Case Based Pediatrics For Medical Students and Residents
Department of Pediatrics, University of Hawaii John A. Burns School of Medicine
Chapter VI.29. Cat Scratch Disease
Judy Makowski Vincent, MD
August 2002

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A four year old girl presents to the pediatric clinic with a chief complaint of a slowly enlarging mass in her right armpit for the past two weeks. She has had no fever, but has had some loss of appetite. The mass was initially small and did not hurt; however, it has now grown to the size of an orange and has become painful. She cannot lower her arm due to the pain from the mass, and she carries her arm extended at 90 degrees to her body. Movement of her arm exacerbates the pain. She does have a 3 month old kitten at home that she "rescued from a sewer". It was covered with fleas when she found it. It playfully bites and scratches her. Three weeks ago it scratched her right thumb. The scratch healed, but a small "wart" has developed in the line of the scratch. There is a scab on the wart and her mother has tried to squeeze the wart, but no pus has come out.

ROS: Non-contributory. No cough. No weight loss. No change in activity other than being unable to use her right arm well.

Exam: VS T 37.2, RR 18, P 102, BP 100/60. She is alert and very cooperative. HEENT is negative. Neck is supple without adenopathy. Chest is clear. Heart regular without murmur. Abdomen exam is normal without hepatosplenomegaly. Neurologic exam is normal (mental status, gait, strength, and reflexes). Her right axilla reveals an 8x8 cm firm, tender, mobile, warm, non-erythematous, non-fluctuant mass that is consistent with an enlarged axillary lymph node. Her right thumb has a 1 cm linear, non-inflamed, healing scar that is consistent with a kitten scratch. In the middle of the linear scar, there is a 3 mm brownish-red papule with a small central crust.

Lab: CBC WBC 8.0, 62% segs, 10% bands. Ultrasonography of the mass reveals that it is a matted group of about 5 lymph nodes which are mostly solid in appearance. There is evidence of a small amount of necrosis at the periphery of one of the lymph nodes.

Impression: Lymphadenopathy due to cat scratch disease.

Clinical course: Because the axillary node is enlarged and painful, you elect to treat her with oral azithromycin at a dose of 10 mg/kg/day for the first day and 5 mg/kg/day for the next 4 days. Serology for Bartonella henselae is obtained, and the result returns one week later with an IgG of 1:512 (a positive result is a value greater than 1:64). The node remains the same size for a week and then begins to get smaller. The adenopathy resolves in one month.

It is now known that cat scratch disease (CSD) is a multisystem disease caused by a small Gram negative bacillus named Bartonella henselae, formerly known as Rochalimaea henselae. As early as 1932, physicians in the United States recognized patients with CSD, but the cause of the disease eluded detection until 1983 when researchers at the Armed Forces Institute of Pathology at Walter Reed Army Medical Center in Washington, D.C. detected the organism in lymph node tissue from patients with clinical CSD. Identification of the causative organism has allowed researchers to identify the epidemiology and transmission of the disease, identify atypical forms of CSD, develop serologic diagnostic tests, and perform placebo-controlled treatment trials.

Jameson et al, recently reported the results of a survey of 33 geographic regions throughout North America and showed that increasing prevalence of antibody to B. henselae in cats paralleled increasing climatic warmth and annual precipitation (1). Seroprevalence was highest in regions with warm humid climates which also have a higher incidence and degree of cat flea infestation. The southeastern United States, Hawaii, coastal California, the Pacific Northwest and the south central plains had the highest average B. henselae antibody prevalences. Alaska, the Rocky Mountains-Great Plains region, and the Midwest had the lowest average B. henselae antibody prevalences.

CSD is generally a benign, self-limited disease in immunocompetent hosts. Although CSD may be associated with significant morbidity, no deaths have been reported in immunocompetent persons with typical CSD proven by positive skin test, positive serology, or by DNA testing (2). Deaths have been reported rarely in immunocompromised patients. Several members of a family may develop clinical CSD, whereas some have asymptomatic infection as evidenced by development of B. henselae antibody. Infection appears to confer lifelong immunity, because reports of recurrences of clinical CSD are rare (2).

B. henselae bacteremia occurs in flea-infested well appearing kittens usually less than one year old, and less commonly in older cats. The organism is transmitted among cats by the cat flea. It is transmitted to humans by a cat scratch, bite or other intimate contact. The pathologic response to infection with B. henselae varies significantly with the status of the host immune system. In immunocompetent hosts, the response is granulomatous and suppurative. In immunocompromised hosts, the response is vasculoproliferative (2).

Organisms are not seen in routinely stained tissue preparations. In Warthin-Starry or Brown-Hopp's tissue-stained CSD lymph node preparations, Gram negative argyrophilic (i.e., it takes up silver stains, so it shows up better with silver staining) non-acid-fast, pleomorphic bacilli may be seen in the tissues. The bacilli are very small and are seen primarily in the walls of blood vessels, in macrophages lining the sinuses, in or near germinal centers, and in microabscesses. Here they may appear as single organisms, or in chains, or clumps.

B. henselae may be grown in standard microbiology laboratories by plating the sample (patient's lymph node aspirate or blood from suspected-bacteremic kittens) directly onto chocolate agar, then streaked and incubated under 6% CO2 at 35 degrees C for 60 days. The organism is fastidious in its growth. Therefore the plates should be left in the CO2 incubator and not examined or exposed to room air for the first 14 days. After 14 days, B. henselae manifests as grayish-yellow pinpoint-sized colonies that are best seen when the plate is held tangentially to the light. If no growth occurs within 60 days, the results may be interpreted as negative.

CSD occurs as both typical and atypical disease (2). Typical CSD in an immunocompetent host is manifested by a characteristic and highly predictable clinical course. In nearly all cases, patients give a history of a scratch, bite, contact or intimate association with a cat, most often a newly acquired kitten. In some patients, a round, red-brown, nontender papule develops in the scratch line after 3 to 10 days. It may vary in size from 1 to several millimeters and may persist for only a few days or for as long as 2 to 3 weeks. In the next 1 to 2 weeks, one or more regional lymph nodes gradually enlarge. The most commonly involved lymph nodes are the anterior cervical, axillary, inguinal, femoral, preauricular, supraclavicular, and epitrochlear nodes; however any node can be involved if it is in the path of lymphatic drainage from a site that has been inoculated with B. henselae.

CSD lymph nodes tend to be large with an average diameter of 4 to 6 cm at the time of maximum size, but can be as large as 10 to 13 cm. After 1 to 2 weeks of growth, they remain the same size for 2 to 3 weeks and then resolve over an additional period of 2 to 3 weeks, with the usual course of the disease lasting for 2 to 3 months. Some cases are more severe and more protracted, lasting up to 6 to 7 months. Although most of the nodes are moderately tender, some are nontender. Most patients with typical CSD remain afebrile and are not ill-appearing. Some patients experience anorexia, malaise, headache, arthralgia, and abdominal, neck, back or extremity pain.

A very useful clinical feature that distinguishes CSD from acute pyogenic lymphadenopathy, is that CSD lymphadenopathy only rarely develops overnight. In our experience, most patients with CSD tend to seek medical care after lymphadenopathy has been present for 7 to 14 days. In contrast, most patients with acute pyogenic adenopathy present for care within 24 hours of onset of the adenopathy. CSD lymphadenopathy is unilateral and isolated to a regional group of lymph nodes in immunocompetent patients. Therefore, if a patient has disseminated lymphadenopathy, or bilateral lymphadenopathy, a diagnosis other than CSD should be sought.

Late in the course of CSD, about 10% of lymph nodes develop overlying erythema and fluctuation and may suppurate if they are not drained. Needle aspiration usually provides satisfactory drainage for suppurative CSD. If pus reaccumulates, the nodes may require open surgical drainage. The incision should be left open, with closure by granulation. Chronic fistulous tracts do not develop if CSD lymph nodes are incised and drained. This is a common misconception. In Hawaii where CSD is highly prevalent, we have followed many patients with large CSD-infected lymph nodes that progressed to suppuration, reaccumulated after needle aspiration, and required open surgical drainage. All CSD-infected lymph nodes treated with incision and drainage have healed completely without fistulae.

CSD can be diagnosed reliably with serologic testing. In a seroepidemiologic study of CSD, rigid criteria were applied for the clinical diagnosis of CSD, and all of 38 patients had positive serology (sensitivity 100%), compared to only 1 of 48 controls with no direct cat exposure in the previous 2 years who had positive serology (specificity 98%) (3). Serology was performed by the CDC. In this study, 24 of 38 patients (84%) had positive titers in their initial serum obtained 1 to 2 weeks after onset of clinical CSD; the other 6 patients (16%) developed positive titers in serum obtained 4 to 8 weeks later.

Prior to the development of a confirmatory serologic test for CSD, intradermal skin testing was used for the diagnosis of CSD. However with the development of specific laboratory tests to confirm the diagnosis, the CSD skin test is no longer recommended (which was less sensitive, less specific, poorly standardized, not readily available, not approved by regulatory authorities, and is considered by some to be unsafe).

Primary care physicians should be familiar with the atypical forms of CSD, as well as the typical form. A fairly common presentation of atypical CSD is Parinaud's oculoglandular syndrome (POGS), which consists of unilateral conjunctivitis with adjacent preauricular lymphadenopathy. The palpebral conjunctivae of the involved eye displays a characteristic granulomatous lesion that measures 2 to 3 mm to >1 cm in diameter, or there may be a scratch near the eye. Although POGS can be caused by other infections, including tuberculosis, tularemia, syphilis, and lymphogranuloma venereum, it has become well established that POGS is a common form of atypical CSD (2). Infection of the eye with B. henselae may be contracted with inoculation of the organism indirectly into the eye, rather than by direct contact through a scratch, as in typical CSD. POGS is a predictable self-limited infection with a good outcome in essentially all cases.

Hepatosplenic CSD is an atypical form of CSD which occurs in immunocompetent patients who present with fever of unknown origin (4). These patients have daily high fevers, often in the range of 40 degrees (104 degrees F), and some patients will have been febrile for a month before the diagnosis is finally made. Many of these patients complain of abdominal pain. In many cases, the care provider has neglected to ask about cat exposure until the patient has been febrile for several weeks. Physical examination is remarkably benign. Although these patients usually have a few well-healed cat scratch scars, these are often overlooked. Only about half of these patients have lymphadenopathy. They do not have hepatosplenomegaly or jaundice, and liver function tests are usually normal. The ESR may be moderately elevated, in the range of 40 to 70 mm/hr, but other screening laboratory tests are usually normal. Diagnosis is made by the presence of lytic lesions in the liver and/or spleen on ultrasound or CT scan, and B. henselae titers are positive, often markedly so. Fever usually resolves with a day or two of starting treatment with an intravenous aminoglycoside; however fever may not resolve for a month, even with adequate treatment (2).

CSD encephalopathy (CSDE) was first reported in 1952 and has recently been extensively reviewed (2). Convulsions occur in about half of cases, and may last only a few minutes or may last 3 to 4 hours, requiring intubation and intensive care. Another neurologic form of atypical CSD is a distinctive type of neuroretinitis, called Leber's stellate neuroretinitis. It presents with painless unilateral, rarely bilateral, loss of vision with central scotomata, optic disc swelling, macular star formation and complete recovery of vision within 1 to 3 months (2).

Both CSDE and CSD neuroretinitis are unusual forms of atypical CSD and are not well known to the average clinician. Immunosuppressed patients with B. henselae infection may have widespread and occasionally fatal disease (2). As these clinical syndromes become better known, along with the knowledge that laboratory tests are now available to confirm the diagnosis, these and other atypical manifestations of CSD may become more widely appreciated.

Typical CSD is a self-limited disease in immunocompetent hosts and will usually resolve spontaneously in 1 to 3 months. Recently we performed the first double-blind placebo-controlled antibiotic trial for treatment of CSD at Tripler Army Medical Center (5). Lymph node volume was measured by clinical measurement with palpation and a tape measure and by ultrasonography. This study showed that 7 of 14 (50%) azithromycin-treated patients had significant resolution of lymphadenopathy at 30 days compared to 1 of 15 (7%) of placebo-treated controls (p=0.026), as measured by ultrasonography. It should be noted that the two treatment groups had no difference in lymph node volume until the fourth week of treatment, and that clinical response at 30 days was only observed in 50% of patients in the azithromycin group. Therefore if a clinician makes a clinical diagnosis of CSD and elects to offer treatment with azithromycin (standard 5 day course), he or she should instruct the patient not to expect overnight resolution of symptoms. Azithromycin-treated patients have a 50% likelihood of having significant lymphadenopathy for 2 months or longer, despite treatment (5).

B. henselae has been reported to be sensitive to gentamicin in vitro, and anecdotal reports have supported its use in hepatosplenic disease; however the only placebo-controlled efficacy study has been with azithromycin for typical CSD lymphadenopathy.

The only way to prevent CSD is to avoid exposure to cats, particularly flea-infested cats that have had exposure to other cats, and kittens less than one year of age. There is currently no CSD vaccine for cats or humans, and antibiotic prophylaxis of humans or cats is not recommended.


1. True/False: Cat scratch disease is usually transmitted by flea-infested kittens.

2. True/False: Cat scratch disease is more common in dry, desert-like areas, as compared to humid climates.

3. True/False: Adenopathy due to cat scratch disease usually develops rapidly, within a few hours.

4. True/False: When patients have hepatosplenic cat scratch disease, their liver function tests are always abnormal, and they always have concomitant lymphadenopathy.

5. True/False: Azithromycin is the only antibiotic that has been shown to be effective in the treatment of typical CSD lymphadenopathy in a double-blind, placebo-controlled trial.

6. True/False: Serology is the diagnostic test of choice for cat scratch disease.


1. Jameson P, Greene C, Regnery R, Dryden M, Marks A, Brown J, Cooper J. Prevalence of Bartonella henselae antibodies in pet cats throughout the regions of North America. J Infect Dis 1995;172:1145-1149.

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. Demers DM, Bass JW, Vincent JM, Person DA, Noyes DK, Staege CM, Samlaska CP, Lockwood NH, Regnery RL, Anderson BE. Cat scratch disease in Hawaii: etiology and seroepidemiology. J Pediatr 1995;126:23-26.

4. Dunn MW, Berkowitz FE, Miller JJ, Snitzer JA. Hepatosplenic cat-scratch disease and abdominal pain. Pediatr Infect Dis J 1997;16:269-272.

5. Bass JW, Cary-Freitas B, Freitas AD, Sisler CL, Chan DS, Vincent JM, Person DA, Claybaugh JR, Wittler RR, Weisse ME, Regnery RL, Slater LN. Prospective randomized double-blind placebo-controlled evaluation of azithromycin for treatment of cat-scratch disease. Pediatr Infect Dis J 1998;17:447-452.

Answers to questions

1. True.

2. False. Cat scratch disease is more common in humid climates because humidity is necessary for the existence of cat fleas.

3. False. Cat scratch disease adenopathy develops slowly, usually over 10-14 days.

4. False. With hepatosplenic CSD, LFTs are usually normal, and only 50% of patients have concomitant lymphadenopathy.

5. True.

6. True.

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