Cat scratch disease (CSD) is a zoonotic infection caused predominantly by Bartonella henselae, usually transmitted to humans through scratches or bites from infected cats, particularly kittens. The disease commonly presents with a primary inoculation lesion followed by regional lymphadenopathy, low-grade fever, malaise, and fatigue. Although most immunocompetent patients experience a self-limited illness, atypical manifestations involving the eyes, nervous system, liver, spleen, bones, or heart may occur. We report the case of a 16-year-old male who presented with fever, fatigue, and progressively enlarging tender right axillary lymph nodes approximately two weeks after being scratched by a kitten. Examination revealed a healing papule at the site of inoculation and tender axillary lymphadenopathy. Laboratory investigations demonstrated elevated inflammatory markers, while Bartonella henselae serology was positive. Ultrasound of the axilla demonstrated enlarged lymph nodes with inflammatory changes. The patient was diagnosed with cat scratch disease and managed with symptomatic therapy and antibiotic treatment. His fever and systemic symptoms improved, followed by gradual regression of lymphadenopathy during follow-up. This case highlights the importance of obtaining a detailed history of animal exposure when evaluating unexplained regional lymphadenopathy.
Cat scratch disease is a bacterial zoonotic infection caused primarily by Bartonella henselae. Cats, particularly kittens, serve as an important reservoir, with transmission to humans occurring most commonly through scratches or bites contaminated with infected flea feces.
The typical clinical presentation consists of a papule or pustule at the site of inoculation, followed approximately 1–3 weeks later by regional lymphadenopathy. Fever, malaise, fatigue, and headache may accompany lymph node enlargement. The axillary, cervical, epitrochlear, and submandibular lymph nodes are commonly involved depending on the site of inoculation.
Most cases in immunocompetent individuals are self-limited. However, atypical or disseminated disease can involve the eye, liver, spleen, central nervous system, bones, or heart. Ocular complications include Parinaud oculoglandular syndrome and neuroretinitis, while neurological involvement may present as encephalopathy or other neurologic syndromes.
Diagnosis is often clinical in patients with a compatible history and characteristic lymphadenopathy. Serologic testing can provide supportive evidence, while molecular testing of lymph node tissue or aspirate may be useful in selected atypical cases.
We report a case of cat scratch disease presenting with fever and regional axillary lymphadenopathy following a kitten scratch.
A 16-year-old male presented with a two-week history of low-grade fever, fatigue, and progressively increasing swelling in the right axillary region.
Approximately two weeks before presentation, the patient had been scratched on the right forearm by a domestic kitten while playing with it. The scratch initially appeared superficial and was managed at home with local cleansing. Several days later, a small erythematous papule developed at the site of injury and subsequently began to heal.

Approximately one week after the appearance of the skin lesion, the patient developed low-grade fever, malaise, and tenderness in the right axilla. Over the following several days, the axillary swelling progressively increased in size and became painful.

There was no history of chronic illness, immunosuppression, recent travel, tuberculosis exposure, weight loss, night sweats, or contact with individuals with known infectious disease.
On examination, the patient was febrile but hemodynamically stable. A small healing papule was observed on the right forearm at the site of the previous cat scratch. Examination of the right axilla revealed enlarged, tender lymph nodes with mild overlying erythema. No generalized lymphadenopathy was identified.

The remainder of the systemic examination was unremarkable. There were no clinical features suggestive of ocular, neurological, hepatosplenic, or cardiac involvement.
Laboratory investigations demonstrated mild leukocytosis with elevated inflammatory markers. Serologic testing for Bartonella henselae demonstrated positive antibodies, supporting the diagnosis of cat scratch disease. Ultrasonography of the right axilla showed enlarged lymph nodes with inflammatory changes consistent with regional lymphadenitis.

Based on the characteristic history of kitten exposure, inoculation lesion, regional lymphadenopathy, fever, and positive Bartonella henselae serology, a diagnosis of cat scratch disease was established.
The patient was managed with supportive care and antibiotic therapy based on the clinical severity and treating physician's assessment.
Medical management included:
Most uncomplicated cases of cat scratch disease are self-limited. Antibiotic treatment may shorten the duration of lymph node swelling in some patients, while treatment is particularly important in immunocompromised patients and those with severe or disseminated disease.
The patient's fever and constitutional symptoms gradually subsided. The axillary lymph nodes decreased in size and tenderness over subsequent follow-up, and no evidence of systemic dissemination or secondary complications was identified.
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Cat scratch disease should be considered in patients presenting with unexplained regional lymphadenopathy, particularly when there is a history of exposure to cats or kittens. The disease is caused primarily by Bartonella henselae, an intracellular gram-negative bacterium associated with cats and flea transmission.
The characteristic sequence in uncomplicated CSD consists of an inoculation lesion followed by regional lymph node enlargement approximately 1–3 weeks later. The lymphadenopathy may persist for several weeks to months, even after systemic symptoms have resolved.
In the present case, the temporal relationship between the kitten scratch, development of a local papule, and subsequent axillary lymphadenopathy was strongly suggestive of CSD. The location of the lymphadenopathy was also consistent with lymphatic drainage from the affected upper limb.
The differential diagnosis of regional lymphadenopathy is broad and includes bacterial lymphadenitis, tuberculosis, atypical mycobacterial infection, toxoplasmosis, tularemia, viral infections, lymphoma, and other malignancies. A detailed history of animal exposure can provide an important diagnostic clue and may prevent unnecessary invasive investigations.
Diagnosis is frequently clinical in patients with a typical presentation. Serology can support the diagnosis, although interpretation requires consideration of the timing of testing and potential cross-reactivity. Bartonella henselae is difficult to culture, and cultures may require prolonged incubation. Molecular testing, including PCR, can be useful in selected cases, particularly when tissue or lymph node aspirate is available.
Ultrasonography may demonstrate enlarged lymph nodes and can be useful when evaluating painful or persistent lymphadenopathy. Lymph node aspiration or biopsy is generally reserved for cases in which the diagnosis remains uncertain, significant suppuration develops, or alternative diagnoses such as malignancy need to be excluded.
Although CSD is usually benign, clinicians should remain alert for atypical manifestations. Ocular involvement can result in Parinaud oculoglandular syndrome or neuroretinitis, while neurological complications can include encephalopathy and other central nervous system manifestations. Hepatosplenic disease, osteomyelitis, and endocarditis are less common but potentially serious complications.

Treatment depends on disease severity and host factors. Most uncomplicated cases in immunocompetent individuals resolve without antimicrobial therapy, although antibiotics may be used to shorten symptom duration or in patients with more significant disease. The CDC notes that immunocompromised patients and individuals with severe manifestations should receive antimicrobial treatment, with longer or combination regimens often required for disseminated disease.
The present case demonstrates the importance of recognizing the classic clinical triad of cat exposure, inoculation lesion, and regional lymphadenopathy. Early recognition can help establish the diagnosis and avoid unnecessary investigations for other causes of lymphadenopathy.
The prognosis of uncomplicated cat scratch disease is generally excellent in immunocompetent individuals. Most patients experience spontaneous clinical recovery, although regional lymphadenopathy can persist for several weeks or months.
Patients with immunosuppression or disseminated disease require closer monitoring because of the possibility of ocular, neurological, hepatosplenic, skeletal, or cardiovascular complications. Severe manifestations may require prolonged antimicrobial therapy and specialist management.
Long-term follow-up is generally unnecessary following complete resolution of uncomplicated disease, but patients should be advised to seek medical evaluation if recurrent fever, persistent lymphadenopathy, visual symptoms, neurological symptoms, or other systemic manifestations develop.
Cat scratch disease is an important cause of regional lymphadenopathy following exposure to cats or kittens. The typical presentation includes a localized inoculation lesion followed by tender regional lymphadenopathy, often accompanied by fever and constitutional symptoms.
This case highlights the importance of obtaining a detailed history of cat exposure in patients presenting with unexplained lymph node enlargement. Clinical assessment supported by appropriate serologic or molecular testing can establish the diagnosis in most cases.
Although cat scratch disease is usually self-limited in immunocompetent patients, recognition of atypical and disseminated manifestations is essential. Appropriate supportive care, selective antibiotic therapy, and follow-up can result in complete recovery and help prevent complications.
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5. Bergmans AMC, Peeters MF, Schellekens JFP, Vos MC, Sabbe LJM, Ossewaarde JM, Verbakel H, Hooft HJ, Schouls LM. Pitfalls and fallacies of cat scratch disease serology: evaluation of Bartonella henselae-based indirect fluorescence assay and enzyme-linked immunoassay. J Clin Microbiol. 1997;35(8):1931-1937. https://pubmed.ncbi.nlm.nih.gov/9230358/
6. Mazur-Melewska K, Mania A, Kemnitz P, Figlerowicz M, Służewski W. Cat-scratch disease: a wide spectrum of clinical pictures. Postepy Dermatol Alergol. 2015;32(3):216-220.
https://pubmed.ncbi.nlm.nih.gov/26161064/
7. Reed JB, Scales DK, Wong MT, Lattuada CP Jr, Dolan MJ, Schwab IR. Bartonella henselae neuroretinitis in cat scratch disease: diagnosis, management, and sequelae. Ophthalmology. 1998;105(3):459-466.
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