Pedersen S S, Høiby N, Espersen F, Koch C
Statens Seruminstitut, Department of Clinical Microbiology, Copenhagen, Denmark.
Thorax. 1992 Jan;47(1):6-13. doi: 10.1136/thx.47.1.6.
Chronic bronchopulmonary infection with mucoid, alginate producing Pseudomonas aeruginosa occurs characteristically in patients with cystic fibrosis. Alginate may be a virulence factor for P aeruginosa infection in such patients.
Forced vital capacity (FVC), nutritional state and the antibody response to P aeruginosa were determined at regular intervals from three years before chronic P aeruginosa infection to 10 years afterwards in 73 patients with cystic fibrosis. All patients were treated intensively with antipseudomonal chemotherapy during the study period.
FVC was reduced in all patients who subsequently developed P aeruginosa infection before they acquired the infection, indicating significant pre-existing lung damage when compared with patients who remained free of P aeruginosa. Lung function and nutritional state remained unchanged after 10 years of infection, except in the patients who died of P aeruginosa lung infection. The FVC and height and weight of patients infected with nonmucoid strains of P aeruginosa were similar to those of uninfected patients. Patients infected with mucoid strains had poorer lung function and nutritional state for the first five years after infection compared with patients with nonmucoid strains. Such infection was also associated with greater IgG and IgA antibody responses to P aeruginosa standard antigen compared with nonmucoid infection. Concentrations of antibody to alginate were similar in patients with non-mucoid and mucoid infection. Noticeably increased concentrations of IgA antibodies to P aeruginosa standard antigen were observed early after the onset of infection in patients who subsequently died.
Alginate producing P aeruginosa infection is associated with a hyperimmune response and poor clinical condition, suggesting that alginate production is a virulence factor in such infections in patients with cystic fibrosis.
黏液样、产藻酸盐的铜绿假单胞菌慢性支气管肺部感染典型地发生于囊性纤维化患者。藻酸盐可能是此类患者铜绿假单胞菌感染的一种毒力因子。
对73例囊性纤维化患者从慢性铜绿假单胞菌感染前3年至感染后10年定期测定用力肺活量(FVC)、营养状况及对铜绿假单胞菌的抗体反应。在研究期间所有患者均接受了强化抗假单胞菌化疗。
所有随后发生铜绿假单胞菌感染的患者在感染前FVC就已降低,表明与未感染铜绿假单胞菌的患者相比,存在明显的既往肺损伤。感染10年后肺功能和营养状况保持不变,但死于铜绿假单胞菌肺部感染的患者除外。感染非黏液样菌株的患者的FVC、身高和体重与未感染患者相似。与感染非黏液样菌株的患者相比,感染黏液样菌株的患者在感染后的前5年肺功能和营养状况较差。此类感染与对铜绿假单胞菌标准抗原的IgG和IgA抗体反应增强也有关,与非黏液样感染相比,对藻酸盐的抗体浓度在非黏液样和黏液样感染患者中相似。在随后死亡的患者中,感染后早期观察到对铜绿假单胞菌标准抗原的IgA抗体浓度明显升高。
产藻酸盐的铜绿假单胞菌感染与超敏反应及不良临床状况相关,提示藻酸盐产生是囊性纤维化患者此类感染中的一种毒力因子。