Cat Scratch Disease
Cat Scratch Disease
ABSTRACT & COMMENTARY
Synopsis: Cat scratch disease, usually caused by Bartonella henselae, causes adenopathy in many parts of the world. Serologic tests aid in the diagnosis.
Source: Karpathios T, et al. Cat scratch disease in Greece. Arch Dis Child 1998;78:64-66.
During a six-year period in athens, serologic testing was done on 18 children who were diagnosed clinically to have cat scratch disease. Serum was tested at presentation, 15 days later, and six months later. An indirect fluorescent antibody test (done on samples transported frozen to the CDC in Atlanta) confirmed the diagnosis in 15 of the patients (83%). In three positive patients, the initial titer was high enough to indicate infection, while the other 12 showed a marked rise in titer over the course of testing.
COMMENT BY PHILIP R. FISCHER, MD
History and Global Epidemiology
Our current understanding of cat scratch disease results from experience and investigation in diverse parts of the world. Similarly, the problem of cat scratch disease and the reservoirs of its etiologic agent span the globe.
Robert Debré followed cases of suppurative adenitis associated with cat scratches in Paris from the 1930s through the 1950s but was unable to identify an etiologic agent. The savvy sleuthing and silver staining by Wear and colleagues at the Armed Forces Institute of Pathology identified a potential causative organism in the early 1980s. Then, further investigation in California and in Oklahoma identified and confirmed that, in fact, a different microbe was actually responsible for most cases of cat scratch disease; this organism is now known as Bartonella henselae.
Long before the etiologic agent was identified, the association with cats was demonstrated. Most all cat scratch disease patients have known contact with a cat, usually a kitten, in the drainage site where adenitis develops. The exact route of transmission, however, is not clear. Usually, the kitten contact consists of a scratch that breaks the victim's skin, but cases have been reported in which cats bit subjects or just licked a pre-existing abrasion. Some association with flea-infested cats has been reported, but the exact role of fleas in transmitting cat scratch disease is not clear.
Kittens are often bacteremic with B. henselae. Older cats, though less commonly bacteremic, show serologic evidence of past infection. Infected, and even bacteremic, animals are usually not symptomatic, but some association between infection and both stomatitis and urinary tract disease has been reported.
While B. henselae (and the resultant cat scratch disease) exists worldwide, the prevalence does vary geographically. In Europe, feline seroprevalence rates vary from 8% in Switzerland to 54% in the Netherlands. In the United States, pet cats show a seroprevalence of 28%, but infection is more common in warm, humid areas (55% in southeastern United States, 47% in Hawaii, 40% in coastal California, 34% in the Pacific Northwest, 7% in the Midwest, 5% in Alaska, and 4% in the Rocky Mountain and Great Plains region). In South Africa and Zimbabwe, approximately 23% of cats are infected. In Australia, where cat scratch disease is relatively uncommon, feral cats are more likely to be culture positive for B. henselae than are domestic cats (40% vs 16%).
Cat scratch disease, in the Greek report, was more common in boys than in girls. This could relate to gender-specific variations in the risk of being scratched by a cat. As noted in Greece, cat scratch disease is most common during the first two decades of life; infection usually results in lifelong immunity. The seasonal variation of human infection noted in Greece and other temperate areas, with infection most common during Autumn and Winter, probably relates to the facts that kittens are often born in late Spring and that these kittens usually become infected during the early months of life.
Clinical Presentations
The typical case of cat scratch disease begins with a papule or pustule that develops at the site of the primary inoculation a few days after the exposure; these primary lesions may persist for up to eight weeks and are often present at the time of diagnosis. Fever and malaise accompany the presenting signs in about half of patients, and more than 80% of patients present with lymphadenopathy. The study from Greece involved a clinical diagnosis of cat scratch disease based on regional lymphadenopathy, history of cat contact, and negative studies for other causes of lymphadenopathy. Certainly, mycobacterial causes of adenopathy would need to be excluded when evaluating returned travelers with enlarged lymph nodes.
Among patients with cat scratch disease, 10-20% will have atypical clinical manifestations of their infection. Ocular infection, usually initiated by rubbing the eye with a hand that has had contact with a cat, presents as a conjunctival granuloma and preauricular adenopathy. Swelling and discoloration may be dramatic, but pain and discharge are not common. Fever and abdominal pain are common in patients who present with hepatic and/or splenic abscesses due to cat scratch disease. Neurologic manifestations are also possible and vary from encephalitis to meningitis to myelitis to radiculitis to Bell's palsy. Encephalopathy is more common in infected school-aged children than in infected individuals of other ages. Pulmonary and musculoskeletal manifestations have been reported. In immunocompromised patients, cat scratch disease can present with bacillary angiomatosis, bacillary peliosis hepatis, or fever with bacteremia.
Diagnosis
As reported in the Greek study, a clinical diagnosis is usually based on the presence of animal contact, regional lymphadenopathy (usually beginning about 2 weeks after the feline exposure), and the lack of another known cause of such findings. As rightly emphasized in the Greek report, laboratory evaluation can be useful.
A cat scratch skin test has been used for several years. It is both sensitive and specific and is used in a manner similar to the way a tuberculosis skin test (PPD) is used. Some hesitation in its use has resulted, however, from concern about injecting material that originates from the pus of another patient. Lymph node biopsy is usually not necessary but can demonstrate granulomas and multinucleated giant cells. Organisms are often visible using the Warthin-Starry silver stain. Culture of B. henselae is possible but requires specialized techniques and extended incubation times (up to 3 weeks).
Serology seems to be the most practical and useful diagnostic test. As noted in the study from Greece, some patients are strongly seropositive at the time of their initial presentation, and most others have seroconverted within the subsequent two weeks. The indirect fluorescent antibody test is reported to have a sensitivity of 88% and a specificity of 97%.
Polymerase chain reaction (PCR) testing holds promise of becoming the most useful means of diagnosing cat scratch disease. This testing is rapid and reliable. To date, however, it has not become widely available.
Treatment
Cat scratch disease is usually self-limited, but it can require several months to be fully resolved. Antibiotic therapy is often used (as in 14 of the 18 Greek patients), but patients usually recover without sequelae whether or not they receive antibiotics. As it is not clear whether antibiotics actually aid in the recovery of cat scratch disease patients, immunocompetent individuals who present only with adenitis should not be subjected to antibiotic treatment. Needle aspiration might provide symptomatic relief in patients with painful suppuration.
Complicated patients who are either severely ill, who have atypical presentations, or who are immunocompromised might benefit from a trial of antibiotics. Trimethoprim-sulfamethoxazole (cotrimoxazole) has been used in the past to prevent suppuration of infected lymph nodes (and was noted in a New England Journal of Medicine case report earlier this year), but it has been associated with a high rate of treatment failure. Macrolides, ciprofloxacin, rifampin, and aminoglycosides are usually considered to be the best treatment choices for patients in whom antibiotic therapy is deemed necessary.
Prevention
Travelers are usually informed of the risks of animal contact in foreign countries. Avoidance of animal contact should be extended to include direct contact with cats, even domestic pets, when possible.
Reviews
1. Anderson B, Edwards K. Cat-scratch disease: A mystery solved. Contemp Pediatr 1995;12(11):17-32.
2. Bass JW, Vincent JM, Person DA. The expanding spectrum of Bartonella infections: II. Cat-scratch disease. Pediatr Infect Dis J 1997;16:163-179.
3. Margileth AM. Antibiotic therapy for cat-scratch disease. Pediatr Inf Dis J 1992;11:474-478.
4. Midani S, Ayoub EM, Anderson B. Cat-scratch disease. Adv Pediatr 1996;43:397-422.
5. Shenep JL. Cat-scratch disease and Bartonella henselae infections in children. Pediatr Ann 1996;25:518-523.
6. Zangwill KM. Bartonella infections. Sem Pediatr Inf Dis 1997;8:57-63.
Instructive Case
1. An 11-year-old boy with a seizure. N Engl J Med 1998; 338:112-119.
Geographic Epidemiology
1. Africa. J S Afr Vet Assoc 1996;67:182-187.
2. Australia. Med J Aust 1997;166:532-535; Pathology 1996;28:262-265.
3. Japan. Microbiol Immunol 1996;40:671-673.
4. Netherlands. J Clin Microbiol 1997;35:2256-2261.
5. Switzerland. J Clin Microbiol 1997;35:2883-2885.
6. United States. J Infect Dis 1995;172:1145-1149.
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