Etiology and Signs.

Congenital disorders including pharyngeal cysts of respiratory epithelial origin, nasal cysts, cystic nasal conchae, skull anomalies, laryngeal malformations, and branchial cysts have been observed in calves and adult cows. Inspiratory dyspnea with audible snoring sounds or stertorous breathing is a sign common to most of these problems. The condition may be present at birth or is most often observed within the first few months of life. The degree of dyspnea associated with these abnormalities tends to be progressive as a result of either enlargement of the lesion (cyst) or worsening upper airway edema and swelling from the mechanical overwork associated with respiratory efforts to move air through an airway narrowed by malformations.

Diagnosis.

Specific diagnosis requires physical examination, including visual inspection of the nares and oral cavity, endoscopy, and skull radiographs (Figure 4-2). In addition, aspiration for cytology and cultures may be indicated for cystic lesions. Most cystic lesions will be secondarily infected.

Figure 4-2 Radiograph of a conchal cyst in a 6-month-old heifer.

Treatment.

Method of treatment depends on the specific lesions found. Cystic conditions may be the most treatable because surgical removal offers some hope of being curative. Simple drainage or drainage with cautery of cystic lesions is not likely to be successful. Therefore referral of such cases to veterinary surgeons experienced in upper airway surgery is recommended so that complete excision of the secretory epithelium can be completed. Other conditions such as laryngeal malformations and skull anomalies have a poor prognosis.

Regardless of cause, symptomatic or supportive treatment may be necessary before diagnostic procedures are performed in calves with severe dyspnea, lest the stress of examination or endoscopy induce anoxia. A tracheostomy should be considered to allow safe diagnostic manipulation. Misinterpreting anoxic patient struggling as wildness requiring additional physical restraint is a frequent, and potentially fatal, error in judgment made by inexperienced clinicians. When a dyspneic animal struggles during examination, usually it is anoxic, frightened, and extremely anxious. All restraint of the head and neck should be relaxed, and the animal should be allowed to “get its breath.” Continued restraint during these situations will result in asphyxiation of the animal.

Although the prognosis for congenital lesions varies with the specific diagnosis, generally it is guarded to poor.

Etiology and Signs.

Acquired mechanical or obstructive lesions of the upper airway may occur in calves or adult cattle. Most of the lesions represent enlargement or inflammation of tissues and structures external to the airway itself. Impingement into the upper airway by soft tissue masses such as pharyngeal abscesses, retropharyngeal cellulitis, necrotic laryngitis, pyogranulomatous swellings (e.g., wooden tongue), enlarged lymph nodes, neoplasms, foreign bodies, or enlarged maxillary sinuses compose the majority of lesions. Pharyngeal abscesses and necrotic laryngitis are probably the most common acquired causes of obstruction. Pharyngeal abscesses and retropharyngeal cellulitis may occur following traumatic injury to the mouth when an animal is treated with oral medication or may arise in calves with no history of pharyngeal trauma.

Regardless of cause, progressive inspiratory dyspnea is the primary sign observed in affected cattle. Fever may be present with pharyngeal abscesses or chronic maxillary sinusitis. Unilateral nasal discharge or reduced airflow from one nostril may be present with maxillary sinusitis or unilateral neoplasms of the nasal pharynx or maxillary sinus. Lymphadenopathy may be present as a primary sign in neoplastic conditions, such as juvenile lymphosarcoma and adult lymphosarcoma (Figures 4-3 and 4-4), or as a secondary sign, in cases of soft tissue infections. Unilateral Horner’s syndrome and progressive exophthalmos have been observed in slow-growing adenocarcinomas of respiratory epithelial origin in the nasal pharynx (Figure 4-5). Cattle with unilateral nasal obstruction often show more obvious respiratory signs during hot weather. One cow with Horner’s syndrome would demonstrate open mouth breathing on hot days because of the nasal mucosal vasodilation and edema (Figure 4-6). A fetid odor may exist on the breath caused by chronic inflammation or tumor necrosis in some cattle. The owner may report a progressive course of stertorous breathing eventually leading to open mouth breathing. Inflammatory lesions often have a more acute course than neoplasms, but this is a generality rather than a rule. Obvious external swelling may be present in certain conditions such as chronic maxillary sinusitis, pharyngeal or retropharyngeal abscesses, and lymphosarcoma.

Figure 4-3 Juvenile lymphosarcoma in a 4-month-old Milking Shorthorn calf presented because of inspiratory dyspnea.

Figure 4-4 Adult Holstein with lymphosarcoma mass in the pharyngeal area that caused inspiratory dyspnea.

Figure 4-5 Aged Jersey cow with an adenocarcinoma of respiratory epithelial origin. The mass caused reduced airflow through the left nasal passage, left-sided Horner’s syndrome, and exophthalmos. The eyelids have been sutured together to protect the eye.

Figure 4-6 Open mouth breathing in a 5-year-old cow with unilateral Horner’s disease (etiology unknown). The cow had no respiratory difficulties during the winter months.

Diagnosis.

A complete physical examination followed by manual and visual inspection of the oral cavity is the first diagnostic procedure. Relative equality of airflow and the odor of the breath should be evaluated at the nostrils. If chronic maxillary sinusitis is suspected, the upper premolar and molar teeth should be examined closely for abnormalities.

Endoscopy should be performed in an effort to identify a specific lesion or the anatomic region of impingement of tissue into the airway. When performing endoscopy in a calf or cow with severe upper airway dyspnea, most of the mucosal surfaces (e.g., soft palate, larynx, and respiratory pharynx) will be edematous from exertional or labored respiratory efforts. This edema should not be misinterpreted as the causative lesion (see video clips 3 to 5).

Skull radiographs may be necessary if physical examination and endoscopy fail to identify a lesion. Radiographs are helpful for definitive diagnosis of sinusitis, nasal or sinus cyst, and for identifying the location of soft tissue masses such as abscesses or tumors. In addition, radiographs would help to identify abscessed tooth roots in cases of chronic maxillary sinusitis and metallic foreign bodies.

Diagnostic ultrasonography, if available, may help in the assessment of soft tissue swellings. This technique also has been used to locate retropharyngeal abscesses and nonmetallic foreign bodies so that external drainage may be performed safely.

In the case of obvious or palpable swellings of the head or pharynx, aspirates for cytology and culture are indicated. Similarly, biopsies for histopathology are indicated for solid masses or enlarged lymph nodes.

Treatment and Prognosis.

Treatment is most successful when external compression of the upper airway can be cured through treatment of an inflammatory lesion. Pharyngeal or retropharyngeal abscesses should be drained with liberal incisions that avoid vital structures. Internal drainage is preferred unless the abscess is close to the skin surface. External drainage is technically difficult in deep pharyngeal abscesses located more than a few centimeters below the skin surface. Vagus nerve damage, salivary duct laceration, and acute cellulitis are potential complications associated with opening the abscess. If drainage is not liberal, abscesses tend to recur. If recurrence is obvious, culture and sensitivity coupled with drainage through multiple sites are indicated. Daily flushing of the drainage sites is important. Systemic antibiotics should be administered for 1 to 2 weeks following drainage; Arcanobacterium pyogenes (A. pyogenes) and Fusobacterium spp. are the most common organisms cultured, so penicillin is the most commonly used antibiotic.

Chronic maxillary sinusitis should be treated by trephination of the sinus, removal of any teeth that have infected roots, daily flushing of the sinus with dilute disinfectants or sterile saline, and appropriate systemic antibiotics for 1 to 2 weeks.

In general, neoplasms have a hopeless prognosis, and the animal should not be treated. Juvenile lymphosarcoma often causes upper airway dyspnea via enlarged pharyngeal lymph nodes. Occasional adult-form lymphosarcoma cases have one or more very large (10 to 20 cm diameter) pharyngeal or mediastinal lymph nodes that will cause dyspnea. Lymphosarcoma usually results in death within 1 to 6 months of diagnosis. Adenocarcinomas originating in the respiratory pharynx in older cattle (i.e., more than 8 years of age) may have an insidious but progressive course over months to years. Therefore unlike cattle with lymphosarcoma, these animals may be allowed to survive for some time to deliver another calf or to undergo superovulation and embryo transfer. Only if the animal stops eating, develops severe respiratory distress, or is suffering from exposure damage from an exophthalmic eye will euthanasia be necessary. Cattle affected with primary squamous cell carcinoma, metastatic squamous cell carcinoma, or osteosarcoma originating in a sinus, bone, or periocular location occasionally may have enough tumor mass or lymph node metastases to develop inspiratory dyspnea. Cattle with squamous cell carcinomas frequently have a fetid breath odor from the primary tumor and should not be made to suffer unduly.

Etiology and Signs.

Actinobacillus lignieresii granulomas within the nasal cavity usually are unilateral masses within the external nares and appear as red, raised, fleshy masses that bleed easily and look very similar to Rhinosporidium granulomas (Figure 4-7, A and B). Signs include a progressively enlarging mass in one nostril and inspiratory dyspnea as the lesion enlarges to occlude the nostril completely. The granulomas may originate at the site of nose-lead lesions of the mucosa near the nasal septum or at other mucosal sites of soft tissue injury from foreign bodies or fibrous feed. Progressive inspiratory dyspnea and nasal discharge are found in patients having granulomas deeper in the nasal cavity, larynx, pharynx, or trachea. Actinomyces bovis was responsible for multiple tracheal granulomas in a cow treated at our clinic.

Figure 4-7 A, Necropsy specimen of nasal turbinate region showing Rhinosporidium granulomas. B, Actinobacillus nasal granuloma in a Holstein cow.

Diagnosis.

Granulomas can be confused with tumors on gross inspection. Therefore diagnosis requires biopsy for histopathology and tissue culture. Sulfur granules may be observed grossly on cut surfaces of these granulomas and suggest the diagnosis. Although usually found near the external nares, granulomas caused by A. lignieresii or A. bovis could occur anywhere in the upper airway or trachea because these opportunists reside in the oral cavity and pharynx. When soft tissue infection occurs following injury to the mucosa, both organisms produce similar granulomas. Endoscopy and radiographs are necessary to identify granulomas at locations other than the external nares.

Treatment.

Treatment for granulomas caused by A. lignieresii consists of excisional biopsy to debulk the mass to the level of nasal mucosa and sodium iodide therapy until iodism is observed. Usually this requires IV sodium iodide (30 g/450 kg) initially and at 2- to 3-day intervals for several treatments, or oral organic iodide (30 g/450 kg) daily following the initial IV dose. Cryosurgery has been used successfully on these granulomas following debulking. In severe or recurrent cases, antibiotic therapy may be necessary in addition to sodium iodide. Penicillin and ampicillin have been used to treat infection caused by A. lignieresii. Whenever possible, an antibiotic should be selected based on organism culture and sensitivity results. Usually the prognosis is good.

Granulomas caused by A. bovis are much more difficult to treat because this organism is poorly responsive to sodium iodide therapy. Treatment with penicillin (22,000 U/kg intramuscularly [IM], once a day), in conjunction with sodium iodide, may be effective. Surgical debulking of soft tissue granulomas also is indicated. The prognosis for those with lesions caused by A. bovis is guarded because of the limited clinical knowledge regarding treatment of this organism, and many owners may not treat for a sufficient time.

Etiology and Signs.

Frontal sinusitis in calves and adult cattle may be acute or chronic. Acute frontal sinusitis is more common and usually follows sharp dehorning techniques. Calves and cattle dehorned by laypeople are most at risk because of nonsterile equipment and techniques. Signs of acute sinusitis include fever (103.0 to 106.0° F/39.4 to 41.1° C), unilateral or bilateral mucopurulent nasal discharge, depression, and headache pain characterized by partially closed eyes, extended head and neck, head pressing or resting the muzzle on support structures (interestingly cattle with severe skeletal pain can often be found pressing their muscle against an object, which suggests this must be a pain relief point), and sensitivity to palpation on percussion of the sinus. When acute sinusitis follows recent dehorning, purulent drainage or heavy scabs may be observed at the wound in the cornual portion of the sinus. A multitude of bacteria such as A. pyogenes, Pasteurella multocida, Escherichia coli, and anaerobes may contribute to acute frontal sinus infection. Tetanus is another possible complication of acute frontal sinusitis if wound debris or scabs occlude the cornual opening to allow an anaerobic environment.

Chronic frontal sinusitis does not develop until months to years following dehorning and may be completely unassociated with dehorning because it occasionally occurs in animals dehorned by noninvasive techniques, polled animals, or animals with horns. Ascending respiratory tract infections, as in other species, are a cause of chronic frontal sinusitis and usually are caused by P. multocida. Chronic frontal sinusitis associated with old dehorning complications such as low-grade infection, bony skull fragments, or sequestra typically is associated with infection by A. pyogenes or mixed infections that may include A. pyogenes, P. multocida, anaerobes, or miscellaneous gram-negative organisms. Signs of chronic frontal sinusitis include gradual loss of condition and production that may be constant or intermittent; unilateral nasal discharge usually is observed, again as a persistent or intermittent complaint. Additional signs include head pressing, an extended head and neck, partially closed eyes, or resting of the muzzle on inanimate objects, all of which signal headache or pain. Intermittent or consistent fever is present. Bony expansions of the sinus may occur, causing asymmetric facial distortion—especially in cattle that do not have significant nasal discharge because of occlusion or obstruction of the ethmoidal meatus opening into the nasal cavity. In fact, some cattle will have intermittent bony swelling of the sinus that becomes less apparent during times of sinus drainage with subsequent nasal discharge. Palpation or percussion of the frontal bone overlying the affected sinus causes pain, and the patient is extremely apprehensive when the examiner approaches the head. Bony expansion of the sinus may result in ipsilateral exophthalmos and decreased air movement through the ipsilateral nasal passage (Figure 4-8). Neurologic complications, including septic meningitis, dural abscesses, and pituitary abscesses, are possible in neglected cases as a result of erosion of the bony sinus. Tetanus is another potential complication. Occasionally cattle with chronic frontal sinusitis have developed orbital cellulitis, pathologic exophthalmos, or facial abscesses from infectious destruction of the postorbital diverticula of the sinus, allowing soft tissue infection of the orbit (Figure 4-9).

Figure 4-8 Chronic frontal sinusitis in a mature bull. The bull died from septic meningitis caused by the sinusitis.

Figure 4-9 Orbital cellulitis, exophthalmos, and facial abscesses secondary to extension of chronic frontal sinusitis into the orbital soft tissue.

Diagnosis.

In acute cases, diagnosis is based on signs, history, and palpation and percussion of the sinus. Ancillary data are limited to bacterial culture and susceptibility testing to ensure proper antibiotic selection.

Diagnosis of chronic cases may be possible based only on clinical signs coupled with palpation and percussion of the sinus in selected cases. When mature animals are affected, however, it is important to rule out neoplasia and other differentials. Skull radiographs are helpful when available. Drilling into the sinus with a Steinmann’s pin and collection of purulent material for cytology and bacterial cultures will confirm the diagnosis (Figure 4-10). Sedation and local anesthesia allow this procedure to be performed with minimal patient discomfort.

Figure 4-10 Sinus trephination with Steinmann pin to facilitate sample collection in a bull with chronic sinusitis. Note caudal trephination flap that has already been made in the dehorning site to facilitate sinus lavage.

Treatment.

In those with acute frontal sinusitis, treatment requires cleansing of cornual wounds, lavage of the sinus with saline or saline and mild disinfectant solutions, and appropriate systemic antibiotics for 7 to 14 days. Penicillin usually suffices, but selection of a systemic antibiotic is better based on culture and susceptibility testing. Tilting the patient’s head to allow the sinus to fill and then twisting the head to empty the sinus facilitate lavage and drainage. Systemic analgesics such as aspirin or flunixin meglumine greatly aid patient comfort. The prognosis is good.

Treatment of chronic frontal sinusitis requires trephination of the sinus at two sites to allow lavage and drainage. One site is at the cornual portion of the sinus, and the second is located over the affected sinus approximately 4.0 cm from midline and on a transverse line connecting the caudal bony orbits (Figure 4-11, A and B). A third site caudodorsal to the rim of orbit and medial to the temporal ridge has been recommended, but we have found this site to be dangerous because it occasionally results in orbital soft tissue infection as compromised softened bone is penetrated. Further caution regarding trephination of the sinus should be practiced in animals less than 2 years of age because the rostral and medial rostral portions of the sinus may not be developed in younger animals. Attempts to establish rostral-medial drainage in these animals may risk invasion of the calvarium. Drains may be placed to communicate the two trephine sites and prevent premature closure of the wounds. Trephine holes should be at least 2.0 to 2.5 cm in diameter or they will close prematurely. Liquid pus is a positive prognostic sign, and pyogranulomatous or solid tissue in the sinus is a grave prognostic sign. Antibiotic selection must be based on culture and susceptibility testing and should be continued for 2 to 4 weeks. Analgesics such as oral aspirin are used to improve the patient’s comfort.

Figure 4-11 A, Trephination sites surgically created to treat chronic frontal sinusitis in a 4-year-old Holstein cow. B, Trephination sites surgically created to treat chronic frontal sinusitis in a 3-year-old Holstein bull.

Prognosis is fair to good with appropriate therapy as described above unless neurologic signs have been observed. Neurologic signs and orbital cellulitis constitute severe and usually fatal complications of chronic frontal sinusitis. On several occasions, especially in animals less than 18 months of age, Dr. Rebhun performed enucleation successfully to allow orbital drainage necessitated by severe orbital cellulitis and ocular proptosis in addition to trephination of the affected sinus. Long-term wound care, antibiotics, and nursing are essential if treatment is elected for such complicated cases.

Etiology and Signs.

Necrotic laryngitis represents an atypical site of infection by the anaerobe Fusobacterium necrophorum, the organism responsible for calf diphtheria. Calf diphtheria is an infection of the soft tissue in the oral cavity following mucosal injury caused by sharp teeth in calves of 1 to 4 months of age. Calves affected with calf diphtheria usually have abscesses in the cheek region, have mild salivation, and may refuse solid feed (Figure 4-12). The infection spreads among calves fed from common utensils or those in such close contact that they may lick one another. When the larynx becomes infected in the atypical form of this disease, the affected calf develops a progressive inspiratory dyspnea. Low-grade fever (103.0 to 104.5° F/39.44 to 40.28° C) may be present along with a painful short cough that is observed when the calf attempts to drink or eat. As the condition worsens over several days, both inspiratory and expiratory dyspnea may be apparent, but the inspiratory component always will be worse. A necrotic odor may be present on the breath.

Figure 4-12 Typical cheek abscess observed in calf diphtheria.

Audible inspiratory efforts are heard. Harsh sounds of airway turbulence will be heard when a stethoscope is placed over the larynx; these sounds will be referred down the tracheobronchial tree to confuse auscultation of the lower airway.

Diagnosis.

Endoscopy is helpful in confirming the diagnosis. In some calves, the lesions can be seen by using an oral speculum, but endoscopy is much easier and less stressful for the patient. If the calf is in extreme dyspnea or is anoxic or cyanotic, a tracheostomy should be performed before endoscopy. The larynx will be found to be uniformly swollen and may appear to have cartilaginous deformities in chronic cases (Figure 4-13). The laryngeal opening always is narrowed, and mucosal necrosis will be present in acute cases. Chronic cases may have laryngeal deformity and airway narrowing, but the necrotic, infected cartilage may be covered by normal mucosa (see video clips 6 to 8).

Figure 4-13 Endoscopic view of laryngeal deformity and profoundly narrow laryngeal airway in a 3-month-old Holstein calf that had necrotic laryngitis and chronic laryngeal cartilage infection caused by F. necrophorum.

Treatment.

Long-term therapy is required because infection of cartilaginous structures usually exists. Acute cases should be treated with penicillin (22,000 U/kg IM, twice daily). A tracheostomy is essential for treatment of calves that have severe dyspnea. This will provide a patent airway and rest the infected larynx from further exertional irritation while the infection is controlled. The prognosis for acute cases is fair.

Chronic cases have a poor prognosis because laryngeal deformity and cartilaginous necrosis or abscesses within the laryngeal cartilage already have developed. Treatment is similar to that described for acute cases but should be extended to 14 to 30 days in patients valuable enough to warrant treatment, or the necrotic cartilage should be surgically removed or debrided. A tracheostomy may be necessary for the reasons listed above, and some clinicians recommend concurrent treatment with sodium iodide in the hope of penetrating the deep-seated infection of cartilage. A. pyogenes frequently contributes to or replaces F. necrophorum as the causative organism in chronic infections because these two organisms are synergistic. For valuable cattle with the chronic form, referral to an expert surgeon familiar with the tracheolaryngostomy technique described by Gasthuys should be considered.

Etiology and Signs.

M. haemolytica is a gram-negative rod that may be a normal inhabitant of the upper airway but is not cultured from the upper airway of normal cattle as frequently as P. multocida. Several properties of M. haemolytica contribute to its pathogenicity. These include a capsule that provides defense against phagocytosis; production of an exotoxin (leukotoxin) lethal to alveolar macrophages, monocytes, and neutrophils; cell wall–derived endotoxin that helps to initiate complement and coagulation cascades; and the ability to reside in the upper airway among other nonpathogenic serotypes and then convert and/or overgrow under stressful stimuli to a pathogenic serotype, A1, that is more virulent. The cytotoxicity of the leukotoxin is associated with its ability to bind and interact with B2 integrin leukocyte function-associated antigen 1. Currently M. haemolytica is a leading cause of death as a result of respiratory infection in dairy cattle and calves in most areas of the United States. This organism is a primary pathogen not always needing assistance from other viral or Mycoplasma agents to establish lower airway infection, although it is well demonstrated that bovine herpesvirus 1 (BHV1) infection can activate genes that will increase leukotoxin binding, cytotoxicity to bovine mononuclear cells, and the severity of M. haemolytica infection. When a virus such as IBR, bovine respiratory syncytial virus (BRSV), or bovine virus diarrhea virus (BVDV) does infect a herd, mortality will be greatly increased if M. haemolytica bronchopneumonia is superimposed. In this situation, the bacteria may cause death because the viral infection compromises mechanical and cellular defense mechanisms. Mortality may approach 30% to 50% when a virulent M. haemolytica infection is superimposed on a preexisting viral infection (e.g., BHV1 or BVDV) in a herd. Cattle that are stressed are at great risk of M. haemolytica pneumonia because stress triggers both activation of the organism to a more virulent form, permits greater colonization of the virulent strain, and compromises the host defense mechanisms. Thus M. haemolytica is frequently isolated as the cause of “shipping fever pneumonia” associated with shipment of cattle, transport of cattle to shows, or recent purchase of replacement animals. Classic signs of pneumonia generally develop 1 to 2 weeks following any of these stresses. The morbidity and mortality percentages tend to be much greater for M. haemolytica pneumonia outbreaks than if P. multocida is found as the cause of shipping fever.

A great deal of variation in pathogenicity and antibiotic resistance exists for various isolates of M. haemolytica. Therefore the veterinarian must accept the fact that signs produced by these types will vary from mild to severe. Mild infections or less pathogenic M. haemolytica may mimic P. multocida with respect to clinical signs and response to therapy, whereas severe infections may be so drastic as to cause death within hours of the first clinical signs. In rare instances the death can be so peracute that toxicity is expected. A less pathogenic form has been seen causing high fever in recently fresh cows, all of which had a remarkably quick recovery following treatment with ceftiofur.

Signs of acute M. haemolytica pneumonia include fever, depression, anorexia, markedly decreased milk production, salivation, nasal discharge, moist painful cough, and rapid respirations (Figure 4-15). The fever may be as high as 108.0° F (42.22° C) but usually ranges between 104.0 and 107.0° F (40.0 to 41.67° C). Auscultation of the lungs reveals moist or dry rales in the anterior ventral lung fields bilaterally. Bronchial tones indicative of consolidation in the ventral lung fields are observed much more frequently than with acute P. multocida infections (Figure 4-16). Pleuritic friction sounds may be ausculted in some cases because of stretching or compression of fibrinous adhesions between the parietal and visceral pleura. The dorsal lung fields may sound normal on auscultation of animals with mild to moderate M. haemolytica pneumonia. In more severe cases, however, the dorsal lung may be forced to overwork because of the ventral lung consolidation. This overwork creates interstitial edema or bullous emphysema on occasion, and these pathologic changes cause the dorsal lung to be abnormally quiet on auscultation. Auscultation of the trachea will reveal coarse rattling or bubbling sounds caused by the inflammatory exudate free in the trachea. Palpation of the intercostal regions over the pneumonic lung causes the animal pain. Occasional cases will have an accumulation of transudative or exudative pleural fluid in the ventral thorax unilaterally or bilaterally that will cause a total absence of sounds when auscultation is performed.

Figure 4-15 Calf affected with M. haemolytica pneumonia showing anxious expression, extended head and neck to minimize upper airway resistance, and ventral edema caused by both albumin loss into the severely infected lungs and gravitational edema.

Figure 4-16 Thoracic radiograph of calf affected with severe M. haemolytica pneumonia. Cranioventral consolidation is highlighted by air bronchograms. Such lesions give rise to bronchial tones when the affected region of the lung is ausculted.

More severe or neglected cases may show open mouth breathing (Figure 4-17), anxious expression, subcutaneous emphysema secondary to tracking of air from bullae rupture in the dorsal lung field, and have harsh bronchial tones ventrally with inaudible lung sounds dorsally. Respiratory dyspnea is marked in such cases and affects both inspiratory and expiratory components, with the expiratory component being the most obvious. An audible grunt or groan may accompany each expiratory effort, and the animals are reluctant to move because of hypoxia and painful pleuritis.

Figure 4-17 Cow affected with severe M. haemolytica pneumonia showing open mouth breathing, pulmonary edema froth at muzzle, anxious expression, dehydration, and extended head and neck to maintain a “straight line” upper airway.

A peracute rapidly consolidating form of M. haemolytica bronchopneumonia occasionally has been observed over the past 10 years in the northeastern United States and has resulted in high morbidity and mortality within affected herds. The causative M. haemolytica has proven extremely resistant to antibiotics. In some instances, it was resistant to all antibiotics approved for use in dairy cows. Signs in acutely affected cattle include high fever (106.0 to 108.0° F/41.11 to 42.22° C), marked depression, salivation, increased respiratory rate (60 to 120 breaths/min), complete anorexia and milk cessation, reluctance to move, absence of rales when the ventral lungs are ausculted, profound bronchial tones bilaterally that indicate consolidation of 25% to 75% of the ventral pulmonary parenchyma (Figure 4-18), and quiet or inaudible sounds in the dorsal lungs where the remaining pulmonary tissue has been subjected to extreme mechanical and physiologic stress to maintain gas exchange. Subcutaneous emphysema and pulmonary edema are common sequelae in these cattle. Ventral abdominal pain can be elicited in the cranial abdomen as a result of the fibrinous pleuritis present. This pain and absence of rumen activity coupled with the other signs have caused many veterinarians to confuse the initial case of rapidly consolidating pneumonia as peritonitis caused by hardware or perforating abomasal ulcer. The major reason for this error is the absence of rales with this form of M. haemolytica. Therefore we have had to “retrain” our ears to auscult carefully for bronchial tones versus normal or harsh vesicular sounds. Careless auscultation of air sounds in the ventral lung field may not discriminate between bronchial tones and vesicular sounds. Acute infection with this form of M. haemolytica will result in progressive dyspnea and death in 12 to 48 hours unless the veterinarian is fortunate enough to choose as the first treatment an antibiotic to which the organism is susceptible.

Figure 4-18 Necropsy view of lungs affected by peracute rapidly consolidating M. haemolytica pneumonia. Consolidation exists over 80% to 90% of the lung parenchyma, and fibrin is obvious on the visceral pleura. The clinical course of the disease was 36 hours.

Diagnosis.

As with P. multocida pneumonia, accurate diagnosis of M. haemolytica bronchopneumonia requires culture of the organisms from tracheal wash specimens collected from acute, untreated cattle (Figure 4-19) or postmortem cultures of lung and lymph node specimens. Because mortality is greater for M. haemolytica than P. multocida, autopsy specimens often are the source of diagnostic material.

Figure 4-19 A cow being restrained with two halters in preparation of a transtracheal wash. This method of restraint helps keep the head and neck straight during the procedure.

Once it is apparent that the disease is epidemic in the herd, the veterinarian should obtain appropriate cultures via tracheal washings or fresh lung tissue at necropsy from several animals so that the delay in accurate diagnosis and bacterial susceptibility to antibiotics is as short as possible.

Tracheal wash, nasopharyngeal swab, or autopsy specimens also should be cultured and/or antigen tested for viral pathogens, H. somni, and Mycoplasma sp. Serum for viral titers should be collected from several acute cases so that it may be compared with convalescent serum titers in the future, if the animals survive. In this way, some viral agents that are difficult to culture, such as BRSV, may be identified as primary or contributing causes of the respiratory outbreak. Having collected these samples for culture, antigen testing, and seroconversion, the veterinarian will now have a basis, albeit retrospective, to identify the pathogens involved and attribute the disease to M. haemolytica alone or combined with other pathogens. This will be of importance for future preventive measures.

Gross pathology specimens show a bilateral fibrinous bronchopneumonia with 25% to 75% or more of the lungs involved. The distribution is anterior ventral in all cases, and the affected lung is firm, meaty, friable, and discolored. Usually fibrin is present on both the visceral and parietal pleura. Increased amounts of yellow or yellow-red pleural fluid are found frequently. In acute cases with advanced pulmonary parenchymal consolidation or in chronic cases, the dorsal lung may have bullous emphysema or interstitial edema present.

A complete blood count (CBC) from acutely infected cattle usually will show leukopenia characterized by a neutropenia with a left shift as neutrophils move to the site of severe infection. Fibrinogen values are elevated.

Radiographs or ultrasonography is only of value for prognosing an individual valuable calf or cow. An estimation of degree of consolidation and subsequent abscess formation may be aided by these techniques and allow accurate prediction of outcome. However, these techniques seldom are necessary given the physical signs present.

Treatment.

Broad-spectrum antibiotics constitute the major therapeutic defenses against M. haemolytica pneumonia. Once again, the veterinarian is forced to use “best guess” judgment when selecting an initial antibiotic in such cases. Following collection of appropriate diagnostic samples, antibiotic therapy should commence immediately. Because life-threatening signs usually appear in at least some of the affected cattle, the veterinarian is more likely to select broad-spectrum antibiotics immediately. The current popular antibiotics for cows and calves are shown in Table 4-1. Even when the causative bacterial organism is known, antibiotic therapy may be unable to cure the patient for a variety of reasons, such as the chosen antibiotic does not reach adequate tissue levels in the lung; the organism is resistant to the antibiotic; the organism is sensitive in vitro but in vitro inhibitory concentrations do not occur in the cow as a result of the dose, frequency of dosage, or other pharmacologic considerations; the drug may not be able to penetrate consolidated tissue or work in purulent tissue; and in vitro susceptibility tests may not reflect in vivo success of an antibiotic against a specific organism—thus the Kirby-Bauer disc assay has been criticized as too gross compared with mean inhibitory or bactericidal concentration tests that can give a concentration of drug that inhibits or kills an organism. This mean inhibitory concentration then can be compared with known achievable blood and tissue levels of the antibiotic in the cow to determine likelihood of successful treatment. The pathology may be irreversible or viral, and Mycoplasma or A. pyogenes pathogens may coexist to complicate the treatment plan. Textbook charts that quote percentages of isolates sensitive to various antibiotics are seldom helpful because both geographic differences in strains and temporal resistance patterns occur. Appropriate withdrawal times for any antibiotic selected for milk and slaughter residues must be known and observed and may shape decisions by the producer as to which antibiotic is chosen so that an immediate slaughter option is maintained.

TABLE 4-1 Dosages and Frequencies of Administration for Selected Antibiotics for Initial Therapy

The industry continues to seek the “silver bullet”—a magic antibiotic that will cure all cases of Mannheimia pneumonia. This silver bullet would take away the need for diagnostic work or preventive medicine, excuse management techniques that predispose to pneumonia, and of course would only be available through veterinarians. As a profession, we persist in overuse of every new antibiotic that becomes available. We ask these antibiotics to do things that cannot be done while ignoring older time-tested antibiotics. The silver bullet does not and will not exist.

Improvement in response to appropriate antibiotic therapy will appear as better attitude and appetite and a decreasing fever within 24 hours. A decrease of 2° F or more should be considered clinically indicative of improvement. The body temperature continues to decrease into the normal range over 48 to 72 hours in most cases that have been treated with appropriate antibiotics. Depending on which antibiotic is used, a minimum of 3 days of antibiotic treatment is often required, and more often 5 to 7 days of continuous therapy are necessary and less likely to result in recurrence.

Antiinflammatory medications are used by many veterinarians in conjunction with antibiotic therapy, as discussed under P. multocida pneumonia. If corticosteroids are used as part of initial therapy, we believe that 20 mg of dexamethasone or a comparable dose of prednisone for an adult cow is the maximum. This should not be used more than once, and it should not be used at all in pregnant cattle. Currently in our clinic, we do not use any corticosteroids in the treatment of M. haemolytica pneumonia. Flunixin meglumine or other nonsteroidal antiinflammatory drugs (NSAIDs) are sound therapeutic agents for use in those with M. haemolytica pneumonia for the first 1 to 3 days of therapy. Excessive dosage of NSAIDs or prolonged treatment with these agents should be avoided. Once again, aspirin is the safest drug for this purpose (at a dosage of 240 to 480 grains orally, twice daily for an adult cow or 25 grains/100 lb body weight twice daily for calves). Flunixin meglumine at 0.50 to 1.0 mg/kg is the most commonly recommended and only approved NSAID for treating bovine pneumonia and has been documented to improve clinical outcomes when combined with antibiotics compared with antibiotic treatment alone.

Antihistamines such as tripelennamine (1 mg/kg twice or thrice daily) are less commonly used these days but are still used by many experienced clinicians as supportive therapy. Atropine may be a useful adjunct in advanced cases showing marked dyspnea, open mouth breathing, or pulmonary edema. Atropine is used at 2.2 mg/45 kg body weight IM or subcutaneously (SQ), twice daily to decrease bronchial secretions and to act as a mild bronchodilator.

In severe cases, dehydration may be a complication because of toxemia and fever causing depression of appetite and water consumption. In addition, some cattle are so dyspneic that they are unable to take time to drink, lest they become more hypoxic. Any IV fluid therapy that excessively expands the intravascular volume may cause or worsen existing pulmonary edema, and the fluid volume administered must be appropriate. Administrating fluids through a stomach tube is safer regarding pulmonary edema, but the procedure is very stressful to an already hypoxic animal. Clinical judgment is required for these decisions, and in most cases, it is best to hope that antibiotic therapy will improve the animal within 24 to 48 hours so that the cow or calf may hydrate itself through adequate water consumption. Adequate water, salt, and small amounts of fresh feeds should be used to promote appetite.

Any management or ventilation deficiencies should be remedied immediately, and fresh air is of the utmost importance. It is better that the animals be in the cold fresh air than in a poorly ventilated or drafty but warm enclosure. The worst environmental effects occur when cattle develop M. haemolytica pneumonia during hot, humid weather because the additional respiratory effort to encourage heat loss complicates existing hyperpnea. Intranasal oxygen is beneficial for affected cattle being treated in a hospital.

Prognosis always is guarded until signs of clinical improvement are obvious. Cattle improving within 24 to 72 hours have a good prognosis, whereas those that take more than 72 hours have a greater risk of chronic lung damage or abscessation.

Following endemic Mannheimia or Pasteurella infection in groups of calves, Drs. King and Rebhun observed occasional calves that developed peracute respiratory distress and dyspnea as a result of proliferative pneumonia 2 to 4 weeks after recovering from confirmed Mannheimia/Pasteurella pneumonia. At autopsy, resolving anterior ventral pneumonia from the previous Mannheimia/Pasteurella infection is observed in anterior ventral lung fields, and the remainder of the lung is diffusely firm, heavy, and wet. Histopathology confirms proliferative pneumonia. Viral cultures, fluorescent antibody (FA) procedures, and serology have been negative for other pathogens, including BRSV, which also may cause a delayed-effect hypersensitivity pneumonia but with different lesions. Following observation of a number of these secondary proliferative pneumonia cases in the necropsy room, they were able to recognize clinically and treat several calves with this problem. The calves had a history of being part of a pneumonia outbreak 2 to 4 weeks previously, then apparently recovering. A sudden onset of extreme dyspnea in one recovered calf typifies the clinical situation. Signs include mild fever, open mouth breathing, and diffusely quiet lungs. Treatment consists of atropine (2.2 mg/45 kg twice daily), furosemide (25 mg/45 kg once or twice daily), broad-spectrum antibiotics, and box stall rest in a well-ventilated area. Response to therapy is slow, but survivors gradually improve over 7 to 10 days.

Etiology and Signs.

P. multocida is a gram-negative normal inhabitant of the upper airway of cattle and calves. The normal defense mechanisms of the lower airway prevent colonization of the lung by P. multocida via physical, cellular, and secretory defenses in the healthy state. P. multocida is, however, a likely opportunist any time lower airway defense mechanisms are compromised. Chemical damage to mucociliary clearance, such as is caused by ammonia fumes in poorly ventilated barns, may allow P. multocida the opportunity to colonize the lower airway. P. multocida also is found in mixed infections of the lung along with H. somni, A. pyogenes, Mycoplasma sp., and various respiratory viruses of cattle. Fusobacterium and other anaerobic organisms may also be present with chronic suppurative pneumonia in adult cattle.

The strains of P. multocida isolated from the lungs of cattle or calves frequently are sensitive to many antibiotics, including penicillin. This is in definite contrast to M. haemolytica, in which antibiotic resistance is much more probable. This difference will be important regarding treatment and prevention of P. multocida pneumonia.

The signs of acute P. multocida pneumonia include fever, depression, mild to severe anorexia, moist cough, increased rate and depth of respiration, and a decrease in milk production commensurate with the degree of anorexia. The fever ranges from 103.5 to 105.5° F (39.72 to 40.83° C) in most cases. Moist and dry rales will be ausculted in the anterior ventral lung field bilaterally and are classical findings in acute cases. Usually the dorsal lung fields are normal. Nasal discharge may be serous or mucopurulent in nature and is more apparent in calves than adult cows. The acute disease may occur in calves and cows of any age but tends to be more common in weaned calves and other grouped animals. When seen in younger animals, the acute disease usually is indicative of poor ventilation, excessive ammonia fumes, failure of passive transfer of immunoglobulins, and/or part of a diarrhea/pneumonia complex. All these predisposing factors are common in dairy calves placed in veal operations or other indoor group housing facilities. P. multocida has been found as the cause of neonatal septicemia in calves receiving inadequate colostrum. These septicemic calves may show signs of meningitis, septic uveitis, septic arthritis, and mucopurulent nasal and ocular discharge (Figure 4-20) in addition to the typical signs of acute P. multocida pneumonia.

Figure 4-20 Neonatal calf with P. multocida septicemia. In addition to pneumonia, signs included fever, hypopyon, and mucopurulent nasal and ocular discharges.

Acute P. multocida pneumonia tends to occur as either an infectious epidemic or endemic disease in groups of housed calves or adult cattle and may affect 10% to 50% of the animals within a group. It is one of the causes of “enzootic pneumonia” in calves, but this is not the preferred term because it gives little information as to the exact cause of pneumonia. During an acute outbreak, the degree of apparent illness and auscultable degree of pneumonia will vary greatly among affected cattle or calves. If only one animal in a group is infected, predisposing causes or stress unique to that animal should be sought when establishing a history (e.g., recent purchase, recent calving, possibility of BVDV-persistent infection [Figure 4-21], transport to a show, sale, or poor ventilatory management).

Figure 4-21 A 3-year-old Jersey bull at a stud facility developed P. multocida pneumonia without any environmental stress factors. The bull was later proven to be persistently infected with BVDV, which likely resulted in immunosuppression.

Chronic pneumonia resulting from P. multocida causes signs similar to the acute disease, but bronchial tones indicative of consolidation frequently are limited to the anterior ventral lung fields. The abnormal area may be missed unless the stethoscope is pushed under the shoulder and the calf or cow forced to take a deep breath. In calves this can be accomplished most easily by holding the mouth and nose shut for a short period (Figure 4-22). Animals affected with chronic pneumonia may have marked exacerbation of dyspnea and an increased respiratory rate ($60 breaths/min) if housed in poorly ventilated areas or where the environmental temperature exceeds 70.0° F (21.1° C). A. pyogenes is a common secondary invader in lungs chronically infected with P. multocida. Following acute epidemic P. multocida pneumonia, occasional affected animals may show signs of chronic pneumonia.

Figure 4-22 An easy method of properly auscultating the lungs in calves. To make the calf breathe deeply, the calf is backed into a corner and one hand is placed over the mouth and nose until the calf struggles, at which time the calf is allowed to breathe. Alternatively, in adult cows a plastic garbage bag can be used over the cow’s nose and mouth to force deep breathing.

Diagnosis.

P. multocida pneumonia may be suspected after obtaining the appropriate history from the cow’s owner and finding typical signs complete with anterior ventral pneumonia and bilateral auscultable rales. However, confirmation requires culture of P. multocida from tracheal wash samples or autopsy specimens of acute, untreated affected animals. Neutrophils predominate the white blood cell components of the tracheal wash fluid, and gram-negative rods may be observed intracellularly in acute cases. The hemogram may show a degenerative left shift typical of acute infection in cattle or may be normal in mild cases. Chronic cases ($2 weeks) may have neutrophilia, and adult cattle may show hyperglobulinemia in the serum.

Gross pathology of fatal acute cases includes bilateral anterior ventral pneumonia with the affected portion of lung being firm and discolored red or blue (Figure 4-23). Palpation of the firm affected lung is the key to gross pathologic diagnosis. Fibrin may coat the surface of the parietal or visceral pleura but tends to be less than that observed with M. haemolytica. Chronic cases will show similar firm, pneumonic lung parenchyma but often have bronchiectasis and pulmonary abscesses.

Figure 4-23 Necropsy findings in a calf that was affected with severe cranioventral pneumonia caused by P. multocida.

Radiographs seldom are necessary but may be helpful for individual chronically infected calves or mature cattle to identify abscesses and degree of consolidation for prognostic purposes. Ultrasound examination will help define the severity of lung involvement.

Treatment.

Antimicrobials and changes in husbandry or management constitute the integral components of effective therapy for P. multocida pneumonia. Many antibiotics have been used, including penicillin, ampicillin, erythromycin, and tetracycline. Sulfa drugs (trimethoprim-sulfa has been used in calves because it can be mixed with milk to bypass the forestomachs) also have been effective when administered either alone or in combination with antibiotics such as penicillin or tetracycline. Ceftiofur, a broad-spectrum cephalosporin, has been approved for use in Pasteurella pneumonia in cattle and has proven to be very effective. Tilmicosin (a macrolide) and florfenicol are also effective but currently not approved for use in adult dairy cattle. The practicing veterinarian must start antibiotic therapy without knowing results of cultures and antibiotic sensitivity tests. Therefore initial treatment is based on previous experience, geographic differences in antibiotic sensitivity, and economic factors. Animals that are febrile, anorectic, and dyspneic require treatment. Other animals that have mild fever and depression but continue to eat and do not act very ill may not require treatment. Individual or small groups of sick animals may be treated empirically if fatalities are not anticipated. However, if an epidemic situation is apparent, it always is best to do transtracheal washes from several animals before any treatment. Having done this, the veterinarian may start empiric therapy assured that definitive antibiotic sensitivity results will be forthcoming in 3 days. Thus if the animals fail to respond to the initial choice of antibiotic, a specific antibiotic may be selected based on the sensitivity results as soon as these are available.

Penicillin, tetracycline, florfenicol, ampicillin, or ceftiofur may be selected for initial therapy. Dosages and frequency of administration are listed in Table 4-1. Regardless of the antibiotic selected, all treated cattle should have temperature and attitudes recorded daily so that 24- and 48-hour evaluations can be assessed. A trend of decreasing temperature into the normal range should proceed at 1 to 2° F per day when an effective antibiotic is used; the attitude, appetite, and degree of dyspnea should improve along with the return to normal body temperature. Hjerpe has done extensive work in feedlot cattle to estimate probable efficacies of various antibiotics in pneumonia outbreaks. This material is an excellent reference, but the veterinarian must remember that geographic variations in bacterial serotypes and antibiotic susceptibility exist and that antibiotic resistance is likely to increase in years to come. Individual treatment generally is easier for dairy animals than beef animals. Antibiotics such as tetracycline, sulfa drugs, and tylosin have been added to feed and water to treat large groups of calves or heifers. This method may be utilized if the animals are not too sick to eat or drink. If affected cattle are completely off feed, this method is ineffective. When faced with an obvious epidemic, the veterinarian may choose to divide the animals requiring treatment into three groups—each group consisting of animals with mild, moderate, and severe signs. Each group then could be treated with a different antibiotic. Twenty-four hours after initial treatment, each group would be evaluated for relative degrees of improvement and all sick animals given the antibiotic that resulted in the most improved group.

Many practitioners use antiinflammatory agents in conjunction with antimicrobial therapy. The goals of antiinflammatory medications are to reduce fever, block specific parts or mediators of the inflammatory cycle, counteract endotoxins released by the cell wall of the causative gram-negative organisms, and result in symptomatic improvement through better appetite and attitude. The two general groups of drugs include corticosteroids and NSAIDs, such as aspirin and flunixin meglumine. Corticosteroids have a marked antiinflammatory and antipyretic activity that often leads to a “steroid euphoria” with resultant improved attitude and appetite within 24 hours. Although corticosteroids have these positive effects and also block several parts of the inflammatory cycle, they are dangerous if used repeatedly or in high dosages. Corticosteroids may reduce some of the chemotactic factors and lysosomal enzymes that cause a vicious cycle of increasing inflammation in the lung and tend to stabilize small vessels. However, they also partially or completely inhibit macrophage activation and antimicrobial peptide expression, which are serious detriments to the defense mechanisms of the lower airway. If the veterinarian elects to use corticosteroids, one treatment of low-dose (10 to 20 mg/450 kg) dexamethasone may be given as part of the initial therapy and should not be used thereafter. This treatment cannot be used in pregnant cows because of the abortifacient qualities of dexamethasone. Corticosteroids have potent antipyretic properties, and this may lead to a false sense of security because the veterinarian may assume that the proper antibiotic has been used based on a decreasing fever 24 hours following treatment when in fact the antibiotic has not been effective and fever will return 24 to 48 hours later. I do not recommend the use of corticosteroids for bacterial pneumonia.

NSAIDs are safer than corticosteroids in the treatment of bacterial bronchopneumonia in cattle but are not without some disadvantages. Advantages include blockage of some prostaglandin-mediated inflammation within the lung, antiendotoxin effects, and antipyretic activity. Disadvantages include inability to gauge response to specific antibiotics based on body temperature alone as a result of the artificial decrease in fever caused by NSAIDs, and the possibility of toxicity manifested by abomasal ulceration or renal damage if treatment is excessive in frequency, dosage, or duration. Aspirin may be the safest of the NSAIDs and is given at 240 to 480 grains orally, twice daily for an adult animal, and flunixin meglumine at 0.50 to 1.0 mg/kg IV, once or twice daily may be the most effective. Occasionally aspirin and flunixin meglumine have caused abomasal ulceration when administered for a prolonged time to sick cattle. Renal toxicity also is a risk—especially in a dehydrated animal in which the cytoprotective and vascular effects of prostaglandins are essential during reduced renal perfusion. I prefer flunixin when NSAID therapy is selected, but similar to corticosteroids, these drugs are adjuncts, not essentials, for the treatment of bronchopneumonia caused by P. multocida.

Bronchodilators such as aminophylline have been used in cattle with pneumonia but do not appear to be beneficial clinically except when given by constant infusion to calves with respiratory distress. Atropine given parenterally or ipratropium by inhalation may be effective bronchodilators. If albuterol could be used in cattle, it might be beneficial because this drug has been shown in other species to act not only as a bronchodilator but also to improve mucociliary clearance. Parasympatholytic bronchodilators have been shown to be more effective in calves than sympathomimetic drugs.

Antihistamines are used as adjunctive therapy in bovine bronchopneumonia by many practitioners. Drugs such as tripelennamine hydrochloride (1 mg/kg IM or SQ, twice or thrice daily) are believed to improve the animal’s attitude and appetite. These symptomatic observations may be valid, but because histamine has not been shown to be one of the major inflammatory mediators in Pasteurella pneumonia, no scientific evidence exists to justify the use of these drugs.

The recognition and correction of management problems or ventilation deficiencies may be as important, if not more so, than any of the previous pharmaceuticals when treating endemic P. multocida pneumonia. Because the organism primarily is an opportunist that gains access to the lower airway following insults to the physical, cellular, or secretory defense mechanisms, predisposing causes should be sought and corrected. In calves, poor ventilation, crowding, and poor husbandry relating to excessive ammonia fumes may be sufficient to allow P. multocida to descend from its normal habitat of the upper airway and colonize the lungs. Examples include changeable temperature and humidity when calves are grouped during the indoor housing season (especially fall, spring, and during winter thaws), broken fans, failure to clean large pens when calves have been in groups for weeks to months, lungworms, and drafts that the confined calves cannot escape. Fresh air is vital to recovery and should be provided even if it means allowing the animals access to outside air in inclement weather.

In adult cattle, all these factors above apply, but ventilation deficiencies predominate. In modern free stall facilities, transition cow management practices that add greater stress to an already changeable/stressful period appear to greatly impact the acquisition of acute pneumonia and progression to chronic disease. Frequent pen moves, overstocking, poor ventilation, and concurrent metabolic disease alongside some of the treatments and therapeutic practices used by producers all substantially increase the chances for postpartum respiratory disease to become a herd problem. Bronchopneumonia caused by P. multocida alone usually is a management problem. Although it certainly is recognized that previous viral infection or mixed infections (e.g., Mycoplasma) could and do predispose to P. multocida pneumonia in calves and cattle, it must be emphasized that management factors are very important. Secondary P. multocida pneumonia, such as that following viral respiratory infection, will be discussed in conjunction with viral diseases. Failure of cattle affected with P. multocida pneumonia to respond to appropriate antibiotic therapy based on culture and susceptibility results should alert the veterinarian to the fact that (1) P. multocida is not the only agent involved in the epidemic (i.e., a virus or Mycoplasma also may be present or was present—therefore viral isolation, paired serology, and so forth are indicated); (2) the predisposing management or ventilation problems have not been corrected; and (3) lungworms should be ruled out.

Vaccinations are included in the prevention section and are discussed on pages 107-109.

Etiology and Signs.

With increasing frequency, H. somni has been identified as a pathogen of the lower airway in dairy cattle. It is occasionally identified as the cause of herd outbreaks of pneumonia in dairy cattle or calves in the northeastern United States. H. somni may be the only pathogen isolated or may be found in conjunction with Mycoplasma spp. or Pasteurella pneumonia in cattle. Although H. somni occasionally is isolated from the upper airway of normal cattle, this gram-negative organism is more commonly isolated in clinical pneumonia patients. A shift in the normal upper airway bacterial flora or stress activation of latent H. somni in the upper airway may contribute to lower airway infection.

The pathogenicity of H. somni and Pasteurella organisms is attributed to several characteristics: (1) an endotoxin derived from the cell wall lipopolysaccharides, (2) exotoxins that are lethal or damaging to alveolar macrophages, neutrophils, and vascular endothelium, and (3) chemotactic factors and possible hemolysins common to H. somni and other bacteria that act as inflammatory mediators. Vasculitis is a predominant feature of H. somni pathology. H. somni–stimulated platelets have also been shown to contribute to endothelial cell damage, which may play a role in pathogenesis of the vasculitis and thrombosis. In addition, H. somni has a propensity to cause disease in the heart muscle and sometimes the central nervous system.

The signs of H. somni bronchopneumonia in calves and adult cattle are indistinguishable from moderate to severe P. multocida pneumonia or mild to moderate M. haemolytica pneumonia. Affected animals have fever (103.5 to 106.6° F/39.72 to 41.44° C), an increased respiratory rate (40 to 80 breaths/min), depression, nasal discharge, occasional salivation, painful cough, and decreased milk production proportional to the degree of anorexia observed. Dyspnea may be marked in some cases, and these cattle will show anxiety and reluctance to move. Neurologic signs or septicemia caused by H. somni observed in feedlot animals is less common in dairy cattle and calves. If, however, any cattle develop neurologic signs during an outbreak of bronchopneumonia in a herd or group of calves, H. somni should be strongly suspected as the cause of the illness.

Auscultation of the lungs typically identifies bilateral anterior ventral pneumonia characterized by moist and dry rales with bronchial tones indicative of ventral consolidation identified in up to 50% of the cases. Tracheal rales may be ausculted as a result of the heavy mucopurulent exudate found in the trachea. Palpation of the intercostal spaces overlying the pneumonic regions may be painful to the animal.

Diagnosis.

Because the signs usually are identical to those of Pasteurella pneumonia, the veterinarian should collect appropriate samples (tracheal washes for culture and bacterial sensitivities or autopsy cultures from lung and lymph nodes) and institute therapy. A failure of response to standard broad-spectrum antibacterial therapy typifies H. somni pneumonia. Usually an exact diagnosis as to etiology has to await culture and sensitivity results from diagnostic samples. CBCs are variable and nonspecific, with either a degenerative or regenerative left shift observed and elevated fibrinogen levels. Acute and convalescent serum may be helpful retrospectively if the diagnostic laboratory utilized for testing has the capability to establish H. somni titers.

Postmortem specimens will show anteroventral firm areas of pneumonia bilaterally. Fibrin may be apparent in the visceral and parietal pleura occupying the areas of pneumonia. In some cases, red blotches or hemorrhage is apparent. White microabscesses may be observed also.

Treatment.

Although H. somni apparently is sensitive in vitro to many antibiotics including penicillin, clinical results in vivo are discouraging. Ampicillin is the drug of choice for H. somni pneumonia in calves and adult cattle. Ampicillin is used at 11 to 22 mg/kg twice daily by injection for 3 to 7 days in most cases. Cephalosporins also may be effective. Enrofloxacin reportedly has good efficacy against Histophilus sp. but currently is not approved for use in dairy cattle in the United States.

Response to ampicillin or other effective antibiotics will be manifested by a progressive decrease in body temperature to the normal range over 24 to 72 hours. For this reason, the treating veterinarian may find it best not to use NSAIDs or corticosteroids in H. somni pneumonia because these drugs decrease the temperature artificially through antipyretic effects and interfere with interpretation of appropriate antibiotic selection.

Just as in Pasteurella bronchopneumonia, ventilation or management factors that predispose to altered lower airway defense mechanisms should be corrected immediately. The prognosis is fair to good unless severe pneumonia and marked dyspnea are present.

Etiology and Signs.

A. pyogenes is a gram-positive coccobacillus that acts as a ubiquitous opportunist capable of establishing chronic pyogenic infections virtually anywhere in the cow’s body. In the lung, it is a secondary invader that usually only establishes infection following suppression of host physical, cellular, or secretory defense mechanisms. Physical factors such as inhalation pneumonia also may allow A. pyogenes to infect the lung, and viral, bacterial, or Mycoplasma agents may precede infection with A. pyogenes. Immunosuppression caused by acute or persistent infection with BVDV has been followed by A. pyogenes pneumonia in calves and adult cows. Similarly, calves affected with bovine leukocyte adhesion deficiency (BLAD) frequently suffered A. pyogenes pneumonia. Pulmonary infection is aided by the proteases and hemolysins that the organism produces. These factors contribute to tissue necrosis and inflammatory events that perpetuate the organism’s existence. Fusobacterium and other pathogenic anaerobic organisms may be found concurrently with A. pyogenes, P. multocida, and Mycoplasma spp.

Signs are indicative of chronic or recurrent infection, the hallmark of A. pyogenes pneumonia. The history usually indicates illness of at least 1 week’s duration or recurrent episodes of pneumonia over weeks to months. There may only be one (usually adult cattle) or a few animals (usually calves) affected out of a group or herd. In adult dairy cattle, it is common for clinical signs to develop following freshening (Figure 4-24). In some cases, there may be severe subcutaneous emphysema over the dorsum, suggesting a rupture of diseased alveoli associated with calving as a cause of the pneumomediastinum, subcutaneous emphysema, and sometimes pneumothorax. Although this should be considered in cattle with dorsal emphysema following calving, similar emphysema may be found sometimes in apparently healthy cattle following calving and of course in cattle with interstitial pneumonia. Affected animals may show low-grade fever (103.0 to 105.0° F/39.44 to 40.56° C), rapid respiratory rate (40 to 100 breaths/min), dyspnea characterized by exaggerated inspiratory and especially expiratory efforts (particularly when stressed), head and neck extension when lying down, cough, nasal discharge (Figure 4-25), rough hair coat, poor body condition, depression, inappetence, or decreased milk production. Some cattle maintain normal respiratory rates but exhibit the other signs. Chronic suppurative pneumonia should always be considered a differential for the “poor doing” cow. Auscultation of the lungs reveals moist and dry rales in the ventral 25% to 50% of both lungs in calves and one or both lungs in adult cattle, bronchial tones indicative of consolidation in the ventral lung fields, and coarse tracheal rales caused by a thick mucopurulent airway exudate. High environmental temperatures, high humidity, and poor ventilation exacerbate the clinical signs. A fetid smell may be present following a cough if anaerobic bacteria are present. Auscultation during rebreathing, paying close attention to the cranioventral lung fields under the triceps musculature for the presence of bronchial tones indicative of consolidation, is important when investigating possible cases of mild to moderate chronic suppurative bronchopneumonia.

Figure 4-24 A 5-year-old cow with cough and respiratory distress following calving 5 days earlier. The cow had chronic suppurative pneumonia with acute onset of respiratory signs associated with stress of calving.

Figure 4-25 A mature Holstein cow presented to the hospital for poor production and weight loss. Although respiratory rate was within normal limits, the cow coughed after rising, had slight head and neck extension when lying down, and, as seen in this photo, had small and intermittent purulent nasal discharge. P. multocida, A. pyogenes, and Mycoplasma spp. were cultured from a tracheal wash. The cow improved dramatically following tetracycline therapy.

Diagnosis.

History and physical signs are very suggestive of A. pyogenes pneumonia, but specific diagnosis requires culture of the organism from tracheal wash samples or lung tissue. There may only be one or a few animals affected with signs of chronic pneumonia following a preceding herd endemic of pneumonia caused by other organisms. Chronic or recurrent cases are referred to as “lungers” by some farmers.

Radiographs or ultrasonography of the thorax is helpful in establishing a prognosis because lung abscesses, bronchiectasis, and consolidation (sometimes remarkably severe in a single lobe) (Figure 4-26) are common in the affected lung (see video clip 9).

Figure 4-26 Radiograph of a cow with chronic suppurative pneumonia and a dramatic lobar consolidation.

A CBC may show neutrophilia or be normal. Serum globulin often is in the high range of normal or elevated ($5.0 g/dl), especially in adult cattle. The animal should be screened for persistent infection with BVDV via buffy coat viral isolation. Gross autopsy of fatal cases reveals anterior ventral consolidation with areas of purulent bronchiectasis and multiple pulmonary abscesses (Figure 4-27).

Figure 4-27 Necropsy view of cut section from the cranioventral lung region of a calf showing bronchiectasis and pulmonary abscesses typical of chronic A. pyogenes pneumonia.

Treatment.

Treatment is frustrating, and the prognosis is poor for pneumonia caused by A. pyogenes. Other causative organisms such as P. multocida, M. haemolytica, Mycoplasma, and/or Fusobacterium also may be cultured from the tracheal wash sample. Penicillin is the drug of choice and should be given at 22,000 U/kg twice daily for 7 to 30 days. Although penicillin is effective against A. pyogenes in vitro, the pulmonary in vivo infection should be likened to an abscess because of the heavy accumulation of A. pyogenes pus in areas of bronchiectasis or encapsulated lung abscesses. If another pathogen, in addition to A. pyogenes, is isolated from the tracheal wash sample, appropriate antibiotic therapy should be selected for this organism as well. Ceftiofur, ampicillin, and tetracyclines are other commonly used therapies. Clinical treatment frequently results in short-term improvement followed by relapse when the animal is stressed or subjected to high environmental temperatures, humidity, or poor ventilation. Signs of improvement will be indicated by normal rectal temperature, improved respiratory function, and improvement in overall body condition and attitude. Many affected animals eventually succumb to the infection or are culled because of poor condition and production.