Evaluation of vitreous levels of gatifloxacin after systemic administration in inflamed and non‐inflamed eyes

Purpose: This study aimed to evaluate the human vitreous penetration of gatifloxacin in inflamed and non‐inflamed eyes after oral administration. Methods: Vitreous penetration of single‐dose (400 mg) oral gatifloxacin was evaluated in patients (n = 33) undergoing vitreous tap during the standard procedure for intravitreal antibiotic injection for acute postoperative endophthalmitis at various time‐points. Vitreous penetration of 400 mg oral gatifloxacin was evaluated in the non‐inflamed eyes of patients (n = 33) undergoing pars plana vitrectomy at similar time‐points. The study was extended to evaluate the vitreous penetration of single‐dose oral (800 mg) gatifloxacin at a single time‐point in inflamed (n = 10) and non‐inflamed (n = 11) eyes. Results: After 400 mg oral gatifloxacin, inflamed eyes showed mean vitreous concentrations of 0.58±0.19μg/ml, 1.33±0.33 μg/ml and 1.30 ± 0.23 μg/ml at 2, 4 and 6 hours, respectively. The levels reached at 2 and 4 hours were found to be significantly increased compared with those in non‐inflamed eyes. At the 800‐mg dose, 4‐hour vitreous levels in inflamed and non‐inflamed eyes were 1.57 ± 0.3 μg/ml and 1.42 ± 0.24 μg/ml, respectively. Although the increased dose of gatifloxacin elevated plasma concentration, it failed to raise vitreous levels significantly higher than the 400‐mg dose at the 4‐hour time‐point. Conclusions: Orally administered gatifloxacin achieves therapeutic levels in both inflamed and non‐inflamed human eyes with a spectrum covering the bacterial species most frequently involved in the various causes of endophthalmitis. However, the levels achieved were below the MIC₉₀ for Pseudomonas aureginosa and Enterococcus.     

Penetration of gentamycin into the aqueous humor of non-inflamed and inflamed human eyes (author's transl)]

The penetration of gentamycin into aqueous humor after parenteral application (i. m., i. v., s. c.) of non-inflamed and inflamed human eyes was investigated. The dose of gentamycin was 80 mg i.m. and i. v. respectively. A doses of 40 mg gentamycin was used by s. c. injection. With Agar-diffusions test it could be demonstrated that the level of gentamycin was higher in inflamed than in non-inflamed eyes.     

Activated complement classical pathway in a murine model of oxygen-induced retinopathy

AIM: To investigate whether the complement system is involved in a murine model of oxygen-induced retinopathy (OIR). METHODS: Forty C57BL/6J newborn mice were divided randomly into OIR group and control group. OIR was induced by exposing mice to 75%±2% oxygen from postnatal 7d (P7) to P12 and then recovered in room air. For the control group, the litters were raised in room air. At the postnatal 17d (P17), gene expressions of the complement components of the classical pathway (CP), the mannose-binding lectin (MBL) pathway and the alternative pathway (AP) in the retina were determined by quantitative real-time polymerase chain reaction (RT-PCR). Retinal protein expressions of the key components in the CP were examined by Western blotting. RESULTS: Whole mounted retina in the OIR mice showed area of central hypoperfusion in both superficial and deep layers and neovascular tufts in the periphery. The expressions of C1qb and C4b genes in the OIR retina were significantly higher than those of the controls. The expression of retinal complement factor B (CFB) gene in OIR mice was significantly lower than those of the controls. However, the expressions of C3 and complement factor H (CFH) genes were higher. The protein synthesis of the key components involved in the CP (C1q, C4 and C3) were also significantly higher in OIR mouse retina. Although MBL-associated serine protease 1 (MASP1) and MASP2 were detected in both the OIR and the control groups, the expressions were weak and the difference between the two groups was not significant. CONCLUSION: Our data suggest that the complement system CP is activated during the pathogenesis of murine model of OIR.     

Distribution of complement anaphylatoxin receptors and membrane-bound regulators in normal human retina

To characterize the distribution of membrane-bound components of the complement system in normal human retina, eyes from eight human donors with no history of ocular disease, ranging in age from 47 to 85 years were examined using immunohistochemistry to localize the C3a receptor (C3aR), C5a receptor (C5aR), CD46, CD55, and CD59 in cryosections prepared from donor posterior segments. The C3aR was identified in the nerve fiber layer in a sawtooth-patterned band. Vimentin, used as a Müller cell marker, produced a similar staining pattern. The C5aR was detected on specific rounded structures in the inner plexiform layer and occasionally in the nerve fiber layer. CD46 produced markedly specific staining of the basolateral surface of the retinal pigment epithelium. CD55 was localized to the nerve fiber layer. Staining for these proteins was consistent across all eyes studied. CD59 was expressed throughout the nerve fiber layer and labeled vessels that extended through the ganglion cell, inner plexiform, and inner nuclear layers, but this pattern was only confirmable in a single subject. Complement anaphylatoxin receptors and regulatory proteins are localized in different but internally consistent patterns in normal adult human retina, independent of the age of the donor. C3aR and C5aR localization only in the inner retina contrasts with previously reported findings in the central nervous system of wide spread diffuse staining. The complement regulators CD55 and CD59 were found primarily on the inner retina, while CD46 was present exclusively in a polarized fashion on the RPE.     

Up-regulation of complement factor B in retinal pigment epithelial cells is accompanied by complement activation in the aged retina

Complement activation is involved in the pathogenesis of age-related macular degeneration. How complement is activated in the retina is not known. Previously we have shown that complement factor H (CFH) is constitutively expressed by retinal pigment epithelial (RPE) cells and the production of CFH is negatively regulated by inflammatory cytokines and oxidative insults. Here we investigated the production and regulation of complement factor B (CFB) in RPE cells. Immunohistochemistry showed that CFB is expressed at low levels on the apical portion of the RPE cells in normal physiological conditions. With age, CFB expression increases and extends to the basal part of RPE cells. Confocal microscopy and real-time PCR of RPE cultures indicated that the production of CFB by RPE cells is positively regulated by TNF-α, IFN-γ and long-term (30 days) photoreceptor outer segments treatments. Increased CFB expression in RPE cells in vivo is accompanied by the accumulation of complement C3 and C3a deposition at the Bruch's membrane and the basal layer of RPE cells. Our results suggest that RPE cells play important roles in regulating complement activation in the retina. Increased complement activation in the aged retina may be important for retinal homeostasis in the context of accumulating photoreceptor waste products.     

Localization of complement 1 inhibitor (C1INH/SERPING1) in human eyes with age-related macular degeneration

Age-related macular degeneration (AMD) is a common degenerative disease resulting in injury to the retina, retinal pigment epithelium and choriocapillaris. Recent data from histopathology, animal models and genetic studies have implicated altered regulation of the complement system as a major factor in the incidence and progression of this disease. A variant in the gene SERPING1, which encodes C1INH, an inhibitor of the classical and lectin pathways of complement activation, was recently shown to be associated with AMD. In this study we sought to determine the localization of C1INH in human donor eyes. Immunofluorescence studies using a monoclonal antibody directed against C1INH revealed localization to photoreceptor cells, inner nuclear layer neurons, choriocapillaris, and choroidal extracellular matrix. Drusen did not exhibit labeling. Genotype at rs2511989 did not appear to affect C1INH abundance or localization, nor was it associated with significant molecular weight differences when evaluated by Western blot. In a small number of eyes (n = 7 AMD and n = 7 control) AMD affection status was correlated with increased abundance of choroidal C1INH. These results indicate that C1INH protein is present in the retina and choroid, where it may regulate complement activation.     

Therapeutic targeting of the complement system in age-related macular degeneration: a review

The last decade has produced pivotal change in our understanding of the molecular mechanisms underlying age-related macular degeneration (AMD), a leading cause of global blindness. In this time, the complement system has featured as a unifying theme for several elements of new evidence: initially, the discovery of complement proteins within drusen and subsequently, the association between AMD and mutations in various complement pathway genes, most notably complement factor H. Increasingly, a wealth of data are pointing towards a role for chronic local inflammation and complement activation in the patho-aetiology of AMD. These findings have paved the way for the exploration of a new paradigm of therapy in AMD management; targeting of specific molecular constituents in the complement pathway thus producing dampening or inhibition of the inflammatory response. Such an approach has the potential to intervene earlier in the disease process and ideally before vision is compromised. In this review we discuss the role of the complement system in AMD, novel therapies in preclinical evaluation and clinical trial, and whether these have a part to play in reducing the burden of disease.     

Hippo/YAP信号通路在眼部作用的研究进展

Hippo-YAP通路在机体发育和疾病发生中均具有重要作用。Hippo-YAP通路的调节紊乱可能导致病理组织过度生长和肿瘤的进展；近年来研究发现，Hippo-YAP信号通路的异常调节可能与眼部疾病相关，如圆锥角膜、Sveinsson 脉络膜视网膜萎缩和视网膜变性等，本文就Hippo/YAP 在眼部作用的研究进展进行系统综述，为眼部疾病的治疗提供理论基础。     

Revisiting the role of factor H in age-related macular degeneration: Insights from complement-mediated renal disease and rare genetic variants

Ophthalmologists are long familiar with the eye showing signs of systemic disease, but the association between age-related macular degeneration and abnormal complement activation, common to several renal disorders, has only recently been elucidated. Although complement activation products were identified in drusen almost three decades ago, it was not until the early 21st century that a single-nucleotide polymorphism in the complement factor H gene was identified as a major heritable determinant of age-related macular degeneration, galvanizing global efforts to unravel the pathogenesis of this common disease. Advances in proteomic analyses and familial aggregation studies have revealed distinctive clinical phenotypes segregated by the functional effects of common and rare genetic variants on the mature protein and its splice variant, factor H–like protein 1. The predominance of loss-of-function, N-terminal mutations implicate age-related macular degeneration as a disease of general complement dysregulation, offering several therapeutic avenues for its modulation. Here, we explore the molecular impact of these mutations/polymorphisms on the ability of variant factor H/factor H–like protein 1 to localize to polyanions, pentraxins, proinflammatory triggers, and cell surfaces across ocular and renal tissues and exert its multimodal regulatory functions and their clinical implications. Finally, we critically evaluate key therapeutic and diagnostic efforts in this rapidly evolving field.     

Imaging the aqueous humor outflow pathway in human eyes by three-dimensional micro-computed tomography (3D micro-CT)

The site of outflow resistance leading to elevated intraocular pressure in primary open-angle glaucoma is believed to be located in the region of Schlemm’s canal inner wall endothelium, its basement membrane and the adjacent juxtacanalicular tissue. Evidence also suggests collector channels and intrascleral vessels may have a role in intraocular pressure in both normal and glaucoma eyes. Traditional imaging modalities limit the ability to view both proximal and distal portions of the trabecular outflow pathway as a single unit. In this study, we examined the effectiveness of three-dimensional micro-computed tomography (3D micro-CT) as a potential method to view the trabecular outflow pathway. Two normal human eyes were used: one immersion fixed in 4% paraformaldehyde and one with anterior chamber perfusion at 10 mmHg followed by perfusion fixation in 4% paraformaldehyde/2% glutaraldehyde. Both eyes were postfixed in 1% osmium tetroxide and scanned with 3D micro-CT at 2 μm or 5 μm voxel resolution. In the immersion fixed eye, 24 collector channels were identified with an average orifice size of 27.5 ± 5 μm. In comparison, the perfusion fixed eye had 29 collector channels with a mean orifice size of 40.5 ± 13 μm. Collector channels were not evenly dispersed around the circumference of the eye. There was no significant difference in the length of Schlemm’s canal in the immersed versus the perfused eye (33.2 versus 35.1 mm). Structures, locations and size measurements identified by 3D micro-CT were confirmed by correlative light microscopy. These findings confirm 3D micro-CT can be used effectively for the non-invasive examination of the trabecular meshwork, Schlemm’s canal, collector channels and intrascleral vasculature that comprise the distal outflow pathway. This imaging modality will be useful for non-invasive study of the role of the trabecular outflow pathway as a whole unit.     

Identification of lymphatics in the ciliary body of the human eye: A novel “uveolymphatic” outflow pathway

Impaired aqueous humor flow from the eye may lead to elevated intraocular pressure and glaucoma. Drainage of aqueous fluid from the eye occurs through established routes that include conventional outflow via the trabecular meshwork, and an unconventional or uveoscleral outflow pathway involving the ciliary body. Based on the assumption that the eye lacks a lymphatic circulation, the possible role of lymphatics in the less well defined uveoscleral pathway has been largely ignored. Advances in lymphatic research have identified specific lymphatic markers such as podoplanin, a transmembrane mucin-type glycoprotein, and lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1). Lymphatic channels were identified in the human ciliary body using immunofluorescence with D2-40 antibody for podoplanin, and LYVE-1 antibody. In keeping with the criteria for lymphatic vessels in conjunctiva used as positive control, D2-40 and LYVE-1-positive lymphatic channels in the ciliary body had a distinct lumen, were negative for blood vessel endothelial cell marker CD34, and were surrounded by either discontinuous or no collagen IV-positive basement membrane. Cryo-immunogold electron microscopy confirmed the presence D2-40-immunoreactivity in lymphatic endothelium in the human ciliary body. Fluorescent nanospheres injected into the anterior chamber of the sheep eye were detected in LYVE-1-positive channels of the ciliary body 15, 30, and 45 min following injection. Four hours following intracameral injection, Iodine-125 radio-labeled human serum albumin injected into the sheep eye (n = 5) was drained preferentially into cervical, retropharyngeal, submandibular and preauricular lymph nodes in the head and neck region compared to reference popliteal lymph nodes (P < 0.05). These findings collectively indicate the presence of distinct lymphatic channels in the human ciliary body, and that fluid and solutes flow at least partially through this system. The discovery of a uveolymphatic pathway in the eye is novel and highly relevant to studies of glaucoma and other eye diseases.     

Retinal pigment epithelial expression of complement regulator CD46 is altered early in the course of geographic atrophy

In geographic atrophy (GA), the non-neovascular end stage of age-related macular degeneration (AMD), the macular retinal pigment epithelium (RPE) progressively degenerates. Membrane cofactor protein (MCP, CD46) is the only membrane-bound regulator of complement expressed on the human RPE basolateral surface. Based on evidence of the role of complement in AMD, we hypothesized that altered CD46 expression on the RPE would be associated with GA development and/or progression. Here we report the timeline of CD46 protein expression changes across the GA transition zone, relative to control eyes, and relative to events in other chorioretinal layers. Eleven donor eyes (mean age 87.0 ± 4.1 yr) with GA and 5 control eyes (mean age 84.0 ± 8.9 yr) without GA were evaluated. Macular cryosections were stained with PASH for basal deposits, von Kossa for calcium, and for CD46 immunoreactivity. Internal controls for protein expression were provided by an independent basolateral protein, monocarboxylate transporter 3 (MCT3) and an apical protein, ezrin. Within zones defined by 8 different semi-quantitative grades of RPE morphology, we determined the location and intensity of immunoreactivity, outer segment length, and Bruch’s membrane calcification. Differences between GA and control eyes and between milder and more severe RPE stages in GA eyes were assessed statistically. Increasing grades of RPE degeneration were associated with progressive loss of polarity and loss of intensity of staining of CD46, beginning with the stages that are considered normal aging (grades 0–1). Those GA stages with affected CD46 immunoreactivity exhibited basal laminar deposit, still-normal photoreceptors, and concomitant changes in control protein expression. Activated or anteriorly migrated RPE (grades 2–3) exhibited greatly diminished CD46. Changes in RPE CD46 expression thus occur early in GA, before there is evidence of morphological RPE change. At later stages of degeneration, CD46 alterations occur within a context of altered RPE polarity. These changes precede degeneration of the overlying retina and suggest that therapeutic interventions be targeted to the RPE.     

Disorganization of the retinal inner layers as a predictor of visual acuity in eyes with macular edema secondary to uveitis

AIM: To assess the correlation between disorganization of the retinal inner layers (DRIL) and best-corrected visual acuity (BCVA) in patients with uveitis and macular edema (UME) who underwent systemic treatment using optical coherence tomography (OCT).METHODS: A retrospective clinical study of 23 patients (30 eyes) with DRIL and 23 patients (31 eyes) without DRIL secondary to UME were included. All patients underwent comprehensive ophthalmic examinations at baseline, 3, 6, and 12mo after local and systemic treatment. The OCT-based parameters included foveal center point thickness (FCPT), mean thickness (MT), and diameters of DRIL in horizontal and vertical directions. BCVA and OCT-based parameters were compared between the two groups. The relationship between each OCT parameter and BCVA was evaluated using linear correlation and regression analysis.RESULTS: At the initial visit, the mean baseline FCPT was 441.03±128.68 μm in the eyes with DRIL and 337.26±99.31 μm in the eyes without DRIL (P=0.001). No significant differences were observed in MT (P=0.357). The mean size of transverse and vertical diameters of DRIL was 684.07±267.51 and 267.07±104.61 μm at baseline, respectively. There was significant improvement in BCVA and OCT-based parameters at 3, 6, and 12mo in all cases (P<0.001 for each timepoint). In addition, significant differences were detected in BCVA and OCT parameters between eyes with and without DRIL at each time point (P<0.01 for each timepoint). A greater DRIL range at baseline was associated with a worse baseline BCVA (transverse diameter of DRIL: r=0.875, P<0.001; vertical diameter of DRIL: r=0.622, P<0.001). The transverse diameter of baseline DRIL was found to be significantly correlated with the final BCVA (P=0.003).CONCLUSION: The improvement in BCVA is associated with DRIL in patients with UME. DRIL is an easy-to-determine and robust imaging biomarker that could help predict BCVA prognosis in eyes with UME.     

Complement factors C1q, C3 and C5b-9 in the posterior sclera of guinea pigs with negative lens-defocused myopia

AIM

To investigate the expression of complement factors in the posterior scleral fibroblasts of guinea pigs with negative lens-defocused myopia.

METHODS

Eighteen guinea pigs were assigned randomly to two groups: the negative lens-defocused group (NLD group, n=9) and the normal control without treatment group (NC group, n=9). The effect of myopic induction was compared in three subgroups: eyes treated with a -10.00 D negative lens in the NLD group (NL group), eyes treated with a plano (0 D) lens in the NLD group (PL group), and untreated right eyes in the NC group (NC group). The following analyses were conducted at four weeks: examination of the refractive error via retinoscopy, assessment of complement C5b-9 expression in the posterior scleral fibroblasts using immunohistochemistry, and measurements of complement C1q and C3 protein levels in the posterior sclera by Western blot.

RESULTS

After an induction period of four weeks, a significant myopic shift was detected in the eyes of the NL group, relative to that of the PL and NC groups (P<0.05). Data analysis showed a significant increase in the percentage of C5b-9 immunopositive fibroblasts in the posterior sclera of the NL group eyes, compared to the PL group (q=11.50, P<0.001). Significantly higher levels of C1q (q=4.94, P=0.01) and C3 (q=4.07, P=0.03) protein were detected in the posterior sclera of NL group eyes, compared to the PL group. There were no significant difference between the PL and NC groups for C5b-9 (q=2.44, P=0.10), C1q (q=1.55, P=0.53) and C3 (q=0.98, P=0.77) in the posterior sclera.

CONCLUSION

The data from present study provide evidence of the up-regulation of C5b-9, C1q and C3 in the posterior scleral fibroblasts in a NLD myopic animal model. The results suggest that the complement system may be involved in the development of myopia.     

On the reactivity of corneal collagen and subcomponent C1q of the complement system with human platelets and IgG-coated latex particles

Collagen was isolated from bovine cornea and tested for reactivity towards platelets and IgG-coated polystyrene latex particles. The corneal collagen caused a dose- and temperature-dependent platelet aggregation in all human platelet-rich plasmas studied. As little as 0 . 31 micrograms of purified corneal collagen could trigger platelet activation. Human C1q, a subcomponent of the first complement component (C1), which shares extensive chemical-structural similarities with collagen, was able to inhibit the platelet aggregation provoked by corneal collagen. This blocking effect could be, however, overcome by increasing collagen doses. In a slide method or in aggregometry both corneal collagen and C1q agglutinated IgG-coated latex particles in a dose-dependent manner. Addition of such latex particles to platelet-rich plasmas or preincubation of the particles with collagen reduced or prevented the platelet action of collagen, suggesting that due to their reactivity with collagen immune complexes may play an inhibitory role in collagen-caused platelet aggregation. The results are discussed in relation to pathological events that lead to collagenolysis and also with respect to wound healing in the injured cornea.     

Retinal disease in the C3 glomerulopathies and the risk of impaired vision

Background: Dense deposit disease and atypical hemolytic uremic syndrome are often caused by Complement Factor H (CFH) mutations. This study describes the retinal abnormalities in dense deposit disease and, for the first time, atypical haemolytic uremic syndrome. It also reviews our understanding of drusen pathogenesis and their relevance for glomerular disease. Methods: Six individuals with dense deposit disease and one with atypical haemolytic uremic syndrome were studied from 2 to 40 years after presentation. Five had renal transplants. All four who had genetic testing had CFH mutations. Individuals underwent ophthalmological review and retinal photography, and in some cases, optical coherence tomography, and further tests of retinal function. Results: All subjects with dense deposit disease had impaired night vision and retinal drusen or whitish-yellow deposits. Retinal atrophy, pigmentation, and hemorrhage were common. In late disease, peripheral vision was restricted, central vision was distorted, and there were scotoma from sub-retinal choroidal neovascular membranes and atypical serous retinopathy. Drusen were present but less prominent in the young person with atypical uremic syndrome due to a heterozygous CFH mutation. Conclusions: Drusen are common in forms of C3 glomerulopathy caused by compound heterozygous or heterozygous CFH mutations. They are useful diagnostically but also impair vision. Drusen have an identical composition to glomerular deposits. They are also identical to the drusen of age-related macular degeneration, and may respond to the same treatments. Individuals with a C3 glomerulopathy should be assessed ophthalmologically at diagnosis, and monitored regularly for vision-threatening complications.     

Association between complement factor I gene polymorphisms and the risk of age-related macular degeneration: a Meta-analysis of literature

AIM: To systematically review the association between complement factors I (CFI) polymorphisms and age-related macular degeneration (AMD) and to explore whether CFI polymorphisms are associated with AMD. METHODS: Meta-analysis of articles published from 1995 to January 2015 of articles involved with AMD and polymorphisms of the CFI gene. Eligible data were pooled in a Meta-analysis, analyzing using STATA software (version 12.0), Review Manager (version 5.2) and different models based on the heterogeneity of effect sizes. Egger’s test, Begg’s rank correlation methods were used to evaluate for publication bias. RESULTS: Thirteen articles were eligible, describing two loci polymorphisms of the CFI gene (of which 12 articles focus on rs10033900T>C and 3 articles focus on rs2285714C>T). For rs10033900T>C, the results of our study revealed that having a mutant allele C, TC, CC and TC+CC was associated with a decreased risk of AMD in all population groups studied (C versus T models, OR=0.84, 95%CI: 0.72-0.99, P=0.04; TC versus TT models OR=0.89, 95%CI: 0.88-0.99, P=0.04; CC versus TT models, OR=0.76, 95%CI: 0.60-0.98, P=0.03; TC+CC versus TT models, OR=0.81, 95%CI:0.65-0.99, P=0.04). We found that C allele were related to lower AMD risk in the Caucasian population by subgroup analysis, but there was no association with AMD under the allele and genotypes comparison in Asian studies. For rs2285714 C>T, the TC, TT genotypes contributed to a higher risk of AMD, compared with the CC carriers and TC+CC (OR=1.34, 95%CI: 1.09-1.63, P=0.004; OR=1.50, 95%CI: 1.25-1.80, P<0.0001). CONCLUSION: This Meta-analysis suggests that CFI rs10033900T>C and rs2285714C>T polymorphisms may contribute to AMD.     

Amycolatopsis sulphurea as the first reported agent of endophthalmitis in a patient after penetrating eye trauma with intraocular foreign body: A case report

We report an Amycolatopsis sulphurea endophthalmitis after the surgical repair of penetrating eye trauma with a metallic intraocular foreign body. A 27-year-old male referred with occupational injury by a nail from his left eye. Endophthalmitis occurred 12 h after the removal of foreign body and repair of the globe. The culture of vitreus samples revealed gram-positive bacillus proliferation, confirming A. sulphurea. Endophthalmitis was eradicated successfully with intravitreal, topical, and systemic antibiotics. To the best of our knowledge, this is the first case, reporting A. sulphurea endophthalmitis.     

Nanopore techniques as a potent tool in the diagnosis and treatment of endophthalmitis: a literature review

Endophthalmitis is a serious ophthalmic disease characterized by changes in the eye’s posterior segment, such as hypopyon and intraocular inflammation, vitritis being a hallmark. Infection-caused endophthalmitis can lead to irreversible vision loss, accompanied by eye pain or eye distention, and in the most severe cases the removal of the eyeball. Microorganisms such as bacteria, fungi, viruses, and parasites typically account for the disease and the entry pathways of the microbial can be divided into either endogenous or exogenous approaches, according to the origin of the etiological agents. Exogenous endophthalmitis can be derived from various occasions (such as post-operative complications or trauma) while endogenous endophthalmitis results from the bloodstream which carries pathogens to the eye. This review aims to summarize the application of new technology in pathogen identification of endophthalmitis so as to prevent the disease and better guide clinical diagnosis and treatment.