**6. Differential diagnosis**

NTM keratitis can often be mistaken with other bacterial infections that cause nonsuppura‐ tive keratitis. Several authors suggest to keep in mind other causative organisms that may present, in the course of disease, similar clinical features such as fungal keratitis, infec‐ tious crystalline keratopathy, Nocardia keratitis, herpes simplex virus, and rarely Acantha‐ moeba keratitis. In our experience at APEC, the principal differential diagnosis must be made between fungal and Nocardia keratitis.

**Fungal keratitis:** Often preceded by history of trauma involving plants or foreign bodies. Like NTM, mycotic keratitis may worsen with the use of topical corticosteroids. These keratitis often do not respond to topical antibiotics, as seen with NTM keratitis. Multiple corneal fungal abscesses may emulate the multifocal presentation of NTM keratitis. Sabo‐ uraud's agar is essential for the identification of the causative fungus. [Figure 6]

**Infectious Crystalline Keratopathy (ICK):** "Cracked windshield" corneal appearance may be also seen in this keratitis caused most commonly by Streptococcus species, but unlike this entity, NTM keratitis presents with this sign transiently early in the course. Gorovoy et al first described Infectious crystalline keratopathy in 1984, describing it as a unique corneal infection characterized by and indolent, progressive course: a paucity of inflammation; and

**Figure 6.** Candida keratitis after penetrating keratoplasty for keratoconus.

post-LASIK infectious keratitis. The most common organisms cultured were nontubercu‐ lous mycobacteria (48%) and staphylococci (33%).. These findings are consistent with Chang's research, where he found that nearly 47% of infectious keratitis cases after LASIK appear to be caused by NTM; 32% being caused by *Mycobacterium chelonei* alone. In con‐ trast to the acute or subacute onset of symptoms generally seen postoperatively in bacteri‐ al and fungal keratitis, rapid growing atypical mycobacteria may present with a slower onset of clinical disease, from 3 to 14 weeks (3.5 weeks in average) after the procedure. It is important to keep in mind that this is not a rule, and more rapidly growing NTM such as the *Mycobacterium chelonae-abscessus* group may present as soon as 10 days posterior to

Innoculation of NTM to the flap-stromal interface probably takes place at the time of sur‐ gery, therefore, it is infrequent to find an epithelial defect, being present in less than half of cases. Corneal infiltrates appear to be entirely within the lamellar flap or at the flap inter‐ face and may be either multiple, tiny, white, granular opacities less than 0.5mm in diame‐ ter or a single white lesion ranging between 0.1-0.2mm in diameter. Anterior extension of infiltrate with ulceration or anterior perforation of the corneal flap or posterior extension in‐ to the stroma is a rare finding and is usually associated with a delay in diagnosis and the beginning of therapy. Anterior chamber reaction is not a common finding, occurring in on‐

NTM keratitis can often be mistaken with other bacterial infections that cause nonsuppura‐ tive keratitis. Several authors suggest to keep in mind other causative organisms that may present, in the course of disease, similar clinical features such as fungal keratitis, infec‐ tious crystalline keratopathy, Nocardia keratitis, herpes simplex virus, and rarely Acantha‐ moeba keratitis. In our experience at APEC, the principal differential diagnosis must be

**Fungal keratitis:** Often preceded by history of trauma involving plants or foreign bodies. Like NTM, mycotic keratitis may worsen with the use of topical corticosteroids. These keratitis often do not respond to topical antibiotics, as seen with NTM keratitis. Multiple corneal fungal abscesses may emulate the multifocal presentation of NTM keratitis. Sabo‐

**Infectious Crystalline Keratopathy (ICK):** "Cracked windshield" corneal appearance may be also seen in this keratitis caused most commonly by Streptococcus species, but unlike this entity, NTM keratitis presents with this sign transiently early in the course. Gorovoy et al first described Infectious crystalline keratopathy in 1984, describing it as a unique corneal infection characterized by and indolent, progressive course: a paucity of inflammation; and

uraud's agar is essential for the identification of the causative fungus. [Figure 6]

the refractive surgery. [1,33,34]

154 Common Eye Infections

ly 20% of cases.[1,29]

**6. Differential diagnosis**

made between fungal and Nocardia keratitis.

the formation of sharply demarcated, gray-white, branching, round, stellate, or needle-like opacities in the corneal stroma. Although the duration of the relatively recalcitrant course of the infectious crystalline keratopathy may mimic NTM keratitis, the crystalline appearance persists in ICK but is transient in NTM keratitis. Among post-LASIK patients, crystalline NTM keratitis occurs rarely (less than 10%).

**Nocardiaasteroides infection:** should also be considered, since it is an acid-fast microorgan‐ ism capable of producing bacterial keratitis. The best way to differentiate Nocardia infection from NTM keratitis is with a Gram stain. Nocardia keratitis is more fulminant than NTM keratitis.[Figure 7]

**Figure 7.** Nocardial keratitis as a differential diagnosis of NTM keratitis.

**Deep lamellar keratitis** can be confused with post-LASIK NTM keratitis. It usually presents within the first 7 days post-LASIK, and unlike NTM keratitis, it clears with topical cortico‐ steroids. If the wrong diagnosis is made, the improper use of such medications contribute to the delay in diagnosis of post-LASIK NTM keratitis.

**Acanthamoeba keratitis** generally presents with out-of-proportion pain in comparison to the clinical findings. It is common to see ring ulcers in Acanthamoeba keratitis. This agent responds, unlike NTM, to topical biguanides and diamidines, and topical corticosteroids may be of some benefit.

**Herpetic keratitis.** In necrotizing stromal keratitis, herpetic keratitis can cause dense white stromal infiltrates that may be confused with NTM keratitis. Special features that are more typically found in herpetic keratitis are decreased corneal sensation and previous or con‐ comitant history of herpes labialis lesions. NTM keratitis may simulate a non-suppurative herpetic keratitis, especially in cases caused by Mycobacterium marinum. There may also be a dendritic or geographic epithelial defect with minimal stromal infiltration, misleading the clinician and prompting treatment with antivirals. This can lead to the development of a se‐ vere, wide corneal infiltrate.
