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Infectious Crystalline Keratopathy due to Abiotrophia Adiacens - Case Study Example

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According to research findings of the paper “Infectious Crystalline Keratopathy due to Abiotrophia Adiacens”, to the best of our knowledge, this is the first published case report of Abiotrophia advances-related infectious crystalline keratopathy following penetrating keratoplasty.  …
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Infectious Crystalline Keratopathy due to Abiotrophia Adiacens
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Case report: Infectious crystalline keratopathy due to Abiotrophia adiacens Micro-organisms of the genus Abiotrophia are known as important causes of bacterial endocarditis, brain abscess and endophthalmitis. In this study, we report a case of crystalline keratopathy caused by the species Abiotrophia adiacens in a 52 year old man with symptoms and signs of infectious keratopathy following penetrating keratoplasty. The isolates were recovered by cultivation of corneal scrapings. The condition responded well to topical ciprofloxacin drops and resolved over a period of 4 weeks. Keywords Abiotrophia adiacens Infectious crystalline keratopathy Penetrating keratoplasty Corneal infections Introduction Infectious crystalline keratopathy is an indolent corneal infection in which needle-like, branching crystalline opacities are seen within the corneal stroma, in the absence of appreciable corneal or anterior segment inflammation1. In most cases it occurs as a complication of corneal surgery and keratitis. It has been detected as a rare complication following penetrating keratoplasty2. The most common cause is Streptococci viridans3. Gram negative and other gram positive bacteria have also been implicated in this condition4. Some studies have indicated fungal infection also5. We have isolated a rare organism Abiotrophia adiacens as a cause of infectious crystalline keratopathy following penetrating keratoplasty. Species of the genus Abiotrophia was initially identified by Frenkel and Hirsh in 1961. They were formerly known as nutritionally variant streptococci6. They are normal inhabitants of the respiratory and oral flora and they cause opportunistic infections. They have been incriminated in bacterial endocarditis, brain abscess, prosthetic infections post total knee arthroplasty, vertebral osteomyelitis, blood stream infections and endovascular infections. In the eye, Abiotrophia species have been implicated in post-operative endophthalmitis, neonatal conjunctivitis, and equine microbial keratitis. In addition, this group of organisms have also been implicated in cirrhosis, pancreatic abscess, otitis media, wound infections, conjunctivitis, and keratitis. They usually appear as small satellite colonies around colonies of associated bacterial species and their growth is usually supported by many gram negative and gram positive bacteria. One important aspect of the cultures of these species is, the microscopic morphology of the organisms is medium dependent and they vary from typical gram positive streptococci to gram variable cocco-bacilli7. The term Abiotrophia means ‘life nutrition deficiency’. This term was adopted only in 1995 to reflect the requirement of supplemental media for the growth of these organisms8. The supplemental media required are pyridoxal hydrochloride and L-cysteine. Some of the common species are A. defective, A. adiacens and A.elegans. The organisms usually appear as small non-haemolytic or alpha-haemolytic satellite colonies9. They gain access through an epithelial break and then they replicate and spread along the plane of dissected collagen lamellae, but do not elicit an inflammatory response. This probably is because of the concomitant use of steroids. Production of a biofilm by certain bacteria also may limit the immune reaction, and bacterial exopolysaccharide production may cause the visible arboreal pattern10. Ormerod et al postulated that the apparent antibiotic resistance is secondary to inductive bacterial factors, produced by variations in nutrient status, and other environmental determinants like pyridoxine (vitamin B6), iron or other nutrients being relatively deficient in the grafted cornea11. Sharma and others have suggested that the eye infections usually suffice with discontinuation of topical steroids and aggressive antibiotic therapy. But continued infection, vascularization, or scar formation may affect visual acuity and may require penetrating keratoplasty12. Case report A 52-year old man with keratoconus presented with uncorrected visual acuity of 1/60 (best corrected visual acuity 6/18) in his left eye, and underwent his third penetrating keratoplasty (PK) in this affected eye for recurrence of disease He had under gone uncomplicated PK in the left eye in 1969 and 1971. He had no pre-existing ocular surface disease. Visual acuity (VA) in his right eye was 6/36. Repeat PK was done using 8 mm host trephine, an 8.75 mm donor button, and 10-0 interrupted nylon sutures. Keflin was administered intra-operatively. His immediate postoperative course was uneventful, apart from his left intraocular pressure being elevated at 26 (right = 21). VA for his left eye was 6/24, BCVA 6/12. The patient was started on an alpha 2–adrenergic agonist (brimonidine tartrate, 0.15%) twice daily. Topical corticosteroid (prednefrin forte, 0.1%) initially was applied four times daily; later tapered to twice daily. Six weeks after corneal transplantation, his uncorrected left visual acuity was noted to have decreased to 6/60 (BCVA 6/36), associated with no other symptoms. Slit lamp examination revealed a focal area of non-suppurative, intrastromal white opacities exhibiting a branching cracked-glass-appearance; this was evident inferiorly, without any epithelial defect. No loose or broken sutures were noted. (Figure1). Corneal scrapings were performed for diagnostic smears and cultures. Topical steroids were withdrawn. The patient was treated presumptively with ciprofloxacin eye drops and non-steroidal eye drops. Provisional microscopic examination of the smears revealed no bacteria on gram stain, and only normal flora was evident after 48 hours of incubation. No fungal elements were detected on stained preparation. One week later, cultures revealed heavy growth of gram-positive cocci, identified as Abiotrophia adiacens. The cultured organisms were sensitive to cephalexin, erythromycin and penicillin. Cultures again were negative for fungi and no inflammatory cells were observed. Ciprofloxacin was continued, while the steroid drops were discontinued. The patient’s ICK responded well to ciprofloxacin (Figure 2) and resolved over a period of 4 weeks. (Figure 3) Visual acuity in the left eye improved to 6/15. Discussion Despite published reports of Abiotrophia species involving eye like endophthalmitis, conjunctivitis and keratitis, these organisms have not been reported as a cause of infectious crystalline keratopathy. In this report, we document a case of infectious crystalline keratopathy following penetrating keratoplasty. The commonest cause of infectious crystalline keratopathy has been reported as Streptococcus viridans. However, post-op eye infections are usually caused by ocular surface micro flora, Staphylococcus species being the commonest. These infections are usually facilitated by pre-operative risk factors such as prosthesis in the eye, contact lens wear, contaminated eye drops, pre-existing subtle conjunctivitis, lacrimal duct obstruction, blepharitis and dacryocystitis13. Abiotrophia species are predominant in oral, pharyngeal and respiratory surfaces. Occasionally, they may be present in ocular surface. This can be expected due to the proximity of regions. They have a tendency to colonise and cause opportunistic infections following surgeries with foreign body implantation. They have also been implicated in the infection of damaged cardiac valves. We diagnosed ICK on the basis of slit lamp findings of hard-edged crystalline opacities in the setting of prior corneal surgery and steroid use. Histopathologically, the crystalline opacities consist of confluent colonies of microbes insinuated between corneal stromal lamellae, along with a notable absence of inflammatory cells. To grow in culture, Abiotrophia species require media with added pyridoxine hydrochloride (0.001%) and L-cysteine (0.01%). Our patient’s ICK responded well to presumptively-prescribed ciprofloxacin, and resolved over a period of 4 weeks. However, response to antibiotic therapy often is slow and may fail, because of the deep stromal sequestration of the organisms. Hence, corticosteroids should be tapered to allow antibiotics to have their full effect. Some infections do not respond to antibiotic therapy, such that patients may require lamellar or penetrating keratoplasty. Intervention with Nd:YAG laser disruption creates a diffuse haze of the protective glycocalyx matrix within the intrastromal crystals, making the bacteria drug-susceptible. This may be considered before more extensive surgical steps are undertaken. Conclusion Abiotrophia adiacens is a very rare cause of infectious crystalline keratopathy in patients who have undergone penetrating keratoplasty. To the best of our knowledge, this is the first published case report of Abiotrophia adiacens-related infectious crystalline keratopathy following penetrating keratoplasty. Prompt and accurate diagnosis of the organism using corneal scrapings can lead to appropriate therapy and resolution of the keratopathy. Works Cited Page Butler TK, Dua HS, Edwards R, Lowe JS. “In vitro model of infectious crystalline keratopathy: tissue architecture determines pattern of microbial spread.” Invest Ophthalmol Vis Sci. 42(6)(May 2001):1243-1246. Frenkel A, Hirsch W. “Spontaneous development of L forms of streptococci requiring secretions of other bacteria or sulphydryl compounds for normal growth.” Nature 191 (1961):728-730. James CB, McDonnell PJ and Falcon MG. “Infectious crystalline keratopathy.” British Journal of Ophthalmology 72 (1988): 628-630. Kawamura Y, Hou X, Sultana J, et. al. “Transfer of Streptococcus adjacens and Streptococcus defectivus to Abiotrophia gen. nov. as Abiotrophia adiacens comb. nov. and Abiotrophia defectiva comb. nov., respectively” Int J Syst Bacteriol. 45(4 (October 1995):798-803. Khater TT, Jones DB, Wilhelmus KR. “Infectious crystalline keratopathy caused by gram-negative bacteria.” American Journal of Ophthalmology 124(1) (July 1997): 19-23. Namdhari H, Kintner K, Jackson BA, et.al. "Abiotrophia Species as a Cause of Endophthalmitis Following Cataract Extraction." Journal of Clinical Microbiology 37(5)(May 1999):1564–1566. Ormerod LD, Ruoff KL, Meisler DM, et al. “ Infectious crystalline keratopathy. Role of nutritionally variant streptococci and other bacterial factors.” Ophthalmology 98(1991):159-169. Sharma N, Vajpayee RB, Pushker N and Vajpayee M. “Infectious Crystalline Keratopathy.” The CLAO Journal 26(1) (2000): 40-43. Sridhar M. “Epithelial infectious crystalline keratopathy.” American Journal of Ophthalmology 131(2): 255-257. Verma K, Vajpayee RB, Tritiyal JS, Sharma N, Nayak N. “Post-LASIK Infectious Crystalline Keratopathy Caused by Alternaria.” Cornea 24(8) (November 2005):1018-1020. Read More

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