Cat Scratch Disease

Cat scratch disease is an infection following the scratch of a cat (usually a kitten) with the organism Bartonella henselae, formerly known as Rochalimaea henselae.
It is a pleomorphic, gram-negative bacillus. It was at one time thought to be caused by the organism Afipia felis, but this has been discounted.¹
Although Bartonella clarridgeiae is also prevalent in some cat populations², its involvement in cat scratch disease has not been proved.³

• Seropositivity levels to Bartonella henselae vary from country to country, and studies have reported figures ranging from 31-61%. Since few patients ever experience symptoms, this suggests that only a minority of exposures result in cat scratch disease.
• Although the majority of patients are children and young adults (80% of patients are under the age of 21)⁴, infections in older people do occur.
  One UK review in 1999 reported a national prevalence of 16.3%, with a slight predominance of males⁵. Analysis by age showed that although rates of infection were highest in the decades 0-9 years (19.4%) and 10-19 years (20.7%), they fell only slightly in the next three decades.
• The incidence is seasonal, with peaks in the autumn and winter, which may be explained by the breeding pattern of cats, or the acquisition of pets at these time of year.¹

• Most patients ( > 90%) present with one or more erythematous lesions at the site of inoculation, 3-12 days after a scratch from a cat, most likely a kitten with fleas⁶.
• The lesion is usually a crusted papule, or rarely a pustule.
• One to three weeks after the appearance of the primary lesion, regional lymphadenopathy appears, usually next to the inoculation site⁷. Lymphadenopathy is present in 90% of patients, primarily involving the axillary nodes, followed in frequency by cervical and inguinal areas. The nodes are often painful and spontaneously suppurate in 25-30% of cases.
• In more than half of cases in one study, systemic symptoms accompanied the lymphadenopathy⁴. These may include fever (in 32 to 60% of patients), malaise (in 29%), headache (in 13%), and anorexia (in 14%)⁷, and often occur in immunocompromised patients.

Atypically, (approximately 5-14% of cases⁷) the following may occur:

• Altered mental status, confusion (encephalopathy)⁸
• Prolonged fever⁹
• Respiratory complaints (atypical pneumonitis)¹⁰
• Myelitis¹¹, paraplegia⁷, cerebral arteritis¹²
• Joint pain (arthritis¹³, synovitis¹⁴)
• Parinaud oculoglandular syndrome - this accounts for up to 20% of reports of Bartonella henselae infection¹⁵. Inoculation is via direct eye contact and characterised by unilateral granulomatous conjunctivitis with ipsilateral suppurative pre-auricular lymphadenitis.
• Neuroretinitis - this occurs in approximately 2% of patients¹⁶. Patients present with unilateral or bilateral acute visual loss. Fundal signs include discrete white retinal/choroidal lesions, optic disc swelling, macular star and branch retinal vein occlusion (in order of frequency)¹⁷
• Abdominal pain - this can occur with associated hepatitis/splenitis, a self-limited granulomatous condition (hepatosplenic granulomatous disease)¹⁸

Other rare conditions:

• Osteolytic lesions¹⁹
• Erythema nodosum²⁰
• Thrombocytopenic purpura²¹

Bacillary angiomatosis can occur in immunocompromised (e.g. AIDS) patients, and represents a severe systemic form of the disease.
It may compromise any tissue, especially the skin, presenting papules, nodules or angiomatous tumors²².

The list of differential diagnoses is long as it can include all known causes of lymphadenopathy. Depending to some extent on a history of exposure or travel to endemic areas, a short list would include brucellosis, mononucleosis, sarcoidosis, Yersinia pestis (plague), tuberculosis lymphogranuloma venereum, tick-borne diseases, syphilis, tularemia, and toxoplasmosis.

Other problems that may need to be considered include: atypical mycobacterium infection, lymphoma, collagen vascular disease, chronic granulomatous disease, pyogenic lymphadenitis, histoplasmosis, spirorotrichosis.

• Haematology may reveal a mild leukocytosis and raised ESR but these are nonspecific and of little value.
• Serology IgG titres will rise in acute infection, although patients may already have high levels at presentation. Titres above 1:64 are supportive of the diagnosis²³.
  • Indirect fluorescent antibody (IFA) for Bartonella is a highly sensitive and specific test although they do not differentiate B. henselae from B.quintana (the organism responsible for trench fever, the urban type of which is sometimes seen in the homeless.²⁴
  • Polymerase chain reaction (PCR) is not widely available, but assays have been developed that differentiate B henselae from B quintana.²⁵
  Other tests which may be indicated in certain clinical situations include:
• Lymph node histopathology - this may be useful in differentiating various causes of lymphadenopathy. It can be further enhanced by combining with immunofluorescent techniques.²⁶
• Cerebrospinal fluid analysis may be performed to exclude other causes of encephalitis. Findings are usually normal, but may show elevated protein or mild pleocytosis.
  Recently, DNA testing of CSF fluid has been used to support the diagnosis in cases of B henselae encephalitis²⁷.
• EEG may demonstrate diffuse slowing in patients with encephalopathy, which like resolves with clinical recovery.
• Imaging is occasionally helpful. CT²⁸ and MRI²⁹ scanning have both proven helpful in specific clinical situations.

• Supportive therapy with antipyretics and analgesics should be given as needed, and local heat may relieve the pain of enlarged lymph nodes.⁷
• Aspiration of fluctuant tender nodes may help to relieve pain, but incision and drainage should be avoided as this may leave scars and fistulae.³⁰
• The condition is usually self-limiting in immunocompetent patients, and in the majority of patients the lymph nodes gradually regress over weeks or months without antibiotics being needed.¹
• Antibiotics are however indicated in immunocompromised patients, and atypical cases involving severe or systemic disease.
  Trimethoprim-sulphamethoxazole, ciprofloxacin or azithromycin are used first line, with gentamicin being reserved for the severely ill patient.¹
• Patients should follow up in 2-6 months for confirmation of symptom resolution.

Complete recovery is usual unless there is severe hepatic or neurological involvement, in which case granulomatous hepatitis, neuroretinitis, and peripheral neuritis can occur³¹.

Recommendations for prevention of cat scratch disease include vigilant elimination of fleas from cats³², and avoiding traumatic injury from cats for immunocompromised patients.³³