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Unusual eruption as a presenting symptom of cat scratch disease
Unusual eruption as a presenting symptom of cat scratch disease Marina Landau, MD,a Yehudith Kletter, PhD,b Boaz Avidor, PhD,b Gabi Ephrat,b Moshe Ephros, MD,c Sarah Brenner, MD,a and Michael Giladi, MDb Tel Aviv and Haifa, Israel Cat scratch disease (CSD) is a common infectious cause of subacute regional lymphadenopathy. Bartonella henselae is the principal etiologic agent. About 10% of CSD patients experience atypical manifestations, including rashes. The most common cutaneous manifestation of CSD is a papule at the inoculation site. We report a case of CSD presenting with an eruption on the upper trunk, reminiscent of Sweet’s syndrome, accompanied by lymphadenopathy, arthralgia, and fever. Response to systemic corticosteroids was remarkable. Histopathologic findings refuted the diagnosis of Sweet’s syndrome. Identification of anti-B henselae antibodies and B henselae DNA in the affected lymph node confirmed the diagnosis of CSD. This is a first report of extensive papuloedematous eruption as a cutaneous manifestation of CSD. Accurate diagnosis is possible due to the availability of serological tests and DNA amplification techniques. (J Am Acad Dermatol 1999;41:833-6.)
CASE REPORT A 32-year-old previously healthy woman was referred to the dermatology outpatient clinic because of fever of 39°C and eruption of 2 days duration. In addition, she complained of pain in the right groin and arthralgia in the right elbow, both knees and ankles, and the left first toe. The eruption, first noted on the upper chest, spread over the next 2 days to involve the shoulders and upper back. Although there was no pruritus, the lesions were accompanied by a mild burning sensation. Her past medical history was uneventful. The patient owned several cats and kittens and was often scratched by them. Examination revealed a well-developed and nourished woman with fever of 38°C. Multiple edematous, pale, reddish papules coalescing to plaques were noted on her upper chest, back, and shoulders (Fig 1). The lesions were surrounded by erythematous halos and some of them had a pseudovesicular appearance. A 2 × 3 cm tender, soft, nonfluctuating lymph node was palpated in the left inguinal area. Multiple scratches were present on both hands and legs. No frank arthritis was found, and ophthalmologic examination was normal.
This supplement is made possible through an educational grant from Ortho Dermatological to the American Academy of Dermatology. From the Department of Dermatologya and the Bernard Pridan Laboratory for Molecular Biology of Infectious Diseases,b Tel Aviv–Elias Sourasky Medical Center, and Sackler School of Medicine, Tel Aviv University, and Department of Pediatrics,c Carmel Medical Center, Haifa. Reprint requests: Marina Landau, MD, Department of Dermatology, Tel Aviv-Elias Sourasky Medical Center 6,Weizman Street,Tel Aviv 64239 Israel. E-mail: [email protected] Copyright © 1999 by the American Academy of Dermatology, Inc. 0190-9622/99/$8.00 + 0 16/4/96950
Fig 1. Edematous plaques and papules, surrounded by erythematous halos on chest of patient.
Complete blood cell count disclosed hemoglobin of 12.9 g/dL, 8,600 leukocytes/mm3 with 83.6% neutrophils, and 192,000 platelets/mm3. Other routine laboratory studies were within normal limits. Serology for HIV was negative. Pending the results of a skin biopsy and on the basis of the clinical findings, a diagnosis of acute febrile neutrophilic dermatosis (Sweet’s syndrome) was considered, and treatment with prednisone 40 mg/day was started. The eruption, arthralgia, and fever improved significantly over the next 5 days. The skin biopsy specimen revealed a normal epidermis with subepidermal edema, a perivascular and focally interstitial infiltrate of lymphocytes, and a few plasma cells and scanty eosinophils (Fig 2). These histologic findings were not consistent with the original clinical diagnosis of Sweet’s syndrome. The history of close contact with cats and the presence of tender regional lymphadenopathy raised the possibility
833
834 Landau et al
J AM ACAD DERMATOL NOVEMBER 1999
Fig 4. Anti-B henselae IgM (closed circles) and IgG (open circles) titers at 1, 6, and 12 weeks after onset of disease, as determined by enzyme immunoassay. Sera were diluted 1:100. Average optical density of triplicate determinations was calculated. Arrows represent cutoff titers for positive tests.
Fig 2. Skin biopsy specimen showing subepidermal edema, perivascular and interstitial infiltrate of lymphocytes, and few plasma cells and eosinophils. (Hematoxylin-eosin stain; original magnification ×40.)
node revealed necrotic material with polymorphonuclear cells, lymphocytes, lymphoblasts, a few macrophages, and histiocytes in a palisading arrangement without granulomas. Warthin-Starry silver stain was negative. The lymph node tissue was subjected to polymerase chain reaction (PCR), amplifying a portion of the B henselae citrate-synthase gene, gltA, followed by digestion with Taq-1 restriction enzyme and electrophoresis on polyacrylamide gel, as previously described. 1 The PCR was positive for B henselae DNA (Fig 3). Follow-up serologic tests obtained 6 and 12 weeks after the onset of disease demonstrated decrease of the anti-B henselae IgM titers with corresponding seroconversion of the anti-B henselae IgG (Fig 4). The patient completed a 3-week course of decreasing doses of prednisone with complete resolution of all symptoms. No antibiotics were given. At a 12-week follow-up visit, she remained free of symptoms.
DISCUSSION
Fig 3. PCR products were digested with Taq-1 and analyzed by polyacrylamide gel electrophoresis. Lanes 1 and 2: patient’s samples, 2 µL and 1 µL, respectively; lane 3: pus specimen from a CSD patient (positive control); lanes 4 (1.0 ng), 5 (10–1 ng), 6 (10–2 ng), and 7 (10–3 ng): B henselae DNA in decreasing amounts; lanes 8 and 9: pus samples of non-CSD patients (negative controls). Numbers on left side indicate size, in base pairs, of digested products.
of cat scratch disease (CSD). Serum obtained 1 week after the onset of disease and tested by enzyme immunoassay, was found positive for anti-Bartonella henselae IgM and borderline for IgG. A fine needle aspiration of the lymph
The history of intense contact with cats, including numerous scratch marks, the presence of tender regional lymphadenopathy, the identification of antiB henselae IgM and IgG, demonstrating a characteristic response of acute infection, as well as the identification of B henselae DNA in the affected lymph node, by PCR, leave no doubt regarding the diagnosis of CSD in our patient. B henselae, and rarely Afipia felis, are considered to be the etiologic agents of CSD.2 The disease affects mainly children and resolves spontaneously in most cases. Typical clinical manifestations include tender lymphadenitis, which is accompanied by fever and malaise in about 50% of the cases. A minority of the patients experience atypical manifestations, including Parinaud’s oculoglandular syndrome, encephalopathy, hepatospleno-
J AM ACAD DERMATOL VOLUME 41, NUMBER 5, PART 2
megaly, neuroretinitis, pneumonia, arthralgia and arthritis, osteomyelitis, and hepatitis.3 Laboratory confirmation of the diagnosis of CSD is not always easy. The histopathology of CSD lymph nodes is not specific, the Warthin-Starry silver stain has low sensitivity, cultures are only rarely positive, and the CSD skin test lacks standardization and carries a potential risk of transmitting infectious agents.2 Recently, however, serologic tests that use either immunofluorescent antibodies or enzyme immunoassay, and PCR have been shown to be specific and sensitive for the diagnosis of CSD.4-6 Various dermatologic manifestations have been described in CSD. Except for a primary inoculation papule found in 60% to 90% of cases,3,7 skin lesions are rare, having been reported in about 5% of CSD patients. They include maculopapular and urticarial eruptions,7-9 granuloma annulare,7 erythema nodosum,3,7,9 erythema marginatum,3 thrombocytopenic purpura,3,10 leukocytoclastic vasculitis,11 multiple granulomatous lesions,12 and erythema annulare.7 Papulovesicular rash was reported in 2 patients, but neither a detailed description nor a photograph of that rash were presented by the authors.7,9 One of these patients experienced systemic manifestations, and the rash lasted for 2 weeks.9 Contrary to most patients with typical (uncomplicated) CSD, whose major complaints center around the tender lymphadenopathy, our patient was most disturbed by the skin eruption, thus, being referred to a dermatologist. The rash appeared similar to the eruption of Sweet’s syndrome. Arthralgia and lymphadenopathy, both present in our patient, have also been described in patients with Sweet’s syndrome, about 10% of whom have associated malignancy, mainly leukemia or lymphoma.13 However, the absence of blood leukocytosis, as well as the presence of a lymphocytic, rather than a polymorphonuclear infiltrate in the skin biopsy, refuted the diagnosis of Sweet’s syndrome. Cat flea bites may also be considered in the differential diagnosis of this rash, because the cat flea has been recently shown to be an important vector for transmission of B henselae.14 However, flea bites usually cause minimal irritation in nonsensitized persons. In persons who have allergic reactions, they may produce extremely itchy urticarial papules, exhibiting central hemorrhagic punctae. In our patient, the eruption was nonpruritic, and there were no central punctae within the lesions. B henselae has been reported to be highly sensitive in vitro to a large number of antimicrobial agents15; however, the value of such treatment in CSD is questionable because, in the majority of cases, symptoms and signs resolve within 2 to 4
Landau et al 835
months regardless of treatment.2 In 1 recent comparative study, azithromycin was shown to accelerate the decrease of the affected lymph node size.16 No other prospective controlled study of antibiotic treatment in CSD is available. The prolonged course of CSD, the presence of manifestations such as arthritis and erythema nodosum, the apparent lack of response to antimicrobial agents, contrary to the expectation in a bacterial infection caused by a susceptible organism, and the presence of granulomas in the affected tissues, raise the possibility that immunologic mechanisms may be involved in the pathogenesis of CSD. The favorable response of our patient to systemic steroids without administration of antibiotics is therefore intriguing. However, definitive conclusions regarding the role of corticosteroids in CSD cannot be drawn from this case, because CSD is usually a self-limited disease. In conclusion, edematous papules, characteristic of Sweet’s syndrome, are probably a rare manifestation of CSD. This and other types of skin lesions may be more common in CSD than currently appreciated because the diagnosis of CSD can be missed, particularly if the chief complaint is an eruption, as was the case in our patient. Increased awareness, a detailed medical history, particularly history of cat contact, and a complete physical examination are needed to identify patients with atypical CSD. Accurate diagnosis is more feasible today because of the increased availability of serologic tests and DNA amplification techniques. REFERENCES 1. Avidor B, Kletter Y, Abulafia S, Golan Y, Ephros M, Giladi M. Molecular diagnosis of cat scratch disease: a two-step approach. J Clin Microbiol 1997;35:1924-30. 2. Anderson BE, Newman MA. Bartonella spp. as emerging human pathogens. Clin Microbiol Rev 1997;10:203-19. 3. Carithers HA. Cat scratch disease: an overview based on a study of 1200 patients. AJDC 1985;139:1124-33. 4. Regnery RL, Olson JG, Perkins BA, Bibb W. Serological response to “Rochalimeae henselae” antigen in suspected cat-scratch disease. Lancet 1992;339:1443-5. 5. Giladi M, Slater LN, Kletter Y, Welch D, Avidor B, Abulafia S, et al. Serodiagnosis of cat scratch disease. 37th Interscience Conference on Antimicrobial Agents and Chemotherapy, September 28-October 1, 1997, Toronto, Canada. Abstract D-5, p. 83. 6. Bergman AMC, Groothedde J-W, Schellekens JFP, van Embden JDA, Ossewaarde JM, Schouls LM. Etiology of cat scratch disease: comparison of polymerase chain reaction detection of Bartonella (formerly Rochalimaea) and Afipia felis DNA with serology and skin test. J Infect Dis 1995;171:916-23. 7. Margileth AM. Dermatologic manifestations and update of cat scratch disease. Pediatr Dermatol 1988;5:1-9. 8. Sundaresh KV, Madjar DD, Camisa C, Carvallo E. Cat scratch disease associated with erythema nodosum. Cutis 1986;38:317-9. 9. Margileth AM,Wear DJ, English CK. Systemic cat scratch disease: report of 23 patients with prolonged or recurrent severe bacterial infection. J Inf Dis 1987;155:390-402.
836 Landau et al
10. Jim RTS. Thrombocytopenic purpura in cat-scartch disease. JAMA 1961;176:1036-7. 11. Hashkes PJ, Trabulsi A, Passo MH. Systemic cat scratch disease presenting as leukocytoclastic vasculitis. Pediatr Inf Dis J 1996; 15:93-4. 12. Calzavara-Pinton PG, Facchetti F, Carlino A, dePanfilis G. Multiple scattered granulomatous skin lesions in cat scratch disease. Cutis 1992;49:318-20. 13. von den Driesch P. Sweet’s syndrome. J Am Acad Dermatol 1994;31:535-56.
J AM ACAD DERMATOL NOVEMBER 1999
14. Chomel BB, Kasten RW, Floyd-Hawkins K, Chi B, Yamamoto K, Roberts-Wilson J, et al. Experimental transmission of Bartonella henselae by cat flea. J Clin Microbiol 1996;34:1952-6. 15. Maurin M, Gasquet S, Duocco C, Raoult D. MICs of 28 antibiotic compounds for 14 Bartonella (formerly Rochalimaea) isolates. Antimicrob Agents Chemother 1995;39:2387-91. 16. Bass JW, Freitas BC, Freitas AD, Sisler CL, Chan DC, Vincent JM, et al. Prospective randomized double blind placebo-controlled evaluation of azithromycin for the treatment of cat-scratch disease. Ped Infect Dis J 1998;17:447-52.
CASE REPORT A 32-year-old previously healthy woman was referred to the dermatology outpatient clinic because of fever of 39°C and eruption of 2 days duration. In addition, she complained of pain in the right groin and arthralgia in the right elbow, both knees and ankles, and the left first toe. The eruption, first noted on the upper chest, spread over the next 2 days to involve the shoulders and upper back. Although there was no pruritus, the lesions were accompanied by a mild burning sensation. Her past medical history was uneventful. The patient owned several cats and kittens and was often scratched by them. Examination revealed a well-developed and nourished woman with fever of 38°C. Multiple edematous, pale, reddish papules coalescing to plaques were noted on her upper chest, back, and shoulders (Fig 1). The lesions were surrounded by erythematous halos and some of them had a pseudovesicular appearance. A 2 × 3 cm tender, soft, nonfluctuating lymph node was palpated in the left inguinal area. Multiple scratches were present on both hands and legs. No frank arthritis was found, and ophthalmologic examination was normal.
This supplement is made possible through an educational grant from Ortho Dermatological to the American Academy of Dermatology. From the Department of Dermatologya and the Bernard Pridan Laboratory for Molecular Biology of Infectious Diseases,b Tel Aviv–Elias Sourasky Medical Center, and Sackler School of Medicine, Tel Aviv University, and Department of Pediatrics,c Carmel Medical Center, Haifa. Reprint requests: Marina Landau, MD, Department of Dermatology, Tel Aviv-Elias Sourasky Medical Center 6,Weizman Street,Tel Aviv 64239 Israel. E-mail: [email protected] Copyright © 1999 by the American Academy of Dermatology, Inc. 0190-9622/99/$8.00 + 0 16/4/96950
Fig 1. Edematous plaques and papules, surrounded by erythematous halos on chest of patient.
Complete blood cell count disclosed hemoglobin of 12.9 g/dL, 8,600 leukocytes/mm3 with 83.6% neutrophils, and 192,000 platelets/mm3. Other routine laboratory studies were within normal limits. Serology for HIV was negative. Pending the results of a skin biopsy and on the basis of the clinical findings, a diagnosis of acute febrile neutrophilic dermatosis (Sweet’s syndrome) was considered, and treatment with prednisone 40 mg/day was started. The eruption, arthralgia, and fever improved significantly over the next 5 days. The skin biopsy specimen revealed a normal epidermis with subepidermal edema, a perivascular and focally interstitial infiltrate of lymphocytes, and a few plasma cells and scanty eosinophils (Fig 2). These histologic findings were not consistent with the original clinical diagnosis of Sweet’s syndrome. The history of close contact with cats and the presence of tender regional lymphadenopathy raised the possibility
833
834 Landau et al
J AM ACAD DERMATOL NOVEMBER 1999
Fig 4. Anti-B henselae IgM (closed circles) and IgG (open circles) titers at 1, 6, and 12 weeks after onset of disease, as determined by enzyme immunoassay. Sera were diluted 1:100. Average optical density of triplicate determinations was calculated. Arrows represent cutoff titers for positive tests.
Fig 2. Skin biopsy specimen showing subepidermal edema, perivascular and interstitial infiltrate of lymphocytes, and few plasma cells and eosinophils. (Hematoxylin-eosin stain; original magnification ×40.)
node revealed necrotic material with polymorphonuclear cells, lymphocytes, lymphoblasts, a few macrophages, and histiocytes in a palisading arrangement without granulomas. Warthin-Starry silver stain was negative. The lymph node tissue was subjected to polymerase chain reaction (PCR), amplifying a portion of the B henselae citrate-synthase gene, gltA, followed by digestion with Taq-1 restriction enzyme and electrophoresis on polyacrylamide gel, as previously described. 1 The PCR was positive for B henselae DNA (Fig 3). Follow-up serologic tests obtained 6 and 12 weeks after the onset of disease demonstrated decrease of the anti-B henselae IgM titers with corresponding seroconversion of the anti-B henselae IgG (Fig 4). The patient completed a 3-week course of decreasing doses of prednisone with complete resolution of all symptoms. No antibiotics were given. At a 12-week follow-up visit, she remained free of symptoms.
DISCUSSION
Fig 3. PCR products were digested with Taq-1 and analyzed by polyacrylamide gel electrophoresis. Lanes 1 and 2: patient’s samples, 2 µL and 1 µL, respectively; lane 3: pus specimen from a CSD patient (positive control); lanes 4 (1.0 ng), 5 (10–1 ng), 6 (10–2 ng), and 7 (10–3 ng): B henselae DNA in decreasing amounts; lanes 8 and 9: pus samples of non-CSD patients (negative controls). Numbers on left side indicate size, in base pairs, of digested products.
of cat scratch disease (CSD). Serum obtained 1 week after the onset of disease and tested by enzyme immunoassay, was found positive for anti-Bartonella henselae IgM and borderline for IgG. A fine needle aspiration of the lymph
The history of intense contact with cats, including numerous scratch marks, the presence of tender regional lymphadenopathy, the identification of antiB henselae IgM and IgG, demonstrating a characteristic response of acute infection, as well as the identification of B henselae DNA in the affected lymph node, by PCR, leave no doubt regarding the diagnosis of CSD in our patient. B henselae, and rarely Afipia felis, are considered to be the etiologic agents of CSD.2 The disease affects mainly children and resolves spontaneously in most cases. Typical clinical manifestations include tender lymphadenitis, which is accompanied by fever and malaise in about 50% of the cases. A minority of the patients experience atypical manifestations, including Parinaud’s oculoglandular syndrome, encephalopathy, hepatospleno-
J AM ACAD DERMATOL VOLUME 41, NUMBER 5, PART 2
megaly, neuroretinitis, pneumonia, arthralgia and arthritis, osteomyelitis, and hepatitis.3 Laboratory confirmation of the diagnosis of CSD is not always easy. The histopathology of CSD lymph nodes is not specific, the Warthin-Starry silver stain has low sensitivity, cultures are only rarely positive, and the CSD skin test lacks standardization and carries a potential risk of transmitting infectious agents.2 Recently, however, serologic tests that use either immunofluorescent antibodies or enzyme immunoassay, and PCR have been shown to be specific and sensitive for the diagnosis of CSD.4-6 Various dermatologic manifestations have been described in CSD. Except for a primary inoculation papule found in 60% to 90% of cases,3,7 skin lesions are rare, having been reported in about 5% of CSD patients. They include maculopapular and urticarial eruptions,7-9 granuloma annulare,7 erythema nodosum,3,7,9 erythema marginatum,3 thrombocytopenic purpura,3,10 leukocytoclastic vasculitis,11 multiple granulomatous lesions,12 and erythema annulare.7 Papulovesicular rash was reported in 2 patients, but neither a detailed description nor a photograph of that rash were presented by the authors.7,9 One of these patients experienced systemic manifestations, and the rash lasted for 2 weeks.9 Contrary to most patients with typical (uncomplicated) CSD, whose major complaints center around the tender lymphadenopathy, our patient was most disturbed by the skin eruption, thus, being referred to a dermatologist. The rash appeared similar to the eruption of Sweet’s syndrome. Arthralgia and lymphadenopathy, both present in our patient, have also been described in patients with Sweet’s syndrome, about 10% of whom have associated malignancy, mainly leukemia or lymphoma.13 However, the absence of blood leukocytosis, as well as the presence of a lymphocytic, rather than a polymorphonuclear infiltrate in the skin biopsy, refuted the diagnosis of Sweet’s syndrome. Cat flea bites may also be considered in the differential diagnosis of this rash, because the cat flea has been recently shown to be an important vector for transmission of B henselae.14 However, flea bites usually cause minimal irritation in nonsensitized persons. In persons who have allergic reactions, they may produce extremely itchy urticarial papules, exhibiting central hemorrhagic punctae. In our patient, the eruption was nonpruritic, and there were no central punctae within the lesions. B henselae has been reported to be highly sensitive in vitro to a large number of antimicrobial agents15; however, the value of such treatment in CSD is questionable because, in the majority of cases, symptoms and signs resolve within 2 to 4
Landau et al 835
months regardless of treatment.2 In 1 recent comparative study, azithromycin was shown to accelerate the decrease of the affected lymph node size.16 No other prospective controlled study of antibiotic treatment in CSD is available. The prolonged course of CSD, the presence of manifestations such as arthritis and erythema nodosum, the apparent lack of response to antimicrobial agents, contrary to the expectation in a bacterial infection caused by a susceptible organism, and the presence of granulomas in the affected tissues, raise the possibility that immunologic mechanisms may be involved in the pathogenesis of CSD. The favorable response of our patient to systemic steroids without administration of antibiotics is therefore intriguing. However, definitive conclusions regarding the role of corticosteroids in CSD cannot be drawn from this case, because CSD is usually a self-limited disease. In conclusion, edematous papules, characteristic of Sweet’s syndrome, are probably a rare manifestation of CSD. This and other types of skin lesions may be more common in CSD than currently appreciated because the diagnosis of CSD can be missed, particularly if the chief complaint is an eruption, as was the case in our patient. Increased awareness, a detailed medical history, particularly history of cat contact, and a complete physical examination are needed to identify patients with atypical CSD. Accurate diagnosis is more feasible today because of the increased availability of serologic tests and DNA amplification techniques. REFERENCES 1. Avidor B, Kletter Y, Abulafia S, Golan Y, Ephros M, Giladi M. Molecular diagnosis of cat scratch disease: a two-step approach. J Clin Microbiol 1997;35:1924-30. 2. Anderson BE, Newman MA. Bartonella spp. as emerging human pathogens. Clin Microbiol Rev 1997;10:203-19. 3. Carithers HA. Cat scratch disease: an overview based on a study of 1200 patients. AJDC 1985;139:1124-33. 4. Regnery RL, Olson JG, Perkins BA, Bibb W. Serological response to “Rochalimeae henselae” antigen in suspected cat-scratch disease. Lancet 1992;339:1443-5. 5. Giladi M, Slater LN, Kletter Y, Welch D, Avidor B, Abulafia S, et al. Serodiagnosis of cat scratch disease. 37th Interscience Conference on Antimicrobial Agents and Chemotherapy, September 28-October 1, 1997, Toronto, Canada. Abstract D-5, p. 83. 6. Bergman AMC, Groothedde J-W, Schellekens JFP, van Embden JDA, Ossewaarde JM, Schouls LM. Etiology of cat scratch disease: comparison of polymerase chain reaction detection of Bartonella (formerly Rochalimaea) and Afipia felis DNA with serology and skin test. J Infect Dis 1995;171:916-23. 7. Margileth AM. Dermatologic manifestations and update of cat scratch disease. Pediatr Dermatol 1988;5:1-9. 8. Sundaresh KV, Madjar DD, Camisa C, Carvallo E. Cat scratch disease associated with erythema nodosum. Cutis 1986;38:317-9. 9. Margileth AM,Wear DJ, English CK. Systemic cat scratch disease: report of 23 patients with prolonged or recurrent severe bacterial infection. J Inf Dis 1987;155:390-402.
836 Landau et al
10. Jim RTS. Thrombocytopenic purpura in cat-scartch disease. JAMA 1961;176:1036-7. 11. Hashkes PJ, Trabulsi A, Passo MH. Systemic cat scratch disease presenting as leukocytoclastic vasculitis. Pediatr Inf Dis J 1996; 15:93-4. 12. Calzavara-Pinton PG, Facchetti F, Carlino A, dePanfilis G. Multiple scattered granulomatous skin lesions in cat scratch disease. Cutis 1992;49:318-20. 13. von den Driesch P. Sweet’s syndrome. J Am Acad Dermatol 1994;31:535-56.
J AM ACAD DERMATOL NOVEMBER 1999
14. Chomel BB, Kasten RW, Floyd-Hawkins K, Chi B, Yamamoto K, Roberts-Wilson J, et al. Experimental transmission of Bartonella henselae by cat flea. J Clin Microbiol 1996;34:1952-6. 15. Maurin M, Gasquet S, Duocco C, Raoult D. MICs of 28 antibiotic compounds for 14 Bartonella (formerly Rochalimaea) isolates. Antimicrob Agents Chemother 1995;39:2387-91. 16. Bass JW, Freitas BC, Freitas AD, Sisler CL, Chan DC, Vincent JM, et al. Prospective randomized double blind placebo-controlled evaluation of azithromycin for the treatment of cat-scratch disease. Ped Infect Dis J 1998;17:447-52.