Case report: Visual acuity loss as a warning sign of ocular syphilis: A retrospective analysis of 17 cases

Abstract

ObjectivesTo define the clinical features of ocular syphilis and analyze the cerebrospinal fluid (CSF) of ocular syphilis patients to determine the co-occurrence of neurosyphilis.MethodsThis was a retrospective study of 17 patients (23 eyes) with ocular syphilis admitted to the Fifth People's Hospital, Suzhou, China from September 2017 to December 2021. Clinical manifestations, laboratory tests, treatment, and clinical outcomes were analyzed, and a review was conducted.ResultsEight males (12 eyes) and nine females (11 eyes) were enrolled. Mean patient age was 49.06 ± 3.47 years. The total manifestation time for ocular symptoms ranged from 10 days to 6 years. The cohort was comprised of three cases of early syphilis, four cases of late syphilis, and ten cases of unknown stage. The primary complaints were decreased visual acuity in 15 cases (21 eyes), ptosis in 1 case (1 eye), and loss of light perception in 1 case (1 eye). Cases were diagnosed as chorioretinitis in 7 cases (8 eyes), optic nerve retinitis in 4 cases (6 eyes), optic neuritis in 4 cases (7 eyes), and oculomotor nerve palsy in 1 case (1 eye), syphilitic stromal keratitis in 1 case (1 eye). Serum HIV antibody was positive in one case(Nos.2). All patients had reactive serum Treponema Pallidum Particle Agglutination (TPPA) and Toluidine Red Unheated Serum Test (TRUST). All patients underwent CSF examination. CSF white blood cell count was ≥5 × 106/L in 13 cases, CSF protein was >500 mg/L in 6 cases, TPPA was reactive in 15 cases, and TRUST was reactive in 5 cases. Eleven cases were also diagnosed with neurosyphilis. Patients were treated with either penicillin G sodium or ceftriaxone sodium. At time of discharge, 12 patients reported improved visual acuity. Abnormal serum or CSF examination improved in ten patients during the 6–12 month follow-up.ConclusionVisual acuity loss is a warning indicator of ocular syphilis. Ocular syphilis primarily manifests as posterior uveitis, involving the choroid, retina, and optic nerve, and often co-occurs with neurosyphilis. Effective treatment should be administered immediately to avoid irreversible visual impairment and other serious adverse outcomes.

Ocular Syphilis as a Primary Manifestation of Neurosyphilis: A Case Report

“…In a retrospective analysis of 17 cases of ocular syphilis in Suzhou, China, seven patients were misdiagnosed with other causes of visual acuity impairment [ 10 ]. The use of symptomatic medication for ocular inflammation, such as steroids, was deemed to be an important cause of misdiagnosis in this investigation [ 10 ].…”

“…In a retrospective analysis of 17 cases of ocular syphilis in Suzhou, China, seven patients were misdiagnosed with other causes of visual acuity impairment [ 10 ]. The use of symptomatic medication for ocular inflammation, such as steroids, was deemed to be an important cause of misdiagnosis in this investigation [ 10 ]. Similarly, our patient was suffering from vision loss and was initially misdiagnosed with the suspicion of GCA for which he received steroids with temporary improvement of his symptoms.…”

Neurosyphilis: insights into its pathogenesis, susceptibility, diagnosis, treatment, and prevention

“…Early neurosyphilis can affect the meninges and central blood vessels, including syphilitic meningitis, meningovascular neurosyphilis and syphilitic gummas, often manifested as headache, nausea, vomiting, blurred consciousness, and neck stiffness; late neurosyphilis affects the spinal cord and brain parenchyma, including general paresis and tabes dorsalis, manifested as ataxia, impaired memory, disorientation, depression, hallucinations, and mania ( 102 , 103 ). Furthermore, as a great imitator, neurosyphilis can mimic a wide range of neurological and psychiatric diseases ( 104 ), including but not limited to autoimmune encephalitis ( 105 ), acute ischemic stroke ( 106 ), status epilepticus ( 107 ), posterior uveitis ( 108 ), asymptomatic optic perineuritis ( 109 ). These phenotypes suggest that T. pallidum can invade and affect one or more components of the CNS.…”