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1 DST/NRF Centre of Excellence for Biomedical TB Research/MRC Centre for Molecular and Cellular Biology/Division of Molecular Biology and Human Genetics, Department of Biomedical Sciences, Faculty of Health Sciences-Stellenbosch University, PO Box 19063, Tygerberg 7505, South Africa;
2 Bacteriology Section, ARC-Onderstepoort Veterinary Institute, Private Bag X05, Onderstepoort 0110, South Africa;
3 Department of Veterinary Tropical Diseases, Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderstepoort 0110, South Africa;
4 Vetpath, PO Box 8464, Pretoria 0001, South Africa;
5 Directorate of Animal Health, Department of Agriculture, Veterinary Investigation Centre, PO Box 12, Skukuza 1350, South Africa
6 Corresponding author (email: pvh{at}sun.ac.za)
ABSTRACT:
We report a case of pyogranulomatous pneumonia due to infection with Mycobacterium goodii in an adult female spotted hyena (Crocuta crocuta). The lungs of the animal showed consolidated, granulomatous lesions, and they were extensively and severely infiltrated. Polymerase chain reaction sequencing of isolated crude lung tissue DNA, and boiled lung culture samples, all confirmed that the causative organism was M. goodii, a recently described fast-growing organism closely related to the nonpathogenic mycobacterial species M. smegmatis. The current study illustrates that this organism can be pathogenic and cause extensive pulmonary disease.
Key words: Mycobacterium goodii, non-tuberculous mycobacterial infection, pulmonary disease, spotted hyena.
In May 2006, an adult female spotted hyena (Crocuta crocuta) was captured in the greater Kruger National Park complex (GKNPC), South Africa (24°55' 24'S, 31°31'30''E), owing to her being a problem animal. The animal was apparently healthy, with no external injuries noted. Her body condition was good, she was within normal weight range of an animal of her age (ca. 4 yr old), and all other vital signs were normal. Upon capture, the hyena was tested with the comparative intradermal tuberculin skin-test as part of the bovine tuberculosis surveillance program in the GKNPC, and diagnosed as a positive reactor to bovine purified protein derivative (PPD) (bovine PPD reaction >2 mm larger than avian PPD reaction, warm and edematous). Because she was a positive reactor and a problem animal, she was euthanized and subjected to postmortem examination according to a standard protocol. On examination of the thoracic organs, confluent, consolidated, granulomatous lesions involving the hilar and ventral regions of the middle and caudal lung lobes were observed (Fig. 1
). Nodular enlargement of the bronchial lymph nodes was also apparent. All other organs and tissues seemed to be macroscopically normal. Tissue samples were taken from the bronchial lymph nodes and the lungs, and from various other lymph nodes in 10% buffered formalin, for histopathology and culture. Histopathologic examination of lung samples showed a pyogranulomatous pneumonia that was chronic and severe in appearance with multifocal-to-confluent inflammatory nodules, often closely associated with larger bronchi (Fig. 2A). The nodules were characterized by central areas of neutrophil infiltration, surrounded by a mixture of neutrophils, lymphocytes, plasma cells, multinucleate giant cells, and some macrophages (Figs. 2B, C). Lymph node tissues, from the mesenteric, gastrointestinal, retropharyngeal, parotid, axillary, popliteal, mandibular, and mediastinal lymph nodes, and the tonsils, seemed histologically within normal limits, with active lymphoid tissue visible. Mammary lymph nodes were less active. Ziehl-Neelsen staining of lung tissue revealed acid-fast bacilli bacteria compatible with Mycobacterium sp. organisms present within the centers of inflammatory nodules.
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enzyme-linked immunosorbent assay (ELISA) using bovine and avian PPD were performed on blood taken before euthanasia (Morar et al., 2007). Although white blood cells of the hyena were reactive (high concanavalin A values), results using bovine and avian PPDs (cattle concentrations) as stimulants were negative (data not shown). Mycobacterium goodii is a recently described fast-growing organism closely related to the mycobacterial species M. smegmatis (Brown et al., 1999). Infections with M. goodii rarely have been reported, but most commonly (79% of described infections) have been associated with panniculitis and wound infection. One case of M. goodii-associated panniculitis was described in a dog, with concurrent endogenous Cushing’s disease (Bryden et al., 2004). Three isolated cases of chronic lung disease in humans were mostly associated with chronic lipoid pneumonia (Brown et al., 1999). Thus far, there is only one report of isolation of M. goodii in Africa (from a pleural effusion in a human immunodeficiency virus-negative human (Buijtels et al., 2005) and only two reports worldwide of nonlipoid granulomatous pneumonia associated with M. goodii infection (Brown et al., 1999). In the previously described pleural effusion case, it is interesting to note that the patient had been treated for pneumonia, which had improved with amoxicillin treatment, a year before diagnosis with M. goodii. This patient also had hookworms in the stool and presented with diarrhea for 3 days. In the case of the hyena described in this study, the axillary lymph node sample and the myocardium showed the presence of Hepatozoon sp. organisms, and tapeworm segments were noticeable in the lumen of intestinal sections on histopathologic evaluation. Although these organisms are usually considered incidental, they may be responsible for some of the inflammation, especially in the myocardium where mild lymphoplasmacytic infiltrates were associated with the Hepatozoon sp. protozoal parasites. Such organisms could thus promote a T-helper (Th)2-type immune system response, as does the helminth infection seen in the human situation (Maizels and Yazdanbakhsh, 2003). It is not known whether this response would allow colonization by M. goodii, although there is evidence to suggest that bacterial colonization and infection takes place more easily under conditions of coinfection by organisms that promote Th2 immune responses (Resende et al., 2007).
The source of M. goodii in this case is unknown; however, the hyena had close contact with a human environment, and food and a human source thus cannot be ruled out. Whether M. goodii can be a pulmonary pathogen in the absence of immune system modifications (e.g., coinfections) or in the absence of lipoid pneumonia is currently unknown. The histopathologic findings of a pyogranulomatous pneumonia in the hyena are, however, compatible with lesions found in cases of mycobacterial pneumonia in animals, including the large wild cats. The fact that this animal was infected and diseased with M. goodii and had negative IFN- ELISA test results suggests that the positive skin-test was a false-positive result and may be due to cross-reactivity with the M. goodii antigens. This is significant with regard to the use of skin-test assays for screening of animals for bovine tuberculosis.
Here, we report the first case of M. goodii infection in a nondomestic animal species and in an animal species in Africa. This study shows that this organism can be a pulmonary pathogen, adding to the pathogenic potential for disease reported for this organism.
The authors thank M. de Kock for technical assistance.
BROWN, B. A., B. SPRINGER, V. A. STEINGRUBE, R. W. WILSON, G. E. PFYFFER, M. J. GARCIA, M. C. MENENDEZ, B. RODRIGUEZ-SALGADO, K. C. JOST, JR., S. H. CHIU, G. O. ONYI, E. C. BOTTGER, AND R. J. WALLACE, JR. 1999. Mycobacterium wolinskyi sp. nov. and Mycobacterium goodii sp. nov., two new rapidly growing species related to Mycobacterium smegmatis and associated with human wound infections: A cooperative study from the International Working Group on Mycobacterial Taxonomy. International Journal of Systematic Bacteriology 49: 1493–1511.
BRYDEN, S. L., A. K. BURROWS, AND A. J O’HARA. 2004. Mycobacterium goodii infection in a dog with concurrent hyperadrenocorticism. Veterinary Dermatology 15: 331–338.[Medline]
BUIJTELS, P. C., P. L. PETIT, H. A. VERBRUGH, A. VAN BELKUM, AND D. VAN SOOLINGEN. 2005. Isolation of nontuberculous mycobacteria in Zambia: Eight case reports. Journal of Clinical Microbiology 43: 6020–6026.
HARMSEN, D., S. DOSTAL, A. ROTH, S. NIEMANN, J. ROTHGANGER, M. SAMMETH, J. ALBERT, M. FROSCH, AND E. RICHTER. 2003. RIDOM: Comprehensive and public sequence database for identification of Mycobacterium species. BMC Infectious Diseases 3: 26.[Medline]
MAIZELS, R. M., AND M. YAZDANBAKHSH. 2003. Immune regulation by helminth parasites: Cellular and molecular mechanisms. Nature Reviews Immunology 3: 733–744.[Medline]
MORAR, D., E. TIJHAAR, A. NEGREA, J. HENDRIKS, D. VAN HAARLEM, J. GODFROID, A. L. MICHEL, AND V. P. RUTTEN. 2007. Cloning, sequencing and expression of white rhinoceros (Ceratotherium simum) interferon-gamma (IFN-gamma) and the production of rhinoceros IFN-gamma specific antibodies. Veterinary Immunology and Immunopathology 115: 146–154.[Medline]
RESENDE, C. T., C. S. HIRSCH, Z. TOOSSI, R. DIETZE, AND R. RIBEIRO-RODRIGUES. 2007. Intestinal helminth co-infection has a negative impact on both anti-Mycobacterium tuberculosis immunity and clinical response to tuberculosis therapy. Clinical and Experimental Immunology 147: 45–52.[Medline]
WARREN, R. M., N. C. GEY VAN PITTIUS, M. BARNARD, A. HESSELING, E. ENGELKE, M. DE KOCK, M. C. GUTIERREZ, G. K. CHEGE, T. C. VICTOR, E. G. HOAL, AND P. D. VAN HELDEN. 2006. Differentiation of Mycobacterium tuberculosis complex by PCR amplification of genomic regions of difference. International Journal of Tuberculosis and Lung Disease 10: 818–822.[Medline]
Received for publication 13 June 2007.
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