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EDUCATION

Case Study: Fury of the Furry

Patel Vivek
Presenter: Luv Patel, MD Discussant: Vivek Patel, MD
 

History

  • 34-year-old male with no relevant Past Medical or Ocular History
  • Eight days prior to presentation, he was straining and felt a “pop” in his left eye. Saw floaters immediately afterward. He did not seek medical attention at the time.
  • Four days prior to presentation, the vision in his left eye became noticeably blurrier than his baseline.
  • Denies pain. No travel or exposure to illness. Works as mechanic. Mom’s cat recently had kittens.

Exam Findings

  • Visual acuity: 20/20 right eye; 20/200 left eye
  • Pupils: Relative APD 2+ left eye; color plates 8/8 right eye, 2/8 left eye
  • No intraocular inflammation
  • Normal appearance right fundus
Figure 1
Figure 1: Fundus photograph of left eye showing disc edema with blurred margins, macular edema, intraretinal and preretinal hemorrhages at disc and intraretinal hemorrhages in temporal macula.

 

Figure 2
Figure 2: Optical Coherence Tomography (OCT) macula of left eye at level of the fovea. Note intraretinal edema, subretinal fluid; loss of foveal contour, and edema nasally tracking contiguous with the optic disc.

 

Figure 3
Figure 3: OCT at level of optic nerve showing vitreous tenting, adherent to nasal aspect of nerve with condensation over nerve head.

 

Figure 4
Figure 4: Fluorescein angiography (FA) of left eye, venous phase, showing leakage at supero-temporal disc; no leakage on macula. In later frames, the supero-temporal wedge of leakage progressed modestly.

 

Differential Diagnosis

  • Infectious
    • Bartonellosis
    • Syphilis
    • Lyme
    • TB
    • DUSN (Diffuse unilateral subacute neuroretinitis
    • Toxoplasmosis
    • Toxocariasis
    • Leptospirosis
    • Salmonella
    • Mumps
    • HSV, VZV
    • Ehrlichiosis, RMSF (Rocky Mountain spotted fever)
  • NAION (non-arteritic anterior ischemic optic neuropathy)
  • Infiltrative
    • Sarcoid
    • Leukemia
  • HTN
  • DM2 papillopathy
  • Mechanical – vitreopapillary traction

Additional Investigations

  • Bartonella titer 1:64 IgG, 1:80 IgM
  • One month follow-up visual acuity: OS 20/30; trace relative APD OS; color plates 8/8 with observation only
Figure 5
Figure 5: Fundus photo of left eye one month later showing exudates in macular star pattern, resolved disc edema and peripapillary hemorrhages.
Figure 6
Figure 6: OCT macula of left eye at one month follow-up showing resolved intraretinal fluid, minimal subretinal fluid and restoration of foveal contour. Note exudates in outer plexiform layer.

 

Diagnosis

  • Bartonella neuroretinitis

Pathophysiology

  • Caused by bartonella henselae, Bartonella neuroretinitis is an ocular manifestation of cat scratch disease. Patients will sometimes have an erythematous pustule at site of the scratch three to 10 days later. Systemic manifestations include fever, lymphadenopathy. Ocular manifestations occur in five to 10 percent of cases and commonly include unilateral conjunctivitis. One to two percent is thought to manifest with neuroretinitis, an acute inflammation of the optic nerve extending to the macula causing signs of optic nerve dysfunction (RAPD, color vision dysfunction) and decline in visual acuity.
  • This case provided an additional interesting twist in that the patient noted a sudden “pop” sensation followed shortly by vision loss. We demonstrated the apparently firm vitreoretinal interface adhesions at the level of the optic nerve in light of a recent editorial offered by Parsa and Hoyt offering that the pathophysiology of NAION is related to sudden release of vitreopapillary traction resulting in sheering of axons and capillaries at the site of separation, rather than the traditionally purported theories involving ischemia and venous congestion. We would not expect to see subretinal and extensive intraretinal macular fluid accumulation in NAION, hence admit that the patient’s “pop” sensation was likely coincidental. However, it may be possible that the evolving bartonella-associated retinitis could have resulted in a mild degree of posterior vitreal inflammation, over the optic nerve, promoting a PVD, accounting for his subjective sensation.

Treatment

  • Clinical practice is to treat confirmed cases with one month course of doxycycline (or macrolide if tetracycline contraindicated). Rifampin can be added for severe cases. Steroids have also been used in extreme cases of visual dysfunction. Retrospective studies have shown no benefit in visual acuity outcome with respect to treatment from steroids or antibiotics. However, treatment is often favored to prevent systemic sequelae.

Prognosis and Future Directions

  • The disease is generally self-limited. Most cases improve even without treatment. Retrospective analyses have shown that greater than 50 percent of cases have a visual acuity of 20/40 or better at last follow-up. Better initial visual acuity confers a better final visual acuity prognosis. However, the presence of systemic symptoms (fever, lymphadenopathy) suggests a worse prognosis.

References

  • 2016-2017 Basic and Clinical Science Course, Section 09: Intraocular Inflammation and Uveitis, Chapter 7. Read RW. American Academy of Ophthalmology.
  • Chi SL, et al. Clinical characteristics in 53 patients with cat scratch optic neuropathy. Ophthalmology. 2012 Jan;119(1):183-7.
  • Parsa C, Hoyt WF. Nonarteritic Anterior Ischemic Optic Neuropathy (NAION): A Misnomer. Rearranging Pieces of a Puzzle to Reveal a Nonischemic Papillopathy Caused by Vitreous Separation. Ophthalmology. 2015 Mar;122(3):439-42.

Contact

Section Editors

 

Produced by: Monica Chavez, John Daniel, Joseph Yim and Dr. Vivek Patel
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