Neuroretinitis; Acute vision loss OS; 1+ Optic disk swelling/ optic disc edema; Rare blot hemorrhages; superior macular retinal edema with arterial narrowing consisting with a cilioretinal artery; superior macular retinal edema with arterial narrowing consisting with cilioretinal artery occlusion OS/ macular edema OS; superior macular retinal edema with arterial narrowing consisting with a cilioretinal artery; superior macular retinal edema with arterial narrowing consisting with a cilioretinal artery; Intraretinal thickening; Mild tortuosity; Relative afferent pupillary defect OS; Cecocentral scotoma OS; Horizontal "dark red line" across his left eye vision while awakening and that line had turned gray by the time of presentation; Visual acuity decreased; Papillophlebitis; This case was reported in a literature article and described the occurrence of neuroretinitis in a 15-year-old male patient who received Men B NVS (Meningococcal B vaccine) for prophylaxis.  On an unknown date, the patient received Meningococcal B vaccine. On an unknown date, less than 2 weeks after receiving Meningococcal B vaccine, the patient experienced neuroretinitis (serious criteria GSK medically significant), unilateral vision loss (serious criteria GSK medically significant), optic disc engorgement (serious criteria GSK medically significant), retinal blot hemorrhages (serious criteria GSK medically significant), retinal edema (serious criteria GSK medically significant), macular edema (serious criteria GSK medically significant), retinal artery narrowing (serious criteria GSK medically significant), retinal artery occlusion (serious criteria GSK medically significant), retinal thickening (serious criteria GSK medically significant), retinal vein tortuosity (serious criteria GSK medically significant), relative afferent pupillary defect, scotoma, chromatopsia, visual acuity decreased and papillophlebitis. The patient was treated with methylprednisolone and prednisone. On an unknown date, the outcome of the neuroretinitis, unilateral vision loss, retinal artery narrowing, retinal thickening, relative afferent pupillary defect, scotoma, chromatopsia and papillophlebitis were unknown and the outcome of the optic disc engorgement, retinal artery occlusion, retinal vein tortuosity and visual acuity decreased were recovering/resolving and the outcome of the retinal blot hemorrhages, retinal edema and macular edema were recovered/resolved.   The reporter considered the neuroretinitis, unilateral vision loss, optic disc engorgement, retinal blot hemorrhages, retinal edema, macular edema, retinal artery narrowing, retinal artery occlusion, retinal thickening, retinal vein tortuosity, relative afferent pupillary defect, scotoma, chromatopsia, visual acuity decreased and papillophlebitis to be related to Meningococcal B vaccine.  Additional information was provided as follows: This case was reported in a literature article and described the occurrence of acute vision loss in a 15-years old male patient, who was vaccinated with unspecified Meningococcal B Vaccine (Manufacturer unknown) for prophylaxis. The patient was previously healthy. The patient's medical, surgical, social and family histories were unremarkable. The patient was taking no medications. No information on patient's current condition was provided. On an unspecified date, the patient received unspecified Meningococcal B Vaccine (Route and site of administration unspecified; batch number not provided, dosage unknown). The age at vaccination was not provided. On an unspecified date, 2 weeks following administration of the unspecified meningococcal B vaccine the patient presented with acute vision loss OS. The patient stated that he saw a horizontal "dark red line" across his vision in the left eye on awakening that had changed to "gray" by the time of presentation. The patient denied any flashes of light, eye pain, headache, nausea, vomiting or fever. The patient's best-corrected vision was 20/25 oculus dexter (OD) and counting fingers at 5 feet oculus sinister (OS). No relative afferent pupillary defect was noted oculus uterque (OU). No abnormalities were found on slit-lamp examination. Intraocular pressure measured 14 mm Hg OU. Funduscopic examination OD was within normal limits. There was 1+ optic disk swelling, rare blot hemorrhages and superior macular retinal edema with arterial narrowing consistent with a cilioretinal artery occlusion OS. Automated perimetry (24-2 Humphrey visual field) showed no abnormalities OD and cecocentral scotoma OS with a mean deviation of -12 dB. Optical coherence tomography of the macula revealed intraretinal thickening consistent with macular edema OS. The patient was diagnosed with neuroretinitis and was treated with a 5-day course of intravenous methylprednisolone 1000 mg daily followed by an oral prednisone taper that consisted of 40 mg daily for 5 days and 20 mg daily for 5 days. Follow-up examination 11 days later revealed mild improvement in visual acuity (20/400 OS), but a mild relative afferent pupillary defect was noted OS. Four weeks after the onset of symptoms, the patient experienced improvement of vision to 20/30 OS. Funduscopic examination OS revealed resolving optic disc edema and mild tortuosity and dilatation of veins, but the retinal hemorrhage and cilioretinal artery distribution macular edema resolved. The 24-2 Humphrey visual field mean deviation was -8 dB. Extensive laboratory tests including C-reactive protein, rapid plasma reagin, rheumatoid factor, anti-neutrophil cytoplasmic antibody, anti-nuclear antibody, Bartonella henslae titer (IgM and IgG) and West Nile virus were negative. Chest x-ray was normal. Magnetic resonance imaging of the brain and orbit with and without contrast material was unremarkable. Follow-up at 1 year demonstrated 20/30 vision OS. The authors commented, "The pathogenesis of vaccine-induced optic neuritis is unknown, primarily because an association between optic neuritis and vaccines has not been officially established. It is theorized that there is an autoimmune reaction to either the pathogen itself or to a vaccine adjuvant used to induce immune response. Specifically, it has been proposed that this reaction results in immune complex formation that attacks the retinal vasculature, leading to hyperpermeability and inflammation. In this case, macular edema and retinal hemorrhages without exudate supported a diagnosis of inflammatory disease of the retina and optic nerve (neuroretinitis). Several causation criteria have been proposed to try to establish a cause-and-effect relationship between triggering events and visual loss. These include a biologically plausible mechanism; a close temporal relationship between cause and effect coherent with the pharmacokinetics or pathogenesis of the purported cause; analogy from prior animal model or human cases; specificity of effect; exclusion of alternative etiologies including chance alone; dose-response gradient; and dechallenge/rechallenge. In our case, the presumed biologically plausible mechanism is believed to be autoimmune inflammatory disease triggered by the vaccine. The onset of symptoms and signs within 2 weeks is consistent with an immunologic mechanism that requires mobilization and activation of inflammatory lymphocytes. There is analogy for optic neuritis after vaccination with other vaccines. No other etiology for the optic neuritis and retinal findings was found despite a complete laboratory evaluation and neuroimaging. The most common alternative etiologies were not present, including multiple sclerosis or other antibody-mediated causes of optic neuritis. Although there was no rechallenge, a dechallenge led to improvement of symptoms and signs without recurrence. The presence of the optic disc edema in conjunction with the retinal findings is an atypical finding for idiopathic or demyelinating optic neuritis, retinal vein occlusion, or retinal artery occlusion. The presence of optic disc edema, retinal venous dilatation, retinal hemorrhages and a concomitant cilioretinal artery occlusion suggests a partial retinal vein occlusion as the unifying mechanism in our case. The lower perfusion pressure of the cilioretinal artery in the setting of central retinal venous backpressure is the presumed mechanism for the ophthalmoscopic appearance in our case."