Department of Microbiology, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA.
Curr Eye Res. 2010 Sep;35(9):787-98. doi: 10.3109/02713683.2010.492462.
The pneumococcal capsule is required for pathogenesis in systemic infections, yet reports show most conjunctivitis outbreaks are caused by nonencapsulated pneumococci, while keratitis infections are caused by encapsulated strains. This study aims to determine the effect of capsule in pneumococcal keratitis and conjunctivitis in rabbit models of infection.
A capsule-deficient isogenic mutant was created using homologous transformation. Parent and mutant strains were injected within the upper bulbar conjunctiva (conjunctivitis) or into the corneal stroma (keratitis) of New Zealand white rabbits. Clinical examinations were performed 24 and 48 hr post-infection at which time corneas or conjunctivae were removed, homogenized, and plated to determine the recovered bacterial load. Whole eyes were removed for histological examination. The neuraminidase activity was determined following in vitro and in vivo growth.
There were no significant differences in clinical scores between the eyes infected with the parent or mutant for either infection, nor was there a difference in the amount of bacteria recovered from the cornea. In the conjunctivae, however, the mutant strain was cleared by the host faster than the parent strain. Histological examination showed slightly more infiltrating polymorphonuclear leukocytes (PMN) and macrophages in the conjunctivae infected with the parent strain. The neuraminidase activity of both strains was not significantly different when the strains were grown in vitro. However, the neuraminidase activity of the parent was significantly less than that of the mutant at 3 and 12 hr post conjunctival infection.
Although more outbreaks of pneumococcal conjunctivitis are tied to nonencapsulated S. pneumoniae strains, this study showed that an encapsulated strain was capable of establishing conjunctivitis in a rabbit injection model and survive attack by the host immune system longer than its nonencapsulated isogenic mutant. Nonetheless, the nonencapsulated pneumococci had an increased neuraminidase activity level in vivo when compared to the parent strain.
肺炎球菌荚膜对于全身感染的发病机制至关重要,但报告显示,大多数结膜炎暴发是由非荚膜肺炎球菌引起的,而角膜炎感染则由荚膜菌株引起。本研究旨在确定荚膜在兔感染模型中肺炎球菌性角膜炎和结膜炎中的作用。
使用同源转化创建了一个荚膜缺陷的同源突变体。将亲本和突变株注射到新西兰白兔的上球结膜(结膜炎)或角膜基质(角膜炎)中。在感染后 24 和 48 小时进行临床检查,此时取出角膜或结膜,匀浆并接种以确定回收的细菌负荷。取出整个眼睛进行组织学检查。在体外和体内生长后测定神经氨酸酶活性。
在两种感染中,亲本或突变株感染的眼睛之间的临床评分没有显着差异,从角膜中回收的细菌数量也没有差异。然而,在结膜中,突变株比亲本株更快地被宿主清除。组织学检查显示,亲本株感染的结膜中有更多浸润的多形核白细胞(PMN)和巨噬细胞。当在体外培养时,两种菌株的神经氨酸酶活性没有显着差异。然而,在结膜感染后 3 和 12 小时,亲本的神经氨酸酶活性明显低于突变体。
尽管更多的肺炎球菌性结膜炎暴发与非荚膜肺炎球菌菌株有关,但本研究表明,一种荚膜菌株能够在兔注射模型中建立结膜炎,并比其非荚膜同源突变体更长时间地在宿主免疫系统的攻击下存活。尽管如此,与亲本株相比,非荚膜肺炎球菌在体内具有更高的神经氨酸酶活性水平。