Slitlamp examination showed conjunctival chemosis of the left eye with corneal edema without an epithelial defect. The anterior chamber had a fibrinous reaction with a 1-mm hypopyon.
Khurana RN, Leder HA, Nguyen QD, Do DV. Enterococcus casseliflavus Endophthalmitis Associated With a Horse Tail Injury. Arch Ophthalmol. 2009;127(11):1547-1553. doi:10.1001/archophthalmol.2009.282
Enterococcus casseliflavus is a gram-positive bacteria that has been rarely reported in human infection. We describe the first case to our knowledge of E casseliflavus endophthalmitis associated with a human's injury by a horse's tail.
A 37-year-old healthy man had pain and decreased vision in his left eye. Two days earlier while working on a horse farm, he was whipped across the face by the tail of a horse. The next day, his eye became painful. He denied any fever or chills. On examination, his visual acuity was 20/20 OD and light perception OS. There was no relative afferent pupillary defect. Extraocular movements were intact. There were skin abrasions on his forehead and cheek. Results from slitlamp and fundus examinations of the right eye were unremarkable. Slitlamp examination of the left eye revealed +2 conjunctival chemosis and +2 corneal edema without an epithelial defect (Figure). The anterior chamber had a fibrinous reaction with a 1-mm hypopyon. Dilated funduscopic examination of the left eye showed dense vitritis. Contact B-scan ultrasonography of the left eye showed vitreous opacities without retinal detachment. The patient underwent a diagnostic vitrectomy with injection of vancomycin hydrochloride (1 mg/0.1 mL) and ceftazidime (2 mg/0.1 mL) for presumptive endophthalmitis. Vitreous cultures grew E casseliflavus that was sensitive to ampicillin but resistant to vancomycin. The blood culture results were negative.
The patient's pain and anterior segment inflammation resolved 1 week after surgery. Three weeks postoperatively, his visual acuity was hand motions OS. A white cataract and vitreous debris were present. Eight weeks after his initial visit, he underwent a pars plana lensectomy and vitrectomy. Intraoperatively, after the vitreous debris was removed, there was an advanced rhegmatogenous and tractional retinal detachment with proliferative vitreoretinopathy. The retinal detachment was inoperable owing to the advanced proliferative vitreoretinopathy and necrotic retina. His last visual acuity was light perception OS.
E casseliflavus is a particular strain of enterococcus commonly found in the gastrointestinal tract of livestock such as cattle and horses.1 It has rarely been associated with human infection. There have been a few cases involving polymicrobacterial bacteremia with biliary tract disease in humans.2 A PubMed search of the literature from 1951 to 2008 revealed no reports of E casseliflavus and eye infection. In this case, the etiology of the E casseliflavus endophthalmitis is not clear. The blood culture results were negative and the patient was afebrile, making endogenous endophthalmitis less likely. The horse tail injury may have introduced the pathogen. E casseliflavus is the most common strain found in fresh and dry horse manure,1 the likely source of infection. However, the mechanism is unclear as there was no entry site for the bacteria (ie, no evidence of a ruptured globe, corneal ulcer, or corneal perforation). The conjunctiva was chemotic, but on surgical exploration there was no evidence of a gross perforation. The horse tail injury might have caused a self-sealing microperforation through the cornea or the conjunctiva, which may explain how the bacterial strain entered the eye. The patient did have abrasions around his face from the horse tail whip, suggesting that the tail could have hit the eye as well. Animal tail whip injuries have been reported to cause traumatic subconjunctival crystalline lens3 and intraocular penetration with the animal hair.4 Ophthalmologists must be aware that tail whip injuries can have serious visual consequences.
Correspondence: Dr Do, Retina Division, Wilmer Eye Institute, Johns Hopkins University School of Medicine, 600 N Wolfe St, Maumenee 742, Baltimore, MD 21287 (firstname.lastname@example.org).
Financial Disclosure: None reported.
Funding/Support: Dr Khurana is a Ronald G. Michels Fellow and is supported by the Ronald G. Michels Foundation.