Cat-scratch disease

Joseph R Berger MD (

Dr. Berger of the Perelman School of Medicine, University of Pennsylvania, received honorariums from Amgen, Biogen, Celegene, Encycle, ExcisionBio, Genentech/Roche, Inhibikase, Merck/Serono, Millennium/Takeda, Novartis, Sanofi/Genzyme, and Shire for his role as a consultant.

John E Greenlee MD, editor. (Dr. Greenlee of the University of Utah School of Medicine has no relevant financial relationships to disclose.)
Originally released March 17, 1994; last updated October 11, 2020; expires October 11, 2023


Cat-scratch disease is a rare but important cause of neurologic and ophthalmologic disease. The diagnosis of this treatable disease, which results from Bartonella henslae, a Gram-negative bacterial infection, is often initially misdiagnosed. In this article, the author highlights the manifold clinical manifestations of the disorder and effective therapeutic regimens.

Key points


• Cat-scratch disease results from infection with Bartonella henselae.


• The organism is transmitted to humans typically from a scratch or bite from an infected cat in the two weeks preceding symptom onset.


• Most infections are characterized by localized lymphadenopathy and low-grade systemic features that clear spontaneously.


• Seroepidemiologic studies suggest that large percentages of some populations have been infected by the causative organism at some time in their life.


• On rare occasion, encephalopathy, seizures, and other neurologic manifestations may accompany cat-scratch disease.


• Neuroretinitis and a variety of other ocular problems also occur with this infection.


• Antibiotic treatment is curative.

Historical note and terminology

The original description of cat-scratch disease was made by Debre (Debre and Lamy 1950) from observations in France dating to the 1930s. The association between contact with cats and chronic lymphadenopathy had been widely appreciated by the last quarter of the 20th century. Numerous descriptions in the medical literature defined the spectrum of recognized clinical manifestations, clarified the epidemiology, refined the diagnostic criteria, and described the associated pathology (Carithers 1970; Carithers 1985; Margileth 1993). However, despite these often thorough descriptions of the clinical and pathological features, the etiology and pathogenesis of cat-scratch disease remained enigmatic. Although a number of potential micro-organisms had been proposed as etiologic agents, including viruses and chlamydia, the identification of a bacterial organism from the tissue of a patient with cat-scratch disease by Wear and colleagues in 1983 was a major advance (Wear et al 1983). Five years later this organism, a Gram-negative bacillus, was cultured and classified in the laboratory as a member of the class Proteobacteriacae and named Afipia felis (English et al 1988). Shortly thereafter, a similar-appearing bacillus, Rochalimaea henselae, also a member of the class Proteobacteriacae, but of the order Rickettsiales, was also found in tissues and cultured from blood from patients with cat-scratch disease (Margileth 1993; Zangwill et al 1993). R henselae, now referred to as Bartonella henselae, was also isolated from cats suspected of transmitting cat-scratch disease. Subsequently, serologic studies of patients with cat-scratch disease provided further evidence that B henselae was the etiologic agent of this disease (Regnery et al 1992; Zangwill et al 1993).

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