The diagnosis of fungal corneal ulcers is difficult and should generally be made from the following three aspects. 1, medical history: one of the following conditions, should be further pathogenic examination. a, rural patients, a history of agricultural trauma such as rice, or history of keratitis, or history of picking foreign bodies before the onset of the disease. b. Longer period of time with drops or subconjunctival injection of multiple antibiotics and the ulcer is not controlled. 2.Signs and symptoms a.White, yellowish-white or grayish-white ulcers often accompanied by pus accumulation in front, and the degree of development is relatively chronic compared with the course of the disease. b. Eye irritation symptoms are relatively mild compared with the size of the ulcer. 3, Pathogen: a, ulcer necrosis tissue scraping examination, can find fungal mycelium; scraping inoculated on fungal medium, can have fungal growth. b. Cell culture is generally negative, or there is only miscellaneous fungal growth. Generally speaking, the necrotic tissue of fungal ulcers is “mossy”, loose in texture and lacking in adhesiveness, while the necrotic tissue of bacterial ulcers is “jelly”, rich in adhesiveness. Treatment: Treatment must be prompt. In the ulcer stage, fungal growth and reproduction is high, so drugs sensitive to fungi should be preferred. Since the fungus is often latent in the corneal tissue and is very stubborn, it is necessary to maintain continuous contact between the drug and the ulcerated surface so that the drug reaches sufficient concentration in the deep tissue to destroy or inhibit the fungal activity. So far, the drugs used to treat fungal corneal ulcers are not ideal. In cases where drug therapy is not effective, corneal transplantation is required. Etiology: Most cases have a history of causative factors at the onset of the disease. The onset of the disease is mostly closely related to vegetative lobular injuries sustained during agricultural work. Plant leaf abrasions and dust and other foreign bodies into the eye, but also in long-term patients with other nature of keratitis secondary to fungal infection. Some people abroad believe that it is related to ocular abuse of antibiotics or corticosteroids. Corneal trauma causing epithelial breakage. Fungus is often present on injury-causing materials such as rice, plant branches, leaves, or dust. When the corneal epithelium is broken at the same time, the fungus can be inoculated into the cornea and cause the disease. The incubation period is usually 1 to 4 days, with an average of 2.4 days. Clinical manifestations: a. At the beginning, there is only ocular scratch sensitivity or irritation, accompanied by blurred vision. In those with a history of trauma, ulcers appear within a few days of injury and develop more slowly, differing from Pseudomonas aeruginosa corneal ulcers that develop rapidly after trauma. b. Early irritation symptoms such as eyelid erythema and photophobia and tearing vary in severity, and most of the irritation symptoms in the severe stage are seen to be milder in contrast. The congestion is often severe, mainly mixed, and in some cases there may be a small amount of grayish-white discharge. c. Due to the different strains of fungi, the duration of infection and individual differences, the morphology of ulcers seen clinically is very inconsistent. Typical early ulcers are grayish or creamy white, often irregular in shape. The surface is rough, dense, and slightly elevated above the plane. The density of the ulcer and infiltrate is not uniformly distributed, the ulcer is mostly clearly demarcated from the healthy area of the cornea, and the ulcer margin is often untidy. d. Larger ulcers are often yellowish-white, mostly irregularly rounded, with a dry, rough surface that appears to be “mossy”. The stroma is densely infiltrated, and the edges of the ulcer are slightly elevated. If the lesion develops, a nodular or tree-root-like stromal infiltrate is seen around the ulcer. Commonly used names for fungal keratitis describe: 1. Mycelial tesserae: Mycelium and necrotic tissue attached to the surface of the ulcer. White opaque, slightly elevated, clearly demarcated from the healthy area of the cornea. Can be scraped off, scraped off the ulcer surface is more transparent. 2, mycelial foci: is a fungal mycelium into the corneal stroma of the lesion. The surface is slightly elevated dry and rough. The density of infiltration in the cloudy area is not uniform. The texture is hard, and when scraping with a knife, the scraping material attached to the tip of the knife is sparse. After scraping the ulcer is still cloudy and opaque. 3, mycelial foci edge: some ulcers edge hairy and uneven. Sometimes extend the root infiltration, called “pseudo-foot”; or in the ulcer around the appearance of isolated nodular round infiltrate point, called “satellite foci”. 4, reaction ring: in the mycelial foci around a circle of inflammatory bacterial infiltration, generally not too wide, about 1 to 2 mm, is the body’s defense response to the mycelium. Some people call it “immune ring”. 5, the demarcation groove: located in the middle of the mycelial foci and reaction ring. Here the most inflammatory cell infiltration, is a shallow tissue necrosis, mildly depressed and shallow grooves. Slit lamp examination of fungal corneal ulcers: 1. The ulcer develops from superficial to deep. Early ulcers are superficial, with little change in corneal thickness. The bottom of the ulcer is a dense stromal infiltrate that can reach 0.2, 0.4, or 0.6 of the full corneal layer. Stromal edema, although mild, is often total. The endothelium directly behind the mycelial foci is often edematous and rough and thickened, accompanied by folds, which some people call “endothelial plaques. Sometimes the entire cornea appears diffuse foggy edema, suggesting that the ulcer is developing. 2, the development process of ulcers, often first in the surrounding or bottom of the infiltration, followed by the formation of pus ulcers, pus ulcers necrosis and ulcers, ulcer surface necrotic tissue constantly melting off, so that the cornea gradually thinning, and finally lead to perforation. 3, perforation is generally slow, the location, size and shape is variable. The perforation is often slightly elevated, with the iris showing every time, and the cornea is slightly conical in the central perforation. The incidence of perforation is about 10%. 4, sometimes the necrotic tissue is not shed, the cornea is already “leaky” phenomenon, so that the anterior chamber disappears unknowingly. Sometimes in the necrotic corneal tissue, a little iris tissue is revealed, which is also another E image of ulcer perforation. Once the ulcer is perforated, the inflammation is gradually reduced, but the anterior chamber is difficult to form again in most perforations of greater size. The necrotic tissue of the ulcer is continuously shed, which can expose the transparent posterior elastic layer and make the iris clearly visible, and as it cannot resist the normal intraocular pressure, it develops into a localized or total corneal chyloma. 6. When the ulcer tends to heal, eye pain is reduced, irritation improves, mucous discharge disappears, ulcer color changes from yellowish white to grayish white, ulcer surface is clean, surrounding epithelium grows inward, and fluorescein staining is reduced in scope. Anterior chamber pus accumulation and Tyndall’s phenomenon as well as posterior corneal deposits were reduced. After the ulcer heals, the corneal stroma remains infiltrated and edematous, often taking several months to absorb. 7, the ulcer healing process can have new blood vessels into. Slender single branches are rare, and dense thick and short ones are seen around the foci of mycelium, rather like a smaller cornea and an inward shift of the corneal edge. 8, severe iridocyclitis reaction, is one of the characteristics of fungal corneal ulcer. About 50% of cases can have pus accumulation in the anterior chamber, since 1 mm or 2-3 mm, a few cases of pus accumulation up to more than half of the anterior chamber, or even fill the entire anterior chamber. The pus accumulation is milky or yellowish in color, the former being an early phenomenon of ulceration, while the latter often represents the development of inflammation to a severe stage. The pus is viscous and does not move easily. Ulcers, pus ulcers and pus accumulation in the anterior chamber are morphologically integrated and can be easily confused, and slit lamp examination is required to differentiate them. 9, there are two types of posterior corneal sediment, one is brownish gray powder or fine granular, every seen in the early stage of ulceration, small area of the case, the anterior chamber mostly no pus or a small amount of pus accumulation. The other type is a yellowish paste-like flake, or a grayish-white patch, attached to the rough endothelial surface of the cornea, usually accompanied by pus accumulation in the anterior chamber. If the anterior chamber pus is not absorbed, it eventually forms a mechanized film on the anterior chamber angle, iris, and lens surface. Treatment: a. The disease is often accompanied by a severe iritis reaction, and the pupil must be adequately dilated with atropine. Corticosteroids have a spreading effect on ulcers and should not be used either locally or systemically. b. In cases of perforated ulcers or posterior elastosis, the conjunctival sac should be bandaged with pressure to promote ulcer healing after placement of gold and brown toxin ophthalmic ointment or dicloxacin B ophthalmic ointment. c. In cases where drug therapy fails, conjunctival flap masking or penetrating corneal transplantation may be performed. In penetrating corneal transplantation, the ulcer and its adjacent unhealthy tissues must all be removed; if an infected cornea is left, it can instead accelerate the expansion of inflammation.