**6. Corneal innate defense**

**e. Multiplication capability.***Streptoccoccus penumoniae* shows an accelerated multiplication rate and leukocytes chemotactic factors synthesis that may originate a huge inflamma‐ tory cell accumulation in anterior chamber. *Enterobacteriaceae* like *Serratia, Enterobacter, Escherichia* etc. have a multiplication rate of two hours for each generation cell, and its growth is exponential. Depending on the adaptability and the capability of the invading microorganism, like quick reproduction and production of toxic substances as results of his own metabolism, both factors known as virulence, the keratitis caused by the bacte‐ rium mentioned above rapidly progress to corneal edema,epithelial ulcer, and dense in‐

**f. Bacterial corneal invasion.** The bacterial invasion to corneal epithelium or corneal stro‐ ma is the first step to a severe inflammatory process, with the attraction of inflammato‐ ry substances and the initiation of edema and disruption of cellular union on the corneal epithelial cells. Yi [8] demonstrated that Gram negative bacteria lipopolysac‐ charide attaches on Occludin ZO-1 and ZO-2 disrupting the tight cellular junction in rat

**a. Fungal adhesive mannoproteins.** The mannoproteins regulate the attachment of yeast and filamentous fungi to corneal epithelial cells. The cell wall of Candida albicans is composed mainly by the polysaccharides mannan, glycan and chitin, in this yeast the ligands proteins for the attachment cell are mannoproteins too. The presence of large

The outer fibrilar layer in filamentous fungi and yeast is composed by mannoprotein descri‐ bed as an external coat, which regulates the attachment; this coat is sloughed off during the

In *Aspergillus fumigatus* keratitis have been demonstrated toll-like2 and 4 (TLR2, TLR4) cell receptors as participants in inflammatory response as key of innate immune system that

**b. Fungal corneal penetration.** Fungal corneal infections always begin in the surface where traumatic events happen, then the fungal cells grow in the surface because the fungi are mainly aerobic microorganism; however, pathogenic Candida can reach deep corneal stroma in his hyphae cell form. In some cases, contaminated trauma involve deep cornea, the fungal cells reach the corneal surface after, in both cases the arrival of polymorphonuclear leukocytes and fibrin make a dense infiltrate after the third week of

**c. Fungal toxins.** The investigations about the harmful action of fungal toxins or micotox‐ ines in corneal infections are beginning nowadays. In keratitis due to *Aspergillus flavus* have been demonstrated aflatoxin B1 in 80% of strains isolated from human corneal in‐ fection, and only in 40 % of *Aspergillus flavus* strains isolated from the environment. [10]

filtrate. [7]

64 Common Eye Infections

**5. Fungal pathogenesis**

invasive phase in a corneal infection.

the inflicted cornea.

corneal epithelium and human cultured cells.

quantities of mannoprotein reveals its pathogenic capability.

triggers host defensive responses inducing interleukins IL-1β and IL-6. [9]


**Figure 1.** *Streptococcus pneumoniae* fagocitized in the protoplasm of Polymorphonuclear leucocyte in Gram stained smear of corneal ulcer. 1000 X magnification.
