01Approach to the Critical Patient/attcp48

Immediate threats and stabilization

›Sight-threatening emergency indicators

›Severe unilateral vision loss worse than 20/200

›Urgent ophthalmology consultation within hours

›IV methylprednisolone consideration for rapid vision loss

›Bilateral visual involvement

›Present in ~5% of CSD neuroretinitis cases

›Escalate urgency of workup and treatment

›Encephalopathy or seizures

›CSD encephalitis occurs in ~0.5% of cases

›Seizures present in 68% of those with CSD encephalitis

›If encephalitis suspected, emergent CT head then LP

›Neurologic emergency flags

›Status epilepticus

›IV benzodiazepine as first-line

›Emergent neurology consultation

›Altered mental status with fever

›Meningitis and encephalitis on differential

›Blood cultures prior to antibiotics

›Focal neurologic deficits

›Emergent brain imaging required

Consult triggers

›Ophthalmology consultation

›All suspected cases of neuroretinitis require urgent dilated exam

›Disc edema and macular star confirmation

›OCT and visual field testing

›Same-day or next-day when vision loss is moderate to severe

›VA worse than 20/40 in affected eye

02History/hx63

Presenting symptoms

›Core visual complaints

›Subacute unilateral vision loss developing over days

›Painless or mildly painful

›Central scotoma

›Blurred vision and dyschromatopsia

›Color vision changes in affected eye

›Floaters

›Mild periorbital discomfort

›Absence of pain with eye movement distinguishes from demyelinating optic neuritis

›Systemic preceding symptoms

›Fever and malaise preceding ocular symptoms by 2 to 8 weeks

›May have resolved by time of ocular presentation

›Lymphadenopathy draining inoculation site

›Skin papule or pustule at scratch or bite site

›May have healed prior to presentation

›Headache

›May accompany optic disc inflammation

Exposure and risk history

›Animal contact history

›Cat scratch, bite, or lick on broken skin

›Single most important historical element

›Present in ~90% of confirmed cases

›Kitten exposure specifically

›Kittens under 12 months old are more likely bacteremic

›Higher risk than adult cat contact

›Flea exposure in household

›Cat fleas transmit B. henselae between cats

03Physical Exam/exam63

Vital signs and general assessment

›Stability snapshot

›Temperature

›Low-grade fever common in active CSD

›High fever suggesting systemic or disseminated involvement

›Blood pressure

›Baseline assessment

›Hypertension as alternative cause of disc edema

›General appearance

›Toxic-appearing patient suggests disseminated disease

›Well-appearing patient consistent with isolated neuroretinitis

Ophthalmologic examination

›Visual acuity testing

›Snellen acuity in affected and unaffected eye

›Ranges from 20/40 to counting fingers at presentation

›33% present with good VA >20/40

›44% with moderate loss 20/40 to 20/200

›23% with severe loss <20/200

›Near vision and reading vision assessment

›Color vision and pupillary exam

›Ishihara color plates or red desaturation testing

›Dyschromatopsia in affected eye is characteristic

›Relative afferent pupillary defect (RAPD)

›Present in affected eye

›Confirms optic nerve dysfunction

›Fundoscopic examination

›Optic disc edema

›Swollen, hyperemic disc

04Differential Diagnosis/ddx46

Infectious causes of neuroretinitis

›Bartonella henselae (CSD)

›ICD-10 A28.1 (cat scratch disease)

›Most common infectious cause of neuroretinitis

›Accounts for ~64% of neuroretinitis cases in series

›Classic triad: cat exposure, disc edema, macular star

›Syphilis

›ICD-10 A52.71 (syphilitic chorioretinitis)

›Must exclude in all cases of neuroretinitis

›RPR/VDRL + FTA-ABS required

›Uveitis, optic neuritis, and neuroretinitis all possible

›Lyme disease

›ICD-10 A69.22 (Lyme disease with optic neuritis)

›Relevant in endemic areas

›Lyme serology required in appropriate geographic context

›Toxoplasmosis

›ICD-10 B58.01 (toxoplasma chorioretinitis)

›Focal retinochoroiditis with overlying vitritis

›Toxoplasma IgG/IgM for differentiation

›Tuberculosis

›ICD-10 A18.53 (tuberculous chorioretinitis)

›QuantiFERON or TST in endemic populations

Non-infectious optic nerve conditions

›Demyelinating optic neuritis

›ICD-10 H46.0

›Pain with eye movement is distinguishing feature

›Macular star does NOT occur

›Associated with MS risk; neuroretinitis is NOT

05Laboratory Tests/lt52

Bartonella-specific diagnostics

›B. henselae serology (IFA)

›IgG and IgM antibody titers

›IgG >= 1:256 is suggestive of infection

›IgG >= 1:512 is more specific for active infection

›IgG >= 1:800 is a major Duke criterion for Bartonella endocarditis

›Performance characteristics

›Sensitivity approximately 64% for neuroretinitis patients

›Antibodies may not be detectable for up to 6 weeks after acute infection

›Convalescent titers 2 to 4 weeks later; 4-fold rise confirms diagnosis

›PCR for B. henselae DNA

›Specimens: blood, lymph node tissue, aqueous humor

›Most sensitive in first week of illness

›Lower sensitivity later in course

›Role in diagnosis

›Useful when serology is negative or equivocal early

›mNGS emerging as option when conventional tests inconclusive

Exclusionary serologies

›Syphilis serology

›RPR or VDRL as screening

›FTA-ABS for confirmation

›Mandatory in all cases of neuroretinitis

›Neurosyphilis consideration

›LP for CSF VDRL when neurologic involvement suspected

›Lyme serology

›ELISA with Western blot confirmation

›In endemic geographic areas

›Two-tier testing per CDC guidelines

06Diagnostic Tests/dt73

Scoring Systems

›Visual acuity classification at presentation

›Good vision: VA better than 20/40 in approximately 33% of cases

›Generally favorable prognosis

›Moderate loss: VA 20/40 to 20/200 in approximately 44% of cases

›Antibiotic plus corticosteroid combination often indicated

›Severe loss: VA worse than 20/200 in approximately 23% of cases

›Aggressive treatment with combined therapy recommended

›OR 7.0 for >= 3-line improvement with combined antibiotics plus prednisone versus antibiotics alone

›Dissemination risk stratification

›Standard CSD: lymphadenopathy dominant

›~90% of cases

›Ocular CSD: neuroretinitis dominant manifestation

›Requires ophthalmology-directed management

›Disseminated CSD: hepatosplenic or neurologic or cardiac involvement

›~2% of cases

›Encephalitis in ~0.5% with seizures in 68% of those cases

MRI

›MRI brain and orbits with contrast

›Indications

›Exclude demyelinating disease (MS-related optic neuritis vs neuroretinitis)

›Exclude compressive optic neuropathy

›Assess for CNS involvement in encephalitis presentation

›Expected findings in CSD neuroretinitis

›Normal brain MRI (no demyelinating white matter lesions)

›Optic nerve enhancement possible

›Normal brain MRI supports CSD over MS-related diagnosis

›When to order

›Atypical presentation without classic macular star

›Pain with eye movement suggesting demyelinating etiology

›Neurologic symptoms beyond visual loss

›MRI limitations in CSD neuroretinitis

›Not required in classic presentation with positive serology

›Saves cost and time when diagnosis is clinically clear

›Fundoscopy and OCT are primary diagnostic tools

›MRI complements when clinical uncertainty present

CT

›CT head

›Indications in CSD neuroretinitis

›Encephalitis presentation with altered mental status

›Seizures to exclude structural cause before LP

›Suspected raised ICP before lumbar puncture

›Not indicated for isolated uncomplicated neuroretinitis

›Classical presentation does not require CT head

›CT abdomen/pelvis

›Hepatosplenic CSD

›Multiple hypoechoic or hypodense microabscesses in liver and spleen

›Indications: fever with abdominal pain, hepatomegaly, elevated liver enzymes

›Sensitivity for hepatosplenic microabscesses

›CT superior to ultrasound for small lesions

›Contrast-enhanced preferred

›CT chest

›If pulmonary sarcoidosis on differential

›Bilateral hilar lymphadenopathy in sarcoidosis

Ultrasound

›Ocular ultrasound (B-scan)

›Vitreous evaluation

›Vitreous opacification or vitritis assessment when fundoscopy limited

›Pre-retinal membranes or hemorrhage

›Posterior segment imaging when media opacity limits fundoscopy

›Subretinal fluid

›Optic disc elevation

›Abdominal ultrasound

›Hepatosplenic involvement screening

›Multiple small hypoechoic lesions in liver and spleen suggest microabscesses

›Less sensitive than CT for small lesions

›First-line imaging when concern for hepatosplenic CSD

›Lymph node assessment

›Regional lymphadenopathy characterization

›Internal necrosis or suppuration in nodes

›OCT (optical coherence tomography)

›Primary diagnostic tool for monitoring

›Quantifies disc edema and subretinal fluid

›Macular exudate mapping for macular star confirmation

›Serial monitoring

›Treatment response assessment over 4 to 6 weeks

›Subretinal fluid resolution tracking

07Disposition/dispo51

Admission criteria

›Indications for inpatient management

›Severe bilateral vision loss

›IV methylprednisolone consideration

›Close ophthalmologic monitoring

›CSD encephalitis or seizures

›Neurologic monitoring and IV antibiotics

›Neurology and ID consultation

›Disseminated disease

›Hepatosplenic CSD with systemic decompensation

›Bartonella endocarditis

›Bacteremia in immunocompromised host

›Immunocompromised host with any CSD manifestation

›HIV/AIDS, transplant, or biologic immunosuppression

›Risk of rapid progression to disseminated disease

›Need for IV antibiotics or IV corticosteroids

›Inability to take oral medications

›Failure of outpatient oral therapy

Outpatient management criteria

›Criteria for safe outpatient management

›Isolated neuroretinitis with stable vision

›VA 20/200 or better in affected eye

›Monocular involvement

›Immunocompetent host

›No HIV, transplant, or immunosuppressive therapy

›Able to take oral medications reliably

›Doxycycline BID tolerated

›Confirmed ophthalmology follow-up within 1 to 2 weeks

08Treatment/t77

Antibiotic therapy

›First-line regimen for neuroretinitis

›Doxycycline oral 100 mg twice daily

›Duration 4 to 6 weeks

›Mainstay treatment for CSD neuroretinitis

›Take with full glass of water; remain upright 30 minutes to prevent esophagitis

›Addition of rifampin consideration

›Rifampin 300 mg twice daily for 4 to 6 weeks

›Combined doxycycline plus rifampin when severe or if monotherapy fails

›Rifampin is a potent CYP inducer — reduces plasma levels of both doxycycline and prednisone

›Avoid combining rifampin with concurrent systemic corticosteroids

›Azithromycin alternative

›Azithromycin 500 mg on day 1 then 250 mg daily for 4 days

›IDSA-recommended for uncomplicated CSD lymphadenopathy

›Less evidence base for neuroretinitis than doxycycline

›Consider when doxycycline is contraindicated

›Children under 8 years old

›Pregnancy (first and second trimester)

Corticosteroid therapy

›Adjunctive oral corticosteroids

›Oral prednisone indication

›Significant vision loss (VA worse than 20/40 or moderate to severe loss)

›Combined antibiotics plus oral prednisone associated with significantly better outcomes

›Odds ratio 7.0 for achieving >= 3-line visual improvement versus antibiotics alone

›Prednisone dosing protocol

›Oral prednisone 1 mg/kg/day (typical range 40 to 60 mg/day)

›Taper over 2 to 4 weeks during antibiotic course

›Do not co-administer with rifampin (CYP induction reduces prednisone levels)

›Timing of corticosteroids

›Initiate during acute inflammatory phase

›Taper as disc edema and VA improve

›IV corticosteroids for severe cases

›IV methylprednisolone 1 g daily for 3 days

›For vision loss worse than 20/200 or rapid deterioration

›Followed by oral prednisone taper

›Inpatient monitoring required for IV steroid administration

Treatment for specific populations and complications

›CNS involvement (encephalitis)

›Doxycycline 100 mg orally or IV twice daily

›Plus rifampin 300 mg twice daily

›Duration minimum 4 to 6 weeks

›Seizure management

›Standard anticonvulsant therapy

›Neurology consultation for seizure protocol

›Immunocompromised patients

›Extended antibiotic duration minimum 3 months

›HIV/AIDS with CD4 <200 requires long-term suppressive therapy

›Doxycycline 100 mg twice daily plus rifampin 300 mg twice daily

›Consider prophylactic doxycycline for heavily immunocompromised

›Bartonella endocarditis

›Doxycycline 100 mg twice daily plus gentamicin 3 mg/kg/day IV

›Gentamicin for first 14 days of treatment

›Total doxycycline course 6 weeks (native valve) or 6 months (prosthetic valve)

›Cardiac surgery consultation for valve destruction

›Topical adjunct therapy

›Topical ketorolac 0.5% twice daily

›For macular edema and inflammatory control

›Topical difluprednate 0.05% four times daily

›Reported beneficial in severe ocular cases

›Tapered as inflammation resolves

Treatment monitoring and response

›Response assessment milestones

›2 to 4 weeks: initial visual acuity improvement expected

›Disc edema beginning to resolve

›Macular star may persist longer than disc edema

›4 to 6 weeks: most patients show significant improvement

›80% of patients achieve final VA better than 20/40

›Macular star resolution may take weeks to months

›Monitoring parameters during treatment

›Liver function tests if rifampin used

›Hepatotoxicity monitoring at 2 and 4 weeks

›Visual acuity at each visit

›VA worsening despite treatment requires reassessment

›CBC with prolonged doxycycline or rifampin

›Baseline and monitoring for cytopenias

›Treatment failure considerations

›Seronegative status not excluding CSD

›Repeat serology at 2 to 4 weeks

›Alternative diagnoses requiring different therapy

›Syphilitic neuroretinitis: IV penicillin G

›Toxoplasmosis: pyrimethamine plus sulfadiazine plus leucovorin

09Special Populations/sp80

Pregnancy

›Pregnancy-specific considerations

›Antibiotic selection in pregnancy

›Doxycycline contraindicated in second and third trimester

›Risk of dental staining and fetal skeletal effects

›Preferred alternatives

›Azithromycin 500 mg day 1, then 250 mg daily x 4 days

›Erythromycin or alternative macrolide as second option

›Short course macrolide favored over prolonged tetracycline exposure

›First trimester and early pregnancy

›Azithromycin preferred; doxycycline may be acceptable for brief courses in early first trimester in severe cases

›Consult ID and obstetrics for guidance

›Fetal and maternal risk

›Bartonella infection in pregnancy

›Limited data on fetal outcomes; maternal treatment recommended

›Severe maternal infection may affect fetal perfusion

›Imaging in pregnancy

›OCT and fundoscopy: no radiation risk; use freely

›MRI brain/orbits: acceptable without gadolinium in first trimester

›CT reserved for life-threatening indications; fetal shielding

›Corticosteroids in pregnancy

›Short course prednisolone acceptable if vision loss severe

›Use lowest effective dose

›Avoid prolonged high-dose corticosteroid exposure

Geriatric

›Older adult considerations

›Presentation differences

›Cat exposure may be underrecognized in older patients

›Systemic symptoms (fever, lymphadenopathy) may be attenuated

›Higher prevalence of comorbidities confounding diagnosis

›Differential diagnosis in older adults

›AION more common in older age group

›Giant cell arteritis (GCA) must be excluded when disc edema plus systemic symptoms

›ESR and CRP markedly elevated in GCA; temporal artery biopsy if suspected

›Medication considerations in older adults

›Doxycycline in renal impairment

›No dose adjustment required; hepatically cleared

›Adequate hydration to prevent renal stone risk

›Rifampin drug interactions

›Review full medication list for CYP3A4 substrates

›Particular concern with anticoagulants, statins, cardiac medications

›Corticosteroid adverse effects

›Higher risk of hyperglycemia, osteoporosis, psychiatric effects in older adults

›Blood glucose monitoring during steroid course

›Bone protection with calcium and vitamin D

›Functional and disposition considerations

›Visual impairment impact

›Falls risk from unilateral visual loss

›Driving restriction if VA severely affected

›Home safety assessment for monocular vision loss

›Adherence support

›Pill organizer or dose assistance for 4 to 6 week course

›Follow-up closer to every 2 weeks for older patients

Pediatrics

›Pediatric epidemiology and presentation

›Peak incidence in ages 5 to 14 years

›Children and young adults most affected

›Cat and kitten exposure common in household

›Hepatosplenic CSD more common in pediatric population

›Abdominal pain, fever, and hepatosplenomegaly

›Pediatric patients more likely to present with systemic forms

›Antibiotic dosing in children

›Doxycycline contraindicated in children under 8 years

›Risk of permanent dental staining and skeletal effects

›Short courses (5 days or less) increasingly used for tick-borne diseases; apply caution for 4 to 6 week CSD course

›Azithromycin preferred for children under 8 years

›10 mg/kg on day 1 (maximum 500 mg)

›Then 5 mg/kg daily on days 2 to 5 (maximum 250 mg/day)

›Azithromycin for children 8 years and older when preferred

›Same dosing as above; doxycycline an acceptable alternative in older children

›Rifampin pediatric dosing if needed

›10 to 20 mg/kg/day divided every 12 hours (maximum 600 mg/day)

›Combined with azithromycin or doxycycline for severe pediatric cases

›Pediatric-specific monitoring

›Visual acuity testing in young children

›Age-appropriate charts (Allen cards, HOTV) for preverbal children

›Patching or preferential looking technique for infants

›OCT in pediatric patients

›Feasible in cooperative children over approximately 5 years

›Sedation rarely needed for fundoscopy

›Immunization and prevention

›No vaccine available for Bartonella

›Flea control and avoiding rough kitten play as primary prevention

10Background/b88

Epidemiology

›Incidence and prevalence

›Cat scratch disease overall

›Approximately 12,000 outpatient diagnoses annually in the United States

›Approximately 500 hospitalizations annually in the United States

›Neuroretinitis as manifestation of CSD

›Accounts for ~64% of infectious neuroretinitis cases in published series

›Most common infectious cause of neuroretinitis overall

›Geographic and seasonal distribution

›Higher incidence in southern US states

›Seasonal peak in autumn and winter (January peak)

›Correlates with kitten birth season and human-animal contact

›Demographics

›Age distribution

›Peak incidence ages 5 to 14 years in pediatric range

›Young adults 15 to 29 years also commonly affected

›Cat owners of any age at risk

›Animal reservoir

›Cats are primary reservoir for B. henselae

›Kittens under 12 months more likely to be bacteremic

›Cat fleas (Ctenocephalides felis) are the vector between cats

›Cat exposure present in ~90% of confirmed human cases

›Atypical manifestations frequency

›Neuroretinitis approximately 1 to 2% of all CSD cases

›Most common ocular manifestation

›Encephalitis approximately 0.5% of CSD cases

›Seizures in 68% of CSD encephalitis cases

›Hepatosplenic involvement approximately 2% of CSD cases

›Endocarditis: rare but life-threatening manifestation

Pathophysiology

›Organism and transmission

›Bartonella henselae: fastidious gram-negative rod

›Facultative intracellular organism

›Infects erythrocytes and endothelial cells

›Inoculation route

›Cat scratch or bite introduces organism from contaminated saliva or claws

›Flea feces (frass) inoculated by cat scratch into human skin

›Fleas transmit B. henselae between cats but not directly to humans

›Host immune response

›Primary lymphadenopathy

›Organism travels via lymphatics from inoculation site to regional nodes

›Granulomatous inflammation with stellate necrosis in lymph nodes

›Warthin-Starry silver stain demonstrates bacilli in tissue

›Bacteremia

›Transient or sustained bacteremia seeds distant organs

›Immunocompromised hosts at risk of prolonged bacteremia

›Mechanism of neuroretinitis

›Optic disc inflammation

›Bacteremic seeding of optic disc vasculature

›Inflammatory disruption of inner blood-retinal barrier

›Disc edema from vasculitis and nerve fiber swelling

›Macular star formation

›Protein-rich fluid leaks from optic disc into peripapillary retina

›Lipid-rich exudates accumulate in Henle fiber layer of macula

›Forms characteristic stellate pattern radiating from fovea

›Develops 1 to 2 weeks after disc edema onset

Therapeutic Considerations

›Rationale for antibiotic therapy

›Natural history

›Self-limited disease in most immunocompetent hosts

›Visual recovery often occurs spontaneously without treatment

›Most experts favor early antibiotics to limit progression and ensure eradication

›Evidence for treatment benefit

›Combined antibiotics plus corticosteroids: OR 7.0 for >= 3-line visual improvement

›No randomized controlled trials; evidence from retrospective series and expert consensus

›IDSA guidelines support antibiotic treatment for CSD neuroretinitis (Level B-III recommendation)

›Corticosteroid rationale

›Mechanisms of benefit

›Reduces optic disc inflammation

›Limits lipid exudate deposition in macula

›Mitigates immune-mediated retinal damage

›Risk-benefit in CSD

›Acceptable when combined with antibiotic coverage

›Avoid monotherapy steroids without antibiotic coverage for infectious etiology

›Rifampin interaction reduces prednisone levels via CYP3A4 induction

›Drug interaction considerations

›Rifampin as CYP3A4 inducer

›Reduces plasma levels of doxycycline by approximately 50 to 70%

›Reduces prednisone plasma levels significantly

›Avoid triple combination of rifampin plus doxycycline plus prednisone simultaneously

›Doxycycline absorption interactions

›Dairy products and antacids reduce absorption via chelation

›Space antacids and calcium-containing products by at least 2 hours

›Long-term outcomes

›Visual prognosis

›80% of patients achieve final VA better than 20/40

›Macular star resolves over weeks to months with treatment

›Residual mild optic neuropathy in some patients (subtle color or contrast sensitivity deficits)

›Recurrence risk

›Recurrent neuroretinitis possible; carries worse visual prognosis

›Re-exposure to cats or kittens is the major modifiable risk factor

11Patient Discharge Instructions/pdi50

copy discharge instructions

›Diagnosis explanation

›Cat scratch disease with eye nerve involvement (neuroretinitis)

›Caused by Bartonella henselae bacteria from cat scratch or bite

›Infection affects the optic nerve at the back of the eye

›Causes temporary vision blurring and changes

›Expected course with treatment

›Most patients (80%) recover vision better than 20/40

›Improvement typically seen over 4 to 6 weeks of treatment

›The white star pattern (macular star) on eye exam resolves over weeks to months

›Medication instructions

›Doxycycline 100 mg twice daily for 4 to 6 weeks as prescribed

›Take with full glass of water

›Remain sitting or standing upright for 30 minutes after taking (prevents esophagitis)

›Avoid dairy products, antacids, and calcium supplements within 2 hours of dose (reduces absorption)

›Avoid prolonged sun exposure; use SPF 30+ sunscreen (photosensitivity risk)

›If prescribed prednisone (steroid):

›Take in the morning with food

›Do not stop abruptly; taper as directed by your doctor

›Monitor blood sugar if diabetic

›If prescribed rifampin:

›May turn urine, sweat, and tears orange-red; this is expected and harmless

›Do not take with concurrent steroids unless specifically instructed

›Activity and prevention

›Cat and flea prevention measures

›Apply flea control product to your cat as recommended by a veterinarian

›Wash cat scratches or bites promptly with soap and water

›Avoid rough play with kittens; they are more likely to carry the bacteria

12References/r25

Guidelines and key sources

›Primary evidence sources

›Shi J, Danesh-Meyer HV, Bhatti MT. Neuroretinitis: A Comprehensive Review on Aetiologies, Clinical Manifestations, and Treatment Options. Eye. 2025. PMID 39537838

›Comprehensive review of neuroretinitis etiology and management

›Abdelhakim A, Rasool N. Neuroretinitis: A Review. Current Opinion in Ophthalmology. 2018. PMID 30148725

›Clinical review covering diagnosis and treatment

›Reed JB, Scales DK, Wong MT, et al. Bartonella Henselae Neuroretinitis in Cat Scratch Disease. Ophthalmology. 1998. PMID 9499776

›Foundational series establishing visual outcomes and treatment data

›Cunningham ET, Koehler JE. Ocular Bartonellosis. American Journal of Ophthalmology. 2000. PMID 11020414

›Definitive review of ocular manifestations and corticosteroid evidence

Infectious disease guidelines

›IDSA guidelines and references

›Stevens DL, Bisno AL, Chambers HF, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update. Clinical Infectious Diseases. 2014. PMID via academic.oup.com/cid/article-lookup/doi/10.1093/cid/ciu296

›IDSA guidance on Bartonella including antibiotic recommendations

›Benson C, Brooks J, Dhanireddy S, et al. Guidelines for Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV. IDSA/OARAC 2025. clinicalinfo.hiv.gov

›HIV-specific Bartonella management guidance

›Biousse V, Newman NJ. Diagnosis and Clinical Features of Common Optic Neuropathies. Lancet Neurology. 2016. PMID 27839652

›Optic neuropathy differential diagnosis framework

Supporting references

›Epidemiology and pediatric sources

›Sandoval AC, Reyes FT, Prado MA, et al. Cat-Scratch Disease in the Pediatric Population. Pediatric Infectious Disease Journal. 2020. PMID 32404788

›Pediatric CSD series with serology performance data

›Nawrocki CC, Max RJ, Marzec NS, Nelson CA. Atypical Manifestations of Cat-Scratch Disease, United States, 2005-2014. Emerging Infectious Diseases. 2020. PMID 32568056

›National data on CSD atypical presentations

›Suhler EB, Lauer AK, Rosenbaum JT. Prevalence of Serologic Evidence of Cat Scratch Disease in Patients With Neuroretinitis. Ophthalmology. 2000. PMID 10811077

›Establishes CSD as most common infectious cause of neuroretinitis

›Yakubovsky M, Kadar L, Katchman E, et al. Cat Scratch Disease Encephalitis. International Journal of Infectious Diseases. 2026. PMID 41544843

›CSD encephalitis rate and seizure data

Evidence & Review