Abstract
Oral necrobacillosis or “lumpy jaw” is a common cause of morbidity and mortality affecting captive macropods.1,3,6,8,9 Dental disease remains the most common disease presentation for macropods at Melbourne Zoo despite a long understanding of the risk factors for its development. Oral cavity disease seen in macropods at Melbourne Zoo can be categorized as follows:
1. Endodontal disease: pulp cavity exposure with or without infection, usually following traumatic injury
2. Soft tissue abscessation: resulting from foreign body penetration (generally grass awns)
3. Periodontal disease: characterized by calculus accumulation, gingivitis and periodontitis without development of osteitis
4. Classic lumpy jaw: the most frequent presentation, characterized by osteitis (severe necrosis and lysis of bone) as well as acute inflammation of soft tissues.
Lumpy jaw may occur as a consequence of progression of periodontal lesions or endodontal disease. A number of etiologic agents have been implicated in the development of lumpy jaw. The most important pathogens are anaerobic bacteria, predominantly Fusobacterium necrophorum.2,9 Macropods are not considered to be inherently susceptible to infection with F. necrophorum; however, they are frequently exposed to important predisposing factors for necrobacillosis.12 Predisposing factors identified as contributing to development of lumpy jaw in Melbourne Zoo macropods include the process of molar progression, features of the captive diet, and environmental stressors.
The Process of Molar Progression
Sanson classifies macropods as “grazer grade,” “intermediate browser/grazer grade,” or “browser grade” marsupials, based on tooth form and function.11 In each jaw quadrant, an adult grazing macropod has three upper incisors and one large lower incisor, a reduced permanent premolar that is relatively rapidly lost through molar progression, and four molars. The mandibular tooth row is curved, so that only the anterior molars are in occlusion. The grazing molar of macropods operates at maximum efficiency when relatively unworn. Molar progression facilitates the migration of unworn teeth anteriorly into wear to replace worn teeth, thus providing a mechanism by which fewer teeth are maintained in the tooth row.10 The dental formula of browsing macropods is identical to that of grazing macropods; however, the premolar is larger and, to a certain extent, prevents forward progression of the molars. It has been hypothesized that abnormalities of tooth wear and shedding contribute to the occurrence of lumpy jaw. A number of authors have proposed that captive diets that are insufficiently abrasive will delay the process of molar progression, or result in retention of post-functional teeth in grazing macropods.5,7,8 This may predispose to development of lumpy jaw. Food impaction associated with molar progression has also been proposed as an initiating factor.8 Butler reported that lumpy jaw lesions often developed at the site of erupting molars, but these lesions did not appear to be associated with abnormalities in tooth shedding.4 In many cases of lumpy jaw affecting red kangaroos (Macropus rufus) and red-necked wallabies (Macropus rufogriseus banksiana) at Melbourne Zoo, lesions have developed in the anterior molars at the time of shedding of the premolar.
Diet of Captive Animals
Trauma to periodontal tissue, resulting in establishment of the etiologic agent in the jaw, is also believed to initiate development of lumpy jaw, and may occur as a result of feeding stalky hays or sharp-awned grasses.1,4,5 It has also been suggested that a plaque-initiated periodontitis may provide the necessary gingival defect that allows invasion by F. necrophorum,8 and that a low fibre, high residue diet in captivity may result in greater proliferation of dental plaque than the free-ranging grazing diet.2 We believe that plaque-initiated periodontitis contributes to the development of lumpy jaw lesions in Melbourne Zoo macropods.
Environmental Stressors
Lumpy jaw has been reported in wild macropods, but is generally considered a disease of captivity. Environmental stressors (e.g., cold stress/exposure, high stocking density, high levels of interaction with zoo visitors) are believed to be contributors to disease development. Bacterial contamination of feeding areas (e.g., as a consequence of overcrowding or poor feeding and/or enclosure hygiene practices) also predisposes to development of disease in macropod groups. Environmental stressors are considered key risk factors for the development of lumpy jaw lesions in Melbourne Zoo collection macropods. Factors that have recently been identified as contributing to disease occurrence in red kangaroos (1995–2005) include the incidence of fighting among males, the availability of suitable shelter areas for animals, enclosure stocking density, and enclosure screening from vehicle noise.
The most common presentation for Melbourne Zoo macropods with lumpy jaw is unilateral facial swelling. Hypersalivation and “mouthing” are frequently observed, and animals are usually obtunded. Initial assessment of affected animals is carried out under anesthesia. Diagnostic techniques include a dental examination, diagnostic radiographs (with the head in a lateral oblique position to optimise views of the affected dental arcade), and blood collection for routine hematology and biochemistry. Treatment consists of extraction of any mobile teeth and curettage of necrotic bone. The extraction site is flushed with sterile saline, benzylpenicillin 150 mg/ml solution (BenPen, CSL Ltd, Parkville, VIC, Australia) and/or metronidazole 5 mg/ml solution (Metrin Solution, Parnell Laboratories Australia Pty Ltd, Alexandria, NSW Australia). The site may be left open or packed with either Orabase Protective Paste® (ConvaTec Ltd, Bristol-Myers Squibb, Noble Park, VIC, Australia) or, if the defect is large, cotton umbilical tape coated with a zinc oxide-eugenol paste. Other authors have suggested placement of antibiotic-impregnated polymethylmethacrylate beads into the bony defect.6 Parenteral antibiotics (long-acting penicillin 1 ml per 10 kg i.m. (Norocillin LA injection, Norbrook Laboratories Australia Ltd, Gisborne, VIC, Australia) are given, and analgesia (ketoprofen 1–2 mg/kg SC (Ilium Ketoprofen Injection, Troy Laboratories Pty Ltd, Smithfield, NSW Australia) and/or buprenorphine, 0.01 mg/kg SC (Temgesic Injection, Reckitt Benckiser, West Ryde, NSW, Australia) is provided.
Affected animals are housed in an off-exhibit enclosure during the treatment course, in order to facilitate treatment and minimise contamination of the display environment with causative organisms. Antimicrobial treatment with clindamycin hydrochloride 11 mg/kg p.o. b.i.d. (Antirobe capsules, Pharmacia and Upjohn Pty Ltd, Rydalmere, NSW, Australia), ceftiofur 2 mg/kg i.m. s.i.d. or long-acting penicillin 1 ml per 10 kg i.m. every other day is continued. Animals are anesthetized once weekly, for reassessment and debridement, until healing of the extraction site has occurred. Neuroleptic drugs such as azaperone 0.2–0.5 mg/kg i.m. (Stresnil Neuroleptic Injection for Pigs, Boehringer Ingelheim Pty Ltd, North Ryde, NSW Australia) and fluphenazine decanoate 2.5 mg/kg i.m. (Modecate, Bristol-Myers Squibb Australia Pty Ltd, Noble Park, VIC, Australia) may be used to reduce anxiety during hospitalization and treatment. In cases of severe and extensive osteomyelitis, or when animals have had repeated episodes of disease, euthanasia is considered appropriate.
Literature Cited
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