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it is frequently associated with systemic infections such as measles , mumps , chicken pox , pertussis , infectious mononucleosis , and immunizations .
less common causes include multiple sclerosis or part of a more diffused demyelinating disorder such as acute disseminated encephalomyelitis or neuromyelitis optica .
poor vision secondary to optic atrophy in patients with biotinidase deficiency has been described in the literature.17 this report is on a young boy with biotinidase deficiency who suffered an acute attack of optic neuritis in both eyes .
rapid clinical diagnosis and prompt management are essential in preventing devastating visual loss in this rare entity .
a 6-year - old malay boy who had been diagnosed with biotinidase deficiency endured sudden reduced vision in both eyes within a period of 5 days .
based on further questioning , it was discovered that he had retro - orbital pain and a headache .
he had no history of fever , symptoms of upper respiratory tract infection , recent vaccination , bleeding tendencies , or trauma .
he was diagnosed with biotinidase deficiency at 18 months of age when he presented with generalized impetigo , delayed developmental milestone , and recurrent episodes of seizure .
he was started on a 6 mg daily dose of oral biotin , however the compliance was poor .
he was also suffering from bronchial asthma with a history of recurrent acute exacerbation , and was prescribed a metered - dose - inhaler of salbutamol .
there had been no seizure attacks for the past 3 years and his anticonvulsant treatment was discontinued . on examination ,
the anterior segment examination was unremarkable in both eyes except for the presence of a mild relative afferent pupillary defect in the right eye .
funduscopy revealed swollen and hyperemic optic discs in both eyes ( figure 1a and b ) .
examination of the lower limbs revealed numerous scars from previous impetigo , healed eczema , and dry scaly skin .
the biotinidase activity in dried blood spots was less than 0.1 pmol / min/l ( normal range : 6.39.3 pmol / min/l ) .
cerebrospinal fluid analysis was within normal range for cell counts , protein , sugar , and gamma globulin levels .
he was started on intravenous methylprednisolone 125 mg 6-hourly for 3 days , followed by oral prednisolone 1 mg / kg daily for 11 days .
both fundi showed normal and a well - defined margin of the optic discs ( figure 1c and d ) .
his case was followed up for 1 year and visual acuity in both eyes remained good with no sign of recurrence .
deficiency of biotinidase enzyme causes loss of biocytin in urine and progressive depletion of biotin which results in multiple carboxylase deficiency .
classically , it is presented with hypotonia , seizures , ataxia , dermatitis , alopecia , and recurrent infections during the first year of life.8 progressive neurological damage such as sensorineural hearing loss , optic atrophy , ataxia , and mental retardation has been described in older children.810 salbert et al described 51% ophthalmic abnormalities in 78 symptomatic children with biotinidase deficiency.1 this included 30% infections , 13% optic neuropathies , 13% motility disturbances , 4% retinal pigment changes , and 1% pupillary findings , while the most common features were optic atrophy and keratoconjunctivitis.1 table 1 summarizes cases of optic neuropathy in children with biotinidase deficiency published in pubmed11 from 1997 to 2011 . our search was made on keywords of  optic neuropathy ,  
we documented seven patients , and reviewed their age , gender , ocular features , funduscopy , systemic features and onset of biotinidase deficiency , treatment received , and their final visual outcome .
six of seven patients ( 85.7% ) presented with optic atrophy in both eyes , while the remaining one patient ( 14.3% ) displayed normal looking optic discs bilaterally.25,910 unfortunately , the final visual outcome was poor in 71.4% ( five patients).25 in contrast , puertas et al reported a 12-year - old boy with biotinidase deficiency and presented symptoms of acute retrobulbar neuritis in both eyes.9 similarly , our patient also exhibited acute papillitis in both eyes .
these two patients were identified during the acute attack , and they were successfully treated with a combination of intravenous corticosteroid and oral biotin .
his biotinidase activity was confirmed low ( less than 0.1 pmol / min/l ) , and this supports the diagnosis of biotinidase deficiency .
raised urinary levels of organic acids 3-hydroxyisovalerate and 3-hydroxypropionate suggest multiple carboxylase deficiencies in our patient .
there are possible explanations regarding the occurrence of optic neuritis in children with biotinidase deficiency ( figure 3a and b).12,13 decreased amount of biotin causes reduction of methylcrotonyl - coa carboxylase activity .
this leads to the accumulation of 3-methylcrotonyl - coa , and subsequently the formation of 3-methylcrotonic acid .
accumulation and storage of these two acids in the retinal ganglion cells directly affects the intracellular metabolism and leads to retinal ganglion cells apoptosis.12,13 due to high energy demand and the long course of their axons , retinal ganglion cells are very susceptible to intracellular metabolic defect . in biotinidase deficiency ,
this leads to the accumulation of propionyl - coa which can be converted later into propionic acid resulting in acidosis.12,13 in addition to that , propionyl - coa can be processed into methylcitrate by an enzyme in the citric acid cycle .
this causes limited energy production in the retinal ganglion cells and subsequently , results in cell apoptosis .
the above factors may lead to optic neuropathy and consequently result in irreversible optic atrophy.12,13 corticosteroid is the standard modality for treatment of optic neuritis .
it acts to decrease inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability .
children with profound biotinidase deficiency have less than 10% of mean serum biotinidase enzyme activity , while children with partial biotinidase deficiency have 10%30% of mean serum biotinidase enzyme activity .
it is important for ophthalmologists and pediatricians to be aware of this diagnosis when a child with biotinidase deficiency presents symptoms of acute visual loss .
prompt diagnosis and early treatment is mandatory to avoid irreversible visual loss in these children .
the combination of systemic corticosteroid and biotin treatment seemed an effective treatment with our patient .
optic atrophy has often been reported in children with biotinidase deficiency . 
 the visual prognosis is usually poor . 
 this report is of a 6-year - old boy with an early onset of biotinidase deficiency who presented with acute profound visual loss in both eyes . 
 fundoscopy revealed swollen discs in both eyes , and the imaging was consistent with bilateral optic neuritis . 
 he was treated with systemic corticosteroid , and commenced on oral biotin . 
 the final visual outcome was promising .