兽研1. 引言
猫皮肤分枝杆菌病是一种不常见的感染性疾病，由多种分枝杆菌属物种引起，包括结核分枝杆菌复合群（MTBC）成员、苛养型或麻风样分枝杆菌以及非结核分枝杆菌（NTM）[1,2,3,4,5,6,7,8]。这些微生物为革兰氏阳性、需氧、抗酸杆菌[1,2,5,9]，其特征是细胞壁富含脂质和分枝菌酸，这有助于其抵抗热、消毒剂以及在抗酸染色过程中酸-酒精的脱色作用[5,9]。
鼻疽分枝杆菌是一种属于NTM群的快速生长菌种[10,11,12]。它于1973年首次被描述为牛鼻疽的病原体，这是一种慢性化脓性肉芽肿性疾病，影响东非和中非瘤牛的皮肤和淋巴管[10,11,13,14,15,16]。感染通常通过皮肤创伤后的皮肤接种、伤口污染或外科手术发生；土壤、水和腐烂植被是这些细菌的主要环境来源[1,2,3,5,6,7,8,9,17,18]。临床病变通常表现为皮下结节、不愈合伤口和多条引流窦道，分布于腹侧腹部和腹股沟区域[1,2,5,7,8,9,17,18,19,20]，该微生物在富含脂质的组织中复制[1,2,3,8,9,18]。在某些病例中，病变还可能延伸至骨盆肢和尾根[5,8]。
治疗通常需要长期给予双联或三联抗菌药物[3,4,21]，新一代氟喹诺酮类药物如pradofloxacin或莫西沙星、大环内酯类药物如克拉霉素或阿奇霉素以及多西环素也可考虑作为某些快速生长分枝杆菌菌种的治疗选择[1,2,5]。通常建议联合抗菌治疗以降低抗菌药物耐药风险[1,2,4,22,23]。然而，体外药敏试验并不总是与临床反应相关[5,24]。治疗应在病变完全消退后至少继续一至两个月[1,2,3,4,5,9]。手术切除在选定病例中可能有益，但可能因伤口裂开和愈合延迟而复杂化[1,2,5,8,9]。
关于人和动物鼻疽分枝杆菌感染的报道仍然罕见，文献中描述了散发性人类病例[11,12,13]。迄今为止，仅在一篇在线教育病例报告中描述了一例猫鼻疽分枝杆菌感染[25]。本病例报告描述了由鼻疽分枝杆菌引起的一只猫的皮肤分枝杆菌病，并记录了尽管对所用抗菌药物之一存在体外耐药，但治疗成功。据作者所知，这是亚洲首例报道的由鼻疽分枝杆菌引起的猫皮肤分枝杆菌病。
2. 病例描述
2.1. 病史
一只4岁绝育雌性家养短毛猫被转诊至Kasetsart大学兽医教学医院，以评估涉及左大腿外侧和左腹股沟区域的8个月慢性不愈合引流伤口病史。左大腿外侧的病变在猫咬伤后出现，对常规伤口管理、经验性抗菌治疗和反复伤口灌洗均无反应。转诊兽医进行的需氧细菌培养未产生细菌生长。
初次咬伤后三个月，在左腹股沟区域和邻近左侧第五乳腺处发现组织肿胀。细针抽吸细胞学检查提示伴有炎症的梭形细胞肿瘤，促使手术切除和组织病理学检查。手术时，对大腿伤口进行了清创并放置了手术引流管。拆线后，乳腺手术切口出现伤口裂开并伴有黏液脓性分泌物，而大腿伤口尽管使用阿莫西林-克拉维酸（16 mg/kg PO q12h）、泼尼松龙（0.5 mg/kg PO q24h）和常规伤口护理治疗，仍持续引流。切除组织的组织病理学检查显示严重的坏死性脓肉芽肿性乳腺炎和皮炎。由于两处病变的进行性、不愈合性质，该猫被转诊进行进一步诊断检查和管理。
2.2. 体格检查
初次就诊时，该猫精神警觉、反应灵敏。生命参数在正常范围内，体况评分为5/9。体格检查发现左腹股沟区域先前手术部位有一处慢性不愈合伤口，其特征为皮下肿胀、多条引流窦道和黏液脓性分泌物。左大腿外侧还存在两处额外的引流伤口。
2.3. 诊断方法
对腹股沟病变进行细针抽吸，采用Wright–Giemsa染色进行细胞学检查。采集两处引流窦道的渗出物用于细菌培养和抗菌药物敏感性试验。样本接种于绵羊血琼脂、麦康凯琼脂、哥伦比亚血琼脂和巧克力琼脂，于37 °C、5% CO2条件下培养；培养2天后首次观察到菌落。对可见菌落进行抗酸染色，并经传代纯化后，通过基质辅助激光解吸/电离飞行时间质谱（MALDI-TOF MS；Bruker Biotyper，Bruker Daltonics，Bremen，Germany）进行菌种鉴定。使用分离菌的纯培养物，通过实验室改良的纸片扩散法进行抗菌药物敏感性试验[26]。简要而言，将调整至0.5麦氏标准的细菌悬液涂布于补充5%绵羊血的Mueller–Hinton琼脂上，贴加抗菌药物纸片，平板于37 °C、5% CO2条件下培养48小时后测量抑菌圈直径[27]。由于尚无经过验证的M. farcinogenes菌种特异性折点[27]，抑菌圈直径在可获得时采用CLSI兽医解释标准[28]进行判读，对于无兽医特异性折点的药物，则采用人医CLSI[29]或EUCAST[30]标准作为替代标准。在等待实验室结果期间，处方阿莫西林-克拉维酸19 mg/kg口服，每12小时一次（Amoxclamed®，BIC Chemical Co.，Ltd.，Bangkok，Thailand）。
2.4. 实验室结果
细胞学检查显示大量中性粒细胞和巨噬细胞，符合化脓性肉芽肿性炎症（图1）。两处病变采集样本的细菌培养均生长出M. farcinogenes，这是一种快速生长的非结核分枝杆菌（NTM），在猫中罕有报道。培养2天后首次可见菌落，样本提交后5天报告菌种鉴定结果。分离菌抗酸染色显示大量抗酸阳性杆菌，经MALDI-TOF MS鉴定为M. farcinogenes。
2.5. 抗菌药物敏感性试验
两处病变的抗菌药物敏感性试验显示对阿米卡星、庆大霉素、亚胺培南、美罗培南、马波沙星和普拉沙星敏感，对阿莫西林-克拉维酸和恩诺沙星中介，对其余受试抗菌药物耐药（表1）。由于尚未建立经过验证的M. farcinogenes抑菌圈直径折点，这些解释分类应视为初步表型指导，而非标准化敏感性分类[27]。
2.6. 治疗
根据抗菌药物敏感性结果，处方普拉沙星6.6 mg/kg口服，每24小时一次（Veraflox®，Elanco (Thailand) Ltd.，Bangkok，Thailand），以及5%硫酸阿米卡星外用凝胶（Likacin® gel 5%，S Charoen Bhaesaj Trading，Bangkok，Thailand）每日一次涂抹于病变内。尽管体外试验耐药，治疗方案中仍加用了阿奇霉素8.2 mg/kg口服，每24小时一次（Azith®，Siam Bheasach Co.，Ltd.，Bangkok，Thailand）。
2.7. 治疗结果
病变随时间逐渐改善，腹股沟开放性伤口愈合后于第21天停用阿米卡星凝胶，治疗24周后达到完全临床缓解（图2）。随访期间进行的血液学和血清生化分析均在正常范围内。未观察到与治疗相关的不良反应，猫在整个治疗期间保持临床健康。
3. 讨论
猫皮肤分枝杆菌病是一种不常见的感染性疾病，由多种分枝杆菌属物种引起，包括快速生长的非结核分枝杆菌（NTM）。尽管由快速生长NTM——如脓肿分枝杆菌、耻垢分枝杆菌和偶发分枝杆菌复合群成员——引起的散发性猫感染已有报道，但由产鼻疽分枝杆菌引起的感染似乎极为罕见。产鼻疽分枝杆菌是一种环境快速生长NTM物种，最初被认为是牛鼻疽的病原体，牛鼻疽是一种影响热带地区牛的慢性肉芽肿性疾病，以化脓性淋巴管炎和皮肤病变为特征[10,11,13,14,15,16]。然而，牛鼻疽主要在撒哈拉以南非洲有报道；尽管在南亚和东南亚部分地区有历史记载，但泰国或邻近亚洲国家的牲畜或水牛中尚无病例报道[15]。在牛中，血清学检测已被研究作为辅助诊断方法，全细胞抗原ELISA显示出对产鼻疽分枝杆菌所致牛鼻疽的血清学诊断和流行病学筛查的潜在效用[31]。然而，该方法对猫NTM感染，特别是产鼻疽分枝杆菌的适用性仍未确定。伴侣动物尤其是猫的感染报道仍然极为有限，关于其在猫中的致病性、临床行为和最佳治疗的信息也很匮乏。据作者所知，这是亚洲首例报道的由产鼻疽分枝杆菌引起的猫皮肤分枝杆菌病病例。本病例为该罕见感染在猫中的表现、诊断和治疗提供了额外的临床信息。
本病例的病变分布与猫皮肤分枝杆菌病一致，该病通常侵犯富含脂质的皮下组织[1,2,3,8,9,18]，引起脂膜炎、结节、溃疡和引流窦道。这些病变常见于腹侧腹部、腹股沟区、尾根和骨盆肢[1,2,5,7,8,9,18,19,20]。在本病例中，初始病变在报道的猫咬伤后发生于左大腿外侧，随后在左腹股沟区出现第二处病变。尽管无法确定确切的传播途径，但已知快速生长分枝杆菌沿皮下组织平面延伸，窦道在临床上可能并不总是明显。因此，原有感染的延伸可能导致了术后伤口裂开。慢性咬伤也可能使环境中的病原体得以污染伤口。本病例表明，将分枝杆菌感染纳入猫慢性不愈合伤口的鉴别诊断十分重要。在临床可行的情况下，术前诊断和处理可以优化抗菌治疗并预防伤口裂开或愈合延迟等并发症。
猫皮肤分枝杆菌病的诊断仍然具有挑战性[1,3,4,5,25]，因为临床表现通常非特异性，且可能与其他慢性皮肤病学状况极为相似，包括细菌感染、深部真菌感染、异物反应、免疫介导性疾病和肿瘤[2,8,32,33]。在本病例中，转诊前对乳腺肿块进行的细针穿刺（FNA）细胞学检查最初被解释为提示梭形细胞肿瘤伴并发炎症，促使进行了手术切除。组织病理学检查显示严重的坏死性化脓性肉芽肿性乳腺炎和皮炎，无肿瘤证据。在慢性化脓性肉芽肿性炎症和脂膜炎中，反应性成纤维细胞和肌成纤维细胞可能在纤维增生过程中增殖，并在细胞学上表现为梭形细胞，可能模仿间叶性肿瘤[34]。因此，提示梭形细胞肿瘤的细胞学发现应谨慎解读，尤其是伴有明显炎症时，并应与组织病理学和微生物学发现结合解读。此外，化脓性肉芽肿性炎症应促使使用特殊染色排查感染性病因，如针对分枝杆菌的抗酸染色和针对真菌病原体的过碘酸-雪夫（PAS）染色或Gomori六胺银（GMS）染色。在本病例中，由于组织在转诊前已经处理，未对组织病理学标本进行这些染色。细胞学涂片也未进行抗酸染色，因为本实验室皮肤细胞学不常规使用该染色。这是本报告的一个局限性。在化脓性肉芽肿性炎症病例中，尤其是怀疑分枝杆菌感染时，应考虑进行抗酸染色。
通过细菌培养和菌种鉴定确立了明确诊断。本病例中一个有趣的发现是转诊前后细菌培养结果的差异。转诊兽医进行的初次培养未长出细菌，而重复培养成功从两处病灶中分离出Farcinogenes分枝杆菌。这一发现提示，细菌培养阴性并不能排除分枝杆菌感染。样本质量、采样深度、细菌载量、运输条件和实验室操作等因素均可能影响培养结果[1,2,5]。因此，当初次培养结果为阴性但仍怀疑分枝杆菌感染时，应考虑由专业实验室进行重复细菌培养。在本病例中，五天内即可见细菌生长，这与快速生长型非结核分枝杆菌的特征一致，此类细菌通常在常规培养基上七天内形成菌落[5,13]。细菌早期生长使得基质辅助激光解吸/电离飞行时间质谱（MALDI-TOF MS）能够及时进行菌种级鉴定，支持其作为兽医分枝杆菌学中快速、准确且经济有效的诊断工具的价值[11,35,36]。由于尽管临床怀疑，细菌培养偶尔仍可能为阴性，因此在条件允许时还应考虑PCR和靶向测序，尤其是在抗酸染色阴性或培养结果不确定时[1,2,4]。尽管MALDI-TOF MS在常规诊断流程中提供了快速的菌种级鉴定，但16S rRNA基因测序仍是确认少见分枝杆菌菌种的决定性方法[4,13,17,23]。在本回顾性报告中，由于治疗后未保留培养分离株，无法进行16S rRNA测序。在今后的病例中，应考虑增加16S rRNA基因测序以进一步确认菌种鉴定。
猫皮肤分枝杆菌病的治疗通常疗程较长，一般需要联合抗菌药物治疗以提高治疗成功率并降低抗菌药物耐药风险[1,2,3,4,5]。在本病例中，在诊断为皮肤分枝杆菌病之前曾使用泼尼松龙进行伤口处理。因此，在疑似分枝杆菌感染时应避免使用皮质类固醇治疗，因为免疫抑制可能损害细胞介导免疫，阻碍对胞内分枝杆菌的有效控制[1,2,37,38]。
在本病例中，普拉多沙星、局部阿米卡星凝胶和阿奇霉素治疗24周后实现完全临床缓解，且无不良反应。选择普拉多沙星是基于体外药敏结果及其对快速生长型非结核分枝杆菌的既定疗效[1,2,5]，并得益于其在深部化脓性肉芽肿性病灶中良好的组织穿透性[39]。尽管全身性阿米卡星（包括以10 mg/kg皮下注射、每日一次的给药方式）是分枝杆菌感染的重要治疗选择，但本病例选择局部阿米卡星凝胶作为可及性引流病灶的辅助治疗，同时避免长期全身性氨基糖苷类暴露及其相关肾毒性风险。然而，局部给药对较深皮下组织的穿透可能有限，因此对于广泛或深部组织受累的病例，可考虑全身性阿米卡星并配合适当监测。
关于阿奇霉素，尽管该分离株在体外显示耐药，但最初仍作为经验性多药方案的一部分用于广泛皮下病变[1,2,3,4,5]。阿奇霉素具有免疫调节特性，可能通过调节巨噬细胞功能促进临床改善[40]。然而，鉴于快速生长分枝杆菌药敏试验的可靠性，体外耐药使阿奇霉素发挥主要作用的可能性降低。尽管如此，分枝杆菌感染中已有体外药敏与临床反应不一致的报道[5,24]，因此本病例中阿奇霉素的辅助贡献不能完全排除。普拉多沙星被认为最可能是临床消退的主要贡献药物，因为该分离株对其敏感，且该药在整个治疗期间全身给药。局部阿米卡星也可能在局部发挥作用，尽管在21天后停用。由于同时使用了多种抗菌药物，无法确定每种药物的个体贡献。在没有正式协同试验的情况下，也无法确定阿奇霉素与普拉多沙星之间的协同活性。本病例强调利用体外药敏结果指导确定性抗菌药物选择的重要性，同时在病变范围、组织穿透、抗菌药物联合及个体宿主免疫反应等更广泛临床背景下解读治疗反应[41]。整个治疗期间未观察到不良反应；连续血液学和血清生化评估均在正常范围内。尽管随访期间维持完全消退且无复发，但由于猫NTM感染已知的复发可能性以及关于M. farcinogenes在猫中长期临床行为的数据有限，仍建议进行长期监测。
总体而言，本病例强调应将分枝杆菌感染纳入猫慢性不愈合伤口、复发性伤口裂开或多条引流管的鉴别诊断，尤其是当经验性抗菌治疗失败时。重复采样、菌种鉴定和抗菌药物药敏试验对于制定适当的治疗计划具有重要价值。由于猫M. farcinogenes感染的报道仍然有限，本病例提供了可能对类似病例有用的额外临床信息。
4. 结论
本报告记录了亚洲首例由Mycobacterium farcinogenes引起的猫皮肤分枝杆菌病确诊病例。本病例强调，对于表现为慢性不愈合伤口和多条引流管的猫，尤其是经验性治疗失败时，应考虑分枝杆菌感染作为鉴别诊断。在本病例中，经过长期多药治疗实现了完全临床缓解，尽管无法确定每种抗菌药物的个体贡献。早期识别、菌种水平鉴定和药敏指导的治疗可能有助于患病猫获得良好的临床结局。
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1. Introduction
Feline cutaneous mycobacteriosis is an uncommon infectious disease caused by several species of Mycobacterium, including members of the Mycobacterium tuberculosis complex (MTBC), fastidious or lepromatous mycobacteria, and non-tuberculous mycobacteria (NTM) [1,2,3,4,5,6,7,8]. These organisms are Gram-positive, aerobic, acid-fast bacilli [1,2,5,9] characterized by a cell wall rich in lipids and mycolic acids, which contributes to their resistance to heat, disinfectants, and decolorization by acid–alcohol during acid-fast staining procedures [5,9].
Mycobacterium farcinogenes is a rapid-growing species belonging to the NTM group [10,11,12]. It was first described in 1973 as the causative agent of bovine farcy, a chronic suppurative granulomatous disease affecting the skin and lymphatic vessels of zebu cattle in East and Central Africa [10,11,13,14,15,16]. Infection generally occurs through cutaneous inoculation following skin trauma, wound contamination, or surgical procedures; soil, water, and decaying vegetation are the primary environmental sources of these bacteria [1,2,3,5,6,7,8,9,17,18]. Clinical lesions are typically characterized by subcutaneous nodules, non-healing wounds, and multiple draining tracts, distributed on the ventral abdomen and inguinal regions [1,2,5,7,8,9,17,18,19,20], where the organism replicates within lipid-rich tissues [1,2,3,8,9,18]. In some cases, lesions may also extend to the pelvic limbs and tail base [5,8].
Treatment usually requires prolonged administration of dual or triple antimicrobial agents [3,4,21], newer-generation fluoroquinolones such as pradofloxacin or moxifloxacin, macrolides such as clarithromycin or azithromycin, and doxycycline may also be considered treatment options for some rapid-growing mycobacterial species [1,2,5]. Combination antimicrobial therapy is generally recommended to reduce the risk of antimicrobial resistance [1,2,4,22,23]. However, in vitro susceptibility does not always correlate with clinical response [5,24]. The treatment should be continued for at least one to two months beyond complete lesion resolution [1,2,3,4,5,9]. Surgical excision may be beneficial in selected cases but can be complicated by wound dehiscence and delayed healing [1,2,5,8,9].
Reports of M. farcinogenes infection in both humans and animals remain rare, sporadic human cases were described in the literature [11,12,13]. To date, only one feline case of Mycobacterium farcinogenes infection has been described in an online educational case report [25]. The present case report describes cutaneous mycobacteriosis caused by M. farcinogenes in a cat and documents successful treatment despite in vitro resistance to one of the administered antimicrobial agents. To the authors’ knowledge, this is the first reported case of feline cutaneous mycobacteriosis caused by M. farcinogenes in Asia.
2. Case Description
2.1. History
A 4-year-old spayed female domestic shorthair cat was referred to the Kasetsart University Veterinary Teaching Hospital for evaluation of an 8-month history of chronic non-healing draining wounds involving the left lateral thigh and left inguinal region. The lesion on the left lateral thigh developed following a cat bite wound and failed to respond to routine wound management, empirical antimicrobial therapy, and repeated wound lavage. Aerobic bacterial culture performed by the referring veterinarian yielded no bacterial growth.
Three months after the initial bite injury, tissue swelling was identified in the left inguinal region and adjacent to the left fifth mammary gland. Fine-needle aspiration cytology was suggestive of a spindle cell tumor with inflammation, prompting surgical excision and histopathological examination. At the time of surgery, the thigh wound was debrided and a surgical drain was placed. Following suture removal, the mammary surgical incision developed wound dehiscence with mucopurulent discharge, while the thigh wound remained persistently draining despite treatment with amoxicillin-clavulanic acid (16 mg/kg PO q12h), prednisolone (0.5 mg/kg PO q24h), and routine wound care. Histopathological examination of the excised tissue revealed severe necrotizing pyogranulomatous mastitis and dermatitis. Due to the progressive, non-healing nature of both lesions, the cat was referred for further diagnostic investigation and management.
2.2. Physical Examination
At the initial presentation, the cat was bright, alert, and responsive. Vital parameters were within normal limits, and the body condition score was 5/9. Physical examination revealed a chronic non-healing wound at the previous surgical site in the left inguinal region, characterized by a subcutaneous swelling, multiple draining tracts, and mucopurulent discharge. Two additional draining wounds were also present on the left lateral thigh.
2.3. Diagnostic Methods
Fine-needle aspiration of the inguinal lesion was performed for cytological examination using Wright–Giemsa staining. Exudate from the draining tracts at both sites was collected for bacterial culture and antimicrobial susceptibility testing. Samples were inoculated onto sheep blood agar, MacConkey agar, Columbia blood agar, and chocolate agar and incubated at 37 °C in 5% CO2; colonies were first observed after 2 days of incubation. Visible colonies were subjected to acid-fast staining and, following purification by subculture, to species identification by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS; Bruker Biotyper, Bruker Daltonics, Bremen, Germany). A pure subculture of the isolate was used for antimicrobial susceptibility testing by a laboratory-adapted disk diffusion method [26]. Briefly, a bacterial suspension adjusted to a 0.5 McFarland standard was spread onto Mueller–Hinton agar supplemented with 5% sheep blood, antimicrobial disks were applied, and plates were incubated at 37 °C in 5% CO2 for 48 h before measuring zone diameters [27]. Because validated species-specific breakpoints for M. farcinogenes are not available [27], zone diameters were interpreted using CLSI veterinary interpretive criteria [28] where available, and human CLSI [29] or EUCAST [30] criteria as surrogate standards for agents without veterinary-specific breakpoints. Pending laboratory results, amoxicillin-clavulanic acid at 19 mg/kg PO q12h (Amoxclamed®, BIC Chemical Co., Ltd., Bangkok, Thailand) was prescribed.
2.4. Laboratory Results
Cytological examination revealed numerous neutrophils and macrophages, consistent with pyogranulomatous inflammation (Figure 1). Bacterial culture of samples collected from both lesions yielded growth of Mycobacterium farcinogenes, a rapid-growing non-tuberculous mycobacterium (NTM) that has been rarely reported in cats. Colonies were first visible after 2 days of incubation, and species identification was reported 5 days after sample submission. Acid-fast staining of the isolate demonstrated numerous acid-fast-positive bacilli, and the organism was identified as M. farcinogenes by MALDI-TOF MS.
2.5. Antimicrobial Susceptibility Testing
Antimicrobial susceptibility testing from both sites demonstrated susceptibility to amikacin, gentamicin, imipenem, meropenem, marbofloxacin, and pradofloxacin, with intermediate susceptibility to amoxicillin-clavulanic acid and enrofloxacin, and resistance to the remaining antimicrobial agents tested (Table 1). Because validated zone-diameter breakpoints for M. farcinogenes have not been established, these interpretive categories should be regarded as preliminary phenotypic guidance rather than standardized susceptibility classifications [27].
2.6. Treatment
Based on the antimicrobial susceptibility results, pradofloxacin at 6.6 mg/kg PO q24h (Veraflox®, Elanco (Thailand) Ltd., Bangkok, Thailand) and topical amikacin sulfate 5% gel (Likacin® gel 5%, S Charoen Bhaesaj Trading, Bangkok, Thailand) applied once daily into the lesions were prescribed. Azithromycin at 8.2 mg/kg PO q24h (Azith®, Siam Bheasach Co., Ltd., Bangkok, Thailand) was additionally included in the treatment protocol despite in vitro resistance.
2.7. Treatment Outcomes
The lesions gradually improved over time, amikacin gel was discontinued on day 21 after inguinal open wound was healed, and complete clinical remission was achieved after 24 weeks of treatment (Figure 2). Hematological and serum biochemical analyses performed during follow-up remained within normal limits. No adverse effects associated with treatment were observed, and the cat remained clinically well throughout the treatment period.
3. Discussion
Feline cutaneous mycobacteriosis is an uncommon infectious disease caused by a diverse group of mycobacterial species, including rapid-growing non-tuberculous mycobacteria (NTM). Although sporadic feline infections caused by rapid-growing NTM—such as Mycobacterium abscessus, Mycobacterium smegmatis, and members of the Mycobacterium fortuitum complex—have been reported, infection caused by Mycobacterium farcinogenes appears to be exceptionally rare. M. farcinogenes is an environmental rapid-growing NTM species originally recognized as the causative agent of bovine farcy, a chronic granulomatous disease affecting cattle in tropical regions characterized by purulent lymphangitis and cutaneous lesions [10,11,13,14,15,16]. However, bovine farcy has been primarily reported in sub-Saharan Africa; although historical accounts exist in parts of South and Southeast Asia, no cases have been reported in livestock or water buffaloes in Thailand or neighboring Asian countries [15]. In cattle, serological testing has been investigated as an ancillary diagnostic approach, with whole-cell antigen ELISA demonstrating potential utility for the serodiagnosis and epidemiological screening of bovine farcy caused by M. farcinogenes [31]. However, the applicability of this approach to feline NTM infections, particularly M. farcinogenes, remains undetermined. Reports of infection in companion animals, particularly cats, remain extremely limited, and information regarding its pathogenicity, clinical behavior, and optimal treatment in cats is scarce. To the authors’ knowledge, this is the first reported case of feline cutaneous mycobacteriosis caused by M. farcinogenes in Asia. This case provides additional clinical information on the presentation, diagnosis, and treatment of this rare infection in cats.
The lesion distribution in this case is consistent with feline cutaneous mycobacteriosis, which typically targets lipid-rich subcutaneous tissues [1,2,3,8,9,18], causing panniculitis, nodules, ulceration, and draining tracts. These are commonly found on the ventral abdomen, inguinal region, tail base, and pelvic limbs [1,2,5,7,8,9,18,19,20]. In the present case, the initial lesion developed on the left lateral thigh following a reported cat bite wound, and a second lesion subsequently developed in the left inguinal region. Although the exact route of spread could not be determined, rapidly growing mycobacteria are known to extend along subcutaneous tissue planes, and sinus tracts may not always be clinically apparent. Therefore, extension of a pre-existing infection may have contributed to the postoperative wound dehiscence. The chronic bite wound may also have allowed environmental contamination with the organism. This case demonstrates the importance of including mycobacterial infection as a differential diagnosis for cats with chronic, non-healing wounds. When clinically feasible, presurgical diagnosis and management can optimize antimicrobial therapy and prevent complications such as wound dehiscence or delayed healing.
Diagnosing feline cutaneous mycobacteriosis remains challenging [1,3,4,5,25] because the clinical presentation is often non-specific and may closely resemble other chronic dermatological conditions, including bacterial infections, deep fungal infections, foreign-body reactions, immune-mediated diseases, and neoplasia [2,8,32,33]. In the present case, fine-needle aspiration (FNA) cytology of the mammary mass performed before referral was initially interpreted as suggestive of a spindle cell tumor with concurrent inflammation, prompting surgical excision. Histopathological examination revealed severe necrotizing pyogranulomatous mastitis and dermatitis without evidence of neoplasia. In chronic pyogranulomatous inflammation and panniculitis, reactive fibroblasts and myofibroblasts may proliferate during fibroplasia and appear as spindle-shaped cells on cytology, potentially mimicking a mesenchymal neoplasm [34]. Therefore, cytological findings suggestive of spindle cell neoplasia should be interpreted cautiously, particularly when accompanied by marked inflammation, and should be interpreted together with histopathological and microbiological findings. In addition, pyogranulomatous inflammation should prompt investigation for infectious causes using special stains such as acid-fast staining for mycobacteria and periodic acid–Schiff (PAS) or Gomori methenamine silver (GMS) stains for fungal pathogens. In this case, these stains were not performed on the histopathology specimens because the tissue had already been processed before referral. Acid-fast staining was also not performed on cytological smears because it is not used routinely for skin cytology in our laboratory. This represents a limitation of the present report. Acid-fast staining should be considered in cases of pyogranulomatous inflammation, particularly when mycobacterial infection is suspected.
A definitive diagnosis was established by bacterial culture and species identification. An interesting finding in this case was the difference in bacterial culture results before and after referral. The initial culture performed by the referring veterinarian yielded no growth, whereas repeat culture successfully isolated Mycobacterium farcinogenes from both lesions. This finding suggests that a negative bacterial culture does not rule out mycobacterial infection. Factors such as sample quality, sampling depth, bacterial load, transport conditions, and laboratory procedures may affect culture results [1,2,5]. Therefore, repeat bacterial culture performed by a specialized laboratory should be considered when mycobacterial infection is still suspected despite an initial negative result. In the present case, visible growth was detected within five days, consistent with the characteristics of rapidly growing NTM, which typically produce colonies within seven days on routine culture media [5,13]. Early bacterial growth enabled prompt species-level identification by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), supporting its value as a rapid, accurate, and cost-effective diagnostic tool for veterinary mycobacteriology [11,35,36]. Because bacterial culture may occasionally be negative despite clinical suspicion, PCR and target sequencing should also be considered, when available, especially if acid-fast staining is negative or culture results are inconclusive [1,2,4]. Although MALDI-TOF MS provided rapid species-level identification during routine diagnostic workflow, 16S rRNA gene sequencing remains the definitive for confirming uncommon mycobacterial species [4,13,17,23]. In this retrospective report, 16S rRNA sequencing could not be performed as the culture isolate was no longer retained post-treatment. In future cases, additional 16S rRNA gene sequencing should be considered to further confirm species identification.
Treatment of feline cutaneous mycobacteriosis is often prolonged and typically requires combination antimicrobial therapy to improve treatment success and reduce the risk of antimicrobial resistance [1,2,3,4,5]. In the present case, prednisolone had been administered for wound management before the diagnosis of cutaneous mycobacteriosis. Corticosteroid therapy should therefore be avoided in suspected mycobacterial infections, as immunosuppression may impair cell-mediated immunity and hinder effective control of intracellular mycobacteria [1,2,37,38].
In the present case, treatment with pradofloxacin, topical amikacin gel, and azithromycin resulted in complete clinical remission after 24 weeks without adverse effects. Pradofloxacin was selected based on in vitro susceptibility and its established efficacy against rapidly growing non-tuberculous mycobacteria [1,2,5], supported by its favorable tissue penetration in deep pyogranulomatous lesions [39]. Although systemic amikacin, including administration at 10 mg/kg SC once daily, represents an important therapeutic option for mycobacterial infections, topical amikacin gel was selected in this case as an adjunctive treatment for the accessible draining lesions, while avoiding prolonged systemic aminoglycoside exposure and its associated risk of nephrotoxicity. However, topical administration may provide limited penetration into deeper subcutaneous tissues, and systemic amikacin may therefore be considered in cases with extensive or deep tissue involvement, with appropriate monitoring.
Regarding azithromycin, although the isolate demonstrated in vitro resistance, it was initially prescribed as part of an empirical multidrug regimen for the extensive subcutaneous lesions [1,2,3,4,5]. It has immunomodulatory properties that may contribute to clinical improvement through modulation of macrophage function [40]. However, given the reliability of susceptibility testing for rapidly growing mycobacteria, the in vitro resistance makes a major contribution from azithromycin less likely. Nevertheless, discrepancies between in vitro susceptibility and clinical response have been reported in mycobacterial infections [5,24], and a supportive contribution from azithromycin cannot be completely excluded in this case. Pradofloxacin was considered the most likely principal contributor to clinical resolution because the isolate was susceptible and the drug was administered systemically throughout treatment. Topical amikacin may also have contributed locally, although it was discontinued after 21 days. Because multiple antimicrobial agents were used concurrently, the individual contribution of each drug cannot be determined. Synergistic activity between azithromycin and pradofloxacin also cannot be established without formal synergy testing. This case emphasizes the importance of using in vitro susceptibility results to guide definitive antimicrobial selection while interpreting treatment response within the broader clinical context of lesion extent, tissue penetration, antimicrobial combinations, and individual host immune responses [41]. No adverse effects were observed throughout the treatment period; serial hematological and serum biochemical evaluations remained within normal limits. Although complete resolution was maintained without recurrence during the follow-up period, long-term monitoring remains advisable due to the known potential for recurrence in feline NTM infections and the limited data regarding the long-term clinical behavior of M. farcinogenes in cats.
Overall, this case emphasizes that mycobacterial infection should be included in the differential diagnosis of cats with chronic non-healing wounds, recurrent wound dehiscence, or multiple draining tracts, particularly when empirical antimicrobial therapy is unsuccessful. Repeated sampling, species identification, and antimicrobial susceptibility testing were valuable for establishing an appropriate treatment plan. As reports of feline M. farcinogenes infection remain limited, this case provides additional clinical information that may be useful in similar cases.
4. Conclusions
This report documents the first confirmed case of feline cutaneous mycobacteriosis caused by Mycobacterium farcinogenes in Asia. The case highlights the importance of considering mycobacterial infection as a differential diagnosis in cats presenting with chronic non-healing wounds and multiple draining tracts, particularly when empirical treatment fails. In this case, complete clinical remission was achieved following prolonged multidrug therapy, although the individual contribution of each antimicrobial could not be determined. Early recognition, species-level identification, and susceptibility-guided treatment may contribute to favorable clinical outcomes in affected cats.