The genus Burkholderia comprises metabolically diverse and adaptable Gram-negative bacteria, which thrive in often adversarial environments. A few members of the genus are prominent opportunistic pathogens. These include Burkholderia mallei and Burkholderia pseudomallei of the B. pseudomallei complex, which cause glanders and melioidosis, respectively. Burkholderia cenocepacia, Burkholderia multivorans, and Burkholderia vietnamiensis belong to the Burkholderia cepacia complex and affect mostly cystic fibrosis patients. Infections caused by these bacteria are difficult to treat because of significant antibiotic resistance. The first line of defense against antimicrobials in Burkholderia species is the outer membrane penetration barrier. Most Burkholderia contain a modified lipopolysaccharide that causes intrinsic polymyxin resistance. Contributing to reduced drug penetration are restrictive porin proteins. Efflux pumps of the resistance nodulation cell division family are major players in Burkholderia multidrug resistance. Third and fourth generation β-lactam antibiotics are seminal for treatment of Burkholderia infections, but therapeutic efficacy is compromised by expression of several β-lactamases and ceftazidime target mutations. Altered DNA gyrase and dihydrofolate reductase targets cause fluoroquinolone and trimethoprim resistance, respectively. Although antibiotic resistance hampers therapy of Burkholderia infections, the characterization of resistance mechanisms lags behind other non-enteric Gram-negative pathogens, especially ESKAPE bacteria such as Acinetobacter baumannii, Klebsiella pneumoniae and Pseudomonas aeruginosa.

属伯克霍尔德包括代谢多样和适应性强的革兰氏阴性细菌，其在茁壮成长往往对抗环境。该属的一些成员是突出的机会病原体。这些包括鼻疽伯克霍尔德氏菌和类鼻疽伯克霍尔德菌的的B.假单胞菌分别复合物，其原因鼻疽和类鼻疽，。Burkholderia cenocepacia，Burkholderia multivorans和viknamiensis属于Burkholderia cepacia复杂，多为囊性纤维化患者。由这些细菌引起的感染由于明显的抗生素抗性而难以治疗。伯克霍尔德氏菌物种中对抗抗生素的第一道防线是外膜渗透屏障。大多数伯克霍尔德菌都含有引起固有的多粘菌素抗性的修饰的脂多糖。限制的孔蛋白是导致药物渗透减少的原因。耐药结节细胞分裂家族的外排泵是伯克霍尔德菌多药耐药的主要参与者。第三代和第四代β-内酰胺类抗生素在治疗伯克霍尔德氏菌方面具有开创性感染，但几种β-内酰胺酶和头孢他啶目标突变的表达削弱了治疗效果。改变的DNA促旋酶和二氢叶酸还原酶靶分别引起氟喹诺酮和甲氧苄啶抗性。尽管抗生素耐药性阻碍了伯克霍尔德氏菌感染的治疗，但耐药机制的表征仍落后于其他非肠道革兰氏阴性病原体，尤其是ESKAPE细菌，如鲍曼不动杆菌，肺炎克雷伯菌和铜绿假单胞菌。