29 April 2023: Articles
Neuroretinitis: There Is More to Cat Scratch Disease than Meets the Eye
Challenging differential diagnosisRaina Saxena12ADEF*, Nishan Gajjar13ADE, Bernard Karnath3ADEF, You Zhou4BCDEF
Am J Case Rep 2023; 24:e938380
BACKGROUND: Cat scratch disease (CSD) is a self-limited infection caused by Bartonella henselae that causes lymphadenitis, fevers, skin changes at the inoculation site, headache, nausea, and ocular symptoms. Bartonella neuroretinitis is a form of CSD that presents with ocular symptoms, such as a central scotoma, rather than the typical lymphadenopathy of CSD. Bartonella neuroretinitis is the most common cause of infectious neuroretinitis leading to painless vision loss. Symptoms can mimic the more common optic neuritis, which can lead to under-diagnosis. Early diagnosis of Bartonella neuroretinitis and initiation of appropriate treatment is crucial to prevent vision loss and shorten recovery time.
CASE REPORT: A 47-year-old man presented to the Emergency Department with nonspecific symptoms of headache, fevers, and visual changes. He was noted to have adopted a cat 2 months prior to presentation. A dilated fundus examination revealed grade 3 optic disc edema with small disc hemorrhages bilaterally without lymphadenopathy, and Bartonella henselae serologies returned positive for the disease. The patient was treated with doxycycline and rifampin at discharge. At his follow-up outpatient ophthalmology visit, the patient had symptomatically improved vision, with dilated fundus examination supporting reduced optic disc edema in the right eye.
CONCLUSIONS: Early recognition and treatment of Bartonella neuroretinitis is essential to prevent vision loss and shorten recovery time. The current standard of treatment is doxycycline and rifampin for 4 to 6 weeks, and a growing body of literature indicates the supplementation of corticosteroids with these antibiotics.
Keywords: Bartonella henselae, Cat-Scratch Disease, Retinitis
A healthy 47-year-old man with no significant past medical history presented to the Emergency Department with a 2.5-week history of fever, night sweats, intractable headaches, and gradual left ocular vision loss. The patient reported having a COVID-19 infection 1 month prior to presentation. He had mild symptoms of COVID-19, including a fever, that lasted for 2 weeks but did not require hospitalization. After being asymptomatic for 1 week, he developed recurrent fevers and constant headaches 1 week prior to admission. At home, he took over-the-counter acetaminophen and ibuprofen, which temporarily alleviated his symptoms. After retesting for COVID-19 with a negative result, the patient visited his primary care provider, who suggested his symptoms were related to post-COVID-19 syndrome. On his drive back from the primary care provider, the patient experienced abrupt painless vision loss with an associated inferonasal field defect in the left eye. This was complicated by photophobia and left eye pain with extraocular movement. He also experienced an onset of throbbing headaches that were associated with fever, nausea, and vomiting. He denied neck stiffness, weakness, numbness, tingling, or rashes. One week after fever onset, he arrived at the University of Texas Medical Branch’s Emergency Department after experiencing abrupt painless vision loss in his left eye. Initial evaluation with a complete blood count, comprehensive metabolic panel, COVID-19 rapid test, influenza A/B test, urinalysis, Epstein Barr virus test, and PCR respiratory panel was unremarkable. Chest X-ray and computed tomography of the head were unremarkable. He was admitted to the inpatient neurology service for headaches and vision loss. Besides a recent COVID-19 infection, the patient was previously healthy, with no sick contacts. He previously lived in North Texas and California before moving to Galveston, TX. There was no relevant family medical history. He did not take any prescription medications and had no known allergies. He was a former smoker who quit 6 years ago, with an indeterminate pack-year smoking history. He denied alcohol or other recreational drug use but reported that he occasionally used marijuana and vaped e-cigarettes. He had adopted a cat 2 months prior to admission and noted his cat would frequently scratch his arms. On admission, the patient was afebrile, his blood pressure was 134/84 mmHg, his pulse rate was 78 beats per min, and his respiratory rate was 18 breaths per min. On ophthalmic examination, the patient’s visual acuity was 20/25 and 20/100, without correction, in the right and left eye, respectively. Intraocular pressures were 8 mmHg bilaterally, and pupillary examinations were within the normal limits. A confrontational visual field examination demonstrated an inferonasal field defect in the left eye. Aside from the presence of trace cells (indicating inflammation) in the anterior chamber of the left eye, the slit lamp examination was unremarkable bilaterally, including the absence of anterior chamber inflammation in the right eye. A dilated fundus examination revealed grade 3 optic disc edema with small disc hemorrhages bilaterally.
Additionally, small, discrete white choroidal lesions were present in close proximity to the nerve, without evidence of obvious macular edema or macular star formation. A non-ophthalmic examination did not reveal any skin changes or the presence of lymphadenopathy. His liver enzyme levels were elevated, with an aspartate transaminase level of 79 U/L (reference range: 13–40 U/L) and alanine aminotransferase level of 146 U/L (reference range: 5–50 U/L). He also presented with an elevated erythrocyte sedimentation rate of 41 mm/h (reference range: 0–10 mm/h) and elevated C-reactive protein level of 8.1 (reference range: <0.8). The initial differential diagnosis was concerning for meningitis owing to nonspecific symptoms of high fevers, headache, and nausea, with venous sinus thrombosis and other inflammatory causes. The patient was empirically started on intravenous vancomycin, ceftriaxone, and acyclovir initially for concerns of meningitis. A computed tomography angiogram of the head revealed 2 internal carotid artery aneurysms up to 4 mm and 7×5 mm. Lumbar puncture results demonstrated an elevated white blood cell count of 10 (reference range: 0–5/mm3). The meningitis panel, Gram stain from the lumbar puncture, and cryptococcal antigen test were negative. The syphilis IgG/IgM test was positive, but his rapid plasma reagin test was nonreactive, and his treponema pallidum particle agglutination test was negative. Infectious work-up was obtained, including typhus, cytomegalovirus, toxoplasmosis, West Nile virus, hepatitis B/C, and
It is important to recognize
Here we present a case of a patient presenting with nonspecific symptoms of headache, fevers, and visual changes who was found to have optic disc edema without lymphadenopathy and was eventually diagnosed with
FiguresFigure 1.. Humphrey visual field 30-2. Stim III, SITA FAST exam. Some details were removed to hide patient identifiers. (A) Left eye, reliable testing, dense inferonasal field defect respecting the horizontal and vertical meridian (arrow). (B) Right eye, reliable testing, non-specific changes noted. Figure 2.. Optical coherence tomography of optic nerve head. (A) Right eye, demonstrating retinal nerve fiber layer (RNFL) thickening, superiorly, nasally, and inferiorly, sparing the temporal side, which is consistent with grade 1 optic disc edema. (B) Left eye, demonstrating superotemporal and temporal RNFL thinning (arrow), which is consistent with the patient’s inferonasal field defect. Figure 3.. Optical coherence tomography of the macula. (A) Right eye, no intraretinal or subretinal fluid. Preserved outer and inner retinal layers. (B) Left eye, no intraretinal or subretinal fluid. Preserved outer and inner retinal layers.
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