|
|
||||||||||
Short Communications |
1 Unidad de Histología y Anatomía Patológica, Departamento
de Producción Animal, Sanidad Animal y Ciencia y Tecnología de
los Alimentos, Facultad de Veterinaria, Universidad CEU-Cardenal Herrara,
Edificio Seminario s/n, 46113 Moncada, Valencia, Spain
2 Instituto Vasco de Investigación y Desarrollo, Agraria (NEIKER), 48160
Derio, Bizkaia, Spain
Correspondence: E-mail for correspondence: jmcorpa{at}uch.ceu.es
OSTEOMYELITIS in animals is frequently caused by bacterial infections, and is often predisposed by previous trauma (Thompson 2007). The most commonly involved bacteria are Arcanobacterium pyogenes, Escherichia coli, and Salmonella and Staphylococcus species (McGavin and others 2001, Thompson 2007). Although osteomyelitis can begin in any bone, it is normally localised in the metaphyseal area of the long bones and vertebrae of young animals (McGavin and others 2001). However, mandibular osteomyelitis has also been reported frequently in animals. The disease in cattle, commonly known as lumpy jaw, is caused by Actinomyces species, and occasionally occurs in other species (Hoefs and Bunch 2001, McGavin and others 2001, Thompson 2007, Brookins and others 2008). Lumpy jaw has been reported in wild sheep in North America, in which a secondary bacterial infection may follow oral trauma and induce the lesion (Hoefs and Bunch 2001). In domestic sheep, mandibular osteomyelitis associated with tooth loosening is sometimes detected as a cause of non-specific weight loss. In these cases, plant material has been found between the teeth and the alveolar bone, which provides access for environmental bacteria into the bone (McGavin and others 2001).
|
|
The studied animals came from a farm located in the Valencian Community (east Spain) and included 450 crossbred ewes that grazed extensively in a typical Mediterranean area. According to the farmer, the mandibular and maxillary bones of almost 12 per cent of the ewes, irrespective of age, became severely deformed over a nine-month period. Initially, the affected animals showed anorexia, depression, recumbency and fever. The next phase was characterised by a swelling of the nasomaxillary and mandibular area, as well as a purulent nasal discharge. The animals become cachectic and had poor body condition and hair loss. Death followed in a period of no more than two months. The mortality of the affected animals was 80 per cent. Eight animals were submitted for postmortem examination and the lesions were seen to be limited to the oral cavity. Gross lesions were confined to the cheek and deep zones, and affected the nasomaxillary and mandibular bones. The initial lesions consisted of small gingival ulcers that spread rapidly and sometimes involved deep tissues. The more severe lesions consisted of a dirty necrotic purulent abscess, surrounded by a zone of acute inflammation inside the alveolar tooth cavity, which caused a deformed bone structure (Fig 1). The submandibular and retropharyngeal lymph nodes were enlarged and congested, with severe oedema. Samples of the mandibular and maxillary bones were collected and fixed in 10 per cent buffered formalin. The fixed and decalcified samples were embedded in paraffin wax, sectioned (4 µm), and stained with haematoxylin and eosin, Masson's trichrome and Gram stains. Microscopically, the gross lesions corresponded to some extensive necrotic areas within the trabecular bone. This histological finding was accompanied by a mixed population of inflammatory cells consisting of neutrophils, macrophages, lymphocytes and plasma cells. The swelling lesions were also due to exuberant fibrous tissue surrounding the necrotic zones (Fig 2). Additionally, swabs of the abscesses were collected for bacterial culture. Five per cent sheep blood agar and McConkey's agar plates were inoculated and incubated aerobically at 37°C for 24 to 48 hours. Abundant Gram-negative bacteria were found in the necrotic material. P aeruginosa was isolated in heavy, pure cultures from all of the swabs taken. The antibiotic susceptibility of the isolates was studied by determining the minimum inhibitory concentration in a solid medium. The isolates were sensitive to ciprofloxacin and gentamicin, and resistant to clavulanic acid, amoxicillin, cefoxitin, sulfamethoxazole, trimethoprim, cloramphenicol and doxycycline.
In domestic animals, mandibular osteomyelitis can be caused by opportunistic bacteria such as Actinomyces species when tissues have been injured previously (McGavin and others 2001, Thompson 2007). The same pathology has been reported in wild sheep. Nevertheless, there are other isolated aetiological agents, such as A pyogenes, Fusobacterium necrophorum or Staphylococcus aureus (Hoefs and Bunch 2001). Even oral flora can produce mandibular osteomyelitis in domestic sheep that present with oral trauma resulting from the ingestion of rough feed (Thompson 2007). However, to the authors' knowledge, there have been no previous reports of mandibular osteomyelitis caused by P aeruginosa in domestic animals. Mandibular and maxillary osteomyelitis has been documented in four red kangaroos (Macropus rufus) from which a mixed population of bacteria was cultured, but Pseudomonas species predominated in all of the isolates (Brookins and others 2008). On the other hand, Pseudomonas species appear to be important, given their ubiquity, the ease with which they grow and their resistance to many antibiotics (Krieg and Holt 1984, El-Sukhon 2002). P aeruginosa causes infections in external organs, such as the mammary glands, skin, nasal cavity or ears. In these cases, contaminated water has been reported to be the origin of the bacteria (Kingsford and Raadsma 1997, Las Heras and others 1999, El-Sukhon 2002, Watson and others 2003, Leitner and Krifucks 2007). In the present study, drinking water was also the likely source of the bacterial infection because no further cases occurred after the drinking trough was cleaned and the water supply changed. However, the water was not submitted for microbiological analysis.
P aeruginosa should therefore be considered as a cause of nasomaxillary and mandibular osteomyelitis in sheep. In these cases, water should not be ruled out as a source of the bacteria. The high bacterial load associated with non-specific mucosal trauma, facilitated by the ingestion of rough feed that is usual in intensive feeding systems, could favour bacterial infection and the development of disease. A combination of antibiotic treatment, the prevention of oral abrasions by avoiding coarse forage and elimination of the source of the bacteria could curb the disease.
Acknowledgements
This study was supported by the Copernicus Program (CEU-UCH and Banco de Santander).
Provenance: not commissioned; externally peer reviewed
References
EL-SUKHON, S. N. (2002) Isolation and characterization of Pseudomonas aeruginosa from sheep with fleece rot in northern and middle Jordan. Veterinary Dermatology 13, 247-251[Medline]
HOEFS, M. & BUNCH, T. D. (2001) Lumpy jaw in wild sheep and its evolutionary implications. Journal of Wildlife Diseases 37,39 -48[Abstract]
KINGSFORD, N. M. & RAADSMA, H. W. (1997) The occurrence of Pseudomonas aeruginosa in fleece washings from sheep affected and unaffected with fleece rot. Veterinary Microbiology 54,275 -285[Medline]
KRIEG, N. R. & HOLT, J. G. (1984) Pseudomonadaceae. In Bergey's Manual of Systematic Bacteriology. Vol 1. Williams & Wilkins. pp140 -218
LAS HERAS, A., DOMÍNGUEZ, L., LÓPEZ, I. & FERNÁNDEZ-GARAYZÁBAL, J. F. (1999) Outbreak of acute ovine mastitis associated with Pseudomonas aeruginosa infection. Veterinary Record 145,111 -112
LEITNER, G. & KRIFUCKS. O. (2007) Pseudomonas aeruginosa mastitis outbreaks in sheep and goat flocks: antibody production and vaccination in a mouse model. Veterinary Immunology and Immunopathology 119,198 -203[Medline]
MCGAVIN, M. D., CARLTON, W. W. & ZACHARY, J. F. (2001) Inflammation of bone. In Thompson's Special Veterinary Pathology. 3rd edn. Mosby. pp441 -443
THOMPSON, K. (2007) Bones and joints. Inflammatory diseases of bones. In Jubb, Kennedy, and Palmer's Pathology of Domestic Animals. Vol 1. 5th edn. Ed M. Grant Maxie. Elsevier Saunders. pp 92-105
WATSON, P. J., JIRU, X., WATABE, M. & MOORE, J. E. (2003) Purulent rhinitis and otitis caused by Pseudomonas aeruginosa in sheep showered with contaminated 'shower wash'. Veterinary Record 153,704 -707
| ||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | CURRENT ISSUE | TABLE OF CONTENTS | ARCHIVE | SEARCH | SUBSCRIPTIONS | JOBS | FEEDBACK | HELP |