Introduction

Catscratch disease is a benign infectious disease caused by the intracellular bacterium Bartonella Henselae. Cats are the main reservoir of this bacterium.^[1], ^[2] Dogs., monkeys and rabbits are also reservoirs other than cats ^[3].CSD is typically a self limiting disease primarily presenting with regional lymphadenopathy following approximately one to three weeks after cat bite.^[1]

Case Report

The patient was a 23 year old lady, postgraduate student, a known case of Systemic Lupus Erythematosus (SLE) diagnosed 1 year back. She was on treatment with Mycophenolate mofetil, Hydroxychloroquine and Wysolone .She presented to Rheumatology OPD with high grade intermittent fever for 1 month ,left sided neck swelling and pain for 1 month. On general Examination, patient was febrile with a temperature of 101 degree F .There were palpable cervical lymphnodes. Left retroauricular node was 3 x 3 cm, firm, tender. Left jugulodigastric nodes were palpable and tender. There were no throat or dental lesions. Systemic examination was unremarkable .Laboratory investigations showed Total count– 7700 (P86 L 7), Platelet count – 3.12 lac/cmm, Creatinine – 0.6 mg/dl, ESR – 101mm/1^st hour, CRP- 8.3. Urine routine was within normal limits. Anti ds DNA – 40 (negative).Blood cultures were negative. Interferon gamma release assay was negative. USG showed no hepatosplenomegaly. Chest X-ray was within normal limits.

Initially she was managed on OPD basis with short course antibiotics- Amoxicillin Clavulanate FNAC of left retroauricular lymph node was done but the results were inconclusive. Since her symptoms persisted, she was admitted for detailed evaluation. Infectious Disease opinion was sought. Excision biopsy from Left retroauricular lymph node was done.

Histology showed lymphnode with histiocytic collections forming granulomas and foci of suppuration. Special stains for AFB and fungi were negative. Warthin Starry stain demonstrated the bacilli, thus confirming the diagnosis of Catscratch disease. On the patient's next visit, a history of catscratch was elicited by the clinician thus supporting the diagnosis. Our patient was treated with Azithromycin and the neck swelling regressed in size.

Discussion

Cat scratch disease (CSD) is a common zoonosis in children caused by Bartonella henselae (B. henselae)which is transmitted through cat bites or scratches.^[4] This organism was first described by Henri Perinaud in 1889.^[5] Typical CSD, which occurs in 90%  of cases, is characterized by low grade fever and subacute regional lymphadenitis following a recent history of cat contact.^[6] Usually a unilateral lymphadenitis near the scratch bite site develops 2-3 weeks after infection, which is usually in the head, neck, axilla, or supraclavicular region. Atypical manifestations include mammary, oculoglandular, hepatosplenic, cardiopulmonary, central nervous system, and bone involvement. The disease has a self-limited course and usually resolves without the use of antibiotics.^[7] However, immunosuppression is a known risk factor for the development of serious and atypical forms of disease.

There are very few reports of CSD in SLE patients. In immunocompromised patients there can be local or systemic complications including suppurative lymphadenitis, retinitis, endocarditis and hepatosplenic disease.^[1]  B. henselae is a small, aerobic, intracellular gram-negative pleomorphic bacillus, microscopically identified by Warthin-Starry stain. The bacillus is very difficult to grow; hence culture is not routinely recommended. Serological testing is an inexpensive tool to diagnose B. henselae with 95% sensitivity and  98% specificity. In the presence of a positive history of cat contact and relevant clinical findings, titers are reliable and sensitive which can lead to prompt diagnosis and initiation of appropriate treatment, thus avoiding unnecessary invasive investigations.^[7]

Culture is not reliable for the diagnosis.^[8] Histopathological examination of lymph nodes is crucial for exclusion.^[9] Typical histopathological findings include necrotising granulomas, central microabscesses with neutrophils, rare multinucleate giant cells. Warthin starry and Brown Hopps stains demonstrate small gram negative bacilli.^[10] These bacilli are usually distributed focally, with hundreds of organisms in one area and none in others. Differentials include Suppurative lymphadenitis caused by bacteria. Gram stain reveals the microorganisms. In tuberculosis, necrosis is caseous with less nuclear remnants or tissue debris. Acid fast staining can demonstrate the bacilli. Fungal lymphadenitis can show neutrophils, but can be demonstrated using PAS or GMS stains. Lymphogranuloma venereum has similar histologic appearance. Demonstration and identification of microorganisms by IFA and serology are necessary. Kikuchi lymphadenitis lacks neutrophils and definite granulomas. Since our patient was an SLE patient, lupus lymphadenitis was also a differential. SLE lymphadenopathy can show paracortical necrosis, nuclear debris, vasculitis with fibrinoid necrosis. But granulomas and neutrophils are absent. ^[11] The major criteria for diagnosis of CSD have been exposure to cat bite or scratch, an inoculation site, regional lymphadenopathy, typical histopathology on lymph node biopsy, negative tests for other infections, and a positive delayed hypersensitivity skin test using CSD antigen.

Conclusion

In SLE patients presenting with fever and lmphadenopathy, Catscratch disease should be considered among the differentials. Appropriate investigations need to be done as this is a treatable condition and a course of antibiotics resolves the disease.

Conflict of Interest

None.

Source of Funding

None.