, is expected to accompany acute pneumonias.
Laryngeal and tracheal hemorrhages may occur as a result of infection, trauma, violent coughing, etc. Laryngeal hemorrhages occur in many septicemic diseases (hog cholera, salmonellosis, etc.). In the trachea, agonal hemorrhages are often times associated with severe dyspnea and hypoxia. Such hemorrhages are produced by small extravasations in the submucosal lymph follicles and tend to spread in a linear fashion.
Edema of the larynx is usually inflammatory and part of the picture of acute respiratory infection. Also, laryngeal edema may be associated with allergic reactions, inhalation of irritants, insertion of tracheal tubes, etc. In the tracheal lumen, foamy fluid is commonly observed. Such foamy fluid is associated with severe pulmonary edema. The foams are actually formed in the alveoli (refer to the section on pulmonary edema).
Even though the diseases discussed in this section may involve all levels of the air passages, they are included at this time as a matter of convenience.
Calf diphtheria is an infectious disease of young calves characterized by necrosis of the larynx and trachea (necrotic laryngitis and stomatitis). Fusiformis necrophorus is considered to be an important primary cause; however, traumatic injury of the involved mucosa is a common predisposing factor. Grossly, necrotic ulcerative lesions are found in mucous membranes of the oral cavity, larynx and pharynx. Croupous and diphtheric membranes may develop. Clinical signs include depression, anorexia, fever, loud wheezing, protrusion of the tongue and salivation. Aspiration pneumonia may occur in severe cases.
Laryngeal hemiplegia (also referred to as "roaring") is a disease of horses characterized by paralysis of the intrinsic muscles of the larynx resulting in audible inspiratory dyspnea. The condition is usually associated with injury to the left recurrent laryngeal nerve (which is the motor nerve to the intrinsic muscles of the larynx). In laryngeal hemiplegia, paralysis of the muscles occurs and the aryntenoid cartilage drops inward into the lumen of the larynx upon inspiration. Therefore, during the act of inspiration, the aryntenoid cartilage and the relaxed vocal cords vibrate in the air stream, resulting in the sound referred to as roaring. The condition may be mild or severe, unilateral or bilateral. In any case, inspiration efforts are increased and the animal is considered unsound. Numerous causes have been suggested to explain laryngeal hemiplegia (pounding of the heart and aorta on the recurrent laryngeal nerve, inflammatory lesions, trauma, toxins, neoplasms, etc.). Regardless of the cause, something must happen to the nerve to cause it to degenerate resulting in a loss of function.
Infectious bovine rhinotracheitis (IBR) is an infectious disease of cattle caused by a herpesvirus. The term infectious bovine rhinotracheitis refers to the respiratory form of the disease. However, the virus (herpesvirus) of IBR has been incriminated as the cause of:
Is most prevalent in large concentrations of cattle (feedlots, large commercial dairies, etc.). Clinical signs include fever, depression, anorexia, profuse salivation, conjunctivitis, serous to mucopurulent nasal discharge and respiratory distress. Grossly, the nasal passages, paranasal sinuses, trachea and bronchi are inflamed and edematous with excessive exudation. Thick mucopurulent exudate may cling to the mucosa. A bronchopneumonia may complicate this form. Microscopically, intranuclear inclusion bodies are found in epithelial cells of the affected mucosa during the early stages of infection (inclusions are difficult to find after about 72 hours). The morbidity ranges from 15 to 100% and the mortality rarely exceeds 5%.
Is characterized by a condition referred to as "infectious pustular vulvovaginitis." Infectious pustular vulvovaginitis is an acute contagious disease of cattle characterized in the female by inflammation, focal necrosis, and pustule formation on the mucosa of the vulva and vagina (occasionally, similar lesions may develop on the skin of the prepuce and penis of bulls). Microscopically, necrosis is prominent and intranuclear inclusion bodies develop within epithelial cells. In the absence of secondary infection. the genital lesions usually heal in 10 to 14 days; however, repeated attacks may occur.
Usually follows the upper respiratory form of the disease or the use of modified live IBR vaccine (two weeks to 2 months after the respiratory disease, or vaccination, up to 60% of a herd may abort). Abortion may occur at any stage of pregnancy, but it is most frequent during the third trimester. Also, abortion is rarely complicated by genital tract infection, and the breeding efficiency of aborting cattle does not appear to be affected. Microscopically, focal necrosis occurs in the fetal liver, spleen, lymph nodes, and kidneys. Intranuclear inclusion bodies may be found in each of these tissues.
The septicemic form of infectious bovine rhinotracheitis is an acute, often fatal generalized infection which occurs in very young calves. Lesions consist of widespread focal necrosis in visceral organs (liver, kidneys, spleen, lymph nodes, mucosa of the oral cavity, esophagus, forestomach, etc.).
The enteric form of infectious bovine rhinotracheitis occurs in young calves and may occur in conjunction with or independently of the septicemic form.
The feline upper respiratory disease complex is composed of a group of respiratory diseases with somewhat similar clinical manifestations (sneezing, ocular and nasal discharges, conjunctivitis, rhinitis, salivation, oral ulcerations, and high morbidity). This disease complex can be caused by a variety of viral and other agents. However, feline viral rhinotracheitis (herpesvirus) and feline calicivirus infection (calicivirus) account for 85% to 90% of all infections. Feline pneumonitis (Chlamydia psittaci) and mycoplasmal infections are of lesser importance. The exact role and importance of reovirus. parainfluenza virus, and feline syncytia-forming virus have not been completely elucidated. The several etiologically and pathologically distinct upper respiratory disease entities cannot be differentiated on the basis of clinical signs since each may be manifested by varying severity of sneezing, coughing, ocular and nasal discharges, conjunctivitis, rhinitis, oral ulcerations, etc. Identification of the etiologic agent is a prerequisite for a specific diagnosis.
9.9.4.1 FELINE VIRAL RHINOTRACHEITIS:
Significant gross lesions consist of focal necrosis and a mucoid or mucopurulent exudate in the nasal passages and turbinates. The nasal mucosa and conjunctiva are reddened and swollen. Also, the laryngeal, pharyngeal, and tracheal mucosa may be mildly inflamed. Ulcerative stomatitis (glossitis, etc) may occur. The lungs may be congested with small areas of consolidation (however, pneumonic lesions are usually not remarkable). Microscopically, acidophilic intranuclear inclusion bodies are found in epithelial cells of the nasal septum, tonsils, epiglottis, trachea and nictitating membranes. These inclusions are transitory and may be difficult to find in cats that die after being ill for 3 to 4 weeks. The epithelial surfaces of infected tissues are often ulcerated and necrotic. In general, mortality is low and the prognosis is usually good, except in young kittens and aged adults.
9.9.4.2 FELINE CALICIVIRUS INFECTION:
The gross lesions are similar to those described for feline viral rhinotracheitis. However, ulceration of the oral mucosa is a more prominent feature. Also, inclusion bodies are absent in calicivirus infections. The signs and lesions observed may vary in severity depending on the strain of calicivirus.
9.9.4.3 FELINE PNEUMONITIS:
The most prominent clinical signs are rhinitis and conjunctivitis. Grossly, the laryngeal and tracheal mucosa are inflamed and the tracheal lumen may contain a mucopurulent exudate. Focal areas of consolidation may be found in the anterior lung lobes. Microscopically, the areas that appeared grossly consolidated consist primarily of collapsed alveolar walls (atelectasis). Elementary bodies are found in the cytoplasm of epithelial and mononuclear cells of the conjunctiva and lungs. Recent evidence suggest that the prevalence of feline pneumonitis and the disease-producing ability of Chlamydia psittaci need reappraisal.
Infectious laryngotracheitis is an acute, highly contagious respiratory disease of chicken and pheasants characterized by severe dyspnea, coughing and rales. A subacute form of the disease may occur with excessive lacrimation, tracheitis, conjunctivitis, and mild rales. The disease is caused by a herpesvirus. Clinically, in the acute form, gasping, coughing and extension of the neck during respiration is seen. Gross lesions occur most consistently in the tracheal and laryngeal tissues. Tissue changes may vary from mucoid inflammation in the early stages to extensive degeneration of the mucosa resulting in necrosis and hemorrhages in the later stages. Expulsion of blood clots may occur during violent coughing. Intranulcear inclusion bodies occur in epithelial cells.
Syngamus trachea is a nematode that inhabits the trachea and lungs of many domestic and wild birds. These parasites are oftentimes referred to as "gapeworms" and they tend to cause serious economic loss in range-reared pheasants and turkeys (gapeworms are not a serious problem in confinement reared poultry). Clinical signs include gasping, choking, head shaking, inanition, emaciation, and suffocation. On gross inspection, adult gapeworms are found obstructing the lumen of the trachea and bronchi. The blood red females are usually attached to much smaller, paler males. There is a tendency for the male's head to become permanently embedded deep in the host tissue. However, the females may become detached from the males and feed freely within the lumen, or be coughed up and discharged from the body.
Many diseases and/or conditions that affect the bronchial tree are similar to those of the larynx and trachea, whereas others are an integral part of the diseases described for the lungs. Therefore, in this section, the discussion is limited to inflammation, stenosis, and bronchiectasis.
Inflammation of the bronchi and bronchioles occurs with frequency. However, the consequences of inflammation of the large bronchi may be quite different from those of inflammation of smaller bronchi and bronchioles. The larger bronchi, for example, lie in interstitial tissue outside of the lung lobules. The epithelium is pseudostratified and well supplied with mucous-secreting and ciliated cell and the peribronchial connective tissue is abundant. The lumen is large enough to remain patent even in the presence of copious exudate and such exudate can be expelled by an effective cough reflex. By contrast, the small bronchi and bronchioles lie within the lung parenchyma and there is a paucity of peribronchial connective tissue. The epithelium is simple and the ciliated and mucous-secreting cells decrease in number and disappear from the smallest branches. The walls are thin and the small lumens are easily occluded by exudate which may be too far distal for the cough reflex to be particularly effective. Therefore, inflammation of larger bronchi may or may not have significant consequences for the lung, but inflammation of small bronchi and bronchioles almost inevitably leads to occlusion with extension of inflammation to the lung parenchyma (bronchopneumonia).
The causes of bronchitis/bronchiolitis are the same as those of bronchopneumonia (to be given later) and include chemical agents, bacteria, viruses, helminths, etc. Even though irritants usually reach the bronchi/bronchioles by way of the upper air passages, an ascending development from established pulmonary lesions is also of considerable consequence and frequency.
The condition may be acute or chronic, focal or generalized and characterized by a catarrhal, purulent, fibrinous or pseudomembranous exudation. Grossly, bronchitis/bronchiolitis are usually accompanied by hyperemia of the mucosa and exudation of materials into the lumen (inflammatory cells, desquamated epithelial cells, bacteria, fibrin, etc.). If fibrin is present, this mass of material may solidify and form a "cast" within the lumen.
Stenosis (narrowing of the lumen) may result from many causes (inflammation, parasites, foreign bodies, peribronchial pressure, etc.). There may be partial or complete closure of the bronchial lumen (increased resistance in the airways). If there is partial obstruction, greater effort is required to force air into the alveoli on inspiration. During this difficult and slow passage of air, the alveolar walls are momentarily stretched. If this process is repeated over a prolonged period, this continued over-stretching of the alveolar walls eventually causes them to break resulting in a condition referred to as emphysema (emphysema will be discussed in more detail later). Then upon expiration, not all of the air is expelled. This results in incomplete exchange of gases.
If complete stenosis/obstruction of the smaller bronchioles occurs, at first the air is trapped in the alveoli (because it cannot escape during expiration). Eventually, the body will absorb the air. As air is absorbed from the alveoli, they collapse and this area of the lung is no longer functional (atelectasis is the term used to refer to collapsed areas of the lung). This process leads to partial stasis of blood in the alveolar capillaries, and mild edema
The term "bronchiectasis" refers to dilatation of bronchi and bronchioles. Some "authors" state that chronic inflammation must always be present for bronchiectasis to occur and that this bronchitis must be undrained and destructive. In the presence of chronic inflammation (chronic bronchitis) there is repeated coughing. Therefore, there is a continuous over-stretching of the alveolar walls as well as over-dilatation of the bronchioles as they stretch to accommodate the cough. As this over-distention and over-stretching is repeated over long periods of time, the smooth muscle in the wall of these bronchioles loses its tone and undergoes degeneration. Eventually, the lumens remain open instead of contracting as they do when they are relaxed and not being used. The mucosa gradually becomes thinner and the walls are gradually destroyed and replaced by fibrous connective tissue. This connective tissue helps to tie the walls of these bronchioles to the surrounding tissue, which in turn aids in keeping them over-dilated. In summary, loss of smooth muscle as well as proliferation of connective tissue causes bronchioles to remain open and thus less functional. Bronchiectasis results in difficult respiration and incomplete exchange of gases. The animal gradually deteriorates until general debilitation occurs.
It is impossible to overemphasize the importance of lung diseases in the overall perspective of pathology and clinical medicine. This organ is constantly insulted by dust, smoke, toxic gas, bacteria, etc. The oxygen exchanging membranous pneumocytes of alveoli are protected from much of this by the pulmonary defense mechanisms (mucociliary system, IgA activity, alveolar macrophages, etc.). However, massive exposure to noxious particles or virulent organisms may overwhelm the capacity of the pulmonary defense mechanisms. The following conditions affecting the lungs are discussed: atelectasis. emphysema, congestion/ edema, inflammation (pneumonia/pneumonitis). and some important diseases and conditions characterized by lung changes.
Atelectasis is a term that comes from the Greek word meaning imperfect or incomplete expansion (the lungs contain no air and nothing else). Atelectasis may be focal or involve entire lobes. It may be classified as fetal or acquired. Atelectasis occurs in all species except birds where the rigid structure of the parabronchi prevents collapse of the alveoli.
9.11.1.1 IN FETAL ATELECTASIS,
The lung is dark-red, liver-like, and will not float in water. There may be a small amount of fluid in the alveoli, but this is not inflammatory edema. The walls of alveoli do not touch (there is a narrow open space where each alveolus is located). If the lungs of a newborn are not inflated, it can be assumed that it was born dead (this point is important to those who own horses to determine if the foal was born alive). However, a newborn animal may take a few breaths and then die. In this case, areas of the lungs will be partially inflated while other areas remain atelectatic (the atelectatic areas must be differentiated from areas of pneumonia).
Extensive neonatal atelectasis may occur in newborn foals (because of their clinical behavior, these foals are known as "barkers'' or "wanderers"). In this condition, the umbilical cord is usually broken too soon and the newborn is deprived of the rather large pool of blood normally present in the placenta. If the foal is deprived of this pool of blood, he will have a deficient blood volume, and therefore, a deficiency in oxygen-carrying capacity. At the same time, fetal atelectasis remains because of lack of vigor and activity. These two factors combined work together to deprive the foal of needed oxygen. Since the brain is also deprived of oxygen, these foals will be stupid when they mature. Of course, the foals may die soon after birth.
9.11.1.2 ACQUIRED ATELECTASIS
May be caused by either compression or obstruction. Compression atelectasis is due to pressure on the lungs due to fluid, air, neoplasms, etc., which drives air out of the lungs resulting in collapse of the walls of alveoli. Grossly, the lung tissue is deflated, depressed, dark red, and will not float in water (there is no interference with bronchial function). If the cause is removed, the lung tissue will reinflate and no damage will follow. Respiratory distress is not noticeable unless a considerable portion of the lung tissue is involved. Obstructive atelectasis is due to an accumulation of material in the bronchioles (mucus, etc.). If the airway is completely obstructed, air cannot enter the alveolus and it collapses. The effect on the body depends on the size of the affected area.
Remember,
Careful distinction must be made between atelectasis and pneumonia. In pneumonia, the lung may be airless also. It may or may not be dark-red in color and it may or may not float in water (depending on the severity). The alveoli are not collapsed. They remain open but filled with some form of material that has appeared as a result of inflammation. Pneumonia (consolidation) will be discussed in more detail later.
Emphysema is a term taken from the Greek word meaning to inflate. There are two types of emphysema based on anatomical location (alveolar and interstitial emphysema).
9.11.2.1 ALVEOLAR EMPHYSEMA
Is characterized by over-inflation of the alveoli with air. The walls of the over-inflated alveoli may or may not rupture. In alveolar emphysema, air is momentarily trapped in the alveoli (because the bronchioles are partially obstructed by mucus, exudate, etc.). The trapped air cannot be readily expelled on expiration because of the obstruction. However, more air can be drawn into the alveoli, past the obstruction, by increased inspiratory effort. Gradually, air accumulates in alveoli and the alveoli gradually become enlarged or stretched. As the alveolar walls are stretched, the affected lung lobules gradually becomes elevated above the surface of the surrounding tissue (an emphysematous area is usually paler than the surrounding lung tissue because of stretched capillaries. Stretching of the capillaries reduces the capillary lumen and thus blood flow). Continued stretching of alveolar walls causes them to degenerate. In addition, there is reduced air flow and reduced oxygen-carbon dioxide exchange. Gradually, degeneration of the alveolar walls continue until they weaken to the point of rupture. When alveolar walls break or rupture, they retract slightly. The alveoli then become confluent and a large open space is formed. The broken ends of these alveolar walls heal by the formation of a small connective tissue scar along the tips.
Chronic diffuse alveolar emphysema of horses (heaves) is a specific disease entity that occurs as a result of the process just described. The cause of "heaves" is not completely understood, but it may be the result of sensitization from exposure to hay dust, molds, or stable dust (allergy). Your textbook suggests that hard work with a stomach full of roughage may be a factor. Regardless of the cause (according to Nieberle and Cohrs), "heaves" must always be preceded by chronic bronchitis. Because of incomplete gas exchange in heaves, the animal makes an added effort to empty the lungs by bringing the abdominal muscles into play (actually, the expiratory part of the respiratory cycle is lengthened). Eventually, this over-exertion of the abdominal muscles causes them to undergo hypertrophy. Subsequently, a condition known as "heaveline" develops along the costal arch at the ends of the ribs. The hypertrophied muscles form a ridge that is exaggerated by the confining effect of the ends of the ribs. In addition, heaves is always characterized by a chronic cough which is explosive, dry, and nonproductive. The coughing constantly aggravates the condition described above. Heaves interferes with the ability of the animal to exercise and work efficiently. Eventually. interstitial emphysema and dilatation of the right heart may occur. All of these factors reduce blood flow to the lungs. At necropsy the lungs are expanded to fill the entire thoracic cavity. They do not collapse when air pressure in the thoracic cavity is equalized and they appear extremely pale.
9.11.2.2 INTERSTITIAL EMPHYSEMA
Is characterized by the escape of air into the interstitial spaces (from ruptured alveoli and bronchioles). If this leakage of air continues over a prolonged period of time, it tends to dissect through the interstitial tissue as well as along the peribronchial and perivascular tissues toward the points of least resistance (which is toward the mediastinum. Once air reaches the mediastinum,
- (1) it may move out of the thoracic cavity via the thoracic inlet eventually reaching the subcutaneous tissues of the skin or
- (2) the air may move posteriorly along the aorta toward the kidneys and accumulate in the loose connective tissue around the (kidneys and posterior intestine). Air in the interstitial tissue forms small round spaces, confined by thin transparent sheets of connective tissue (beading). If the volume of air is large and under pressure, it may interfere with venous return to the heart and be associated with dyspnea and cyanosis.
Remember,
Interstitial emphysema may be terminal or agonal. It sometimes occurs during terminal violent respiratory efforts, especially if the animal is stunned by a blow to the head.
Pulmonary congestion and edema develop acutely in a variety of diseases. Chronic congestion and edema are usually attributable to some functional defect in the left heart (the left ventricle and atrium are prevented from clearing the blood that comes from the lungs). Hypostatic congestion develops due to the effects of gravity on blood flow through the lungs. If an animal lies on one side for a long period of time and is relatively inactive, the flow of blood through the lungs gradually slows, respiration becomes shallow, and oxygenation is interfered with. All of these factors contribute to reduced efficiency and function of the lungs. Gradually, blood accumulates in the lower lung. The affected lung will be nonfunctional, extremely heavy, dark-red, and firm to the touch. In contrast, the upper lung will be pale, inflated, and light in weight. An area of hypostatic congestion provides an ideal location for infection to start. Chronic pulmonary congestion results in the condition known as brown induration of the lungs.
Pulmonary edema is the accumulation of fluid (plasma protein filtrate) in alveoli. This is due to:
Grossly, the lungs are doughy, heavy, firm, and foamy. Fluid flows from the cut surface. Microscopically, the alveoli are filled with fluid that is high in albumin content.
Pneumonitis is the correct term for inflammation of the lungs. However, pneumonia is the conventional term for lung inflammation (correctly, the term pneumonia refers to filling of alveoli with cellular exudate). There is a tendency to use the term pneumonitis to refer to those inflammatory lesions which are characterized by cellular infiltration and proliferation of the alveolar walls rather than exudation. In other words, pneumonitis tends to be synonymous with interstitial pneumonia. In this section, the term pneumonia is used to refer to inflammation of the lungs. The term pneumonitis is not used except as accepted names of specific diseases (feline pneumonitis, etc.).
The causes of pneumonia are numerous and may include bacteria, viruses, aspirated foreign matter, fungi, parasites, etc. Pneumonias can be classified in a number of ways, including:
Traditionally, bronchopneumonias caused by bacterial agents have been divided into four successive stages:
However. present day effective antibiotic therapy frequently alters the progression so that the anatomic changes at necropsy may not conform to the classical stages.
The initial stage of congestion represents the developing bacterial infection and lasts for approximately 24 hours. Microscopically, it is characterized by hyperemia (vascular engorgement), fluid within the alveoli (edema), a few neutrophils, and often by the presence of numerous bacteria.
Grossly, the involved lung is heavy, boggy, and red (the affected areas are not consolidated).
The stage of red hepatization is characterized by increasing numbers of neutrophils and precipitation of fibrin to fill the alveolar spaces. Affected areas of the lungs are consolidated (liver-like in consistency). Completely consolidated lung tissue sinks in water. Extravasation of erythrocytes causes the red color observed on gross examination. Grossly, involved lung is distinctly red, firm, and airless, with a liver-like consistency.
The stage of gray hepatization is characterized by a continuing accumulation of fibrin, associated with progressive disinte-gration of neutrophils and erythrocytes. The hyperemia is decreased and erythrocytes have disappeared from the alveolar contents. Mononuclear cells and fibrin predominate, with fewer neutrophils. Thus, grossly, the affected lung tissue appears grayish (or less red). Tissues are still consolidated (liver-like) and will sink in water.
The stage of resolution is the final stage. In untreated cases, this stage supervenes in 7 to 10 days after the onset of pneumonia and a favorable outcome may follow. During this stage, the exudate within alveoli (fibrin, inflammatory cells, etc.) undergoes progressive enzymatic digestion to produce a semifluid debris that is either reabsorbed, ingested by macrophages, or coughed up. In favorable cases, the normal lung parenchyma is restored to its normal state. However, complete resolution may not occur and complications develop. These complications may include organization of the exudate by fibrous connective tissue, abscess formation, and dissemination of bacterial agents by the bloodstream to various organs and tissues.
Bronchopneumonia is the most common form of lung inflammation. It is particularly common in young calves and pigs and in sheep of any age. It is less common in other animal species.
Many species of pathogenic bacteria may cause bronchopneumonia. In calves, pigs, and sheep, Pasteurella spp (P. multocida and/or P. hemolytica) and Corynebacterium pyogenes are usually found. In horses, Streptococcus spp. Staphylococcus spp. and Escherichia coli are important. In cats (in which pneumonia seldom occurs), Pasteurella multocida is isolated most consistently. It is generally agreed that most bacteria associated with bronchopneumonias become pathogenic or are allowed to express their pathogenic potential only when the respiratory environment is suitably altered by other agents (viruses, external environmental factors, etc.). In other words, bacterial agents usually act as secondary invaders.
9.11.7.1 DOGS:
Brucella bronchisepticus bronchopneumonia is usually a complication of canine distemper. The canine distemper virus is considered to be a primary etiologic agent. (Pneumonia in dogs in the absence of canine distemper is not common).
9.11.7.2 HORSES:
Corynebacterium equi may cause a primary respiratory infection in foals. Otherwise, bronchopneumonias in horses are usually a complication of a systemic infection (equine infectious anemia) or a viral infection involving the respiratory tract (equine viral rhinopneumonitis, equine viral arteritis, etc.).
9.11.7.3 SWINE:
Bronchopneumonia is often observed in cases of swine influenza which is considered to be caused by a specific viral agent and Hemophilus influenza suis acting in concert. Pasteurella bronchopneumonia is believed to be initiated by the activity of viral agents (hog cholera virus, etc.).
9.11.7.4 CALVES:
Bronchopneumonia in calves is considered to be a primary viral infection (especially PI3 virus) with Pasteurella spp. and/or other bacterial agents superimposed.
9.11.7.5CATS:
Bronchopneumonia in cats is usually a complication of feline Pneumonitis. However, as a lesion, the bronchopneumonia is usually overshadowed by empyemia of the pleural cavity.
The bacterial agent responsible for the pneumonia causes a bronchitis or bronchiolitis initially. There is subsequent spread of infection through the finer ramifications of the respiratory passage to reach the alveoli. The anterioventral portions of the lungs are primarily involved.
Remember,
The inflammatory process in different lung lobules can be in different stages of development, thus, giving a mosaic pattern to the lungs.
Fibrinous pneumonia is basically a bronchopneumonia characterized by a marked exudation of fibrin (occasionally, fibrinous pneumonia is hematogenous in the course of septicemic salmonellosis). Fibrinous bronchopneumonia is an important disease in cattle, sheep and swine and is usually caused by Pasteurella spp. (P. multocidia and P. hemolytica). However, Mycoplasma spp. may be responsible for this type of pneumonia in sheep and cattle. So-called shipping fever of cattle is a fibrinous bronchopneumonia caused by Pasteurella spp. It occurs with high frequency in animals that have been stressed (shipped, etc.).
Interstitial pneumonia (pneumonitis) is characterized by inflammation of the alveolar walls with an absence or minimum exudation of inflammatory cells (neutrophils, etc.) into alveolar lumens. A diagnosis of interstitial pneumonia depends on the detection of any one of a combination of the following:
The causes of interstitial pneumonia are numerous and include viral infections (feline pneumonitis, canine distemper, equine viral rhinopneumonitis, etc.), chemical toxicosis (ANTU poisoning, turpentine, kerosene, etc.), mycoplasma infection (enzootic pig pneumonia, etc.), and some allergic reactions. In addition, interstitial pneumonia is common in septicemic diseases and/or those characterized by sustained or intermittent bacteremia (colibacillosis, salmonellosis, erysipelas, leptospirosis, etc.).
In summary, an interstitial pneumonia is characterized by exudation into the walls of alveoli. These walls become greatly thickened by infiltrating lymphocytes, macrophages, and plasma cells, as well as by accumulations of serum or fibrin and increased connective tissue. Proliferation and metaplastic changes of alveolar epithelial cells are frequent findings. In some diseases (canine distemper, parainfluenza virus 3 in calves, etc.), multinucleated giant cells are a component of the exudate in alveolar walls and lumens.
Is a chronic, clinically mild, infectious respiratory disease caused by Mycoplasma hyopneumonia and characterized by an interstitial pneumonia. The disease is wide-spread, and the lungs of 30 to 80% of all pigs slaughtered show typical pneumonia lesions. Incidence is highest in growing pigs (2-4 months of age). Immunity to the disease develops slowly. The lung lesions may regress and adult pigs may recover completely. Clinically, the disease is chronic and characterized by coughing and slow weight gain. Grossly, the lungs are grey to plum-colored and lesions are located chiefly in the apical and cardiac lobes. Microscopically, the reaction is limited primarily to the alveolar septa (walls), being characterized by thickening of the septa by infiltrating lymphocytes, macrophages, and plasma cells (interstitial pneumonia).
(Hog flu) is characterized by gross and microscopic lesions similar to those described for enzootic pig pneumonia. However. swine influenza is an acute, contagious respiratory disease caused by concurrent infection with an influenza virus and Hemophilus influenzae suis.
Acting alone, the virus produces only a mild illness and Hemoplilus influenzae suis is a common inhabitant of the upper respiratory tract of normal pigs. Together, under favorable climatic conditions, these agents are capable of producing swine influenza. The disease is characterized by sudden onset, coughing, dyspnea, fever, prostration, and rapid recovery. Lesions develop rapidly in the respiratory system and regress quickly, except in a few complicated cases where a severe bronchopneumonia may be followed by death. Even though the pig is the only commonly known natural host, there is serologic evidence of infection in human beings. Clinically, swine influenza is a herd disease (the entire herd usually becomes ill within a few days). There is loss of appetite, animals are reluctant to move, coughing is prominent, and prostration is common. Mortality is low. The gross lesions of swine influenza and enzootic pig pneumonia are similar. Lesions are found primarily in the anterior lobes and consist of consolidated "plum-colored" areas.
Embolic pneumonia refers to foci of lung inflammation initiated by the lodgement of emboli of pathogenic organisms or septic fragments of thrombi in the pulmonary arteries or capillaries. Most organisms which cause embolic Pneumonia are pyogenic and abscessation is to be expected
The pneumonic foci and/or abscesses are rather evenly scattered throughout all lung lobes, with the greatest concentration being found near the pleural surface (largest proportion of small vessels are in the subpleural location). Microscopically, in the early states, embolic pneumonic foci can be seen spreading outward from blood vessels (not from bronchi as in bronchopneumonia). Emboli pneumonia and hematogenous pulmonary abscesses occur commonly in ruminants and swine, occasionally in horses, but rarely in dogs.
In addition to hematogenous pulmonary abscesses, pyogenic organisms may reach the lung parenchyma by the bronchogenic route or by direct traumatic penetration of the lungs. In animals. lung abscesses are most often bronchogenic in origin (complication of bronchopneumonia).
The following forms and/or types of pneumonia are commonly given special consideration because of peculiar characteristics.
Is not an independent type of pneumonia, but a complication of other forms in which there is necrosis and invasion of lung tissue by saprophytic and putrefactive bacteria. The usual cause of this condition is the introduction into the lungs of materials (medicines, etc.) intended for the gastrointestinal tract (saprophytic and putrefactive bacteria are usually introduced with the foreign material). The severity of the lung lesions is largely dependent on the nature and quantity of the foreign material introduced. Many substances are highly irritating and capable of producing extensive necrosis of lung tissue. At necropsy, the lungs may be yellowish-green to greenish-black, foul smelling, with extensive cavitations.
Occurs when droplets of oil are introduced into the lungs. In general, vegetable oils are not irritating and are eventually absorbed with very little inflammatory reaction. However, oils of animal origin are highly irritative, not capable of being reabsorbed and they provoke a severe inflammatory response. In later stages, there is a monocytic reaction in which giant cells and foamy macrophages predominate (granulomatous lesion).
Refers to lung inflammation that develops subsequent to the accumulation of blood and the inhalation of upper respiratory pathogens in the ventral portions of the lungs. The condition follows hypostatic congestion and occurs in recumbent animals in the terminal stages of many diseases.
Equine viral rhinopneumonitis is caused by equine herpesvirus-I. Pregnant mares may abort 3-weeks to 4-months following clinical disease or asymptomatic infection. Abortion is most common in the 8th and llth month of gestation. In aborted fetuses, the most consistent gross lesion is severe edema of the lungs. The edematous lungs are heavy and rubbery and casts of fibrin are occasionally found in bronchi. The liver contains grayish-white foci of necrosis scattered throughout. The spleen may be enlarged. Petechial and ecchymotic hemorrhages may be found anywhere in the body. Microscopically, acidophilic intranuclear inclusion bodies are found associated with necrotic foci in the liver, spleen, and in bronchial epithelial cells. In uncomplicated cases, pregnant mares usually recover promptly, exhibiting little more than a slight transitory fever. In some outbreaks, however, pregnant mares may exhibit mild to severe central nervous signs which include incoordination, ataxia, and/or paresis of the hind quarters. Microscopically, the CNS lesions are characterized by a myeloencephalitis. Also, it has been suggested that neuritis of the cauda equina is a sequela of equine herpesvirus-I infection. In foals and young horses, equine viral rhinopneumonitis is a highly contagious, mild disease of the respiratory tract characterized by fever, leukopenia, congestion and serous nasal discharge, conjunctivitis, pharyngitis, cough, and inappetence. In uncomplicated cases, recovery occurs within one week of onset.
Is an acute contagious disease of horses characterized by extensive necrosis in the media of small muscular arteries of the intestine, lymphoid tissues, and visceral organs. Initially, the virus destroys the endothelium in the vascular supply (vasa vasorum) of small muscular arteries. Subsequently, there is endothelial swelling and necrosis of the media of small muscular arteries. Grossly, the lesions of equine viral arteritis are attributable to the vascular changes and consist principally of extensive hemorrhages and generalized edema. The distribution of edema in the intestine is considered to be characteristic; edematous segments of the intestine (1 to 3 feet), alternate with segments of normal thickness. Clinically, the disease is characterized by depression, fever, leukopenia, limb edema, abortion of pregnant mares (up to 80%), enteritis, and pneumonic complications.
Is an acute highly contagious febrile respiratory disease with a low mortality in uncomplicated cases. At necropsy, interstitial pneumonia, bronchitis, peribronchitis and perivasculitis may be observed. The disease is usually diagnosed on observation of a fast-spreading disease with rapid onset, high fever, weakness, and cough.
Adenovirus infection occurs frequently in foals, but it is of primary importance only in Arabian foals with combined "B" and "T" lymphocyte immunodeficiency.
Occurs in Arabian foals as a fatal, autosomal recessive, combined B- and T- lymphocyte immunodeficiency. Affected foals are usually asymptomatic during the first 2 to 3 months of life, but become progressively more susceptible to secondary infections after that time (newborn foals receive immunoglobulins from colostrum). Following nursing (colostrum secretion), immunoglobulin levels are normal; however, there is a progressive decrease after that time compared to normal foals (prior to receiving colostrum, IgM is absent or not detectable). Clinically, there is a marked lymphopenia (less than lOOO/cmm). Lesions consist of thymic atrophy as well as a marked depletion of lymphoid elements in the spleen, lymph nodes and Peyer's patches. Foals with combined immunodeficiency are highly susceptible to respiratory disease and usually die with some form of pneumonia. High mortality occurs from adenoviral infections and from Pneumocystis carinii lesions.
Canine distemper is a highly contagious disease caused by a Morbivilli virus. The disease occurs primarily in young dogs and is characterized by a visceral phase as well as by an encephalitic phase. The virus, in combination with bacterial infections, is responsible for the clinical signs observed during the visceral phase (ocular and nasal discharges, pneumonia. enteritis. skin vesicles and pustules, etc.). Dogs that survive the visceral phase may succumb subsequently to central nervous system complications. Significant clinical findings include a diphasic temperature elevation, ocular and nasal discharges, respiratory distress, enteritis, and nervous signs (characterized by chewing movements, excessive salivation, epileptiform seizures, blindness and paralysis).
Gross lesions in the visceral phase depend on the extent and severity of secondary bacterial infections (pneumonia, enteritis. etc.). The virus produces intranuclear and cytoplasmic inclusion bodies in epithelial cells (respiratory, urinary, digestive, etc.). The virus of canine distemper in combination with Brucella bronchiseptica is considered to be the cause of the respiratory lesions associated with this disease. The virus attacks epithelial cells and renders the lungs more susceptible to bacterial invasion. Lung lesions are oftentimes manifested by a purulent bronchopneumonia when secondary bacterial invasion is present. The virus alone stimulates an interstitial reaction with or without multinucleated giant cells. Cytoplasmic and nuclear inclusion bodies are formed in epithelial cell (bronchial epithelial cell, etc.) by the virus.
In the central nervous system, the virus has an affinity for the myelinated portion of the brain and spinal cord; the cerebellar peduncles, anterior medullary velum: myelinated tracts of the cerebellum and the white columns of the spinal cord are the structures most constantly affected. Central nervous lesions consist of demyelination, gliosis, perivascular cuffing, and inclusion bodies within glial cells and neurons. A clinical diagnosis of canine distemper is best confirmed by histopathologic lesions (inclusion bodies, demyelination, etc.) and/or by the fluorescent antibody technique.
Caseous lymphadenitis of sheep and goats (pseudotuberculosis) is caused by Corynebacterium pseudotuberculosis (C. ovis). The disease is usually unapparent clinically, but overt disease and death may occur. Symptoms are seldom noted and the disease is most likely to be encountered as an incidental finding in slaughtered animals. Adult sheep and goats are primarily involved (2-years or older). Lesions are most commonly observed in the lungs and lymph nodes. However, generalized infection may occur. Grossly, the entire lymph node may become enlarged by abscesses (yellowish-green, odorless pus). In chronic lesions, the pus becomes rather dry and firm. This exudate is usually arranged in concentric, "onion ring" layers with a thick fibrous capsule.
Corynebacterium pseudotuberculosis is also the cause of ulcerative lymphangitis of horses. This condition is characterized by nodules, ulcers, and inflammation of the lymph vessels, especially in the region of the fetlock.
Nocardiosis is a chronic infection resulting from soil-borne organisms of the genus Nocardia (N. asteroides) and characterized by generalized purulogranulomatous nodular lesions. The condition occurs most commonly in the dog, but other species may be affected (man, cattle, horses, cats. sheep, goats, birds, etc.). In dogs, infection of the lungs, pleura and skin is most common; however, systemic infection can occur. Grossly, granulomatous and purulent lesions may occur in superficial lymph nodes. The abscesses may rupture. The lungs, bronchial lymph nodes, and pleural cavity frequently contain granulomatous and suppurative lesions. The pleural exudate is dark, muddy brown, and may contain orange-white granules. Microscopically, tangled, gram-positive colonies of organisms surrounded by radiating clubs are found. Treatment during the early stages may be successful. Nocardia is a sporadic cause of mastitis in cattle.
Murine respiratory mycoplasmosis (chronic respiratory disease) is a disease syndrome complex characterized by inflammation of the respiratory tract and middle ear. Clinical signs include chattering and dyspnea in mice, and nasal discharge, snuffing, rales, dyspnea, head tilt, incoordination and circling in rats. The primary etiologic agent is mycoplasma pulmonis; however, Pasteurella pneumontropica, Corynebacterium kutscheri, Bordetella bronchiseptica, streptococci, pneumococci and viruses may act in concert with the primary agent. Gross lesions include suppurative bronchitis, bronchopneumonia, mucopurulent rhinitis, otitis media, and otitis interna. The lungs have discrete or disseminated, red and gray, indurated and somewhat depressed areas. Lung lobes that are completely involved have a rubbery consistency and cobbled surface. Cut surfaces of the lungs reveal cystic dilated, and thick-walled bronchi filled with mucoid material. Microscopically, thick-walled bronchi which are surrounded by a heavy collar of lymphoid cells make up the dominant feature in advanced cases.
Lung infarction occurs infrequently because of two rather efficient arterial system (pulmonary and bronchial arteries). In the absence of significant cardiac failure, the bronchial arteries, of aortic origin, can sustain the vitality of the pulmonary parenchyma when branches of the pulmonary artery are occluded (via emboli, etc.). However, if the pulmonary circulation is already compromised (via heart failure, etc.), the pulmonary arterial branches tend to function as end arteries and embolism would lead to infarction of the lungs.
Calcification of the lungs occurs rather frequently in the dog. It usually occurs as a consequence of vitamin D toxicosis in young dogs, whereas in older dogs, it is usually associated with chronic renal diseases and hyperparathyroidism (metastatic calcification). Grossly, the lungs are gritty, firm to hard, and they do not collapse when the thoracic cavity is opened. Microscopically, calcium concretions are found in alveolar walls.
Melanosis refers to a deposition of melanin pigments in various organs and tissues: the lung is a common site of involvement. There is no change in the texture or consistency of involved tissues, and no tendency toward neoplasia. Affected animals are in a state of normal health.
Pneumomycosis or mycotic pneumonia may be caused by a number of fungal agents. However, Aspergillus fumigatus, Cryptococcus neoformans, Blastomyces dermatitidis, Coccidioides immitis and Histoplasma capsulatum are most frequently encountered. Fungi are major causes of "opportunistic infections" (especially aspergillosis and mucormycosis).
Cryptococcus and the other fungal diseases discussed in this section are usually primary infections, even though they may serve as secondary invaders (opportunistic infections). The growing use of wide-spectrum antibiotics, radiation. and immunosuppressive drugs predisposes animals to these ubiquitous opportunists. It should be remembered that most fungi are harmless soil saprophytes which inadvertently become agents of disease.
Even though the fungal disease discussed in this section may be responsible for lesions in various organs and/or tissues, the lungs and associated structures are major sites of involvement.
9.13.13.1 ASPERGILLOSIS
Fungi of the genus Aspergillus are ubiquitous and exposure to spores occurs on a daily basis. Aspergillus fumigatus is responsible for most infections in animals, birds and man. The fungus may invade already devitalized tissues (virtually as a saprophyte) or induce primary infections, usually of an opportunistic nature, in a compromised (severely debilitated or immunosuppressed, etc.) host. In general, aspergillosis of the respiratory tract of animals appears to be a complication of some other debilitating disease. Infection may develop as an implantation on the mucous membranes of air passages. On mucous membranes, the fungus may be visible to the naked eye, first as a whitish growth, and later as a powdery felt-like growth with a greenish-grey color produced by the spores (such superficial colonies may develop after the animal dies; thus, their significance depends upon accomplishing tissue reactions). The fungus grows in tissues as short, slender, septate, filamentous organisms with branching hyphae. Grossly, lesions are varied in nature. They may occur as abscesses with giant cells along the margins or, nodular granulomatous growths with caseous centers in more chronic cases. Microscopically, tangled masses of organisms are observed within the lesions. In cattle, radiating club-like structures may surround the fungal agent.
9.13.13.2 MUCORMYCOSIS
Mucormycosis appears most commonly as an opportunistic infection and the fungus grows in tissues as a coarse, nonseptate, filamentous organism, with branching hyphae. Disseminated lesions may develop, but the major sites of involvements are lymph nodes, lungs and gastrointestinal tract.
9.13.13.3 CRYPTOCOCCOSlS
Cryptococcosis is a subacute to chronic disease of many animal species as well as man. The causative organism. Cryptococcus neoformans, is a yeast-like fungus which may live in a nonparasitic state in nature. The organism has an affinity for the meninges, respiratory tract and mammary glands; however, generalized infections may occur with involvement of several systems of the body. In dogs, the brain, meninges and paranasal sinuses are most commonly involved. In cats, the nasal cavities and pharynx are the usual sites of infection. Outbreaks of intractable mastitis have been reported in cattle. Cryptococcus neoformans occurs in tissues as a round to oval, thick-walled, yeast-like body surrounded by a wide gelatinous capsule and reproduces by budding. The cell within the capsule is approximately 5 to 20 microns in diameter and the heavy gelatinous capsule increases the overall size to a maximum of 30 microns in diameter. A useful laboratory aid in the identification of this organism is the introduction of India ink into exudate suspected of harboring these fungi. The ink provides a contrast medium which clearly outlines the heavy translucent coat. The fungi are widespread throughout the world and bird droppings are considered to be an important source of infection.
The tissue response to Cryptococcus neoformans is extremely variable. On one extreme, the organism may evoke virtually no inflammatory reaction. Gelatinous masses of fungi may develop as though in a culture medium (apparently evoking little or no protective response). On the other extreme, the fungi induce a chronic inflammatory reaction which consist of macrophages, lymphocytes, and giant cells.
Grossly, the cut-surfaces of affected tissues usually have a definitely mucinous quality and well-defined granulomas may or may not develop. Microscopically, typical organisms can be demonstrated within lesions.
9.13.13.4 BLASTOMYCOSIS
Blastomycosis is a chronic disease caused by Blastomyces dermatitidis and characterized by focal suppurative and granulomatous lesions. The dog is principally affected and the respiratory system is most frequently involved. However, the disease has been reported in a number of animal species, and generalized (systemic) infection may occur. Blastomyccsis is limited primarily to North America (particularly in the Mississippi-Ohio basins and in the Middle Atlantic States). In tissues, Blastomyces dermatitidis assumes a yeast-form, appears round to oval, measures 8 to 20 microns in diameter, reproduces by budding and has a thick refractile (double-contoured) wall.
Gross lung lesions in most cases are manifested by multiple circumscribed gray nodules of consolidation; however, in some cases, lung consolidation may be diffuse or multiple miliary abscesses may develop. Microscopically, the lesions are characterized by an intense infiltration of macrophages, lymphocytes, foci of neutrophils and giant cells. The yeast-form of the fungi can usually be demonstrated within the lesions (free or within macrophages). Systemic dissemination may lead to metastatic sites of infections, especially in the skin, brain, liver, bones, eyes, adrenal, and intestine.
9.13.13.5 COCCIDIOIDOMYCOSIS
Coccidioidomycosis is an acute or chronic disease which bears many similarities to tuberculosis. Granulomatous lesions are usually limited to the lungs and associated lymph nodes (cattle), but a disseminated form of the disease may occur (dogs). Coccidioides immitis is most prevalent in the Southwest and far West of the United States and is particularly common in the San Joaquin Valley of California. In tissue sections, the fungus appears as a thick- walled (double contoured), nonbudding spherule that measures 5 to 50 microns in diameter. Reproduction is by endosporulation (rupture of spherules with release of endospores).
Gross lesions usually appear as discrete or confluent granulomas with or without suppuration and calcification. In cattle, lesions are often limited to small nodules in the lungs and associated lymph nodes. In dogs, multiple lung granulomas with dissemination to other organs and tissues are observed. Microscopically, granulomas without suppuration (neutrophils) occur when there is a slower rate of fungal reproduction. However, in cases where there is florid proliferation of fungi, the response tends to be suppurative. Typical spherules can be demonstrated in the suppurative exudate and/or in macrophages or giant cells within the granulomas. In cattle, the large spherules may be surrounded by a corona of radiating club-like structures.
9.13.13.6 HISTOPLASMOSIS
Histoplasmosis is an infectious mycotic disease of man and lower animals caused by Histoplasma capsulatum. A benign unapparent form and a fatal systemic form may occur. In dogs, the fatal systemic form occurs most commonly and various organs and tissues may be affected. Histoplasmosis is characterized by extensive proliferation of reticuloendothelial cells (macrophages, epithelioid cells) and many of these cells contain "yeast forms" of the causative organism. The yeast-like bodies are cytoplasmic, irregular, egg-shaped, and measure approximately 2 microns in diameter. Histoplasmosis is one of the most frequent systemic fungal diseases encountered in dogs and man. The fungus grows in soil and infection is acquired by inhalation or rarely by the oral route. Acute disseminated histoplasmosis usually is fatal. The disease is especially prevalent in the Ohio and Central Mississippi Valleys and along the Appalachian Mountains in the Southeastern United States where the appropriate climatic conditions are found for growth of the fungus in the soil.
SUMMARY: A diagnosis of the fungal diseases discussed in this section can be established by demonstrating the organisms in characteristic lesions. The fungal agents may stain poorly with routine hematoxylin and eosin; However, they can be demonstrated readily by employing stains for glycogen (Periodic Acid Schiff reaction, Bauer's and Gridley's fungal stains).
Remember,
Branching septate hyphae is a feature of Aspergillus, whereas Mucor is characterized by branching nonseptate hyphae. Blastomyces reproduces by budding and is larger than Histoplasma capsulatum and smaller than Coccidioides immitis (which reproduces by endosporulation). Cryptococcus neoformans reproduces by budding, but it is characterized by the presence of a wide, mucicarmine-staining capsule.
Parasitic diseases of the lungs are discussed in detail in your parasitology course. However, the student should become familiar with the information presented in this section. In animals, there are a number of parasites whose final habitat is the lung. Pulmonary nematodiasis refers to infection of the lungs by parasitic nematodes. Most of these parasites cause direct irritation, stimulate excessive mucus production, and predispose the respiratory tract to secondary bacterial invasion. Dictyocaulus spp. are responsible for the formation of shrunken or raised, "plum-colored" areas in the posteriodorsal diaphragmatic lobe. Filaroides osleri is characterized by nodules in the mucosa of the trachea or bronchi. The important lung worms are:
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At necropsy, lung nematodes can be demonstrated best by opening bronchi and bronchioles leading to the affected areas within the lungs. The term verminous pneumonia refers to lung inflammation caused by parasites.
Most neoplasms encountered in the lungs are metastatic growths (lungs are especially prone to the lodgement of tumor emboli). However, any component of lung tissue can give rise to primary neoplasms. Primary lung neoplasms are rather infrequent; but the incidence is much higher in dogs than in any other species. Bronchiolar carcinoma accounts for approximately 75% of primary pulmonary neoplasms in dogs. It occurs most frequently as a solitary nodule which is well-demarcated, but not encapsulated; however, it may be of multicentric origin. Bronchiolar carcinomas arise in the periphery of the lung lobes, most frequently the diaphragmatic. Only a small proportion of these neoplasms metastasize. Growth occurs by infiltration and expansion. Bronchogenic carcinomas originate from the epithelium of larger bronchi and they are less common than the bronchiolar type.
So-called pulmonary adenomatosis of sheep is a chronic progressive interstitial pneumonia characterized by marked proliferation of alveolar lining cells with thickening of alveolar walls (the bulk of the alveolar spaces may be replaced by thickened alveolar walls). The thickened alveolar lining cells are hyperplastic, but they tend to resemble adenomas (thus, the name, pulmonary adenomatosis).
9.13.16.1 MAEDI
Maedi is a chronic progressive interstitial pneumonia of sheep which is caused by a viral agent (evidence suggests that the same viral agent causes Maedi, Marsh progressive pneumonia. and visna of sheep). This disease occurs primarily in Iceland, Germany, Holland, Norway and Sweden. It has been reported in the U.S.A. as Marsh and/or Montana progressive pneumonia. Maedi occurs principally in sheep (2-years old or older), but it has been reported in goats. The interstitial pneumonia develops very slowly and lesions are quite widespread when clinical signs appear (incubation period of at least 2 years). Grossly, the lungs are larger, and 2-4 times as heavy as normal lungs. They do not collapse completely when the chest cavity is open and appear grey to pink in color. Enlargement of the bronchial and mediastinal lymph nodes is a constant feature. Microscopically, changes are characteristic of a chronic interstitial pneumonia. There is rather uniform thickening of alveolar walls by hyperplastic alveolar lining cells, lymphocytes, and mononuclear cells. Intracytoplasmic inclusion bodies have been reported in mononuclear cells. There is an absence of healing. No treatment has been successful.
9.13.16.2 JAAGSIEKTE DISEASE
Jaagsiekte disease is a chronic progressive interstitial pneumonia of sheep, characterized by rather uniform thickening of alveolar walls and by hyperplastic alveolar lining cells. The disease is similar in character to Maedi (however, adenomatous proliferation is more severe and there is less tendency for metastasis to regional lymph nodes). There is evidence that Jaagsiekte disease is caused by a herpesvirus; however, a mycoplasma is commonly encountered in affected sheep and may play an etiologic role. The disease has been reported from Europe, South Africa, Asia, Britain, Iceland, and Israel; no confirmed cases have been recorded in North America.
Pathologic involvement of the pleura is usually a secondary complication of some underlying disease. Pleuritis (inflammation of the pleura) is the most common condition encountered and it is usually secondary to pneumonia. Noninflammatory pleural collections (fluid, blood, chyle, air) may be observed.
9.13.17.1 PLEURITIS:
Inflammation of the pleura is usually secondary to pneumonia; however, a primary pleuritis is associated with bovine blackleg, Glasser's disease, sporadic bovine encephalomyelitis, etc. When copious exudation into the pleural sacs accompanies the inflammation, the lesion is commonly designated as "pleurisy with effusion." Effusive pleurisy is common in cats. The exudate is voluminous, the diaphragm is depressed, and the lungs are compressed and displaced to the caudodorsal portion of the thorax. Pasteurella multocida, Escherichia coli, and Sterptococci are present in most cases. Also, copious effusion occurs with frequency in horses, and it is a characteristic of pleural tuberculosis in dogs.
The exudates associated with pleuritis include serous, fibrinous, serofibrinous, suppurative (empyema) and hemorrhagic. Serous, serofibrinous and fibrinous are all caused by the same processes (fibrinous exudations generally reflect a later and more severe reaction). The exudates are commonly caused by inflammatory diseases within the lungs. A frank purulent pleural exudate usually implies bacterial or mycotic seeding of the pleural space. Empyemia or pyothorax of the pleural cavities is characterized by frank yellow-green creamy pus.
9.13.17.2 HYDROTHORAX:
The accumulation of serous fluid (transudate) within the pleural cavities is referred to as hydrothorax. It is usually bilateral and the causes are varied. (Review the section on generalized edema in your General Pathology notes).
9.13.17.3 HEMOTHORAX:
The escape of blood into the pleural cavities is known as hemothorax. It is usually associated with traumatic rupture of a blood vessel. A pure hemothorax is readily identifiable by the large clots that accompany the fluid component of the blood.
9.13.17.4 CHYLOTHORAX:
The accumulation of chyle (milky fluid) into the pleural cavities is referred to as chylothorax (chyle is lymph to which an opacity is imparted by highly emulsified fats). Chyle accumulates subsequent to leakage from the thoracic or right lymphatic duct. It can be differentiated from other types of fluid by extraction of the fat content with ether or by staining the droplets with one of the Sudanophilic dyes.
9.13.17.5 PNEUMOTHORAX:
The accumulation of air or gases within the pleural cavities is referred to as pneumothorax. The presence of air in these cavities reduces the "negative" thoracic pressure and this provides a means for detecting its presence. If there is a movement of air into the thorax when its wall is pierced, a normal negative pressure can be assumed to have been present. In small animals, air can be detected by opening the chest under water and observing the escape of air bubbles. Pneumothorax may be traumatic in origin, or it may occur subsequent to the rupture of alveoli. If the air or gas pressure is high, compression atelectasis of the lungs may occur.
9.13.17.6 NEOPLASMS:
Primary and sec