CAT SCRATCH DISEASE

Signs and Symptoms

Neuroretinitis secondary to cat scratch disease.

The patient with cat scratch disease (CSD) is typically younger. Often, there is a history of being scratched by a cat, though this history is not invariably present. However, there will be a history of exposure to cats. The incidence of case presentations tends to be higher during breeding seasons of cats, which are typically fall and winter.

The patient will manifest a regional lymphadenitis with the appearance of a small cutaneous lesion at the site of the inoculation following an incubation period ranging from several days to weeks. The patient will develop fever and flu-like symptoms, which typically resolve within three to six weeks. Vision varies widely, from normal acuity to finger counting, depending upon the severity of ocular manifestations. While patients may be visually asymptomatic, relative afferent pupil defects, dyschromatopsia and field loss may also be present.

Systemic signs may include hepatosplenic infection, encephalopathy, osteomyelitis and endocarditis. The most common ocular syndrome occurring from CSD is Parinaud's oculoglandular syndrome, manifesting as conjunctivitis, retrotarsal conjunctival granulations, regional preauricular and cervical lymphadenitis, and fever. Another common ocular manifestation associated with CSD is neuroretinitis, a combination of disc edema with stellate macular star exudates. Other fundus findings include peripapillary serous macular detachment, discrete foci of retinitis manifested as white retinal or choroidal lesions, vitritis, posterior uveitis, and submacular exudates. Anterior uveitis may also occur.¹

Pathophysiology

Cat scratch disease is caused by the Gram-negative bacillus, Bartonella henselae and, to a lesser extent, Bartonella quintana. The organism is transmitted through the bite or scratch of an infected cat or kitten. Transmission through flea bites has not been reported. Following inoculation, there is an incubation period, which is followed by a period of self-limiting febrile illness with lymphadenopathy.

Management

Proper diagnosis begins with clinical suspicion based upon ocular findings in association with an antecedent febrile illness. Testing for CSD involves obtaining ELISA Bartonella henselae titre. Titres for Bartonella quintana are appropriate as well. An alternate diagnostic modality is a polymerase chain reaction analysis of lymphadenopathy aspirate. This should be considered in a clinical situation in which CSD is strongly suspected and ELISA titers are negative, borderline or otherwise inconclusive.

In immunocompetent individuals, the course of CSD is self-limiting with a good prognosis. As such, medical treatment is generally unnecessary. However, cases with ocular involvement are generally recommended for treatment. The causative organism is susceptible to a number of antibiotics, including penicillins, cephalosporins, aminoglycosides, tetracyclines, macrolides, fluoroquinolones, and rifamicin. Doxycycline 100mg po bid for four weeks is a recommended therapy. This may be used alone or in combination with rifampin 300mg bid.^2­4 Azithromycin is an acceptable substitute.⁵ In cases with vision loss, typically from neuroretinitis, oral prednisone is often employed with antimicrobial therapy.

Clinical Pearls

• CSD should be considered first when encountering neuroretinitis.
• CSD is a benign, self-limiting disease, and the value of treatment in immunocompetent individuals appears to be in shortening the duration of the disease.
• Always question for an antecedent history of febrile illness and lymphadenopathy when encountering patients with painless vision loss with disc edema, as well as retinochoroidal exudates and anterior uveitis.