Abstract

Cat-scratch disease (CSD) is a systemic infection caused by the facultative, rod-shaped, non-motile, Gram-negative, intracellular zoonotic bacillus Bartonella henselae. The bacteria that cause CSD were not discovered until decades after the condition was first characterized in 1931. The prevalence of CSD is more common in warm, humid areas and is typically seasonal, peaking in the fall and winter. The pathogenesis of CSD starts when a tiny wound from an infected cat's bite or scratch allows the bacteria B. henselae to enter the human body. The innate immune system, which includes cells like neutrophils and macrophages, is activated as one of the initial reactions. Histological investigation of skin lesions and lymph nodes in immunocompetent people early in the clinical phase of CSD reveals lymphoid hyperplasia and arteriolar proliferation. The best initial test for CSD is the enzyme-linked immunosorbent assay (ELISA) or indirect fluorescence assay (IFA). Bacteremia is typically asymptomatic in cats that are naturally infected with B. henselae. In humans, B. henselae can spread and infect the liver, spleen, eyes, or central nervous system in certain people. Cat fleas (Ctenocephalides felis) are the main vectors of B. henselae transmission. The zoonotic nature of CSD makes it a public health concern since it can be transmitted from cats to people. Treatment strategies for Bartonella infections differ according to the patient's immunological status and clinical signs. The research on the effectiveness of antibiotics in vitro and in vivo differs significantly. Eliminating fleas from cats and preventing severe injuries from cats are two ways to prevent CSD.

Key words: B. henselae, Cat, CSD, Public health, Scratch