CAT SCRATCH

 

 DISEASE

 

 

Epidemiology

 

Approximately 29.2 million households (31 percent) in the United States own a cat, averaging close to two cats per household, for a total household cat population of 57 million. This large population of domestic cats explain the more than 22,000 cases of CSD reported annually. CSD affects persons of all ages, although 60 percent to 90 percent of cases are reported in children and young adults. CSD is seen worldwide and does not appear to have a racial prevalence. Most patients with CSD recall a history of cat contact, but this is not absolute (90.3 percent to 99.1 percent). The incidence of CSD is slightly higher in males and it occurs seasonally, mostly between July and October.

 

CAT-SCRATCH DISEASE AT

A GLANCE

• Vast majority of cases caused by Bartonella henselae
• Transmitted by the scratch or bite of a cat
• Most common cause of localized, chronic lymphadenopathy in children
• Diagnosis established serologically

CSD is associated with exposure to a cat, usually a kitten. The method of spread from cat to human is usually a scratch or bite. In California, 39.5 percent of cats are bacteremic for B. henselae with a single sampling, indicating a very high

infection rate. Bacteremic cats were more likely to be stray cats, young (less than 1 year old), and flea-infested. Seroprevalence for B. henselae is as high in pet cats as in shelter and feral cats.⁷ The seroprevalence of B. henselae among pet cats in North America is 27 percent overall but highly variable, with a higher seroprevalence in warm rainy regions. When the geographic seroprevalence of B. henselae is compared with predicted estimates of cat flea populations based on temperature and humidity, there is considerable overlap, supporting the role of the cat flea (Ctenocephalides felis) as the arthropod vector maintaining infection in cats. B. henselae can be transmitted from cat to cat via the cat flea, cat fleas contain Bartonella organisms after feeding on infected cats, cat flea feces contains viable Bartonella, and cats can be experimentally infected by the intradermal injection of infected cat flea feces.⁸ The cat flea has not been demonstrated to spread Bartonella infection from cats to humans. Rather, cats' claws and teeth may be contaminated by infected flea feces during scratching and grooming allowing for transmission to humans by scratches.

Etiology and Pathogenesis

B. henselae causes the vast majority (more than 95 percent) of cases of CSD. There is one infectious genotype in the United States and two types in Europe, but the disease caused by all is clinically identical. In the immunocompetent host, the organism is, in the majority of cases, well controlled by the immune system, with containment in the primary skin papule and draining lymph node.

Clinical Findings

 

CUTANEOUS LESIONS

 

The clinical spectrum of CSD has expanded since serologic diagnosis has become possible. Typical CSD exhibits two components, the primary inoculation papule and adenopathy proximal to the inoculation site. The papule appears at the site of inoculation within 3 to 10 days of exposure and progresses through an edematous or vesicular and crusted stage. The primary inoculation papule lasts 1 to 3 weeks. The lymphadenopathy, seen in at least 90 percent of patients with typical CSD, develops on average 2 weeks after inoculation . The inoculation papule is still present in 60 percent to 90 percent when the adenopathy develops, making it a valuable diagnostic finding.⁹ The most commonly affected lymph nodes are axillary, cervical, and submandibular, with 98 percent of patients having involvement of only one anatomic region. The nodes are generally firm, tender and between 1 and 5 cm in diameter . The lymphadenopathy usually remits spontaneously after several months, although in 20 percent of cases, the adenopathy lasts longer than 6 months. Recurrences are uncommon.

Suppuration of clinical significance occurs in less than 10 percent of cases, but when affected nodes are followed with ultrasonography, suppuration is found to be the natural course of resorption of affected nodes in nearly all cases.⁹ Surgical drainage is seldom necessary.

 

RELATED PHYSICAL FINDINGS

 

With improved diagnosis, atypical cases of CSD have increased from fewer than 5 percent of cases to more than 30 percent of cases in some series.¹⁰ The exact prevalence of these atypical presentations is not known, as they are often reported as single cases, and the total number of CSD cases from which they come is unknown. In one pediatric series, atypical mononucleosis with pharyngitis and bilateral cervical adenopathy and thrombocytosis was a common presentation of B. henselae infection.¹¹ Fever of unknown origin with or without endocarditis, hepatic and splenic granulomatosis, and massive lymph node enlargement resembling lymphoma are uncommon presentations.¹⁰ Involvement of the terminal ileum may rarely mimic inflammatory bowel disease and intra-abdominal lymphadenopathy may very rarely obstruct the portal vein.^12,13 Ocular complications of B. henselae infection have been frequently reported and include neuroretinitis, focal retinochoroiditis, arterial and venous occlusion, iridocyclitis, and macular

hole. The most common neurologic complication of CSD is acute encephalopathy, presenting with seizures in 66 percent and status epilepticus in 10 percent of patients

In one study, up to 20 percent of immunocompetent patients with serologically confirmed CSD had PCR positivity for B. henselae in peripheral blood, suggesting bacteremia may be common.¹⁹ Not surprisingly, hematogenous dissemination of B. henselae complicating CSD in immunocompetent persons has been reported to affect bone (osteomyelitis), liver and spleen, lungs (pneumonia, pleural effusion, pulmonary nodules), and the optic nerve.^20-22 These lesions may be markedly symptomatic, or, in one case of pulmonary involvement, completely asymptomatic.²⁰ B. henselae, not infrequently causes endocarditis in persons with known valvular heart disease, usually affecting the aortic valve, and 90 percent of patients require valvular surgery as a consequence of severe damage.

Reactive conditions of the skin and joints may be seen in patients with CSD. Two percent of CSD patients develop erythema nodosum.²⁴ Three percent of patients with CSD suffer a rheumatoid factor-negative arthropathy of the larger joints of the extremities.²⁵ These patients are older than 20 years of age and two-thirds are female. Twenty percent have lesions of erythema nodosum. In 80 percent the arthropathy resolved in 6 weeks, but in 20 percent there is a more chronic course averaging 2.5 years.

 

Laboratory Tests

 

Routine laboratory findings are non-specific and usually not helpful except to exclude other diseases. Patients with CSD may have a slightly elevated white blood cell count and elevated erythrocyte sedimentation rate during the acute phase. Blood cultures are rarely positive when using current testing techniques. PCR of affected lymph nodes may be positive in 30 percent of cases. Between 80 and 90 percent of cases of CSD have positive serology for B. henselae at the time of presentation, and many of the seronegative cases are positive 2 to 8 weeks later. Serologic testing has replaced the CSD skin test as the confirmatory test of choice in cases of CSD.

 

Histopathology

 

Histopathologic examination of CSD lymph node lesions is not specific. Lymph nodes undergo three stages in the formation of a granuloma: (1) enlargement with hypertrophy of the germinal centers and thickening of the cortex; (2) formation of granulomas with invasion of lymphocytes and epithelioid cells; and (3) necrosis and infiltration with neutrophils—all of which may be simultaneously present within a single lymph node. Abscess formation may occur. Organisms can be detected in lymph nodes and primary skin lesions, often in clumps or filaments, usually in or adjacent to areas of necrosis.

In primary skin lesions, microscopic examination reveals necrosis of the epidermis and upper dermis, and dermal inflammation ranging from neutrophil and macrophage infiltration to granuloma formation. Conjunctival lesions have similar histologic findings. In a few cases, conjunctival lesions produce proliferating blood vessels and a homogenous eosinophilic to basophilic granular appearance in the background—features similar to those of BA.

Differential Diagnosis

Treatment

Virtually all cases of CSD remit spontaneously without therapeutic intervention. In a retrospective study of 202 patients with CSD who were treated with antibiotics, commonly prescribed antibiotics, including macrolides, tetracycline derivatives, and cephalosporins, were ineffective.²³ However, antibiotic susceptibility studies have shown that B. henselae is highly sensitive to macrolides, tetracycline derivatives, and second-and third-generation cephalosporins, and is variably sensitive to quinolones. The failure of antibiotics in classic CSD in the immunocompetent host may relate to the small infectious burden and the frequent initiation of therapy once the disease is already improving spontaneously (in its lymphatic phase). In a recent prospective randomized trial, azithromycin for 5 days was demonstrated to reduce the lymph node volume during the first 30 days of observation. Half of azithromycin-treated patients reached 20 percent of baseline lymph node volume by 1 month, as opposed to 7 percent of untreated patients. However, there was no difference in any other symptoms or findings, or in the long-term outcome, and some treated patients had increases in lymph node size after treatment. For complicated CSD of the eye or central nervous system, doxycycline 100 mg twice daily plus rifampin 300 mg twice daily is recommended.

Box 182-1 Differential Diagnosis

Most Likely

• Atypical Mycobacteria (especially M. marinum)
• Sporotrichosis

Consider

• Syphilis
• Tularemia
• Primary inoculation tuberculosis

Rule Out

• Lymphoma