Infectious Keratitis Flashcards

1
Q

• Pseudomonas

A

often in CL wearers, form biofilms.

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2
Q

• Biofilms

A

It can take around 24-48 hours for a biofilm to develop. Washing CLs at least daily can help prevent the buildup of biofilm

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3
Q

• Infectious crystalline keratopathy

A

the bacteria makes its own biofilm and the crystalline part is a biofilm made by the host bacteria. Strep viradans in the most common culprit. Others include alpha hemolytic strep species. Because of the biofilm there is a minimal host response, meaning the eye might not be as red, there may be less corneal edema or necrosis. Associated risk factors include chronic steroid use.

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4
Q

• Group of bugs that can infect through intact corneal epithelium

A

usually they have some sort of enzyme that enable them to tunnel or that CHANLS through intact epithelium—Corynebacterium, Hemophilus Aegyptus, Neisseria, Listeria and Shigella (CHANLS)

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5
Q

• Things you can do in setting of significant corneal thinning/corneal melt

A

a lot of practitioners will start Vitamin C to help with collagen synthesis; or doxycycline for its reported inhibition of matrix metalloproteinase, a key enzyme in the stromal melting process.

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6
Q

• Infectious keratitis caused by atypical mycobacteria

A

common post-lasik or similar refractive surgeries. Pop up on acid fast stains or culturing on Lowenstein-Jensen media. For atypical mycobacteria, it will usually occur 10 days or more after refractive surgery, along with fungal infections.

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7
Q

• Post refractive surgery corneal infections

A

atypical mycobacterial and fungal infections usually occur 10+ days post-op. If less than 10 days post-op, suspect normal bacterial keratitis

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8
Q

• Risk factors for fungal keratitis

A

vegetative matter, contact lenses, frequent topical steroid use, immunocompromised patients. Hints for fungal—not responding to antibiotics, feathery edges (although not a slam dunk), painful, perhaps less focal infiltrates, could be multifocal or satellite lesions/infiltrates.

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9
Q

• Culturing for fungal keratitis:

A

sabaraud or blood agar. Confocal microscopy can also be helpful to see if filaments or septa are branching or not, which can help in differentiation and treatment.

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10
Q

• Treatment of fungal keratitis

A

natamycin has been the go-to treatment for fusarium. IF candida or aspergillus then amphotericin B or voriconazole. People have also trialed intrastromal injection of antifungal agents for recalcitrant fungal infections with varying results. Classically fusarium is more common in the Southern US.

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11
Q

• Acanthamoeba keratitis

A

can exist in dormant cyst form and then transform to trophozoite form. Can spread along the nerves, causing perineural inflammation or infiltrate and pain out of proportion to exam. It can also present as a ring infiltrate. It can grow on non-nutrient agar and along with e. coli and Enterobacter (eats the E. Coli). On confocal microscopy you should be able to see the cysts. Treatment is with a biguanide, including chlorhexidine or polyhexanide. They kill the trophozoite and the cystic form.

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12
Q

• Microsporidia keratitis

A

more common in immune-compromised individuals. Also has been popping up more in southeast Asia in immunocompetent patients. Can be a very painful keratitis. May see punctate epitheliopathy as well as tiny cysts in the areas of epitheliopathy. It doesn’t typically penetrate deep in the stroma or cause a large confluent ulcer. Looks like recalcitrant punctate epitheliopathy. Restoring immune function can usually help clear microsporidiosis; fumagillin has also been shown effective in some but not all cases.

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13
Q

• Epithelial Herpes simplex keratitis:

A

if epithelial, then topical antivirals will help. Trifluridine is very toxic to the cornea and has to be applied very often, has fallen somewhat out of favor. Much preferable is topical ganciclovir. Oral acyclovir or valacyclovir is purportedly as effective as topical therapy. For Valtrex, be careful with immunocompromised patients or those with significant liver problems as one of the side effects is HUS/TTP.

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14
Q

• When to use steroids for herpes keratitis

A

for stromal keratitis or herpetic endotheliitis. If you see whiteish haze to stroma or KNV then think of stromal keratitis. Also think about disciform keratitis which is really a form of endotheliitis, where you have circular areas of endothelial KP and then overlying that because endothelial cells aren’t working you will have an overlying stromal/epithelial edema over that circle.

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15
Q

• Differential for follicles

A

mnemonic is MCHAM– Molluscum, chlamydia, Herpetic (zoster, simplex), adenovirus (or other viruses), medicamentosa. Like MCHammer. Or think of a little pig. MCHam.

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16
Q

• Some HEDS Trial Highlights

A

1) topical steroids reduces the length of stromal inflammation and resulted in better visual outcome. 2) oral acyclovir reduces recurrence over 12-18 months span after the initial episode of stromal keratitis. Oral acyclovir was not found to reduce the time of the average episode of active stromal keratitis, but most providers will still start it to help reduce recurrence rate. 3) no clear risk factors proven to precipitate attacks such as stress, steroids, lifestyle risk factors.