Chapter 00-Repiratory Dx9

7/28/2019 Chapter 00-Repiratory Dx9

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EXAMINATION OF THERESPIRATORY TRACT

POSTMORTEM

Te respiratory tract should always be examined in a systematicashion. o determine whether negative pressure is present in thethoracic cavity, the diaphragm is punctured through the abdominalcavity beore the thoracic cavity has been opened. When the dia-phragm is punctured in a resh carcass, the loss o negative pressurein the thorax causes the diaphragmatic cupola to drop back caudallytoward the abdominal cavity, and at the same time, there is anaudible sound caused by the inrush o air into the thorax. Lack othis movement may be an indication o advanced pneumothorax,pleural eusion, or the presence o uncollapsed lungs caused bypulmonary edema, pneumonia, fbrosis, or emphysema. In carcasses

Web Fig. 9-2 Normal lung, pig.

Te lung parenchyma appears homogeneously pink. Te pale pink appear-ance o these normal lungs is due to exsanguination. Te appearance onormal unexsanguinated lungs is bright pink to red. (Courtesy Dr. A. Lpez,Atlantic Veterinary College.)

that have been dead or a long time, pulmonary air and gas pro-duced by saprophytic bacteria leak into the pleural cavity, reducingthe negative thoracic pressure and collapsing the lung.

Te rib cage must be removed by cutting along the costosternaljoints and along the neck o the ribs (close to the costovertebraljoints) in such a way that pleural adhesions and abnormal thoraciccontents can be observed and grossly quantifed (e.g., 200 mL oclear, yellow uid). Te tongue, pharynx, esophagus, larynx, trachea,and thoracic viscera (lungs, heart, and thymus) should be removedas a unit (oten called the pluck) and placed on the necropsy table.

Te pharynx and esophagus are opened starting at the pharynx

by a single cut with scissors along the dorsal midline and inspectedor ulcers, oreign bodies, and neoplasms. Te larynx and tracheamust be examined by opening both along the dorsal midline romcranial to caudal ends and then extending the incision into thelarge bronchi o the caudal lung lobes. Normal tracheobronchialmucosa has a smooth and glistening pearl-colored surace withempty lumina in airways. Te presence o oamy uid in airwaysindicates pulmonary edema. Feed particles may suggest aspiration;however, careul examination o the mucosa is required becauseaspiration o ingesta rom stomach or rumen into the lungs com-monly takes place agonally or can be displaced into these areas

when the carcass is moved.Te lungs should be examined beore incision. Normal lungs

typically have a homogeneous pink color (Web Fig. 9-2). Exter-

nal changes include the presence o rib imprints on the pleuralsurace when lungs ail to collapse. In addition, the lungs shouldbe inspected or changes in color and texture and distribution olesions. Color changes can be various shades o red, indicatinghypostatic congestion, hyperemia (acute pneumonia), and hemor-rhage; dark blue collapsed lobules or areas are indicative o atelec-tasis; pale pink to white lungs indicate notable anemia, fbrosis, oremphysema; and uniormly or patchy yellow-brown lungs indicatechronic passive congestion and pulmonary fbrosis likely second-ary to chronic heart ailure. Lungs rom exsanguinated animalsare generally paler than the normal pink color because o reducedblood in the pulmonary tissue. A covering o yellowish material onthe pleural surace indicates accumulation o fbrin. Because it is

STRUCTURE AND FUNCTION

Web Fig. 9-1 Ultrastructural morphology o respiratory mucosa.

A, Normal bronchial mucosa, bronchus, rat. Te mucous layer was removedbeore fxation to expose the external surace o the epithelium. Mucosaconsists o ciliated cells and nonciliated secretory cells. Ciliated cells havenumerous slender cilia (arrows). Nonciliated secretory cells have a dome-shaped surace with abundant microvilli (arrowheads). Te proportion ociliated to nonciliated cells varies depending on the level o airways. Cili-ated cells are more abundant in proximal airways, whereas secretory cells

are more numerous in distal portions o the conducting and transitionalsystems. Scanning electron micrograph. Carbon-sputter coating method.B, Normal ciliated epithelium, trachea, cow. Tis trachea was specially fxedto preserve the mucous layer, which consists o an internal, clear, hypophase-uid layer (not visible here) surrounding microvilli and kinocilia and anexternal mucous epiphase at the level o the tips o the kinocilia (cut inboth transverse and longitudinal section here). EM. Uranyl acetate andlead citrate stain. (A courtesy Dr. A. Lpez, Atlantic Veterinary College. B romSims DE, Westall JA, Kiorpes AL, Horne MM: Biotech Histochem 66:173-180, 1991.)

A

B

e71CHAPTER 9 Respiratory System, Mediastinum, and Pleurae

Copyright 2012, 2007, 2001, 1995, 1988 by Mosby, Inc., an affiliate of Elsevier Inc.


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HISTOPATHOLOGY AND BIOPSIES

Microscopic examination o pulmonary tissue is routinely done indiagnostic laboratories. Samples o normal and abnormal lungs,along with other appropriate tissue, should always be submitted in10% buered-neutral ormalin or histopathologic evaluation. Aminimum o our lung samples (let cranial, let caudal, right cranial,

and right caudal) should be taken or histopathologic examinationin animals with a history o respiratory signs. o improve fxation,a paper towel can be placed over the samples o lung oating infxative. When detailed evaluation o the alveolar walls is required,lungs can be fxed by a gentle intratracheal injection o fxative;however, this technique displaces transudates and exudates and canartifcially cause distention o the perivascular and peribronchialspaces. Lung biopsy specimens are taken only sporadically becausecomplications oten outweigh the diagnostic value. However, theuse o new techniques, such as endoscopic-directed biopsies, hasnotably reduced some o these complications. Biopsies o the lungsare recommended in cases o chronic persistent pulmonary diseaseunresponsive to treatment or intrathoracic masses o undeterminedorigin. Endoscopic-directed biopsies o the nasal and bronchial

mucosa are routinely used in clinical practice and generally have amuch better diagnostic value.

impossible to describe the texture o normal lungs, experience inpalpation is required to appreciate the actual texture o a normallung. exture is determined by gently palpating the surace andparenchyma o the lungs. Normal texture can change to frm, hard,elastic (rubbery), or crepitus (with a crackling sound or eeling).For a detailed description o lung texture, see the section on Clas-sifcation o Pneumonias. Palpation o the lungs, which should begentle, also permits detection o nonvisible nodules or abscesses inthe parenchyma. Knowing the distribution o a lesion in the lungsalso acilitates diagnosis because particular etiologic agents causelesions with specifc distribution. Distribution o lesions is generallydescribed as ocal, multiocal, locally extensive, or diuse. Accord-ing to their topography, pulmonary lesions can also be classifed ascranioventral, dorsocaudal, and so on.

Reports must also contain an estimate o the extent o the pul-monary lesions, preerably expressed as a percentage o the volumeo the lungs aected. For instance, a report may read cranioventralconsolidation involving 40% o the lungs. I the lungs have ocallesions, a rough estimate o the number should also be includedin the report. For instance, numerous (approximately 25), small (1to 2 cm in diameter), hard nodules were randomly distributed inall lung lobes.

wo methods are used to examine the nasal structures. Tefrst is making a midsagittal cut through the head and removingthe nasal septum; the second is making several transverse sectionso the nose at the level o the second premolar teeth. Tis lattermethod is preerred when examining pigs suspected o havingatrophic rhinitis or animals suspected o having nasal neoplasms.

Bronchoalveolar Lavage andTracheal Aspirates

wo valuable diagnostic tools in human medicine, bronchoalveolarlavage (BAL) and tracheal aspirates, have in recent years becomemore widely used in veterinary clinical diagnosis o respiratoryailments, particularly in horses, dogs, and cats. Te basis o BAL issampling to determine the cellular and biochemical compositiono the lung in a respiratory patient live animal by inusing andretrieving sterile uid via the trachea. BAL is done by inserting a

DISEASES OF THE RESPIRATORY SYSTEM

NASAL CAVITY AND SINUS MUCOSA

Anomalies of the Nasal Cavity

Localized congenital anomalies o the nasal cavity are rare indomestic animals and are oten merely part o a more extensivecranioacial deormity (e.g., cyclops) or a component o general-ized malormation (e.g., chondrodysplasia). Congenital anomaliesinvolving the nasal cavity and sinuses, such as choanal atresia (lacko communication between the nasal cavity and pharynx), sometypes o chondrodysplasia, and osteopetrosis, are incompatible withlie. Examples o nonatal congenital anomalies include cystic nasalconchae, deviation o nasal septum, clet upper lip (harelip, cheilos-chisis), hypoplastic turbinates, and clet palate (palatoschisis) (Fig.7-1). Bronchoaspiration and aspiration pneumonia are commonsequelae to clet palate. Nasal and paranasal sinus cysts are slowlygrowing and expansive lesions that mimic neoplasia and causesevere cranial deormations in horses. Tese large cysts presum-ably originate congenitally rom dentigerous tissue. As in otherorgans or systems, it is extremely di cult to determine the actual

cause (genetic versus congenital) o anomalies based on pathologicevaluation.

tube directly through the larynx into a bronchus, or transtrache-ally by inserting a tube through a needle percutaneously into thecervical trachea. Microscopic examination o properly collected,stored, and processed samples may reveal many erythrocytes andsiderophages in pulmonary hemorrhage or let-sided heart ailure;inclusion bodies or syncytial cells in viral pneumonias; increasednumber o leukocytes in pulmonary inammation; abundant mucusin asthma or equine heaves (chronic obstructive pulmonary disease[COPD]); presence o pulmonary pathogens, such as parasites,ungi, and bacteria; or tumor cells in cases o pulmonary neoplasia.In the healthy patient, 80% to 95% o the BAL cells are pulmonaryalveolar macrophages (see Fig. 9-10).

Web Fig. 9-3 Suppurative rhinitis, midsagittal section o head, cal.

Te nasal septum has been removed to expose nasal conchae. Te nasalmucosa is covered by yellow-white purulent exudate. Tere is also a large,round ulcer in mucosa o the nasopharynx (arrow). (Courtesy Western Collegeo Veterinary Medicine.)

e72 SECTION 2 Pathology of Organ Systems

Inflammation of the Nasal Cavity

Purulent (Suppurative) Rhinitis



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Web Fig. 9-4 Exophytic granulomatous mass surgically removed romthe nasal mucosa(Rhinosporidium seeberi), mule.Large pedunculated mass o granulomatous tissue containing numeroussporangia (arrows). Inset, Sporangium. Note a large encapsulated cyst flledwith a myriad oRhinosporidium seeberiendospores. H&E stain. (From Ber-rocal A, Lpez A: Can Vet J48:305-306, 2007.)

Other Bovine Rhinitis

Nasal granulomas occur in cattle presumably as a result o repeatedexposure to an as yet unidentifed inhaled antigens. Nasal granu-lomas (atopic rhinitis) are reported mainly in cattle in Austra-lia, South Arica, and the United Kingdom, where aected cattle

develop multiple, small, pink or red, polypoid nodules, starting inthe nasal vestibule that in time extend into the caudal aspect o thenasal septum. Tese nodules are composed o fbrovascular tissuemixed with lymphocytes (granulation tissue) superfcially lined byhyperplastic epithelium with abundant mast cells and eosinophilsin the lamina propria (nasal eosinophilia). Te microscopic ea-tures suggest that hypersensitivity type I (immediate), type III(immune complex), and type IV (delayed) may be involved in nasalgranulomas o cattle. Bovine (idiopathic) nasal granuloma must bedierentiated rom nasal mycetomas, nasal rhinosporidiosis, andnasal schistosomiasis, which also cause the ormation o nodulesin the nasal mucosa o cattle. An eosinophilic material consistent

with the Splendore-Hoeppli phenomenon is occasionally observedin bovine mycotic granulomas. Tis phenomenon seen in some

mycotic or bacterial inections is microscopically characterized by adeeply eosinophilic homogeneous material surrounded by bacteriaor mycelia. It is thought to result rom a localized antigen-antibodyresponse in tissue.

Other Causes of Equine Rhinitis

Te protistan parasite,Rhinosporidium seeberi, causes nasal inectionin humans, horses, mules, cattle, dogs, and cats. Gross lesions varyrom barely visible granulomas to large expansive polypoid nodulesthat may be mistaken as tumors. Tese granulomatous nodules aredetected by direct observation when present in the nasal mucosaclose to the nares or by rhinoscopy when located in the deep nasalcavity. Te oending organism, Rhinosporidium seeberi, is readily

visible in histologic preparations and in impression smears, appear-ing as a large (400 m), oval sporangium containing thousands oendospores (Web Fig. 9-4). Rhinosporidium seeberiwas once consid-ered a mycotic agent, but recent phylogenetic investigations suggestthat it is an aquatic protistan parasite o the class Mesomycetozoea.

Bovine Nasal DiseasesInfectious Bovine Rhinotracheitis

Web Fig. 9-5 Subacute fbrinous laryngitis and tracheitis, longitudinal(dorsal) section o larynx and trachea, cal.

Inectious bovine rhinotracheitis (IBR; bovine herpesvirus 1). Tick plaqueso fbrinonecrotic exudate cover the laryngeal and tracheal mucosae. (Cour-tesy Dr. J.M. King, College o Veterinary Medicine, Cornell University.)

Specific Diseases of the Nasal Cavityand Sinuses

Equine Nasal Diseases




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Linguatula serrata

Linguatula serrata is a rare but highly specialized pentastomidparasite that shares some morphologic eatures with arthropodsand annelids and causes inection when dogs consume uncookedruminant meat containing inective larvae. It occurs primarily incarnivores, although sheep and goats may become aberrant hosts.Humans can also acquire the inection by ingesting raw ovine orcaprine meat. Te adult parasite is ound throughout the nasalpassages and sometimes can reach the sinuses and middle ear bymoving through the exudate in the eustachian tubes. In common

with other nasal parasites, Linguatula serrata acts as an irritant,causing sneezing, catarrhal inammation, and epistaxis. Te eggso this parasite leave the host in the exudate, which is coughed upor swallowed and eliminated in the eces.

Te nasal cavity and paranasal sinuses o dogs can occasionallybe inested with other parasites, including mites (Pneumonyssuscaninum).

Allergic rhinitis

Allergic rhinitis (hay ever; nasolacrimal urticaria), which is socommon in humans sensitized and reexposed to inhaled pollensor allergens, has been reported only sporadically in dogs and cats.Hay ever in humans and animals is a type I hypersensitivity reac-tion in which an IgE-mediated degranulation o mast cells resultsin an acute rhinitis and conjunctivitis. Microscopically the nasalmucosa is edematous and infltrated with numerous eosinophils,neutrophils, and some macrophages. Clinically, allergic rhinitis ischaracterized by prouse serous nasal discharge and lacrimation.

Other Causes of Canine Rhinitis

Aspergillus spp. and Penicillium spp. cause mycotic rhinitis andsinusitis in dogs (canine nasal aspergillosis) (Web Fig. 9-6). Nasalbiopsies reveal extensive necrosis o the nasal epithelium and thickplaques o fbrinopurulent exudate mixed with many ungal hyphae.Cryptococcus neoformansand Rhinosporidium seeberiinections o thenasal cavity occur sporadically in dogs (Web Fig. 9-7). Lesions arecharacterized by mucosal granulomas containing periodic acidSchi (PAS)-positive organisms, and the inection is clinicallycharacterized by mucopurulent nasal discharge.

Canine Nasal Diseases

Web Fig. 9-7 Granulomatous rhinitis (Rhinosporidium seeberi), nasalcavity and nostril, dog.A polypoid granulomatous mass flls the rostral part o the let nasalcavity. (Courtesy Dr. C. Bridges, College o Veterinary Medicine, exas A&MUniversity; and Dr. J.M. King, College o Veterinary Medicine, Cornell University.)

Other Causes of Feline Rhinitis and Sinusitis

Mycoplasma felis, feline leukemia virus, and feline

immunodeficiency virus

Mycoplasma feliscan also cause mucopurulent conjunctivitis anda mild upper respiratory inection, with clinical signs and lesionsoverlapping those seen with chlamydiosis, FVR, and FCR inec-

tions. Respiratory inections and bronchopneumonia in cats mayalso be associated with the immunosuppressive eects o elineretroviruses such as eline leukemia virus (FeLV) and eline immu-nodefciency virus (FIV).

Mycotic rhinitis

Te most common mycotic inection in the eline nasal cavityis caused by Cryptococcus neoformans, but not all animals exposedto this ungus necessarily develop cryptococcosis unless they areimmunosuppressed. Te lesions vary rom discrete nasal granulo-mas to large conuent masses o mucopurulent exudate flling theentire nasal cavity and paranasal sinuses. Microscopic examinationo the exudate reveals the typical thick-walled PAS-positive organ-isms (see the section on Pneumonias o Dogs). Nasal aspergillosis

and allergic rhinosinusitis are sporadically reported in cats (see thesection on Other Causes o Canine Rhinitis).

Feline Nasal Diseases

Web Fig. 9-6 Fibrinonecrotic sinusitis, aspergillosis, dorsal section onasal cavities, dog.

A, Te nasal conchae have been destroyed by chronic granulomatousinammation. Mycotic exudate remaining in the caudal aspect o the nasalcavity is yellow-green and granular. B, Hyphae oAspergillus spp. wereisolated rom the granulomatous inammatory exudate. Note the neutro-phils at the periphery o the ungal matt. H&E stain. (Acourtesy College o

Veterinary Medicine, University o Illinois. B courtesy Dr. M.A. Wallig, College oVeterinary Medicine, University o Illinois.)

AA B




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Mammomonogamus (Syngamus) Laryngeus

Mammomonogamus (Syngamus) laryngeus) is a nematode that isseen attached to the laryngeal mucosa o cattle in tropical Asiaand South America, and cats (gapeworm) in the Caribbean andsouthern United States (US). Occasionally, humans with a per-sistent cough or asthma-like symptoms have the parasite in thelarynx or bronchi.

Oslerus (Filaroides) Osleri

Oslerus (Filaroides) osleri is a nematode parasite o dogs and otherCanidae that causes characteristic protruding nodules into thelumen at the tracheal biurcation. Tey are readily seen on endo-scopic examination or at necropsy. In severe cases, these nodulescan extend 5 cm cranially or caudally rom the tracheal biurcationand even into primary and secondary bronchi. Te disease occurs

worldwide, and Oslerus osleriis considered the most common respi-ratory nematode o dogs.

Te gross lesions are variably sized, up to 1 cm, submucosalnodules that extend up to 1 cm into the tracheal lumen (WebFig. 9-8). Microscopically, a mild mononuclear cell reaction ispresent when parasites are alive, but with the death o the parasite,an intense oreign body reaction develops with neutrophils and

Web Fig. 9-8 Parasitic tracheobronchitis (Oslerus osleri), trachea andmain bronchi, dog.

A, Note the numerous large parasitic nodules on the mucosal surace othe distal trachea and main bronchi. Tese nodules cause clinical signsonly in severe inections.Inset, Filarial orms oOslerus oslerican be seenin the nodule. B, Filarial orms oOslerus oslerican be seen in the laminapropria o the tracheal mucosa. Numerous chronic inammatory cells arealso present. H&E stain. (A courtesy Dr. M.D. McGavin, College o VeterinaryMedicine, University o ennessee. Inset and B courtesy College o Veterinary Medi-

cine, University o Illinois.)

A

B

Subepiglottic and Pharyngeal Cysts

Anomalous lesions, such as subepiglottic and pharyngeal cysts,are occasionally seen in horses, particularly in Standardbred and

Toroughbred race horses. Tese cysts vary in size (1 to 9 cm)

and occur most commonly in the subepiglottic area and to a lesserextent in the dorsal pharynx, larynx, and sot palate. Cysts arelined by squamous or pseudostratifed epithelium and containthick mucus. Large cysts cause airway obstruction, reduced exercisetolerance, or dysphagia and predispose to bronchoaspiration o ood.

Besnoitiosis(Besnoitia Bennetti; Besnoitia Besnoiti)

Besnoitiosis (Besnoitia bennetti; Besnoitia besnoiti) is caused by anapicomplexan coccidian parasite, whose lie cycle is still unknown.

Tis parasite can cause pedunculated lesions on the skin, sclera,mucosa o the nasal cavity, and larynx o horses and donkeys, cattle,and wild animals. Besnoitiosis has been reported rom Arica,Central and South America, and Britain. Grossly, pale, round, exo-

phytic nodules up to 2 cm in diameter can be observed protrudingrom mucosal suraces. Tese nodules microscopically consist ofngerlike projections covered by hyperplastic and sometimes ulcer-ated epithelium containing numerous thick-walled parasitic cysts

with little inammatory response.

Parasitic Diseases of the Larynx and Trachea

Hypoplastic Epiglottis, Epiglottic Entrapment, andDorsal Displacement of the Soft Palate

Anomalies, such as hypoplastic epiglottis, epiglottic entrapment,and dorsal displacement o the sot palate, are important causes orespiratory problems and reduced athletic perormance in horses.

An undersized epiglottis is prone to being entrapped below thearytenoepiglottic old, causing an equine syndrome known as epi-glottic entrapment. Tis syndrome also occurs in horses with lateraldeviation and deormity o epiglottis, epiglottic cysts, or necrosis othe tip o the epiglottis. Hypoplastic epiglottis also occurs in pigs.Dorsal displacement o the sot palate, particularly during exercise,narrows the lumen o the nasopharynx and creates abnormal airturbulence in the conducting system o horses. Epiglottic entrap-ment is clinically characterized by airway obstruction, exerciseintolerance, respiratory noise, and cough.

Brachycephalic Airway Syndrome

Brachycephalic airway syndrome is a clinical term that reers toincreased air-ow resistance caused by stenotic nostrils and nasalmeatuses and an excessively long sot palate. Tese abnormalitiesare present in brachycephalic canine breeds such as bulldogs, boxers,Boston terriers, pugs, Pekingese, and others. Te deects are a resulto a mismatch o the ratio o sot tissue to cranial bone and theobstruction o airow by excessive length o the palatine sot tissue.Secondary changes, such as nasal and laryngeal edema caused byorceul inspiration, eventually lead to severe upper airway obstruc-tion, respiratory distress, and exercise intolerance.

PHARYNX, GUTTURAL POUCHES, LARYNX,AND TRACHEA

Anomalies




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Neoplasms of Guttural Pouches, Larynx,and Trachea

Neoplasms of the Guttural Pouches

Neoplasms o the guttural pouches occur rarely in horses and areusually squamous cell carcinomas.

Neoplasms of the Larynx and TracheaLaryngeal neoplasms are rare in dogs and extremely so in otherspecies, although they have been reported in cats and horses.

Te most common laryngeal neoplasms in dogs are papillo-mas and squamous cell carcinomas. Other less common tumorsare laryngeal rhabdomyoma, previously reerred to as laryngeal

WEB TABLE 9-1 Main Chemical Mediators Involved in Pulmonary Inflammation

Name Source Function in the Lung

Histamine Mast cells, basophils, monocytes Increase vascular permeability, pain

Prostaglandins and

leukotrienes

Cell membranes Increase permeability, platelet aggregation, vasoconstriction or

vasodilation, lung edema, pain

L-selectin Neutrophils, monocytes Leukocyte attachment and migration, homing to areas of pulmonary

inflammation

P-selectin, E-selectin;

ICAM-1, ELAM-1

Venules and capillary endothelium Leukocyte attachment and migration to areas of pulmonary inflammation

IL-1 Alveolar macrophages ELAMs, leukocyte chemotaxis

IL-6 Macrophages Lymphocyte and fibroblast activation in the lung; downregulates TNF and

reduces inflammation

IL-8 Macrophages, fibroblasts Leukocyte and lymphocyte chemotaxis

IL-9 Macrophages, alveolar cells Decreases cytokine production in pulmonary alveolar macrophages

TNF- Alveolar macrophages ELAMs, endothelial adhesion, vascular permeability, lung edema; feverand acute-phase proteins, apoptosis

Eotaxin and IL-5 Lymphocytes Eosinophil chemotaxis, airway eosinophilia, asthma, pulmonary allergies

Epithelial secretory proteins Type I and II pneumonocytes, Clara

cells

Modulation of lung inflammation; regulation of fibroblasts-fibrosis and NO

Surfactant A, B (collectins) Type II pneumonocytes and Clara

cells

Chemotaxis, phagocytosis, immunomodulation, regulation of nitric oxide

NO Pneumonocytes, macrophages,

endothelium

Decreases cytokine production in pulmonary alveolar macrophages,

modulation of apoptosis

TGF- and TGF- Pneumonocytes, macrophages Lung remodeling, deposition of connective tissue, fibrosisNeuropeptides (Tachykinins:

substance P, neurokinins

Macrophages Lung permeability, lung edema, bronchoconstriction, bronchial secretions,

inflammation

ELAM, Endothelial adhesion molecule; ICAM, intercellular adhesion molecule; IL, interleukin; NO, nitric oxide; TGF, transforming growth factor; TNF, tumor necrosis factor.

giant cells. Clinically, it can be asymptomatic, although it mostoten causes a chronic cough that can be exacerbated by exerciseor excitement. Severe inestations can result in dyspnea, exerciseintolerance, cyanosis, emaciation, and even death in young dogs.


LUNGS

General Aspects of Lung Inflammation

oncocytoma, and chondromas and osteochondromas. Lymphomainvolving the laryngeal tissue is sporadically seen in cats.

When large enough to be obstructive, neoplasms may cause achange or loss o voice, cough, or respiratory distress with cyanosis,collapse, and syncope. Other signs include dysphagia, anorexia, andexercise intolerance. Te neoplasm is sometimes visible rom theoral cavity and causes swelling o the neck. Te prognosis is poor,as most lesions recur ater excision.

racheal neoplasms are even more uncommon than those othe larynx. Te tracheal cartilage or mucosa can be the site o anosteochondroma, leiomyoma, osteosarcoma, mast cell tumor, andcarcinoma. Lymphosarcomas in cats can extend rom the medias-tinum to involve the trachea.



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Classification of Pneumonias

Embolic Pneumonia

Mycoplasma BovisPneumonia

Species-Specific PneumoniasPneumonias of CattlePneumonic Mannheimiosis (Shipping Fever)

Pneumonias of PigsPorcine Enzootic Pneumonia

Web Fig. 9-9Acute to subacute embolic pneumonia, lung, dog.

Te lung has numerous circular areas o hemorrhage distributed randomlythroughout all lung lobes (embolic pattern [see Fig. 9-55]). Tese oci ariserom injury to the microvasculature in alveolar septa and the visceral pleurasecondary to lodgment o bacterial or ungal emboli (septic emboli) romvalvular or mural endocarditis in the right heart or rom other bacterial orungal diseases where the bacterium or ungus gains access to the circulatorysystem as occurs in many bacterial and ungal enteritides or pneumoniascaused bySalmonella spp.,E coli, or Aspergillus spp. (Courtesy College o Vet-erinary Medicine, University o Illinois.)

Web Fig. 9-10 Fibrinous bronchopneumonia (pleuropneumonia),pneumonic mannheimiosis (Mannheimia haemolytica), right lung, steer.Note the cranioventral pneumonia involving approximately 85% o thelung parenchyma. Te lung is frm and swollen, and the visceral pleura iscovered with a thick layer o fbrin. (Courtesy College o Veterinary Medicine,University o Illinois.)

Web Fig. 9-11 Caseated granulomas, chronic-active bronchopneumo-nia, cow.

Note the cranioventral pneumonia and the sharp line o demarcationbetween normal (N) and pneumonic lung. Te aected lung is frm andplum colored due to inammation and contains numerous randomly dis-tributed caseated granulomas. Tis cow had a dual bacterial inection with

Mycoplasmasp. andMannheimia haemolytica.(Courtesy Drs. V.E. Valli and S.J.Akare, College o Veterinary Medicine, University o Illinois.)

N

Web Fig. 9-12 Chronic suppurative bronchopneumonia (porcineenzootic pneumonia), lung, pig.

Cranioventral consolidation o 40% to 50% o pulmonary parenchyma.Consolidated lung (C) is frm, and the outlines o the lobules are accentu-ated by edema o the interlobular septa. N, Normal lung. (Courtesy OntarioVeterinary College.)




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Web Fig. 9-14 Schematic diagram o meconium aspiration resultingrom intrauterine hypoxia.

1, Increased peristalsis and relaxation o anal sphincter.2, Meconium con-tamination o amniotic uid. 3, Meconium in the oropharynx. 4, Intra-

uterine gasping with open glottis causing aspiration o meconium andamniotic uid into etal lung. (Redrawn with permission rom Dr. J. Martinez-Burnes, Facultad de Medicina Veterinaria y Zootecnia, Universidad Autnoma de

amaulipas, Mxico.)

Meconium Aspiration Syndrome

Meconium aspiration syndrome (MAS) is an important but pre-ventable condition in human babies that originates when amnioticuid contaminated with meconium is aspirated during labor orimmediately ater birth. Te pathogenesis o MAS is basically thesame as in those o etal bronchopneumonia (see Web Fig. 9-14).Fetal hypoxia, a common event during dystocia or prolonged par-turition, causes the etus to relax the anal sphincter and releasemeconium into the amniotic uid. Aspiration o meconium canoccur directly rom aspirating contaminated amniotic uid beoredelivery (respiratory movements with an open glottis), or immedi-ately ater delivery when the meconium lodged in the nasopharynxis carried into the lung with the frst breath o air. Tis latter orm

o aspiration is prevented in delivery rooms by routine suction othe nasopharynx in meconium-stained babies. MAS is well knownin human babies, but the occurrence and signifcance in animals

Pneumonias in DogsBacterial Pneumonias of Dogs

Web Fig. 9-13Acute to subacute aspiration pneumonia, acute necro-tizing bronchopneumonia, right lung, dog.

Te cranioventral portions o the lung are frm, hemorrhagic, and necrotic.Te necrotic areas are gray-yellow-brown and are caused by gastric content,especially hydrochloric acid, discoloring, coagulating, and digesting proteinsin the tissues o the bronchi, bronchioles, and alveoli. Te red regions aroundthe necrotic oci are areas o active hyperemia in acute inammation. Tisdog had myasthenia gravis and aspirated stomach content secondary to anacquired megaesophagus (M).(Courtesy Drs. C.A. Lichtensteiger and P.J. Roady,College o Veterinary Medicine, University o Illinois.)

M

Fetal and Perinatal Pneumoniasremains largely unknown. MAS has been reported in calves, oals,piglets, and puppies. Although pulmonary lesions are generallymild and transient, aspiration o meconium can be lie-threateningor newborn babies and animal because it typically occurs in com-promised neonates already suering rom intrauterine hypoxia andacidosis. Neonatal acidosis is known to impair colostrum absorp-tion in calves. Common MAS sequels are lobular atelectasis, pul-monary hypertension, and possibly airway hyperreactivity.

In the most severe cases o MAS, ocal (patchy) atelectasis canbe observed grossly in the lung, indicating ailure o the lungs tobe ully aerated because o the mechanical obstruction and thechemical eect o meconium on pulmonary suractant (see Fig.9-34). Microscopically, meconium and keratin exoliated rom skino the etus into the amniotic uid are present in bronchi, bronchi-

oles, and alveoli and accompanied by mild alveolitis characterizedby infltration o leukocytes ollowed by alveolar macrophages andoccasional giant cells.




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SUGGESTED READINGS

Ackerman MR, Brogden KA: Response o ruminant respiratorytract to Mannheimia (Pasteurella) haemolytica: A review,MicrobInfection 2:1079-1088, 2000.

Allan GM, McNeilly F, Kennedy S et al: Isolation o porcinecircoviruslike viruses rom pigs with a wasting disease in theUSA and Europe,J Vet Diagn Invest9:3-9, 1998.

Arceneaux KA, aboada J, Hosgood G: Blastomycosis in dogs:

115 cases (1980-1995),J Am Vet Med Assoc213:658-664, 1998.Beech J: Equine respiratory disorders, Philadelphia, 1991, Lea &Febiger.

Birks EK, Durando MM, McBride S: Exercise-induced pulmonaryhemorrhage, Vet Clin North Am Equine Pract 9:87-90, 2003.

Boy MG, Sweeney CR: Pneumothorax in horses: 40 cases (1980-1997),J Am Vet Med Assoc216:1955-1959, 2000.

Braiman A, Priel Zvi: Eect o mucociliary transport relies one cient regulation o ciliary beating, Respir Physiol Neurobiol163:202-207, 2008.

Brogden KA, Lehmkuhl HD, Cutlip RC: Pasteurella haemolyticacomplicated respiratory inections in sheep and goats, Vet Res29:233-254, 1998.

Caswell JL, Williams KJ: Te respiratory system. In Maxie MG

editor: Jubb, Kennedy and Palmers pathology o domesticanimals, ed 5, vol 2, oronto, 2007, Saunders Elsevier.

Corvol H, Flamein F, Epaud R et al: Lung alveolar epitheliumand interstitial lung disease,Inter J Biochem Cell Biol41:1643-1651, 2009.

Craword PC, Dubovi EJ, Castleman WL et al: ransmission oequine inuenza virus to dogs, Science310(5747):482-485, 2005.

Davenport-Goodall CL, Parente EJ: Disorders o the larynx, VetClin North Am Equine Pract19:169-187, 2003.

De la Concha-Bermejillo A: Maedi-visna and ovine progressivepneumonia, Vet Clin North Am Food Anim Pract13:13-33, 1997.

De las Heras M, Gonzalez L, Sharp JM: Pathology o ovinepulmonary adenocarcinoma, Curr Top Microbiol Immunol275:25-54, 2003.

Delclaux C, Azoulay E: Inammatory response to inectiouspulmonary injury,Eur Respir J Suppl42:10s-14s, 2003.

Demetriou JL, Foale RD, Ladlow J et al: Canine and elinepyothorax: a retrospective study o 50 cases in the UK andIreland,J Small Anim Pract43:388-394, 2002.

Dixon PM, McGorum BC, Railton DI et al: Laryngeal paralysis:a study o 375 cases in a mixed-breed population o horses,Equine Vet J33:452-458, 2001.

Emura M: Stem cells o the respiratory tract, Pediatric RespirReviews3:36-40, 2002.

Fulton RW: Bovine respiratory disease research (1983-2009),AnimHealth Res Rev 10:131-139, 2009.

Hahn KA, McEntee MF: Prognosis actors or survival in catsater removal o a primary lung tumor: 21 cases (1979-1994),

Vet Surg27:307-311, 1998.Johnson LR, Herrgesell EJ, Davidson AP et al: Clinical,

clinicopathologic, and radiographic fndings in dogs withcoccidioidomycosis: 24 cases (1995-2000),J Am Vet Med Assoc222:461-466, 2003.

Johnson LR, Lappin MR, Baker DC: Pulmonary thromboembolismin 29 dogs: 1985-1995,J Vet Intern Med13:338-345, 1999.

Jones DJ, Norris CR, Samii VF et al: Endogenous lipid pneumoniain cats: 24 cases (1985-1998), J Am Vet Med Assoc 216:1437-1440, 2000.

King LG: Respiratory diseases of dogs and cats, Philadelphia, 2004,Saunders.

Web Fig. 9-16 Hydrothorax, pleural cavity, neonatal pig.

Te pleural cavity contains a large amount o a clear yellow transudate. Teuid in the thoracic cavity has compressed the lungs resulting in compres-sive atelectasis. Te cause o the hydrothorax could not be determined.(Courtesy Dr. V. Hsiao, College o Veterinary Medicine, University o Illinois.)

THORACIC CAVITY AND PLEURA

Circulatory and Lymphatic Disturbances

Hydrothorax

Web Fig. 9-15 Metastatic hemangiosarcoma, lung, dog.

Note the red to dark red bulging masses randomly distributed throughoutall lobes o the lung. (Courtesy College o Veterinary Medicine, University oIllinois.)

Neoplasms of the Lungs

Secondary Neoplasms of the Lungs




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Krohne SG: Canine systemic ungal inections, Vet Clin North AmSmall Anim Pract30:963-990, 2000.

Mellanby RJ, Villiers E, Herrtage ME: Canine pleural andmediastinal eusions: a retrospective study o 81 cases,J SmallAnim Pract43:447-451, 2002.

Reneiro CR: Advances in the understanding o pathogenesis, anddiagnosis and therapeutics o eline allergic asthma, Vet J(epub)2010 Elsevier.

Rice JA, Carrasco-Medina L, Hodgins et al:Mannheimia haemolyicaand bovine respiratory disease, Animal Health Res Rev 8:117-128, 2008.

Ru n DC: Mycoplasma inections in small ruminants, Vet ClinNorth Am Food Anim Pract17:315-332, 2001.

Sibila M, Pieters M, Molitor et al: Current prespectives onthe diagnosis and epidemiology oMycoplasma hyopneumoniaeinection, Vet J181:221-231, 2009.

Tacker EL: Diagnosis oMycoplasma hyopneumoniae,Anim HealthRes Rev 5:317-320, 2004.

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sushima K, King LS, Aggarwal NR et al: Acute lung injury review,Internal Med48:621-630, 2009

Ware LB, Matthay MA: Te acute respiratory distress syndrome,N Engl J Med342:1334-1349, 2000.

Wilson DW, Dungworth DL: umors o the respiratory system.In Meuten DJ, editor: Tumors in domestic animals, ed 4, Ames,2002, Iowa State Press.


Chapter 00-Repiratory Dx9

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