MISCELLANEOUS CHRONIC PNEUMONIAS

At least two chronic interstitial pneumonias of uncertain cause have been identified in cattle: fibrosing alveolitis and bronchiolitis obliterans. These are typically chronic diseases of individual animals.

Fibrosing Alveolitis

Fibrosing alveolitis is, by definition, a chronic disease of unknown and possibly multiple causes, characterized by diffuse inflammation of the lung beyond the terminal bronchiole. Approximately 50% of cases produce positive results for precipitating antibody to M. faeni, and it is possible that these cases represent chronic farmer’s lung whereas others (that have negative M. faeni results) may be the chronic stage of hypersensitivity to other unidentified antigens.460 Field investigations have failed to substantiate any connection between fibrosing alveolitis and repeated episodes of ARDS such as ABPEE. Furthermore, recovery from a single dose of 3-MI does not result in lesions typical of fibrosing alveolitis. However, repeated doses of 3-MI at weekly intervals experimentally cause fibrosing alveolitis—like lesions.460 Fibrosing alveolitis occurs in individual adult cattle (usually over 6 years of age) in both housing and pasture conditions. The history is usually that of a chronic progressive respiratory disease several weeks to 2 years in duration. Affected cattle remain bright and alert and continue to eat until the terminal stages of cor pulmonale and heart failure intervene. Signs include marked weight loss; consistent coughing; tachypnea (40 to 70 breaths/min); very marked hyperpnea, even at rest; and dyspnea after mild exertion. Auscultation may reveal crackles in the rostral-ventral lung field and widespread wheezes. Fever is not apparent. The primary differential diagnoses to consider are other chronic respiratory conditions of individual adult cattle. Chronic suppurative pneumonia and metastatic pneumonia can usually be differentiated from fibrosing alveolitis by careful physical examination and detection of depression, anorexia, shallow respiration, thoracic pain, and hemoptysis. ARDS caused by feed-associated pneumotoxins and lungworms are typically group problems, with at least some severe cases in the group. Differentiation from EAA may be impossible if the group outbreak nature of farmer’s lung is not apparent; in fact, at least some cases of fibrosing alveolitis may represent chronic farmer’s lung. At necropsy the lungs are very pale, firm, and heavy throughout. Scattered lobules are gray-red, slightly collapsed, and edematous. Thick mucus may be found in the airways, and there is frequently right ventricular hypertrophy as a result of cor pulmonale. Histologic changes are diffuse and include interalveolar fibrosis and infiltration with plasma cells, lymphocytes, mast cells, and interstitial cells; obliteration of alveolar spaces; mononuclear exudates in alveoli; alveolar epithelial hyperplasia; bronchitis; and bronchiolitis. The epithelioid granulomas characteristic of acute farmer’s lung are absent.460 No treatment exists, and the lesions are irreversible.

Bronchiolitis Obliterans

Bronchiolitis obliterans is a chronic respiratory condition of yearling or young adult cattle characterized by a deep infrequent cough, tachypnea, hyperpnea, and an exaggerated expiratory effort. There is no fever. The cause is unknown; the condition is speculated to be a sequela to viruses (RSV, PI3, IBR), parasites such as Dictyocaulus viviparus, or hypersensitivity pneumonitis. The lungs appear grossly normal at necropsy, except that they do not collapse. Histologic examination reveals extensive bronchiolitis and bronchiolitis obliterans, with epithelium-covered polyps with a connective tissue core projecting into and obstructing the lumen.460

PARASITIC BRONCHITIS AND PNEUMONIA

ANNE M. ZAJAC

Two parasites in cattle (D. viviparus and aberrant migration of Ascaris suum larvae) and three in sheep and goats (Dictyocaulus filaria, Protostrongylus rufescens, and Muellerius capillaris) may cause respiratory disease characterized by alveolar and interstitial pneumonia. Other species of lungworms also parasitize small ruminants but are less widely distributed throughout the world.

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Lungworms of Cattle

Dictyocaulus Viviparus

Definition and Etiology

D. viviparus is a trichostrongylid nematode parasitizing the bovine trachea and bronchi. Adult worms may reach 8 cm in length. The lifecycle of D. viviparus is direct. Adult female worms in the trachea and bronchi lay eggs that hatch almost immediately. First-stage larvae are coughed up, swallowed, and passed in the feces. Larvae develop in a minimum of 5 days (usually longer under normal environmental conditions) to the infective third stage, migrate onto grass, are ingested, penetrate the intestine, and move to the mesenteric lymph nodes, where they molt. Fourth-stage larvae travel through lymph and blood to the lungs and tend to lodge in the pulmonary capillaries of the ventral parts of the caudal lobes. Approximately 7 days after ingestion, they enter the alveoli and molt to the fifth (final) stage in the bronchioles several days later. Egg-laying adults are present in the bronchi 21 to 28 days after ingestion of larvae. Clinically evident infection with D. viviparus typically occurs in young, nonimmune stock (less than 12 months old) or in previously unexposed yearling or adult cattle. A reinfection syndrome can also occur when previously infected (and therefore immune) adults are subjected to massive challenge with infective larvae.529,530

Clinical Signs and Differential Diagnosis

Primary infection with D. viviparus can be broken down clinically into a prepatent phase, a patent phase, and a postpatent phase.531 No signs are associated with the initial penetration of larvae until they reach the alveoli, where they provoke an eosinophilic exudate that blocks small airways. During the prepatent phase (approximately 7 to 25 days after ingestion), there is a gradual onset of coughing and tachypnea (35 to 60 breaths/min), which becomes increasingly apparent from day 14 to day 25. The severity of signs in this stage is proportional to the number of larvae ingested, the rate of ingestion, and the proportion reaching the lungs. Severe illness and death can occur in cases of heavy infection. In the patent phase (approximately 25 to 55 days after ingestion), a parasitic pneumonia with consolidation develops in the ventral areas of the caudal lung lobes as a result of aspiration of eggs and larvae into these areas. Tracheitis and bronchitis associated with the adult worms also develop. Clinical signs vary in severity and range from intermittent to marked coughing, tachypnea (respiratory rate may increase to more than 70 breaths/min), dyspnea, anorexia, and weight loss. Fever may develop with secondary bacterial infection. Auscultation reveals harsh breath sounds and widespread crackles and wheezes. In severe cases animals may exhibit open-mouth breathing, extended head and neck, protrusion of the tongue, and an expiratory grunt. Death is common in untreated, heavily infected animals.530,531

Recovery begins in the late patent phase, and the signs gradually resolve, sometimes over several months. During the postpatent phase (about days 55 to 90), adult parasites are expelled by a self-cure phenomenon. In approximately 25% of severe cases the postpatent phase is characterized by a sudden exacerbation of dyspnea at days 45 to 60 that is often fatal, after secondary bacterial infection or alveolar epithelialization.529,531 The reinfection syndrome occurs 14 to 16 days after adult cattle are placed on heavily contaminated pastures. Signs include acute hypogalactia; severe, frequent coughing; marked tachypnea; and depression. Auscultation reveals only harsh breath sounds with no crackles or wheezes.529,531

Differential diagnosis should be straightforward if both the clinical signs and epidemiologic characteristics of the disease are taken into account, especially in endemic areas. This is a disease of groups of cattle at pasture, typically in late summer or fall in northern temperate climates; the situation thus resembles ABPEE, which differs in clinical signs (i.e., less coughing and fewer adventitious lung sounds). The signs associated with lungworm infection are reminiscent of those of farmer’s lung, which occurs in quite different circumstances. In typically nonendemic areas, outbreaks associated with climatic changes are frequently mistaken for acute bacterial bronchopneumonia.529

Diagnosis

Larvae of D. viviparus are large (390 to 450 μm × 25 μm) and slow moving and contain dark food granules. They are best detected by the Baermann test532 and may also be seen on a transtracheal wash. It is best to check several animals in the herd. Rectal fecal samples are preferred for parasite examination because samples picked up off the ground may contain free-living nematodes that can be difficult to differentiate from lungworm larvae. Recovery of larvae from fecal samples is substantially diminished if the sample is stored at room temperature for more than a few hours. If the Baermann test cannot be set up soon after fecal collection, the sample can be safely refrigerated for 24 to 48 hours without serious larval loss.533 No larvae are detected in the reinfection syndrome. In some European countries an ELISA technique that can detect adult infection is also available534 (Cypress Diagnostics, Langdorp, Belgium). An increase in eosinophils in the peripheral blood may also occur approximately 2 weeks after infection, peaking at 4 to 7 weeks after infection.535

Pathophysiology

Once the fourth-stage larvae enter the alveoli, they incite an eosinophilic exudate that blocks small bronchi and bronchioles, resulting in atelectasis and causing the cough and tachypnea of the prepatent phase. As these larvae mature and migrate up the airways, these lesions may resolve. However, the adult worms produce an inflammatory response in the larger airways, and aspirated eggs and larvae cause a marked macrophage and giant cell response, with consolidation of the ventral caudal lobes; these lesions are the cause of the signs in the patent phase. At any point in the pathogenesis (prepatent, patent, or postpatent stage), complications may occur that account for acute exacerbation and death. These complications are as follows:

image Development of pulmonary edema caused either by heart failure or by extensive alveolar epithelial damage and hyaline membrane formation
image Severe interstitial emphysema from the severe dyspnea
image Alveolar epithelial hyperplasia
image Secondary bacterial infection, which is actually relatively uncommon

In the reinfection syndrome the immune response cannot completely overcome a massive challenge, and a small number of larvae reach the lungs. The signs are caused by the immune reaction to the migrating larvae. Lymphoid nodules develop around dead larvae in the bronchioles.529-531

Epidemiology

Parasitic bronchitis and pneumonia in cattle occur most often in temperate areas with high rainfall or intense irrigation. In the United States, lungworm infection is widely distributed, but disease outbreaks are uncommon, probably because periods of dry summer weather limit larval survival and accumulation on pasture.530 In the southern United States, lungworm transmission is probably greatest in the cool winter months,536 whereas autumn is probably the season of most intense transmission in the northern United States.537,538

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Dictyocaulus infections have been studied extensively in Europe, where the parasite is an important pathogen. Disease outbreaks occur most frequently in first season grazing animals. If large numbers of larvae are present on pasture at spring turnout of calves, disease may develop at that time. Often, however, levels of pasture larvae are too low to cause disease, but lead to low-level primary infections in calves that result in the accumulation of additional larvae on pasture. This second wave of infection may lead to clinical lungworm disease when the primary infection did not produce adequate levels of immunity. If infection levels remain low, disease may not be observed until a third generation of parasites occurs. Immunity develops beginning about 10 days after heavy infection, and patent infections usually persist for only a few months. In the absence of continued exposure to parasites, immunity to reinfection will begin to decline after several months.530,539

Older animals without immunity also develop lungworm disease when exposed to high levels of pasture contamination with larvae. This can occur when animals from a nonendemic area are moved to an endemic area. In recent years outbreaks of primary parasitic bronchitis have become an important cause of respiratory disease in adult dairy cows in Europe. The increased prevalence of disease in this older age-group is likely the result of decreased levels of immunity after the widespread use of powerful suppressive anthelmintic regimens in first and second season grazing animals. Other management factors, such as isolation of calves from adult carrier animals and increased movement of livestock, may also contribute to a decline in levels of immunity.534,540 Beef animals are less often affected than dairy cattle because management practices are more extensive and levels of infective larvae on pastures are generally lower.530 The reinfection syndrome occurs in immune adult animals when, for example, immune cows are placed on a pasture previously contaminated very heavily by calves with patent disease.529,530

In northern temperate climates, the infection is carried from year to year by overwintering of larvae on pasture in some areas, by spreading of manure from infected housed calves in the spring, and by carrier cattle. Lungworm larvae also may be inhibited in the lungs of calves in winter (as with Ostertagia species in the abomasum) and mature in the spring.529,531

Necropsy Findings

In the prepatent phase the lungs are largely normal, with a few atelectatic lobules in the ventral caudal lobes; adult worms are not present until late in this phase, but larvae may be detectable by microscopic examination of smears of bronchial exudate. In the patent phase there is usually bilaterally symmetric red consolidation of the ventral caudal lobes. Adult worms can be recognized on necropsy by their relatively large size and location in the trachea and bronchi. The lesions of the postpatent phase are similar, but no adult worms or larvae are present. In those patients that die of an acute exacerbation, there is extensive pulmonary edema and emphysema, with hyaline membranes and alveolar epithelial hyperplasia.

In the reinfection syndrome the pulmonary lymphoid nodules may be 3 to 4 mm in diameter and thus grossly visible as raised, gray-red to greenish yellow nodules under the pleura. Initially these are composed of a core of eosinophilic parasitic debris surrounded by macrophages, multinucleated giant cells, hyperplastic bronchiolar epithelium, eosinophils, and plasma cells. The lesions eventually mature to lymphoreticular nodules with a germinal center. There is also greenish mucus in the airways and a greenish discoloration to the tissues, both caused by eosinophil infiltration. There is no edema or emphysema, and the rare lungworms that may be found are small and stunted.529

Treatment, Prognosis, Prevention, and Control

D. viviparus infection can be treated with a number of bovine anthelmintics available in the United States and other countries (Table 31-12). Macrocyclic lactone products also have residual efficacy against D. viviparus.541 Animals with only cough and tachypnea respond well, whereas those with dyspnea, fever, anorexia, and depression have a more guarded prognosis; some of these can be expected to die or remain chronically unthrifty.529 Control (see also Chapter 49) involves appropriate pasture management and the strategic use of anthelmintics to prevent buildup of infection in the herd and on pastures. Several strategic deworming programs have been developed in Europe, which effectively suppress lungworm infection throughout the grazing season. These programs include use of ivermectin at 3, 8, and 13 weeks after turnout and use of doramectin or eprinomectin at 0 and 8 weeks. Use of an oxfendazole pulse release bolus (not available in the United States) also provides strategic treatments. Alternatively, use of a continuous-release ivermectin or fenbendazole bolus (not available in the United States) will prevent development of lungworm infection during its period of efficacy.540 A long-acting moxidectin injection product that provides protection from lungworm infection for 120 days is also now available in some countries.542 Anthelmintic treatment with moxidectin or fenbendazole followed by movement of calves to safe pasture 9 weeks after turnout was also effective in controlling lungworm.543 None of these control programs have been extensively tested under the variety of grazing conditions found in the United States.

Table 31-12 Anthelmintics Approved for Treatment of Dictyocaulus viviparus in the United States

image
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Despite concern that suppressive programs may limit exposure to larvae and interfere with the development of immunity to lungworm, several studies conducted in Europe have shown that stimulation of the immune response still occurs, although relative levels of immunity may vary with different management systems and annual variation in the intensity of lungworm challenge.534,544-546 In Europe, methods of control also include an effective irradiated larval vaccine, although use of the vaccine has diminished with the introduction of suppressive anthelmintic programs. Delay of spring turnout is an adjunct to control but should not be relied on as the sole means of control.545 A targeted selective deworming program was successful in controlling lungworm infection in a dairy herd in Sweden. Only cattle testing positive for lungworm by the commercial ELISA test were treated at each sampling date.547

ASCARIS SUUM

Cattle exposed to large numbers of A. suum eggs in areas contaminated by swine may have an interstitial pneumonia. Animals are typically affected approximately 10 days after exposure. Signs include depression, anorexia, fever, tachycardia, tachypnea, dyspnea with an expiratory grunt, variable coughing, ruminal stasis, and bloat. Auscultation of the lungs reveals increased breath sounds without adventitious sounds. Some deaths may occur. Differential diagnosis is difficult. Differentiation from the other interstitial pneumonias depends more on history of exposure to the causative agents (e.g., lush pastures, moldy sweet potatoes, P. frutescens, toxic gases, moldy hay). Differentiation from viral pneumonia (such as that caused by RSV) and D. viviparus reinfection syndrome requires necropsy and demonstration of larvae. Ascarid larvae have characteristic lateral alae in histologic sections. Patent D. viviparus infection can be differentiated by Baermann examination of the feces. In fatal cases the lung lobes are firm and mottled blue, red, and gray. The cut surface oozes thin yellow exudate. There is emphysema in the dorsal diaphragmatic lobes and subpleural hemorrhage with neutrophil infiltration and necrosis of bronchiolar and alveolar epithelium. In chronic cases the cellular infiltrate is lymphocytic, and there are proliferation of bronchiolar epithelium and peribronchial fibrosis. Recommended treatments include corticosteroids (dexamethasone, 0.04 mg/kg IM or IV, or prednisolone 1 mg/kg IM or IV daily) and antibiotics to control secondary bacterial infection.548 Clinical signs resolved after treatment with oxfendazole in one outbreak of suspected A. suum migration.549 Cattle should not be exposed to areas heavily contaminated by swine.

Lungworms of Sheep and Goats

Three species of lungworms are of primary importance in sheep and goats: D. filaria and the two metastrongylid nematodes, M. capillaris and P. rufescens. Other genera of metastrongylid lungworms of minor pathogenic importance in sheep and goats include Cystocaulus, Spiculocaulus, and Neostrongylus. These parasites are rare or absent in North America.550

DICTYOCAULUS FILARIA

D. filaria has a lifecycle essentially identical to that of D. viviparus; the time from ingestion to the appearance of larvae in the feces is about 4 weeks. Mainly young animals are affected, but disease can also occur in adults. Dyspnea, tachypnea and coughing, and loss of condition occur in clinical cases.550,551 Differential diagnosis includes the progressive viral pneumonias. Diagnosis is made by finding larvae in fresh feces by the Baermann test.532 Samples should be tested soon after collection because larval recovery is significantly reduced in stored samples.533 Larvae of D. filaria are similar in size and appearance to those of D. viviparus but also have a distinctive knob on the anterior end. The pathogenesis is similar to that of D. viviparus (see earlier discussion). The adults are found largely in the dorsal-caudal regions of the diaphragmatic lobes. Bronchitis and peribronchitis, along with cone-shaped areas of pneumonia and atelectasis, and emphysema are present. Secondary bacterial infections may also occur.550,551 Levamisole (8 mg/kg), fenbendazole (5 to 10 mg/kg), ivermectin (0.2 mg/kg PO),551 and moxidectin (0.2 mg/kg, PO or SC)552-554 can be used for treatment. When outbreaks occur, all animals should be treated and moved to fresh pasture when possible. Clinical D. filaria infections seem to occur most frequently in areas with warm climates. In temperate areas the parasite overwinters either as arrested larvae in ewes or as larvae on pasture.550

MUELLERIUS CAPILLARIS

M. capillaris is probably the most common of the lungworms of sheep and goats. Infection is more pathogenic in goats than in sheep. Surveys in Maryland and Georgia detected the parasite in 64% and 68% of goats, respectively.555,556 The lifecycle is indirect. First-stage larvae are coughed up, swallowed, and passed in the feces. These larvae are relatively resistant and may survive for several months in the environment. After penetration of an appropriate molluscan intermediate host, the infective third stage develops in a minimum of about 12 days, is ingested with the snail, and passes to the mesenteric lymph nodes. The fourth stage larva proceeds to the lungs, where adults develop in the alveoli. The prepatent period of M. capillaris infection is about 6 weeks.557 Although many infections are subclinical, clinical disease may develop. Goats appear to be more likely than sheep to develop unthriftiness, coughing, and dyspnea. Infection may also predispose to secondary bacterial infection.551,558 The difference in clinical signs between sheep and goats probably results from a difference in the pathogenesis of infection. The adult worms live in the pulmonary parenchyma, particularly the subpleural tissue. In sheep they produce grayish nodules typically 2 to 3 mm in diameter. On palpation at necropsy, these nodules have been described as feeling like “lead shot.”557 Each nodule contains a worm and necrotic leukocytes and pulmonary tissue surrounded by a connective tissue wall and giant cells.550 They may calcify or become secondarily infected with bacteria. Reports of lesions in goats indicate that M. capillaris causes an interstitial pneumonia. The lungs are resilient and firm, fail to collapse, and have tan, yellow, or gray patches located especially in the dorsal diaphragmatic lobes. The histologic lesion in goats is a diffuse thickening of alveolar septa, with a mononuclear cell infiltrate and alveolar epithelial hyperplasia that extends far beyond the area immediately around the parasite. The local reaction around the worm is quite variable and does not appear to produce the nodules seen in sheep.558 Diagnosis is made by Baermann examination of the feces. The larvae are smaller than those of D. filaria and have a kink at the end of the tail with a characteristic subterminal accessory spine.532

Several anthelmintics have been used in the treatment of M. capillaris infections. Moxidectin (0.2 mg/kg in oral or injectable formulation) is effective in treating sheep infected with M. capillaris and other small lungworms (Cystocaulus ocreatus, Neostrongylus linearis, and P. rufescens) and may be equally effective in goats.559 Although larvae may initially disappear in the feces after treatment, they often reappear in fecal samples again after 1 to 2 months, either because anthelmintics are ineffective against immature worms and/or because of resumption of development by inhibited larvae.559 Treatments that appear to eliminate adult parasites in goats include fenbendazole (15 to 30 mg/kg),557,558,560-562 albendazole (10 mg/kg),562 oxfendazole (7.5 to 10 mg/kg),563 and ivermectin (0.3 mg/kg).560,564M. capillaris is largely resistant to levamisole.551 Better control of immature or inhibited larvae with fenbendazole was achieved by administering the drug (1.25 to 5 mg/kg) for 7 to 14 days, although a regimen of 1 week on/1 week off/1 week on appeared to provide the most effective treatment. Albendazole (1 mg/kg) PO daily for 7 to 14 days was also effective.562 Possible teratogenic effects of extended benzimidazole treatment in goats have not been thoroughly investigated, and albendazole should be used cautiously in the first 35 days of pregnancy.560 Administration of ivermectin (0.3 mg/kg) or fenbendazole (15 mg/kg) two or three times at 35-day intervals has also been suggested for treatment.551 Control methods include avoiding wet pastures and treating animals before the start of the grazing season to reduce infection levels in the intermediate host.551

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PROTOSTRONGYLUS RUFESCENS

P. rufescens also uses molluscan intermediate hosts, and adults develop in the small bronchioles of sheep and goats.557 Most infections are probably subclinical or produce only mild signs of chronic bronchitis or bronchopneumonia with nasal discharge and cough. Occasionally P. rufescens may produce severe or even fatal disease.565 The diagnosis of Protostrongylus species infection is made by finding larvae in the feces with the Baermann technique. The larvae are similar to those of Muellerius except Protostrongylus larvae lack the subterminal accessory spine on the tail.532 Fenbendazole, levamisole,565 and moxidectin559 can be used for treatment at the dosages used for Dictyocaulus. Other macrocyclic lactone products may also be effective but have not been tested. Control strategies are identical to those for M. capillaris. Few cases of infection have been reported in the United States, but nonspecific clinical signs, presence of subclinical carriers, and need for a special diagnostic technique may produce an underestimation of the prevalence of P. rufescens infection in sheep and goats.565

PROGRESSIVE BACTERIAL AND VIRAL PNEUMONIAS OF SHEEP AND GOATS

JEANNE LOFSTEDT

Chronic progressive pneumonias are diagnosed with some frequency in mature small ruminants. In sheep, OPP and C. pseudotuberculosis–induced mediastinal lymph node and lung abscesses are the chief causes of chronic progressive pneumonia. Chronic progressive pneumonia in goats is commonly associated with the pneumonic form of CLA, and less frequently with CAE virus (CAEV)–induced lung lesions. Differential diagnoses that should be entertained in sheep and goats exhibiting signs of chronic pneumonia include OPA, chronic suppurative pneumonia, verminous pneumonia, mycotic pneumonia, tuberculosis, and pulmonary neoplasia.

OVINE PROGRESSIVE PNEUMONIA (MAEDI-VISNA)

Definition and Etiology

OPP and maedi-visna (MV) are North American and European names for slow viral diseases of sheep characterized by chronic, progressive, debilitating pneumonia, wasting, and indurative mastitis.566-568 Synonyms are Marsh’s progressive pneumonia, zwoegerziekte, la bouhite, and Graaff-Reinet disease.566,567 The OPP virus (OPPV) and MV virus (MVV) are nononcogenic exogenous retroviruses that belong to the subfamily Lentiviridae.569 These enveloped, single-stranded RNA viruses contain the enzyme RNA-dependent DNA polymerase (RT). With this enzyme they use cellular machinery to transcribe a segment of DNA from a template of single-stranded viral RNA; the DNA strand or provirus is then incorporated into the host genome. Close similarity of causal viruses, clinical signs, and lesions produced in tissues permits discussion of OPP and MV as a single disease entity.567 The ovine lentiviruses (OvLVs) are also related to the CAEV of goats, but differences have been demonstrated through nucleic acid hybridization studies.570

Clinical Signs and Differential Diagnosis

Conditions in sheep attributed to infection with OvLV include progressive emaciation (“thin ewe syndrome”), progressive respiratory failure, indurative lymphocytic mastitis (“hard bag”), posterior paresis, chronic nonsuppurative arthritis, and vasculitis.566-571 In North America progressive pneumonia and aseptic mastitis are the most common clinical manifestations.567 Natural disease is usually observed in 2- to 3-year-old sheep, but adult sheep of any age can be affected.567,568,570 Emaciation despite a good appetite is one of the earliest symptoms. Clinical signs of progressive pneumonia include exercise intolerance, tachypnea, expiratory dyspnea, open-mouth breathing, and occasionally a nonproductive cough. Thoracic auscultation reveals increased breath sounds, but crackles and wheezes are inapparent. Pyrexia and purulent nasal discharge usually indicate the presence of secondary bacterial pneumonia. Affected ewes give birth to small, weak lambs. Death from anoxia or secondary bacterial infection occurs within 6 to 12 months of first appearance of signs.

Chronic pneumonias of sheep that have to be differentiated from OPP include chronic bronchopneumonia caused by M. (Pasteurella) haemolytica, OPA, verminous pneumonia, and pulmonary and lymph node abscesses caused by C. pseudotuberculosis.566,569 Thoracic radiographs, culture of tracheal wash material, and fecal examination by the Baermann technique are useful for antemortem differentiation. Gross and histopathologic evaluations of pulmonary tissues obtained at necropsy are useful for diagnosis of a flock problem.

Diagnosis

Hematologic changes in sheep with OPP are nonspecific and may include lymphocytosis early in the course of disease and mild hypochromic anemia and hypergammaglobulinemia in advanced disease.570 A presumptive diagnosis of OPP can be made on the basis of clinical signs, lack of response to treatment, and serologic test results. Currently available serologic tests are run by different laboratories using different techniques, making comparisons difficult. The serologic tests commonly used to detect antibodies to OvLV in serum are the AGID test and ELISAs.566-568 The simplicity and low cost of the AGID test makes it the test of choice for eradication programs.566,572 Several authors have suggested that ELISA tests are more sensitive than the AGID test.566,572,573 However, in a study comparing the AGID test with 2 recombinant ELISA tests the AGID test was found to have a specificity of 100% and a sensitivity of 11% 2 weeks postinfection, and 100% 5 weeks postinfection.566 In comparison, ELISA tests directed against the OvLV core protein or the OvLV transmembrane protein had mean sensitivities of 88% and 86%, respectively, and mean specificities of 95%.566 ELISA tests may produce false-negative results in recently infected animals as they detect IgG rather than IgM.566 Virus isolation can be used to definitively identify OvLV-infected animals.566,569 Virus isolation, which is time-consuming and expensive, is accomplished by coculture of infected fresh or frozen tissue with indicator cell lines. In culture, retroviruses form characteristic multinucleated syncytia.570 Viral antigens can be detected in these syncytia by use of immunofluorescent staining.570 PCR testing has been used as a research tool to demonstrate OvLV DNA in clinical specimens from naturally infected sheep.574

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Pathophysiology

OvLVs are thought to gain access to the body via the oral or respiratory route. Infection is then established in the monocyte or macrophage cell line and spreads via these infected cells to the lungs, lymph nodes, choroid plexus, spleen, bone marrow, mammary glands, and kidneys.570 The virus is able to persist in the face of humoral and cellular immunity through (1) latent infection of host cells by DNA provirus, (2) long-term nonproductive infection of blood monocytes (virus replicates only on differentiation of monocytes into macrophages), and (3) virus mutation with emergence of new antigenic variants that are not neutralized by preexisting antibody.570

Epidemiology

The seroprevalence of OPP in cull ewes in the United States ranges widely and increases with advancing age.566 With the exception of West Texas, with an infection rate of 0.5%, serologic surveys in cull ewes in other states have revealed infection rates of 30% to 67%. The low seroprevalence in Texas has been attributed to the hot dry climate and extensive grazing practices.570 Limited studies in large mixed-breed flocks have provided evidence that some sheep breeds may be more resistant to infection than other breeds.566 Additional research is required before a particular breed or line of sheep can be viewed as resistant to OvLV infection. The lung and mammary gland are believed to be the main sources of excreted virus.566 Studies conducted in Europe and Iceland have shown that transmission from the ewe to her lambs commonly occurs through the ingestion of infected colostrum and milk.566 In other studies, close confinement of diseased or seropositive sheep with healthy or seronegative sheep resulted in disease or seroconversion in the previously healthy or seronegative animals; these infections were presumed to have occurred via the respiratory route.566 OvLV transmission has been shown to occur through fecal contamination of drinking water.566 It is likely that other fomites (saliva, nasal discharge, urine) contaminating feed and/or water also contribute to the spread of disease.507 Transmission through the uterine wall, or via germ cells, can occur but is rare.566

Necropsy Findings

Lesions may develop in any or all of the following tissues of OPPV-infected sheep: lungs and regional lymph nodes, brain, joints, mammary glands, and blood vessels.567 Changes are most obvious in the lungs, which do not collapse on opening of the thorax.569,570 Vertical rib impressions may be seen on the exterior lung surface. Affected lungs are heavy and have a mottled to uniform pink-brown to gray-blue discoloration. Secondary bacterial pneumonia may cause anterior-ventral pulmonary consolidation. Tracheobronchial and mediastinal lymph nodes are markedly enlarged, bulge on cut surfaces, and are homogeneous, gray-white throughout. Histologic examination reveals a diffuse lymphoproliferative pneumonia characterized by prominent lymphoid follicle formation adjacent to bronchioles and small vessels; discrete nodules of lymphocytes, unrelated to vessels or airways, are also found in the lung parenchyma.567-570 Lymphocytes, plasma cells, and macrophages infiltrate into interalveolar septa, and hyperplasia of alveolar epithelium and terminal bronchial smooth muscle may be seen.

Treatment and Prognosis

OPP is not treatable. Antibiotics can be used to control secondary bacterial pneumonia, but most sheep die within a year of first exhibiting clinical signs.567,568

Prevention and Control

OPPV is difficult to eradicate from a flock once infection is established.570 Control methods include (1) a “test-and-cull” practice and (2) isolation of infected adults and artificial rearing of their offspring.567 With the first method, all sheep are tested annually for antibody, and seropositive animals and their progeny younger than 1 year of age are culled or isolated from the negative flock; culling is preferred because of the danger of cross-contamination. New additions should be seronegative and originate from seronegative flocks. Annual testing should be performed until two consecutive negative herd test results are obtained to be reasonably confident that the flock is virus free. With the second method, progeny are removed from their dams before they nurse and are fed cow’s colostrum and raised in isolation. The clean herd should be kept isolated from infected sheep and goats and from humans and equipment in contact with infected sheep. Herd additions and annual testing should be handled as described for method one.

OVINE PULMONARY ADENOCARCINOMA

Definition and Etiology

OPA (sheep pulmonary adenomatosis or jaagsiekte) is a naturally occurring retrovirus-induced bronchioloalveolar carcinoma of sheep and, rarely, goats that has been associated etiologically with a type B/D retrovirus (JSRV).575,576 OvLVs and herpesviruses have been isolated from OPA tumors; however, they are not consistently present577 and do not induce OPA when inoculated experimentally.578,579 One theory is that these viruses act as cofactors in tumor induction. Defining the role of JSRV in OPA has been complicated by the presence of 15 to 20 endogenous jaagsiekte retroviruses (enJSRVs) that are stably integrated into the genomes of sheep and goats.580,581 Recent research has indicated that exogenous JSRV is likely not of endogenous origin. There has been speculation that the endogenous viruses may modify the genome of exogenous JSRV, either by inducing the expression of an oncogene or by inactivating a tumor suppressor gene.576 Sequence analyses of exogenous JSRV and enJSRV suggest that endogenous viruses do not directly contribute to the pathogenesis of OPA through large-scale recombination events, but small-scale recombination or complementation of gene function has not been definitively excluded.580 There has been speculation that expression of enJSRV in the fetal or neonatal period may influence expression of OPA through induction of immunologic tolerance.580

Clinical Signs and Differential Diagnosis

OPA usually affects mature sheep between 2 and 4 years of age, although lambs as young as 3 months of age have been diagnosed with the disease.576 Clinical manifestations include progressive weight loss, exercise intolerance, tachypnea, dyspnea, occasional cough, and crackles and wheezes on thoracic auscultation. In many cases, presence of abundant watery nasal discharge can be demonstrated by raising the rear limbs and lowering the head of the affected sheep (“wheelbarrow test”).576 Appetite and rectal temperature are usually normal unless secondary infection and intercurrent disease are present. Sheep with OPA typically succumb within a few weeks to months after first exhibiting clinical signs.

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Diagnosis

The only reported laboratory abnormality in sheep with OPA is hypergammaglobulinemia. Some researchers have demonstrated the utility of serologic assays to identify OPA-infected sheep, but other investigators have been unable to demonstrate antibodies to JSRV in the sera of affected sheep.576 PCR tests, capable of demonstrating viral nucleic acids of endogenous JSRV tissues in OPA-infected animals, have been developed.575

Epidemiology

OPA has been reported in many countries in Europe, Africa, and Asia but is a rare occurrence in sheep in Australia and New Zealand.575,576 The prevalence of OPA varies among countries in which the infection occurs; it is endemic in Scotland, Peru, and South Africa, where annual losses range from 2% to 10%. In contrast, OPA is infrequently diagnosed in the United States and Canada, where totals of 11 and 43 cases, respectively, have been reported.575,576

OPA has been reproduced experimentally by intratracheal inoculation of lung homogenates or pulmonary lavage fluids obtained from infected animals.582 Lambs between birth and 5 weeks of age have been shown to be more susceptible to experimental infection than 10-week-old lambs.582 This age-related susceptibility to OPA suggests that natural virus transmission occurs in the neonatal period. Aerosol transmission and contamination of feed and water by respiratory secretions are likely methods of disease spread, particularly in confined sheep.

Necropsy Findings

Lungs of OPA sheep are heavy (two to three times normal weight) and exude clear fluid from the cut surface. The trachea and bronchi often contain clear, foamy fluid. Large, firm, gray masses are commonly encountered in the cranioventral regions of one or both lungs. Smaller (1- to 2-cm) nodules are occasionally visualized in the caudodorsal lung regions.576 Metastasis to regional lymph nodes occurs in approximately 10% of cases, causing pulmonary lymph node enlargement.583 Metastases to cardiac and skeletal muscles are infrequently reported.583 Some cases of OPA are complicated by secondary acute or chronic bacterial pneumonia.

OPA is classified by the World Health Organization (WHO) as a bronchioloalveolar carcinoma arising from alveolar type II pneumocytes or nonciliated bronchiolar cells.583 Neoplastic masses consist of columnar or cuboidal cells arranged in an acinar or papillary pattern. Some tumors are surrounded by areas of fibroplasia.

Treatment and Prognosis

There are no known treatments for this disease. Antibiotics may prolong the life of OPA-affected sheep through control of secondary bacterial pneumonia.576

Prevention and Control

Recently a PCR for JSRV, performed on peripheral leukocytes and tissues of naturally infected sheep, demonstrated that this test could detect virus in live sheep before the onset of clinical disease.575 This may hold promise for instigation of test-and-cull programs in the future. OPA was eradicated from Iceland by slaughtering all sheep in endemic areas.

CAPRINE ARTHRITIS-ENCEPHALITIS

CAE is a persistent lentiviral infection of goats with two major clinical presentations: leukoencephalomyelitis in kids 2 to 6 months of age and chronic, hyperplastic polysynovitis in mature goats.584,585 Mild interstitial pneumonia, which is silent clinically, is a common postmortem finding in goat kids with leukoencephalomyelitis.585 In one study, 60% of goats serologically positive for CAEV had lesions of severe chronic interstitial pneumonia at slaughter.585 Similarly, chronic interstitial pneumonia, accompanied by exercise intolerance and dyspnea, was described in dairy goats originating from herds that had clinical cases of arthritis and leukoencephalomyelitis.586 The lung lesions in these goats resembled those of OPP586,587 and were positive for CAEV. However, CAEV has been recovered from the lungs of goats with advanced arthritis but without pneumonia. In addition, goats inoculated intratracheally with purified CAEV did not develop pulmonary lesions.586 This may indicate that there is no causal relationship between CAEV and interstitial pneumonia in goats, or that the lesions have a multifactorial cause. CAE is discussed in detail in Chapter 35.

CASEOUS LYMPHADENITIS

CLA, caused by C. pseudotuberculosis (previously known as C. ovis), is a worldwide disease of sheep and goats characterized by the development of pyogranulomatous abscesses in lymph nodes and internal organs.588-591 Once established in a herd or flock CLA is difficult to eradicate. The disease responds poorly to treatment, infected animals are difficult to detect via clinical signs or diagnostic testing, and the organism tends to persists in the environment.588,589 CLA most commonly presents as an external form characterized by SC abscesses in superficial lymph nodes.588 The internal, or visceral, form of CLA manifests as internal abscesses in the mediastinal and mesenteric lymph nodes and internal organs, such as the lungs, liver, spleen, kidneys, uterus, and so on.588 Goats are more commonly afflicted with external abscesses, whereas the visceral form of CLA appears to be more common in sheep.588 Visceral CLA may be asymptomatic but is usually associated with ill thrift and significant weight loss.588,592,593 Clinical signs that may accompany abscesses in the lung parenchyma and mediastinal lymph nodes are exercise intolerance, tachypnea, dyspnea, and chronic cough. Because of the encapsulated nature of pulmonary abscesses and lack of exudate in airways, pulmonary crackles are rarely auscultated.591 Nonspecific laboratory findings in sheep and goats with CLA include leukocytosis, hyperfibrinogenemia, hyperproteinemia, and hypergammaglobulinemia; however, laboratory findings are frequently normal in animals with chronic abscesses.591 A definitive diagnosis of visceral CLA with pulmonary involvement can be achieved by demonstrating abscesses in the lungs and mediastinal lymph nodes with thoracic radiography, and by isolating C. pseudotuberculosis from a TTA.588,591 Failure to isolate the organism from tracheal wash fluid, however, does not rule out CLA as the cause of pulmonary disease. Characteristic postmortem findings of the respiratory form of CLA are one to multiple thick-walled, laminated, encapsulated, caseopurulent abscesses in the bronchial lymph nodes, mediastinal lymph nodes, and/or lung parenchyma. The synergistic hemolysis inhibition (SHI) test, which screens for antibodies directed against the phospholipase D exotoxin of C. pseudotuberculosis, was developed to diagnose early infections (before the development of SC abscesses) and to assist in the diagnosis of internal abscesses.594 Any titer higher than 1:4 is suggestive of exposure or early infection.588 Titers of 1:512 and higher are highly correlated with internal abscesses.588 In a field study the SHI test had a sensitivity of 96% in sheep and 98% in goats and detected subclinically affected animals.595 A double-antibody sandwich ELISA directed at C. pseudotuberculosis is being employed in Europe to detect subclinically affected sheep and goats and has contributed to successful disease eradication from some flocks.596 CLA is discussed in more detail in relation to the hemolymphatic system (see Chapter 37).

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OTHER PNEUMONIAS

AMELIA R. WOOLUMS

STEVEN E. WIKSE

ASPIRATION PNEUMONIA

Aspiration pneumonia is caused by inhalation of large amounts of foreign material, often liquids. It is also called gangrenous pneumonia, foreign-body pneumonia, medication pneumonia, or lipid pneumonia. The most common cause is careless drenching or passage of stomach tubes during administration of milk or liquid medication. It also occurs occasionally in pail-fed calves, animals with pharyngeal paresis, animals with necrotic laryngitis, lambs with nutritional myodegeneration, anesthetized animals, sheep that are dipped, cattle that have parturient paresis, and cattle that ingest crude oils or fuel oils.597,598 Meconium aspiration secondary to fetal distress has been recognized as a possible risk factor of neonatal calf mortality.599 The condition is characterized by a mild diffuse alveolitis that results in hypoxia and acidosis, which leads to impaired absorption of colostral antibodies and inadequate passive transfer in affected calves.

If large quantities of fluid are aspirated, death may be almost instantaneous, but generally a gangrenous bronchopneumonia develops as a result of infection and the irritating properties of the inhaled material. Affected animals exhibit depression, polypnea, dyspnea, coughing, and fever and may have putrid breath. Crackles, wheezes, and occasionally pleural friction rubs can be heard on auscultation.

Diagnosis is based on the history, sudden onset, and severe signs. Differential diagnoses include acute bronchopneumonia and septicemia. Necropsy reveals consolidation of the anterior ventral areas of the lungs. Affected areas are severely hemorrhagic in acute cases and contain suppuration and liquefactive necrosis in subacute cases.

The prognosis is guarded in all cases of aspiration pneumonia, but some animals can be saved. Antibiotics combined with antiinflammatory agents should be promptly administered, and long-term antimicrobial therapy is required. Prevention of aspiration pneumonia centers on careful administration of medication and avoidance of other risk factors that may promote inhalation of foreign materials.

MYCOTIC PNEUMONIAS

Ruminants may occasionally have pulmonary infections with C. immitis, Aspergillus species, H. capsulatum, C. albicans, and fungi of the order Mucorales.600 Coccidioidomycosis occurs in cattle and much less commonly in sheep and goats in the southwestern United States. It causes very few clinical signs in ruminants, but the occasional animal may exhibit a chronic cough and weight loss. Differential diagnoses include tuberculosis and CLA. Radiologic evaluation is helpful in establishing the presence of pulmonary masses. The diagnosis may be confirmed by culture, histologic identification of the characteristic spherules, and intradermal and complement-fixation tests. The organism is obtained from the soil and is not easily transmitted from animal to animal or to human, but nevertheless it represents a serious zoonotic disease concern. The major lesion is a granuloma with creamy pus in the bronchial and mediastinal lymph nodes. There is no treatment. Control of dust may lessen the incidence.600

Aspergillosis is a rare condition that usually occurs in housed calves, particularly in those that have had chronic antibiotic or steroid therapy or that are otherwise immunosuppressed or chronically ill. There are three forms. The acute form is characterized by a fibrinous pneumonia with fever, dyspnea, tachypnea, cough, nasal discharge, groaning, and a short course to death. The subacute and chronic forms are less severe and exhibit mainly anorexia, weight loss, and mild respiratory signs. Differential diagnoses include enzootic pneumonia, tuberculosis, and lungworms. Radiographs, transtracheal washings, histopathologic evaluation (with demonstration of branching septate hyphae), and culture of lesions help establish the diagnosis. The subacute and chronic lesions consist of multiple small, white, discrete granulomas with necrotic centers. The acute lesions are those of a severe fibrinous pleuropneumonia.600 Treatment is frequently ineffective; antifungal agents such as nystatin, amphotericin B, and ketoconazole may be tried in individual cases. Doses and withdrawal times for these drugs are not established for ruminants, and because treatment of fungal pneumonia in other species requires months of therapy, treatment is not likely to be economically feasible in most cases.

Histoplasmosis is rare in ruminants. It is a polysystemic disease with chronic emaciation, dyspnea, diarrhea, and anasarca. An intradermal delayed hypersensitivity test, culture, or histopathologic identification of the yeastlike organism helps to confirm the diagnosis. Lesions include ascites, liver enlargement, gut edema, pulmonary emphysema, and pulmonary edema with abscesses. As described for aspergillosis, antifungal therapy may be attempted but is not likely to be economically feasible.

Pulmonary candidiasis has been reported as an outbreak in a feedlot. It was characterized by a chronic pneumonia with severe dyspnea but only moderate fever; a mucopurulent, brown-streaked nasal discharge; diarrhea; a crusted muzzle; and lacrimation without conjunctivitis. Differential diagnoses should include the various upper respiratory viruses, particularly IBR and BVDV, and bacterial bronchopneumonia. The diagnosis is made by the presence of the budding yeastlike organism in smears and cultures. Lesions include lung consolidation and abscesses.600 Treatment has not been investigated.

Zygomycosis, phycomycosis, and mucormycosis are synonyms for a very rare opportunistic disease in ruminants. This is a systemic fungal infection that may affect the lung, stomach, liver, brain, and lymphatic system. Cattle with Mucorales species pneumonia exhibit tachypnea, dyspnea, nasal discharge, fever, and anorexia. The pulmonary lesions are a fibrinous pleuritis with firm, heavy, wet, mottled lungs. Histopathologic demonstration of broad aseptate hyphae in affected tissue and culture are the best means of diagnosis.600 Treatment has not been investigated.

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VENA CAVAL THROMBOSIS AND METASTATIC PNEUMONIA

Definition and Etiology

Metastatic or embolic pneumonia in cattle, also called caudal vena caval thrombosis, pulmonary thromboembolism, and embolic pulmonary aneurysm, is a distinct syndrome associated with multifocal abscessation of the lungs caused by septic thromboembolism of the pulmonary arterial system. The septic emboli arise from septic thrombi of the caudal vena cava (Fig. 31-68) or, less commonly, the cranial vena cava. Vena caval thrombi are in turn a sequela to various septic conditions such as jugular phlebitis, mastitis, metritis, foot rot, or, most often, liver abscesses secondary to rumenitis.601 A variety of bacteria may be involved; those most frequently encountered include F. necrophorum, Arcanobacterium (Actinomyces) pyogenes, staphylococci, streptococci, and E. coli.

image

Fig. 31-68 Postmortem photograph of thrombus in caudal vena cava, which leads to embolic pneumonia demonstrated in Fig. 31-69.

Photograph contributed by Feedlot Health Management Services, Okotoks, AB, Canada.

Clinical Signs

Because of its association with rumenitis, this condition is most commonly seen in feedlot cattle, but any age, breed, sex, and class of cattle may be affected. The problem is unusual in cattle less than 1 year of age. Cattle with metastatic pneumonia usually exhibit respiratory disturbance or weight loss or occasionally thoracic pain. The duration of signs is quite variable, ranging from acute respiratory distress to a chronic history of weight loss and coughing for weeks to months.602,603 The classic presentation includes tachycardia, tachypnea (respiratory rate over 30 breaths/min), expiratory dyspnea and groaning, hyperpnea, coughing, heart murmurs and pale mucous membranes (caused by anemia), widespread wheezes, epistaxis, and hemoptysis.601,602 Other signs, which are more variable, include fever, thoracic pain on deep palpation of the sternum and intercostal spaces, hepatomegaly (indicated by the ability to palpate the caudal edge of the liver in the right paralumbar fossa), SC emphysema, froth at the muzzle, and melena caused by coughing up and swallowing blood.601,602 Nonspecific accompanying signs include depression, anorexia, ruminal stasis, scant feces, and decreased milk production. In chronic cases cor pulmonale may lead to signs of right ventricular failure such as jugular distention and brisket edema.602 The combination of respiratory signs with anemia, widespread wheezes, and especially hemoptysis is generally regarded as pathognomonic for this syndrome.602 Animals usually deteriorate rapidly once hemoptysis becomes evident, and the condition is essentially 100% fatal. Many patients die suddenly with an acute episode of severe intrapulmonary hemorrhage or hemoptysis after a variable course of respiratory disease. Some of these cases in which the respiratory signs were overlooked may account for the reports of sudden death attributed to vena caval thrombosis.602 Caudal vena caval thrombosis can also lead to hepatomegaly and extensive ascites, but most of these animals also have respiratory signs.603 Sudden erosion of a large hepatic abscess into the caudal vena cava may also result in a massive embolic shower, with acute respiratory distress and death.603

In patients with the pathognomonic signs (the majority of cases), no differential diagnoses need be considered. However, many patients are examined before the onset of hemoptysis, and a few may die without exhibiting these signs.603 Differential considerations in such cases, which usually manifest as acute dyspnea, should include anaphylaxis, the various ARDSs, hypersensitivity pneumonitis, lungworms, and acute bronchopneumonia. Patients with right ventricular failure should be differentiated from those with pericarditis, lymphosarcoma, cardiomyopathy, and endocarditis.

Pathogenesis

The classic pathogenesis of this disease begins with the development of rumenitis secondary to lactic acidosis caused by highly fermentable diets such as those used in feedlots, some dairies, and some growing rations. Bacteria such as F. necrophorum and A. pyogenes are then able to penetrate the damaged ruminal epithelium and are transported to the liver in the portal drainage system, where they are filtered out and result in abscesses. If an abscess is located next to the caudal vena cava (where the vessel is closely applied to the left border of the liver), a septic thrombus may form in the vena cava as a result of infiltration of its wall by the abscess (see Fig. 31-68). Septic emboli detach from the thrombus and reach the lungs through the pulmonary arterial system. Alternatives to this classic pathway are rare; they include the following: thrombosis of the cranial vena cava from primary lesions such as jugular phlebitis, thrombosis of the caudal vena cava from other subdiaphragmatic abscesses, right-sided endocarditis, and emboli arising from other septic foci such as mastitis, metritis, and foot rot. Large emboli may block lobar or larger arteries, causing an acute crisis and death. More typically, smaller emboli lodge in arterioles, where they cause arterial thromboembolism, arteritis, endarteritis, and pulmonary abscesses (Fig. 31-69). The widespread arterial embolism also results in pulmonary arterial hypertension. Arteritis and endarteritis weaken the vessel walls and, in combination with pulmonary hypertension, lead to the formation of aneurysms. In some cases a perivascular abscess not only erodes an arterial wall to produce an aneurysm but simultaneously erodes a bronchial wall; when the aneurysm ruptures, the abscess cavity channels the blood into the bronchus, resulting in massive hemoptysis. In other cases, rupture of aneurysms results in large interstitial hematomas. Both processes result in anemia; when coughed-up blood is swallowed, melena may result. Coughing and wheezes are probably caused by blood clots in airways, peribronchial aneurysms and abscesses, and suppurative pneumonia. Pain results from dissecting aneurysms and hematomas.602

image

Fig. 31-69 Postmortem photograph of lung from feedlot steer with embolic pneumonia caused by caudal vena caval thrombosis. Note multiple dark red emboli with raised abscesses scattered throughout lung.

Photograph contributed by Feedlot Health Management Services, Okotoks, AB, Canada.

Epidemiology

Metastatic pneumonia accounted for 1.3% of necropsy diagnoses in one large feedlot survey, with a rate varying between 1.6 and 7.3 cases per 100,000 head on feed. Cases occurred year round and during all stages of fattening, although 68% of cases occurred during the first 90 days on feed.604 The case fatality rate is usually 100%.

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Necropsy Findings

Almost all patients with significant hemoptysis have a thrombus in the posterior vena cava between the liver and the right atrium. There is usually an adjacent hepatic abscess, varying degrees of venous congestion of the liver, and hepatomegaly. The lungs are large, uncollapsed, and firm. Aneurysms may occur in either lung or both. Hematomas associated with ruptured aneurysms are frequently 3 to 10 cm in diameter.604 Large blood clots may be found in the airways, aspirated blood in the alveoli, and swallowed clots in the rumen. Areas of suppurative pneumonia and multiple abscesses are present (see Fig. 31-69).

Diagnosis

The CBC may reveal anemia and a neutrophilic leukocytosis with a regenerative left shift. Hyperglobulinemia is frequently present. Serum chemical analysis may reflect chronic passive congestion of the liver, with elevation of bilirubin and liver-derived enzymes. Radiographs often reveal only an irregular increase in lung density. Small discrete densities (areas of embolic infarction and collapse); large, discrete, spheric opacities (hematomas); cavitating nodules, sometimes with gas-fluid interfaces (abscesses); bullae; and areas of consolidation may be observed in some cases.602,603

Treatment and Prevention

The prognosis is grave, so treatment is rarely indicated, and salvage is the most feasible recommendation. In valuable individuals, antibiotics and supportive therapy may be attempted. Penicillin is the drug of choice for the most common organisms involved; large doses (22,000 U/kg IM or SC twice daily as a minimum) for extended periods (weeks to months) are recommended. Long-acting oxytetracycline and florfenicol are other drugs that are effective against the bacteria likely to be involved. Supportive therapy for cases with acute severe dyspnea includes furosemide (0.5 to 1 mg/kg IV or IM once or twice daily) and flunixin meglumine (1.1 to 2.2 mg/kg once or divided twice daily). One or two doses of corticosteroids (dexamethasone at 0.05 to 0.2 mg/kg IV or IM q 24 h), or atropine (0.04 mg/kg SC daily), may be helpful in cases with severe respiratory distress.

On the basis of the assumption that rumenitis and liver abscesses are the first steps in the pathogenesis of most cases, measures to reduce the incidence of these problems are appropriate. Recommendations include slow adaptation of animals to high-energy rations and feeding of antibiotics to reduce the incidence of liver abscesses.

BOVINE TUBERCULOSIS

MICHAEL S. VANDERKLOK

Definition and Etiology

Mycobacterium bovis, know as bovine tuberculosis, is the most common cause of tuberculosis in cattle. The bacterium belongs to the M. tuberculosis (MTB) complex of organisms, which includes M. tuberculosis, M. africanum,andMycobacterium microti. Mycobacterium bovis has the widest host range of the species included in this complex.605 All species of mammals, including humans, are susceptible to Mycobacterium bovis infection, although the susceptibility of different species is variable. The importance of this organism as a zoonotic agent has led to the institution of long-standing programs for eradication of the disease, especially in developed countries. The occurrence of Mycobacterium bovis as an endemic disease in wildlife populations in mammalian species in numerous countries has created new challenges for control of this disease in domestic livestock.

The organism can affect animals of any age.606 Commonly infected livestock species include cattle, goats, swine, and cervids. Horses have been regarded as relatively resistant, but reports from New Zealand indicate that large numbers of sheep can be affected.607,608 Other Mycobacterium species occasionally cause clinical disease, especially M. avium in swine, but their main importance historically lies in the problems created for control and eradication programs through the reaction of exposed animals to the common tuberculosis tests. Disease caused by M. avium subsp. paratuberculosis (Johne’s disease) has risen as a concern in dairy cattle in recent years.

Clinical Signs and Differential Diagnosis

Signs of Mycobacterium bovis infection can be very nonspecific, and in early stages of the disease are inapparent. Infected animals may not show clinical abnormalities, yet may pose health risks to other livestock and to humans. Patients may have chronic weight loss, variable appetite, and fluctuating fevers, which may be accentuated after calving. Other signs depend on the organs involved. The route of invasion in ruminants is usually respiratory through inhalation; however, recent research and occurrences have demonstrated the capability of ingestion of contaminated feed and other forms of indirect contact to transmit the disease.609-612 Signs related to the respiratory system are relatively common and usually mild, although severe chronic infections can lead to debilitation. Progressive emaciation can occur that is unassociated with other clinical signs, and such occurrences should lead to investigation of potential Mycobacterium bovis infection.606

Specific clinical signs of the disease are determined by the initial location of bacterial introduction to the body. Respiratory signs in ruminants include a soft, moist, chronic cough resulting from bronchopneumonia. Obvious dyspnea, tachypnea, hyperpnea, and adventitious lung sounds occur only in the terminal stages. Lung sounds include crackles, wheezes, and silent spots occupied by granulomas; pleural friction rubs may occur rarely. Enlarged mediastinal nodes may cause bloat. Intestinal ulceration and diarrhea may occur, and enlarged mesenteric nodes may cause transport failure or obstructions. Involvement of retropharyngeal nodes may cause dysphagia, stridor, and salivation. Lesions occur rarely in the peripheral nodes, the reproductive tract (causing infertility, abortion, metritis, and vaginitis), and the mammary gland. Other chronic pulmonary infections should be considered for differential diagnosis (e.g., chronic suppurative pneumonia, Arcanobacterium (Actinomyces) pyogenes abscesses, C. pseudotuberculosis CLA in sheep and goats, and mycotic pneumonias). Pharyngeal lesions should be differentiated from pharyngeal trauma, abscesses, lymphosarcoma or other neoplasia, rabies, botulism, actinobacillosis, necrotic laryngitis, and laryngeal abscesses, trauma, edema, paralysis, and tumors.

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Diagnosis

Mycobacterial organisms in general precipitate a cell-mediated immune response but do not cause an immediate or sustained humoral reaction in mammalian species. The lack of specific antibody production in an exposed or infected animal has made development of serum-based laboratory tests for use in a live animal difficult. The intradermal tuberculin test has been the only clinicopathologic test routinely used. Recent advances in diagnostics have led to the introduction of tests that measure specific IFN-γ production in the blood of exposed or infected cattle.613 In the United States, accredited veterinarians are authorized to administer 0.1 mL of mammalian tuberculin purified protein derivative intradermally in the caudal tail fold (CFT) as a primary diagnostic test. The test result is read in 72 ± 6 hours as negative or suspect. State or federal veterinarians may also use a 0.2-mL cervical test in known infected herds.

Only state or federal veterinarians may use the comparative cervical test (CCT), or state or federal veterinarians and approved accredited veterinarians may use the IFN-γ test (IG), to determine the disposition of cattle determined suspect by the CFT. In the CCT, biologically balanced mammalian and avian tuberculin are injected simultaneously in two sites on the same side of the neck, 12 cm apart and one above the other. The test site is assessed at 72 ± 6 hours and results determined by comparison of the relative increase in skin thickness between time intervals as measured by approved calipers. These relative increases are applied to a normogram to determine the final test result. Alternatively, the IG may be performed on animals suspect to the CFT by collection and submission of a whole blood sample to an approved laboratory for testing.614 This test compares the relative production of specific IFN-γ of cells exposed to MTB antigen and M. avium antigen. The basis for following CFT suspect testing with the CCT or IG tests is that animals infected with mycobacteria other than the MTB complex react to avian antigenic stimulation to a greater degree than to bovine antigens.613 Tests vary in nonbovid species and include application of the intradermal tuberculin test in the axillary area of new world camelids and in the cervical region of cervid species.614

Testing protocols in other countries can vary in relation to the specific composition of tuberculin, interpretation of the tests, and application of tests in different species or situations. The presence of control and eradication programs in most developed countries depend on the ability of these initial test procedures to differentiate herds or animals that may have been exposed to the organism. As there is no economically viable or routinely effective treatment for the disease in livestock, final determination of the presence or absence of Mycobacterium bovis is based on specific identification of the organism, such as via genetic identification or bacteriologic culturing.

Other tests no longer in use include the SC and IV thermal tests, in which a temperature spike to over 40° C (104° F) in 4 to 8 hours is the positive response; and the Stormont test, in which the intradermal test is performed twice in the same area 7 days apart. The response is determined 24 hours after the second test, and an increase in skin thickness of 5 mm or greater is the positive result. A tuberculin test may result in locally increased sensitivity for about 12 days; thereafter there is a temporary generalized hyposensitization. Because of this, follow-up intradermal tests must be performed before 10 days or after 60 days, and the IG test performed within 30 days, after initial CFT injection in the United States.614 A relative hyposensitization also may occur just before and for 4 to 6 weeks after calving.

Animals with chronic disease or advanced pulmonary lesions may be anergic and may not react to immune-based testing.615 False-positive reactions may occur as a result of human or avian tuberculosis, Johne’s disease, saprophytic Mycobacterium species, or other agents such as Nocardia species.613 Radiographs may be helpful in establishing the presence of pulmonary masses in individual cases. Postmortem examination of animals delivered to slaughter facilities inspected by the Food Safety Inspection Service and necropsy are used by control officials to determine the presence or absence of lesions. Histopathologic examination, PCR testing, and bacterial culture are all used to determine the final diagnosis in animals with lesions and suspect or reactor animals.

The accuracy of antemortem diagnostics for Mycobacterium bovis is limited by the organism’s failure to produce a reliable cellular or humoral response, and the prevalence at which animals are exposed to cross-reacting organisms. Sensitivity of the CFT in field trials has been reported to be 63% to 97%, and increased test sensitivity can be seen in cases of individual animals with more extensive lesions and in herds that contain a higher prevalence of Mycobacterium bovis infection.613,615,616 Therefore the test is more valuable in making decisions regarding the presence of Mycobacterium bovis in herds rather than individual animals.617 It has been reported that Mycobacterium bovis strain type may influence the effectiveness of the CFT.605 The specificity of intradermal tuberculin testing has been reported to be 75.5% to 99.0%,613 although accurate estimates are difficult because of differences in research and field trial testing protocols. In areas with a low prevalence of disease, overall testing specificity is enhanced by using a combination of the CFT and CCT or IG tests in sequence.

Determination of Mycobacterium bovis infection through examination of animals presented at slaughter facilities is routinely used in developed countries. Slaughter examination systems have a lowered sensitivity compared with intradermal testing but are seen as a cost-effective surveillance method.618 Sensitivity of postmortem examination is affected by the procedure used and the tissues examined. The most common areas of lesion development in naturally infected cattle are in the lymph nodes that drain the respiratory tract. From 70% to 90% of Mycobacterium bovis lesions are found in the lymph nodes of the head or in the thoracic cavity. In low-prevalence areas, animals may have no, or only one, macroscopically visible lesion.617-619 Because Mycobacterium bovis is difficult to culture, aseptic collection technique and appropriate storage of tissues during transport are critical for appropriate diagnosis.

Pathophysiology

The organism usually enters ruminants through the respiratory route, occasionally by ingestion. The infectious dose has a significant effect on the severity and progression of the disease. Animals exposed to high doses of the organism develop more severe lesions and produce an earlier and more consistent period of bacterial shedding than those exposed to low doses. It has been reported that a dose as small as one CFU can cause disease.619,620

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Inhalation of the organism, the most common method of infection, usually results in a small necrotic granulomatous lesion occurring in the lungs. Granuloma formation is less common when the digestive tract is involved. Infection of the upper respiratory tract or pharyngeal area may also be caused by ingestion of infected feeds.610 From the initial site of entry the organism invades the local lymph nodes (retropharyngeal, tracheobronchial, mediastinal, mesenteric), where it causes necrosis surrounded by a granuloma containing mononuclear cells. Localized lesions stimulate development of a fibrous capsule that varies in severity depending on the rate of development. This combination of lesions at the site of entry and the local lymph nodes forms the primary complex. From there a postprimary dissemination occurs to various organs and can result in diffuse miliary tuberculosis, discrete nodular lesions in various organs, or chronic organ tuberculosis. The disease in cattle is progressive and eventually causes weakness, debility, and death.605,606,610,619 Hypotheses based on knowledge of human tuberculosis have suggested that the majority of cattle exposed to Mycobacterium bovis may have the ability to clear the disease or enter a period of latency.615 If proven true, this could have significant impact on eradication programs.

Epidemiology

Contact with infected animals is the most common source of exposure, and the organism is present in exhaled droplets, sputum, feces, milk, urine, vaginal discharge, semen, and draining nodes. Tuberculous lesions occur in the head or respiratory lymph nodes in 70% to 90% of reactors with confirmed infections. However, lung lesions are found in 1% to 2%, to less than 10%, of these infected animals on postmortem examination.617,618 Animals with no visible signs of organ involvement have historically been regarded as nonexcreters and been determined to be unimportant in transmission of the disease. If careful laboratory examinations are made, over 70% of cattle with lesions in respiratory lymph nodes have small lung lesions, and in 19% of confirmed cases Mycobacterium bovis is present in the tracheal mucus. All cattle with tuberculous lesions are therefore considered potential shedders.621 Research has supported that Mycobacterium bovis adheres to a commonly held belief about many diseases: cattle with more advanced lesions have a higher shedding rate than animals with less extensive disease.622 Feces can remain infective for 6 to 8 weeks, and stagnant water for 18 days. Milk historically was a common route of infection in young animals. Recent research has demonstrated that Mycobacterium bovis can persist on feedstuffs such as corn, carrots, apples, hay, and sugar beets for up to 16 weeks at 0 ° C (Whipple, unpublished data).

Housing and crowding increases the contact of naive animals with secretions of infected animals and can enhance spread of this disease. The disease can also be transmitted by indirect contact through contaminated feed and water, feeding and watering equipment, cleaning equipment, or movements of personnel—anything that can mechanically transfer the organism between locations. Movement of untested infected animals through purchases, sharing of breeding animals, and fenceline contact with other herds have historically been the most common ways of transferring the disease.

Mycobacterium bovis has been found to occur as an endemic disease of wildlife populations in multiple countries. Such occurrences, and associated transmission from wildlife into domestic livestock herds, poses a new challenge to the control and eradication of the disease. Wildlife involvement in the transmission of disease to cattle has occurred with free-ranging white-tailed deer (Odocoileus virginianus) in the United States, badger (Meles meles) in Great Britain, and brushtail possum (Trichosurus vulpecula) in New Zealand, among others. Studies have demonstrated that these species can be reservoirs for transmission to livestock through indirect contact and contamination of feed, water, and environmental substrates.610,611,622 The foraging habits of mammalian herbivores may also contribute to an increased risk of exposure to the organism in areas with wildlife reservoirs.623,624 Movement of infected wildlife species through rehabilitation or reintroduction programs can be an avenue for spreading the disease between areas.

Bovine tuberculosis is an important zoonotic disease because of its potential for spread in nonpasteurized milk from infected animals. The disease may also be spread between animals and humans that are in close association. The incidence of tuberculosis has been greatly reduced by control programs in many developed countries but still persists and presents a potential disease hazard to humans in many areas of the world.605 Within developed countries the residual cases are the most difficult and expensive to detect and remove, and consequently outbreaks still occur. In the United States, fairly large-scale outbreaks have been reported in dairies that were previously free of the disease, and the proportion of feeder animals that accounts for slaughter cases has increased in recent years. Importation of feeder cattle from Mexico has been shown to be a source of disease introduction for the United States.625 Movement of infected cattle is also a contributor to the spread of Mycobacterium bovis in Great Britain.

Necropsy Lesions

The pathognomonic lesion of Mycobacterium bovis infection is the granuloma, which is thought to be a result of chronic antigenic stimulation and an attempt to localize the invading organism.626 Tuberculous lesions primarily occur in the respiratory tract and associated head and thoracic lymphatic tissue but can exist in other areas depending on the initial location of introduction of the organism. It is common that infected cattle may display no grossly visible lesions or may have a visible lesion in only one lymph node.616,617,621 Macroscopic lesions appear as firm encapsulated nodules, with thick, yellow to orange, creamy to caseous pus, and may be calcified. They may occur in any lymph node, but especially the bronchial, mediastinal, and mesenteric nodes, and in a variety of organs, particularly the lungs and liver. The organs may be riddled with small miliary tubercles, and in the lungs these may coalesce into a suppurative bronchopneumonia. Swine may have involvement of the joints of the forelimb or hindlimb.627 Chronic lesions are characterized by a discreet, thickened fibrous capsule containing thick caseous material.606

Histopathologically lesions in lymph nodes or organs are granulomatous with a central area of mineralization and necrosis. Macrophages have a distinctly elongated appearance and can coalesce into multi-nucleated giant cells (Langerhans cells). These fused cells form the center of the developing tubercles. The presence of acid-fast bacteria within these lesions strongly suggests the presence of Mycobacterium bovis, although there may be only small numbers of widely dispersed organisms. Lesion development can be divided into four different stages: stage 1 (no necrosis), stage 2 (minimal central necrosis), stage 3 (central caseous necrosis with minimal necrosis), and stage 4 (extensive multicentric caseous necrosis with mineralization).626 Differentiation between the thickness of the fibrous capsule and the histopathologic stage of development may assist in determining the chronicity of the infection.

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Treatment, Prognosis, Prevention, and Control

In developed countries the disease is not treated in livestock, and affected animals are slaughtered. Species infected with Mycobacterium bovis that are considered valuable as zoologic exhibits or that are rare or endangered have undergone attempted treatment for the disease. These treatments have included human tuberculosis drugs such as isoniazid, streptomycin, paraaminosalicylic acid, and others.606 Outside of these rare cases, treatment for bovine tuberculosis in animals is not considered effective on the disease or practical with regard to cost.

The development of an effective vaccine for bovine tuberculosis has been a desired tool to use in preventing and eradicating Mycobacterium bovis. Vaccines may increase resistance to infection or reduce the disease severity and potential risk of transmission from an infected animal. Much research is now going into development of an effective vaccine, but field study methods need to be developed that mimic natural infection.628,629 The use of a vaccine at the end stages of an eradication program may increase the difficulty in locating the last vestiges of infection, because of the tendency of vaccines to mask disease, which is generally not desired. Much of the vaccine research is aimed toward usage in areas with widespread disease or in wildlife species in areas where the disease is endemic in these populations. Recent results in the United States involving challenge studies in white-tailed deer have demonstrated decreased lesion severity in vaccinated animals.630

Eradication schemes in numerous countries rely on a program of surveillance in livestock and wildlife, testing of animals before movement, and systems to track animals between farms in order to identify animals exposed to the disease and potential sources of infection. More recently, surveillance and control programs for wildlife species deserve consideration as these may also be a source of infection. In the United States, individual farms infected with Mycobacterium bovis are handled through a series of testing protocols intended to eliminate infection through removal of all infected animals, or by whole herd depopulation.614 Because of limitations in the sensitivity of antemortem diagnostic tests for tuberculosis, depopulation of infected herds and other exposed animals is thought to be the most effective way to ensure eradication of the disease.616

When herds are depopulated and the owner intends to repopulate in the future, it is important to remove or thoroughly clean and disinfect facilities and equipment potentially exposed to the organism. The ability of Mycobacterium bovis to survive for extended periods in the environment, and the ineffectiveness of disinfection of organic materials, necessitates that pastures and fields to be used in repopulation schemes be left vacant for a period of time before use. This period of “down time” will be affected by climatic conditions, as the organism is less resistant to sunlight and drying, but can survive for longer periods during certain seasons. Instances of infection that are thought to originate from wildlife sources may precipitate changes in facilities, management, feeding practices, or wildlife control to prevent reinfection. Current experience with endemic Mycobacterium bovis infections in wildlife in numerous countries have demonstrated that eradication of the disease in these species is difficult, and a long-term proposition. More work is needed in the areas of diagnostic testing, environmental sampling, vaccine development, and management practices that may decrease the risk of disease spillover, in order to achieve successful control and eradication of the disease in the future.

DISEASES OF THE THORACIC WALL AND CAVITY

AMELIA R. WOOLUMS

JOHN A. SMITH

PLEURITIS AND PLEURAL EFFUSIONS

Definition and Etiology

Acute, primary pleuritis is rare in ruminants. It is almost always a secondary condition. The most common primary cause is most likely bronchopneumonia caused by M. haemolytica or H. somni. Other possible causes of pleuritis and pleural effusions include traumatic reticulopericarditis, extension from other causes of peritonitis, tuberculosis, liver abscesses, tumors (especially lymphosarcoma), external trauma, fractured ribs, gunshot, perforating injuries, sporadic bovine encephalomyelitis (SBE), contagious bovine and caprine pleuropneumonia, various septicemic conditions, acorn toxicity and other causes of uremia, uroperitoneum, right ventricular failure, hypoproteinemia, ruptured thoracic duct, and hemothorax from trauma or hemangiosarcoma.

Clinical Signs

The signs depend on, and may be overshadowed by, the primary disease process. Pleuritis is a painful, septic process, whereas the signs associated with nonseptic effusions depend largely on the cause. Signs referable to pleuritis itself include anorexia, depression, fever, weight loss, decreased milk production, progressive dyspnea, and a characteristic stance and respiratory pattern, with the head and neck extended, elbows abducted, restricted excursion of the thorax, abdominal breathing, tachypnea, and a grunting or groaning with respiration. The animal may be reluctant to move. If a cough is present, it is often soft and suppressed because of pain. Jugular distention and pulsation may result from interference with venous return.631 Auscultation may reveal creaking or rubbing noises in dry pleuritis or a cranial-ventral masking of sounds caused by effusion. Percussion may reveal dullness ventral to the fluid line and may elicit pain. Differential diagnoses for dyspnea with abnormally quiet lung fields may include the atypical pneumonias, pneumothorax, and space-occupying lesions such as large abscesses, tumors, and diaphragmatic hernia. Once pleuritis or pleural effusion has been identified, the main differential diagnostic consideration is the determination of the underlying cause, as listed previously.

Diagnosis

A CBC helps to separate infectious from noninfectious causes and distinguish relatively acute conditions (with significant left shifts) from those of a more chronic nature (with mature neutrophilia, hyperglobulinemia, and nonregenerative anemia of chronic disease). Serum chemical determinations and urinalysis identify hypoproteinemia and azotemia. A thoracocentesis should be performed and submitted to cytologic and cultural examination for bacteria, mycoplasma, and chlamydia. Nonseptic transudates indicate conditions such as neoplasia, heart failure, hypoproteinemia, and uremia. Effusions of sporadic bovine encephalomyelitis are relatively acellular with high protein and fibrinogen levels, whereas septic exudates high in both cells and protein occur with pneumonia, hardware, peritonitis, abscesses, penetrating trauma, and septicemias. A transtracheal wash is usually indicated because of the common association with pneumonia. Pericardiocentesis, abdominocentesis, and radiographs may indicate the primary source of an infection. Tuberculosis tests, leukemia virus titers, chlamydial titers for SBE, electrocardiography, echocardiographic examinations, ultrasonographic examination of the liver, and exploratory laparotomy may also help to detect other primary processes.

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Treatment

The primary problem should be treated. Effusions should be drained, either periodically or continuously through a Heimlich valve or a suction device fashioned from a syringe with the plunger transfixed with a pin. Effective drainage can be difficult in ruminants because of their propensity for fibrin formation and loculation of the fluid. Intermittent drainage is as effective as continuous drainage and simpler to maintain. Attempts at lavage have rarely been successful because of adhesions. Appropriate antibiotics are indicated in the presence of sepsis. NSAIDs (aspirin, 100 mg/kg PO twice daily; flunixin meglumine, 1.1 to 2.2 mg/kg IV or divided twice daily) are useful to relieve pain, ease respiration, and improve appetite. Rest and good nursing care are essential. The prognosis obviously depends on the extent and duration of the disease. Although many animals that have severe cases survive, such animals often remain chronically underweight.

PNEUMOTHORAX

Pneumothorax is not common in ruminants. Most cases result from the rupture of an emphysematous bulla associated with pneumonia, straining, or coughing or from puncture of the lung by a fractured rib. The bullae that occur in BRSV-induced pneumonia are a common source. Trauma to the pharynx or larynx can also lead to pneumothorax,632 presumably caused by air traveling from the cranial cervical regions through soft tissues and into the thoracic cavity. Penetration from the exterior is possible but less common. A case has been described in a postparturient cow with no other underlying cause found.633 A retrospective study of 30 cattle with pneumothorax presented to a referral hospital found that 18 of the cases (60%) were associated with bronchopneumonia, seven cases were associated with interstitial pneumonia, three cases were associated with laryngeal or pharyngeal trauma, and two cases were associated with neonatal respiratory distress.632 Of interest was the finding that 13 of the 18 cases with bronchopneumonia were chronic, based on history and diagnostic findings; an association between pneumothorax and chronic bronchopneumonia had not been previously reported. The rate of survival for cattle with pneumonia and pneumothorax was lower than for cattle presented with pneumonia without pneumothorax, with an overall survival rate of 60% for cattle presented with pneumothorax.

Clinical signs of pneumothorax include inspiratory dyspnea, sometimes severe, with open-mouth breathing sometimes present.633 One side of the thorax may be relatively collapsed and immobile, with a compensatory increase in the size and excursion of the other side; however, this latter finding is often subtle and difficult to appreciate. Ruminants have a complete mediastinum; thus when pneumothorax occurs it is usually unilateral, and the animal is able to ventilate adequately using the opposite lung. Unless an infectious disease is responsible, affected animals are often alert and anxious. They may attempt to stand with the forefeet elevated. There is a pronounced abdominal component to the respirations. Cyanosis may occur, and airflow may be markedly reduced in severe cases. On auscultation there is an obvious disparity between the two sides; bronchovesicular sounds will be diminished dorsally on the affected side or may be entirely absent. Those lung sounds that are audible have a harsh, high-pitched, large airway character similar to those of a consolidated lung, especially over the carina; these sounds seem to be distant, as if the animal were breathing in a barrel. The point of maximum intensity of the heart may be displaced, and tachycardia is often present. Percussion may reveal an abnormal resonance when compared with that of the normal side, and simultaneous auscultation and percussion may produce a “ping” over the thorax. SC emphysema is a fairly common feature, and pleuritis is often a sequela. Differential diagnoses of the inciting cause should include the various causes of ARDS, bronchopneumonia, viral pneumonias (especially BRSV), pleural effusions, diaphragmatic hernia, other space-occupying lesions (large abscesses, tumors), and clostridial infections.633

Pneumothorax can be diagnosed with radiographs, transthoracic ultrasound, or thoracocentesis632; radiographs and ultrasound will also be useful to characterize the extent of any underlying lung disease. Other diagnostic tests to characterize underlying lung disease as described for infectious bronchopneumonia or interstitial pneumonia are appropriate.

If the affected animal shows signs of significant distress, the air in the pleural space should be evacuated. Evacuation can be accomplished by aseptically placing a teat cannula into the thoracic cavity at the dorsal aspect of the thorax at the tenth intercostal space and withdrawing air by use of an extension set and three-way stopcock. In some cases this method can be successfully used to intermittently remove air; in other cases, continuous removal with a pleural evacuation device (Pleur-evac A-8000, Deknatel Inc., Fall River Mass.) has been more effective.634 If continuous evacuation is attempted the animal must be adequately restrained; this is likely to be possible only with hospitalized animals. Other treatment includes therapy appropriate for underlying acute or chronic pneumonia as described previously for infectious bronchopneumonia or interstitial pneumonia. External wounds allowing air to enter the thorax should also be closed if present.

DIAPHRAGMATIC HERNIA

Definition and Etiology

Diaphragmatic hernias are uncommon in ruminants but have been reported in calves, cattle, sheep,635 and domestic buffalo.636,637 The condition appears to be much more prevalent in the buffalo but otherwise is analogous to that in cattle.638 Hernias may be congenital, but most appear to be acquired, including those occurring in neonates. A congenital weakness in the diaphragm may predispose to some cases. Causes include difficult parturition, external trauma, and, by far the most common cause, traumatic reticuloperitonitis (TRP).

Clinical Signs and Differential Diagnosis

Affected animals can be asymptomatic for a prolonged period.638 Most affected cattle are in late gestation or have calved recently. The history may include decreased milk production, weight loss, capricious appetite, difficulty in swallowing or regurgitation, previous signs of abdominal pain (possibly associated with acute TRP), vomiting, and abnormal posturing of the head and neck on swallowing or regurgitation. Respiratory signs are actually fairly uncommon, with the exception of large congenital hernias, in which there is obvious severe dyspnea and abdominal respiration from birth. Occasional cough and dyspnea have been reported, and auscultation may reveal asymmetric sounds, with lack of lung or heart sounds in the affected area, or splashing sounds similar to those heard with pericarditis. GI signs are actually more common and include bloat, signs consistent with TRP, difficulty or pain on passage of a stomach tube, diarrhea, constipation, and ruminal hypomotility. Some cows may retch or vomit on regurgitation. Pain is evidenced by odontoprisis or grunting on regurgitation. The primary differential diagnoses are TRP, pericarditis, esophageal stricture, esophageal foreign body (choke), neoplasia, and abscessation.638

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Diagnosis

Radiographs are the best means of confirming the diagnosis. The normal outline of the diaphragm and heart may be obscured,636,637 and the honeycombs or foreign objects in the reticulum may be seen in the thorax637 because this organ is most commonly involved. Oral barium may also aid in the radiographic interpretation, particularly in early small hernias that will be missed on plain films. Pleuritis and other masses such as tumors and abscesses can also mimic hernias on plain films.637 Because TRP is frequently involved, the CBC, pleural effusions, and abdominocentesis may reflect the septic process. In cases not associated with TRP, the pleural effusion may be hemorrhagic in acute cases and normal in chronic cases.638

Necropsy Lesions

The hernial ring is usually located at the junction of the musculotendinous portion of the diaphragm, about 12 cm ventral to the vena cava and slightly lateral to the midline. The ring is usually round to oval, with a diameter of 7 to 20 cm. The reticulum is usually herniated, most frequently to the right side of the chest. The liver, spleen, rumen, omasum, abomasum, intestine, and omentum may also be involved. Extensive adhesions usually develop between the herniated organs and the thoracic organs, and evidence of hardware can often be found.639

Treatment and Prognosis

Treatment is surgical. A two-stage approach is usually used. First, a standing left flank laparotomy and rumenotomy are performed; the defect is identified, foreign bodies are removed, and the ruminoreticulum is emptied. Because of the complete mediastinum, ventilatory assistance is rarely needed during this stage. Next, the animal is placed under general anesthesia with positive pressure ventilation. Various approaches have been used for this portion, including ventral midline, paramedian, semilunar postxiphoid, paracostal, and transthoracic with rib resection. The hernia is reduced, and the rent repaired with sutures or mesh grafts. Mesh grafts are contraindicated if infection is present.638

PLEURAL MESOTHELIOMA

Mesotheliomas have been reported in cattle and goats,640 including a congenital form in calves.641 Most are peritoneal, but pleural mesotheliomas also occur.642,643 Mesotheliomas result in the accumulation of large amounts of fluid in the involved body cavity; signs of pleural mesothelioma are therefore related to pleural effusion. They include dyspnea, tachypnea, decreased lung and heart sounds (sometimes unilateral, with a concomitant increase in sounds on the normal side), dullness on percussion, exercise intolerance, cyanosis, tachycardia, anorexia, weight loss, decreased production, cough, and weak pulses. If peritoneal lesions are also present, as is common but not universal, ascites is also present. Radiographs confirm the pleural effusion, and thoracocentesis yields a serous, sometimes blood-tinged or gelatinous fluid. Cytologic examination may reveal reactive mesothelial cells. At necropsy the pleura is thickened and contains multiple nodules of gray to yellowish white tissue measuring several millimeters to several centimeters in diameter. Metastasis is uncommon. The tumor can be difficult to diagnose histologically and may resemble inflammation, pleural tuberculosis (“pearl disease”), or metastasis of another tumor.641 There is no treatment.

MISCELLANEOUS CONDITIONS

JOHN C. BAKER

JOHN A. SMITH

LUNG TUMORS

Lung tumors are uncommon in large animals, with slaughterhouse surveys reporting an incidence of 19 per million cattle.644 Those reported include pulmonary alveolar carcinomas, pulmonary adenomas, pulmonary adenocarcinomas, bronchogenic carcinoma, and pulmonary blastoma.645-647 Malignant forms metastasize to regional lymph nodes and occasionally to other organs. Lymphosarcoma is the most frequent neoplasm to become metastatic to the lung, and uterine and ovarian adenocarcinoma may undergo metastasis to the lung.647 Because many lung neoplasms in cattle are incidental findings at slaughter or necropsy, clinical signs are therefore not well documented. The lesions are typically discrete, round, yellow to gray masses distributed throughout the lung tissue. Tumors are most likely to be detected antemortem by radiographic examination. Differential diagnoses in such cases include pulmonary abscesses, mycotic pneumonias, and tuberculosis.

BRONCHOBILIARY FISTULA

A communication between the bile duct and a cavitating lesion in the lung has been described in a 3-year-old Charolais cow.648 The cow had weight loss of 8 months’ duration, before which she had been normal. Clinical signs were tachypnea, an expiratory press, bilateral crackles and friction rubs in the ventral lung fields, and a greenish yellow nasal discharge. The adventitious sounds were slightly more prominent on the right, and a silent area was detected in the caudodorsal right lung field. Radiographs revealed a cavitation with a fluid line in this area, and thoracocentesis yielded a sterile green fluid. At surgery, pleural-diaphragmatic adhesions and a mass in the right diaphragmatic lobe were found. A drain was installed, and fluid similar to bile, with a bilirubin of 3.1 mg/dL and alkaline phosphatase concentration of 2694 IU/L, was drained. At necropsy the lesion was a smoothlined cyst communicating by way of tracts through the adhesions with the biliary system and the bronchioles. Greenish fluid was found in the airways of both lungs.

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