Clinical History
A 2-month-old Holstein bull calf with a history of droopy ears and poor weight gain was submitted alive for euthanasia and necropsy to the Diagnostic Center for Population and Animal Health at Michigan State University. The owner reported that 6 to 8 calves with similar signs in the same herd had died or been euthanized in the preceding 30 days; some affected calves had additionally developed signs of ataxia prior to death.
Gross Findings
The calf was euthanized with an IV overdose injection of pentobarbital sodium. At necropsy, the calf was markedly emaciated (40.9 kg [90 lb]), with little pericardial, perirenal, and mesenteric fat. The remaining fat around the heart and kidneys was red and gelatinous (serous atrophy). The cranioventral aspects of both lungs were firm and red to purple, with numerous spherical, 3- to 5-mm-diameter nodules (Figure 1). The centers of many of the nodules were white and pasty. Approximately 66% of the right lung and 33% of the left lung were affected, and there was a distinct line of demarcation between the firm, affected areas and the apparently normal, spongy, pink caudodorsal portions. The right tracheobronchial lymph node was enlarged. Both tympanic bullae were soft and collapsed under digital pressure; they were filled with white pasty material. Bony septa within the bullae were not visible.
Photographs of the lung surface (A) and tympanic bullae (B) of a bull calf that was euthanized for necropsy because of droopy ears and poor weight gain. Notice the extensive suppurative bronchopneumonia and the severe bilateral suppurative otitis media.
Citation: Journal of the American Veterinary Medical Association 242, 10; 10.2460/javma.242.10.1351
Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page →
Histopathologic and Microbiological Findings
Sections of affected tissue from the right lung (cranioventral portion) and unaffected right lung (caudodorsal portion) were examined histologically. In affected areas, there was diffuse consolidation of the parenchyma; bronchi and bronchioles were distended with necrotic debris and inflammatory cells, and compression or collapse of surrounding alveoli was evident. The lining epithelium of the ectatic airways was effaced, and the central necrotic luminal contents were partially mineralized (Figure 2). This core of caseous necrotic debris was surrounded by a zone of degenerated and viable neutrophils and macrophages, and the walls of the airways and the peribronchiolar and peribronchial interstitium contained moderate numbers of lymphocytes, plasma cells, and macrophages. Elsewhere in the affected lung tissue, there was consolidation caused by suppurative exudate in airways and alveoli. Inflammation was so severe in these areas that alveolar architecture was obscured or effaced. In grossly nonconsolidated areas of the lung tissue, there was diffuse congestion, and the peribronchial and peribronchiolar interstitium contained increased numbers of mononuclear inflammatory cells. Mycoplasma bovis organisms were detected by immunohistochemical staining in some foci of inflammation (Figure 3) and in the apical portion of numerous intact bronchiolar epithelial cells bordering the areas of inflammatory changes.
Photomicrograph of a section of affected lung tissue from the calf in Figure 1. Notice that eosinophilic granular and partially mineralized material (caseous necrosis) has completely effaced the airways and compressed the surrounding parenchyma. H&E stain; bar = 2 mm.
Citation: Journal of the American Veterinary Medical Association 242, 10; 10.2460/javma.242.10.1351
Photomicrograph of a section of affected lung tissue from the calf in Figure 1. The granular red labeling indicates the presence of Mycoplasma bovis in a focus of pyogranulomatous inflammation characterized by degenerated neutrophils surrounded by macrophages. Immunohistochemical stain for M bovis; bar = 100 μm.
Citation: Journal of the American Veterinary Medical Association 242, 10; 10.2460/javma.242.10.1351
Numerous M bovis and moderate numbers of Pasteurella multocida were cultured from samples of lung tissue. Microbial cultures of samples from the middle ear yielded Acinetobacter sp, nonhemolytic Streptococcus sp, and rare Bacillus sp, in addition to M bovis.
Morphologic Diagnosis and Case Summary
Morphologic diagnosis: severe extensive suppurative bronchopneumonia and bilateral severe diffuse suppurative otitis media.
Case summary: Mycoplasma bovis–associated bronchopneumonia and otitis media in a calf.
Comments
Mycoplasma bovis is a known cause of mastitis, infertility, arthritis, and pneumonia in cattle. Arthritis is the predominant clinical consequence of infection, although it can often be concurrent with mastitis or pneumonia.1 The microorganism can be shed in secretions of the respiratory tract, genital tract, or mammary glands.2 Respiratory tract disease generally develops in calves that are 1 to 4 months old.3 Infected animals often develop signs of disease when debilitated as a result of an underlying condition or when stressed.4 Gagea et al5 reported that M bovis–associated bronchopneumonia was identified in 54 of 99 feedlot beef calves that died or were euthanized; 25 of the 54 calves also had arthritis. Otitis media was diagnosed in 7 of the 99 feedlot calves, but M bovis was isolated from samples of the tympanic bullae of only 3 of those animals.5 In another study,6 16 of 64 (25%) veal calves with pneumonic lesions at slaughter were positive for M bovis (determined on the basis of results of bacterial isolation and immunohistochemical staining).
In the calf of this report, a diagnosis of M bovis infection was tentatively established clinically on the basis of droopy ears and poor weight gain. Additional reported abnormalities associated with M bovis infection include signs of depression, nasal discharge, swollen joints, and reluctance to rise.5,6
At necropsy, the findings of suppurative bronchopneumonia and otitis media supported the presumptive clinical diagnosis of M bovis infection for the calf of this report. Additional gross findings related to M bovis infection may include fibrinous pleuritis and fibrinonecrotizing polyarthritis,7 but these were not evident in this case. Histologically, lesions caused by M bovis are typically characterized by suppurative bronchopneumonia with bronchiectasis, fibrinous pneumonia with irregular areas of coagulative necrosis, or multifocal pyogranulomatous inflammation with centers of caseous necrosis and abscess formation.2,7,8
A definitive diagnosis of M bovis infection requires histologic examination, bacterial culture, PCR assay, ELISA, or immunohistochemical analysis of samples of the lungs and middle ear.3,8,9 For live animals, results of PCR assay or culture of transtracheal wash or bronchoalveolar lavage fluid samples may provide a diagnosis. Bacterial culture of nasal swab specimens has lower sensitivity (21%), compared with culture of bronchoalveolar lavage fluid samples, for prediction of M bovis–associated lung disease.10 In calves with arthritis, affected joints or tendon sheaths can be aspirated to obtain samples for microbiological testing.11 Also, it is not uncommon for bacterial culture of samples to yield M bovis along with other bacteria, as illustrated by the case described in this report. It has been proposed that lesions of fibrinosuppurative bronchopneumonia initiated by infections with Mannheimia haemolytica, Histophilus somni, and P multocida may be secondarily colonized and perpetuated by M bovis, which can also colonize healthy bovine lung tissue without causing pneumonia.5 Thus, it is important to identify not only infection with this organism, but also the presence of characteristic clinical signs or lesions.2
Approved treatments for M bovis infection in calves in the United States include tulathromycin, enrofloxacin, florfenicol, oxytetracycline, streptomycin, tilmicosin, and tylosin3; however, many isolates are resistant to tetracycline, oxytetracycline, and tylosin as well as spectinomycin and lincomycin.12 In addition to antimicrobials, the use of anti-inflammatory drugs can be beneficial because the inflammatory response may contribute to disease associated with M bovis infection.3 Treatment is frequently unrewarding, however, either because it has to be provided over a long period or because the affected calf fails to respond. Thus, calves with M bovis infection usually die or are euthanized.3 Elimination of the disease from a herd often involves culling of infected animals, such as cows with Mycoplasma mastitis. It is important to avoid feeding milk and colostrum from such infected cows to calves. In instances where that procedure is unavoidable, pasteurization of the milk is recommended.3 For calves, inoculation with an experimental quadrivalent inactivated vaccine has been shown to provide some protection against respiratory tract disease caused by M bovis.13 In another study,14 calves administered a saponised inactivated vaccine developed fewer respiratory tract signs and less damage to the lungs and had less weight loss and lower rectal temperatures after challenge with a virulent strain of M bovis, compared with findings in unvaccinated calves. However, these vaccines are not yet available for commercial use. Therefore, currently, the best way to avoid development of M bovis–associated disease in cattle is to maintain a closed herd and keep newly purchased animals under quarantine for a period.
References
1. Maunsell FP, Woolums AR, Francoz Det al., Mycoplasma bovis infections in cattle. J Vet Intern Med. 2011; 25:772–783.
2. Caswell JL, Williams KJ, Respiratory system. Maxie MG, Pathology of domestic animals. Philadelphia: Saunders Elsevier, 2007; 611–614.
3. Maunsell FP, Donovan AG, Mycoplasma bovis infections in cattle. Vet Clin North Am Food Anim Pract. 2009; 25:139–177.
4. Hewicker-Trautwein M, Feldmann M, Kehler Wet al., Outbreak of pneumonia and arthritis in beef calves associated with Mycoplasma bovis and Mycoplasma californicum. Vet Rec. 2002; 151:699–703.
5. Gagea MI, Bateman KG, Shanahan RAet al., Naturally occurring Mycoplasma bovis – associated pneumonia and polyarthritis in feedlot beef calves. J Vet Diagn Invest. 2006; 18:29–40.
6. Radaelli E, Luini M, Loria GRet al., Bacteriological, serological, pathological and immunohistochemical studies of Mycoplasma bovis respiratory infection in veal calves and adult cattle at slaughter. Res Vet Sci. 2008; 85:282–290.
7. Maeda T, Shibahara T, Kimura Ket al., Mycoplasma bovis. J Comp Pathol. 2003; 129:100–110.
8. Shahriar FM, Clark EG, Janzen Eet al., Coinfection with bovine viral diarrhea virus and Mycoplasma bovis in feedlot cattle with chronic pneumonia. Can Vet J. 2002; 43:863–868.
9. Khodakaram-Tafti A, López A, Immunohistopathological findings in the lungs of calves naturally infected with Mycoplasma bovis. J Vet Med A Physiol Pathol Clin Med. 2004; 51:10–14.
10. Thomas A, Dizier I, Trolin Aet al., Comparison of sampling procedures for isolating pulmonary mycoplasmas in cattle. Vet Res Commun. 2002; 26:333–339.
11. Byrne W, Fagan J, McCormack M, Mycoplasma bovis arthritis as a sequel to respiratory disease in bought-in weanling cattle in the Republic of Ireland. Ir Vet J. 2001; 54:516–519.
12. Thomas A, Nicolas C, Dizier Iet al., Antibiotic susceptibilities of recent isolates of Mycoplasma bovis in Belgium. Vet Rec. 2003; 153:428–431.
13. Howard CJ, Thomas LH, Parsons KR, Immune response of cattle to respiratory mycoplasmas. Vet Immunol Immunopathol. 1987; 17:401–412.
14. Nicholas RA, Ayling RD, Stipkovits LP, An experimental vaccine for calf pneumonia caused by Mycoplasma bovis: clinical, cultural, serological and pathological findings. Vaccine. 2002; 20:3569–3575.
