Cat-scratch disease

Cat-scratch disease is a bacterial infectious disorder triggered by exposure to Bartonella henselae, a Gram-negative, facultatively anaerobic, intracellular bacillus ^[1]. Originally described clinically in 1931, the causative organism was identified much later following advances in microbiological detection ^[1]. The pathogen establishes infection in humans primarily through inoculation via feline saliva introduced by bites or scratches, occasionally involving canine vectors ^[2][3].

Initial manifestations typically emerge within three to fourteen days following inoculation and feature a localized vesicular or erythematous papule at the wound site ^[2]. Within one to three weeks, patients commonly develop unilateral regional lymphadenopathy, frequently affecting the axillary, cervical, or inguinal nodes, accompanied by systemic complaints such as low-grade fever, fatigue, headache, and generalized myalgias ^[2]. While most cases remain self-limiting, disseminated involvement may occur in a minority of patients, potentially manifesting as hepatic or splenic lesions, ocular conditions like Parinaud oculoglandular syndrome, or neurological complications including encephalopathy and cerebellar ataxia ^[1][3].

The disease demonstrates a clear geographic and climatic distribution, showing higher prevalence rates in regions characterized by warm and humid environments ^[1]. Incidence follows a pronounced seasonal trend, consistently reaching its highest levels during the autumn and winter months ^[1]. Population-level data indicate an approximate annual incidence of one case per ten thousand individuals, with substantially elevated rates observed among pediatric populations ^[1].

Human infection originates primarily from direct inoculation of Bartonella henselae through breaks in the skin caused by bites or scratches from domestic cats, particularly kittens which harbor higher bacterial loads ^[1][2]. The bacterium circulates within feline populations largely maintained by cat flea vectors, while asymptomatic carrier cats shed the organism in their saliva ^[1][2]. Secondary transmission routes include rare exposures to dogs or indirect contact with contaminated feline feces, underscoring the necessity of mechanical barriers and hygiene practices to interrupt exposure pathways ^[2][3].

Primary prevention strategies center on rigorous environmental management and behavioral modifications to minimize human-feline exposure ^[2]. Implementing consistent ectoparasite control protocols effectively reduces vector-borne bacterial circulation within pet populations, while restricting cats to indoor environments significantly lowers infestation risks ^[2]. Additionally, maintaining strict hand hygiene following any interaction with animals or their waste products serves as a critical barrier against cutaneous inoculation and subsequent disease acquisition ^[2].

1. 1Puspitasari Y et al. Uncovering the truth about cat-scratch disease. Open Vet J. 2025 May. PMID: 40557109. doi: 10.5455/OVJ.2025.v15.i5.5.PubMed: https://pubmed.ncbi.nlm.nih.gov/40557109/
2. 2Wikipedia contributors. Cat-scratch disease - Wikipedia [Internet]. Wikipedia. cited 4 Sept 2026.Available from: https://en.wikipedia.org/wiki/Cat-scratch_disease
3. 3Jurja S et al. The Clinical Profile of Cat-Scratch Disease's Neuro-Ophthalmological Effects. Brain Sci. 2022 Feb 4. PMID: 35203980. doi: 10.3390/brainsci12020217.PubMed: https://pubmed.ncbi.nlm.nih.gov/35203980/