- Email: [email protected]
Posttraumatic endophthalmitis due to a rare pathogen, Alcaligenes faecalis
Correspondence
GCA has been reported to lead to cerebrovascular ischemic events in approximately 3%–4% of patients.2,3 Involvement of extradural internal carotid or vertebral arteries, or both, may cause ischemia from reduced perfusion related to severe occlusion. This case describes an extremely rare occurrence of bilateral cerebellar and occipital infarction due to bilateral vertebral artery occlusion secondary to GCA, resulting in complete left congruous homonymous hemianopia, and right inferior homonymous quadrantanopia. Physicians and neurologists should be aware of this entity because of its potential high mortality in patients. A high index of suspicion should be maintained in patients with symptoms and signs of vertebrobasilar ischemia, headache and (or) myalgias. An ESR and temporal artery biopsy should be performed without delay. Early diagnosis of GCA is necessary for immediate initiation of intensive antiinflammatory and immunosuppressive treatment that may improve prognosis in these cases. REFERENCES
Fig. 1—A, B: Cranial magnetic resonance scans using diffusion-weighted imaging demonstrates bilateral occipital infarction. C: Cranial magnetic resonance angiogram demonstrates nonvisualization of the vertebral arteries bilaterally, secondary to occlusion. D: Humphrey visual field shows complete left congruous homonymous hemianopia and right inferior homonymous quadrantanopia.
weighted images, revealed bilateral cerebellar and occipital infarction (Fig. 1A and 1B). A cranial MR angiogram showed occlusion of the vertebral arteries bilaterally (Fig. 1C), which was also confirmed by cerebral angiography. On neuro-ophthalmic examination, she had a visual acuity of 20/30 in the right eye and 20/25 in the left eye, with normal optic discs in both eyes. Humphrey visual field testing indicated a complete left congruous homonymous hemianopia (consistent with extensive infarction of the occipital cortex on the right) and a right homonymous inferior quadrantanopia (possibly due to predominant involvement of the superior calcarine cortex on the left, Fig. 1D).1 Bilateral temporal artery biopsy specimens were positive for GCA. The patient was managed by rehabilitation and a combination of high dose prednisone and methotrexate therapy.
1. Levin LA. Topical diagnosis of chiasmal and retrochiasmal disorders. In: Miller NR, Newman NJ, Biousse V, Kerrison JB, eds. Walsh and Hoyt’s Clinical Neuro-Ophthalmology. 6th ed. Baltimore, Md: Lippincott Williams & Wilkins; 2005:503–73. 2. Caselli RJ, Hunder GG, Whisnant JP. Neurologic disease in biopsy-proven giant cell (temporal) arteritis. Neurology 1988;38:352–9. 3. Gonzalez-Gay MA, Blanco R, Rodriguez-Valverde V, et al. Permanent visual loss and cerebrovascular accidents in giant cell arteritis: predictors and response to treatment. Arthritis Rheum 1998;41:1497–504.
Sandeep Randhawa, Gregory P. Van Stavern Departments of Ophthalmology, Neurology, and Neurosurgery Kresge Eye Institute, Wayne State University Detroit, Michigan [email protected] Can J Ophthalmol 2007;42:486–7 doi: 10.3129/can.j.ophthalmol.i07-068
Posttraumatic endophthalmitis due to a rare pathogen, Alcaligenes faecalis
A
n 8-year-old boy presented with a 15-day history of an acutely painful red eye with decreased vision. There was a history of penetrating trauma to the left eye with a wooden stick 18 months earlier There was no other significant ocular or systemic history. At presentation to our centre, vision in the patient’s
CAN J OPHTHALMOL—VOL. 42, NO. 3, 2007
487
Correspondence
Fig. 1—Postoperative fundus photograph showing attached retina with formation of an epiretinal membrane and some traction along the inferotemporal arcade.
left eye was light perception with accurate localization of light projection in all 4 quadrants. Ocular findings included diffuse conjunctival injection, ciliary congestion, self-sealed corneal perforation with adherent iris in the upper temporal part of the cornea, 4+ aqueous cells and flare, and white fluffy exudates within the anterior chamber. As the lens was cataractous, fundus glow was absent. On B-scan ultrasound examination, the presence of mild to moderate amplitude spikes was noted in the vitreous, suggestive of exudates. The right eye had a visual acuity of 6/6 and all findings on examination were within normal limits. When topical and systemic therapies with antibiotics and steroids failed to elicit improvement, pars plana vitrectomy with lensectomy was undertaken. Intravitreal ceftazidime and vancomycin were given after the vitrectomy. Intraoperatively, the disc was noted to be pale with macular and retinal edema. After surgery the patient recovered a visual acuity of finger counting at 1 m. The retina was attached but there was an evolving epimacular membrane (Fig. 1). The vitreous biopsy specimen and contents of the vitrectomy cassette were sent for microbiologic culture. Smear examination revealed polymorphs but no organism. Culture showed Alcaligenes faecalis sensitive to most of the tested antibiotics. Fungal culture was negative. Alcaligenes faecalis is a gram-negative, oxidase-positive rod with peritrichous flagella. It grows on MacConkey agar. A. faecalis is the most frequently isolated member of the Alcaligenaceae in the clinical laboratory. A. faecalis exists in the soil and water and has been isolated from various clinical specimens, such as urine, sputum, pus, feces, and blood. It has also been considered responsible for urinary tract infections, typhoid-like fever, and gastroenteritis. The species A. xylosoxidans has been reported to cause
488
CAN J OPHTHALMOL—VOL. 42, NO. 3, 2007
postcataract endophthalmitis rarely.1–3 A. faecalis has even less frequently been cited as the causative organism of ocular infections such as keratitis and postkeratoplasty endophthalmitis.4,5 Recently, one case of postoperative endophthalmitis due to A. faecalis infection has been reported.6 This is the first report to our knowledge of posttraumatic endophthalmitis caused by A. faecalis. Although most A. faecalis infections are opportunistic and acquired from moist items such as nebulizers, respirators, and lavage fluids, in our case infection appears to have been from direct traumatic inoculation with delayed manifestation. It is also possible that the infection may have occurred 18 months after injury as a secondary inoculation with the incarcerated iris in the corneal wound acting as a wick. This report provides additional evidence that A. faecalis is emerging as a low-grade virulent organism with a potential to produce endophthalmitis. REFERENCES 1. Weissgold DJ, Kirkpatrick B, Iverson M. Acute postoperative Alcaligenes xylosoxidans endophthalmitis. Retina 2003;23: 578–80. 2. Rahman MK, Holz ER. Alcaligenes xylosoxidans and Propionibacterium acnes postoperative endophthalmitis in a pseudophakic eye. Am J Ophthalmol 2000;129:813–5. 3. Swart J, Volker-Dieben HJ, Reichert-Thoen JW. Alcaligenes xylosoxidans endophthalmitis 8 months after cataract extraction. Am J Ophthalmol 1999;127:345–6. 4. Khokhar DS, Sethi HS, Kumar H, Sudan R, Sharma N, Nayak N. Postkeratoplasty endophthalmitis by Alcaligenes faecalis: a case report. Cornea 2002;21:232–3. 5. Tayeri T, Kelly LD. Alcaligenes faecalis corneal ulcer in a patient with cicatricial pemphigoid. Am J Ophthalmol 1993; 115:255–6. 6. Kaliaperumal S, Srinivasan R, Gupta A, Parija SC. Postoperative endophthalmitis due to an unusual pathogen: Alcaligenes faecalis. Eye 2006;20:968–9.
Abhas Mehrotra, Ritu Gadia, Pradeep Venkatesh, Niranjan Nayak, Satpal Garg Dr. Rajendra Prasad Centre for Ophthalmic Sciences Department of Ocular Microbiology All India Institute of Medical Sciences New Delhi, India [email protected] Can J Ophthalmol 2007;42:487–8 doi: 10.3129/can.j.ophthalmol.i07-064
GCA has been reported to lead to cerebrovascular ischemic events in approximately 3%–4% of patients.2,3 Involvement of extradural internal carotid or vertebral arteries, or both, may cause ischemia from reduced perfusion related to severe occlusion. This case describes an extremely rare occurrence of bilateral cerebellar and occipital infarction due to bilateral vertebral artery occlusion secondary to GCA, resulting in complete left congruous homonymous hemianopia, and right inferior homonymous quadrantanopia. Physicians and neurologists should be aware of this entity because of its potential high mortality in patients. A high index of suspicion should be maintained in patients with symptoms and signs of vertebrobasilar ischemia, headache and (or) myalgias. An ESR and temporal artery biopsy should be performed without delay. Early diagnosis of GCA is necessary for immediate initiation of intensive antiinflammatory and immunosuppressive treatment that may improve prognosis in these cases. REFERENCES
Fig. 1—A, B: Cranial magnetic resonance scans using diffusion-weighted imaging demonstrates bilateral occipital infarction. C: Cranial magnetic resonance angiogram demonstrates nonvisualization of the vertebral arteries bilaterally, secondary to occlusion. D: Humphrey visual field shows complete left congruous homonymous hemianopia and right inferior homonymous quadrantanopia.
weighted images, revealed bilateral cerebellar and occipital infarction (Fig. 1A and 1B). A cranial MR angiogram showed occlusion of the vertebral arteries bilaterally (Fig. 1C), which was also confirmed by cerebral angiography. On neuro-ophthalmic examination, she had a visual acuity of 20/30 in the right eye and 20/25 in the left eye, with normal optic discs in both eyes. Humphrey visual field testing indicated a complete left congruous homonymous hemianopia (consistent with extensive infarction of the occipital cortex on the right) and a right homonymous inferior quadrantanopia (possibly due to predominant involvement of the superior calcarine cortex on the left, Fig. 1D).1 Bilateral temporal artery biopsy specimens were positive for GCA. The patient was managed by rehabilitation and a combination of high dose prednisone and methotrexate therapy.
1. Levin LA. Topical diagnosis of chiasmal and retrochiasmal disorders. In: Miller NR, Newman NJ, Biousse V, Kerrison JB, eds. Walsh and Hoyt’s Clinical Neuro-Ophthalmology. 6th ed. Baltimore, Md: Lippincott Williams & Wilkins; 2005:503–73. 2. Caselli RJ, Hunder GG, Whisnant JP. Neurologic disease in biopsy-proven giant cell (temporal) arteritis. Neurology 1988;38:352–9. 3. Gonzalez-Gay MA, Blanco R, Rodriguez-Valverde V, et al. Permanent visual loss and cerebrovascular accidents in giant cell arteritis: predictors and response to treatment. Arthritis Rheum 1998;41:1497–504.
Sandeep Randhawa, Gregory P. Van Stavern Departments of Ophthalmology, Neurology, and Neurosurgery Kresge Eye Institute, Wayne State University Detroit, Michigan [email protected] Can J Ophthalmol 2007;42:486–7 doi: 10.3129/can.j.ophthalmol.i07-068
Posttraumatic endophthalmitis due to a rare pathogen, Alcaligenes faecalis
A
n 8-year-old boy presented with a 15-day history of an acutely painful red eye with decreased vision. There was a history of penetrating trauma to the left eye with a wooden stick 18 months earlier There was no other significant ocular or systemic history. At presentation to our centre, vision in the patient’s
CAN J OPHTHALMOL—VOL. 42, NO. 3, 2007
487
Correspondence
Fig. 1—Postoperative fundus photograph showing attached retina with formation of an epiretinal membrane and some traction along the inferotemporal arcade.
left eye was light perception with accurate localization of light projection in all 4 quadrants. Ocular findings included diffuse conjunctival injection, ciliary congestion, self-sealed corneal perforation with adherent iris in the upper temporal part of the cornea, 4+ aqueous cells and flare, and white fluffy exudates within the anterior chamber. As the lens was cataractous, fundus glow was absent. On B-scan ultrasound examination, the presence of mild to moderate amplitude spikes was noted in the vitreous, suggestive of exudates. The right eye had a visual acuity of 6/6 and all findings on examination were within normal limits. When topical and systemic therapies with antibiotics and steroids failed to elicit improvement, pars plana vitrectomy with lensectomy was undertaken. Intravitreal ceftazidime and vancomycin were given after the vitrectomy. Intraoperatively, the disc was noted to be pale with macular and retinal edema. After surgery the patient recovered a visual acuity of finger counting at 1 m. The retina was attached but there was an evolving epimacular membrane (Fig. 1). The vitreous biopsy specimen and contents of the vitrectomy cassette were sent for microbiologic culture. Smear examination revealed polymorphs but no organism. Culture showed Alcaligenes faecalis sensitive to most of the tested antibiotics. Fungal culture was negative. Alcaligenes faecalis is a gram-negative, oxidase-positive rod with peritrichous flagella. It grows on MacConkey agar. A. faecalis is the most frequently isolated member of the Alcaligenaceae in the clinical laboratory. A. faecalis exists in the soil and water and has been isolated from various clinical specimens, such as urine, sputum, pus, feces, and blood. It has also been considered responsible for urinary tract infections, typhoid-like fever, and gastroenteritis. The species A. xylosoxidans has been reported to cause
488
CAN J OPHTHALMOL—VOL. 42, NO. 3, 2007
postcataract endophthalmitis rarely.1–3 A. faecalis has even less frequently been cited as the causative organism of ocular infections such as keratitis and postkeratoplasty endophthalmitis.4,5 Recently, one case of postoperative endophthalmitis due to A. faecalis infection has been reported.6 This is the first report to our knowledge of posttraumatic endophthalmitis caused by A. faecalis. Although most A. faecalis infections are opportunistic and acquired from moist items such as nebulizers, respirators, and lavage fluids, in our case infection appears to have been from direct traumatic inoculation with delayed manifestation. It is also possible that the infection may have occurred 18 months after injury as a secondary inoculation with the incarcerated iris in the corneal wound acting as a wick. This report provides additional evidence that A. faecalis is emerging as a low-grade virulent organism with a potential to produce endophthalmitis. REFERENCES 1. Weissgold DJ, Kirkpatrick B, Iverson M. Acute postoperative Alcaligenes xylosoxidans endophthalmitis. Retina 2003;23: 578–80. 2. Rahman MK, Holz ER. Alcaligenes xylosoxidans and Propionibacterium acnes postoperative endophthalmitis in a pseudophakic eye. Am J Ophthalmol 2000;129:813–5. 3. Swart J, Volker-Dieben HJ, Reichert-Thoen JW. Alcaligenes xylosoxidans endophthalmitis 8 months after cataract extraction. Am J Ophthalmol 1999;127:345–6. 4. Khokhar DS, Sethi HS, Kumar H, Sudan R, Sharma N, Nayak N. Postkeratoplasty endophthalmitis by Alcaligenes faecalis: a case report. Cornea 2002;21:232–3. 5. Tayeri T, Kelly LD. Alcaligenes faecalis corneal ulcer in a patient with cicatricial pemphigoid. Am J Ophthalmol 1993; 115:255–6. 6. Kaliaperumal S, Srinivasan R, Gupta A, Parija SC. Postoperative endophthalmitis due to an unusual pathogen: Alcaligenes faecalis. Eye 2006;20:968–9.
Abhas Mehrotra, Ritu Gadia, Pradeep Venkatesh, Niranjan Nayak, Satpal Garg Dr. Rajendra Prasad Centre for Ophthalmic Sciences Department of Ocular Microbiology All India Institute of Medical Sciences New Delhi, India [email protected] Can J Ophthalmol 2007;42:487–8 doi: 10.3129/can.j.ophthalmol.i07-064