- Email: [email protected]
Pemphigus vulgaris induced by D-penicillamine therapy in a patient with systemic sclerosis
J AM
ACAD DERMATOL VOLUME 42, NUMBER
Brief reports 2,
297
PART 3
based on in vitro susceptibility studies using infected HL cell lines in which antituberculotic drugs, the fluoroquinolones, and the penicillins have proven efficacious (unpublished data). Isoniazid shows activity against the persistent, nonreplicating cryptic body. Levofloxacin, through its inhibition of the bacterial gyrase enzyme, interferes with the metabolically active reticulate body n-Penicillamine, a metabolite of penicillin, can reduce disulfide bonds on the surface of the elementary body eliminating its infectious capability Negative PCR and reduced antibody titers in our patient after 6 months of combination therapy validate the in vivo efficacy of this regimen. This case suggests a possible pathogenic role for C pneumoniae in the evolution or chronicity of PGlike skin ulcers. REFERENCES 1. Powell FC, Su WPD, Perry HO. Pyoderma cation and management. J Am Acad 409.
2. Huang W, McNeely MC. Neutrophilic tissue reactions. Adv Dermatol 1997;13:33-64. 3. Lear JT, Atherton MT, Byrne JPH. Neutrophilic dermatoses: pyoderma gangrenosum and Sweet’s syndrome. Postgrad Med J 1997;73:65-8. 4. Kuo C-C, Jackson LA, Campbell L, Grayston JT. Chlamydia pneumoniae (TWAR). Clin Microbial Rev 1995;8:451-61. 5. Muldowney JAS. Cblamydia pneumoniae: A treatable cause of atherosclerosis? Antimicrob Infect Dis Newsletter 1997;16:1-8. 6. Stratton CW, Mitchell WM. The pathogenesis of systemic chlamydial infections: theoretical considerations of host cell energy depletion and its metabolic consequences. Antimicrob Infect Dis Newsletter 1997;16:33-8. 7. Gupta S, Camm AJ. Chronic infection in the etiology of atherosclerosis: the case for Chlamydia pneumoniae. Clin Cardiol 1997;20:829-36. 8. Hurwitz RM, Haseman JH. The evolution of pyoderma gangrenosum: a clinicopathologic correlation. Am J Dermatopathol 1993;15:28-33. 9. Stratton CW, Mitchell WM. The pathogenesis of Chlamydia species. Antimicrob Infect Dis Newsletter 1996;15:83-90.
gangrenosum: classifiDermatol 1996;34:395-
Pemphigus vulgaris induced by D-penicillamine therapy in a patient with systemic sclerosis Michael Shapiro, MD,a Sergio Jimenez, MD,b and Victoria I! Werth, MDC Philadelphia, Pennsylvania n-Penicillamine-induced pemphigus occurs infrequently, typically in patients with rheumatoid arthritis. We describe a patient with systemic sclerosis who experienced this complication 3 months after starting Dpenicillamine therapy. Nikolsky’s sign, histopathologic findings, and direct immunofluorescence all confirmed the diagnosis. Termination of disease progression required intravenous pulse glucocorticoids, azathioprine, and 3 courses of plasmapheresis. The presentation, treatment, and etiology of Dpenicillamine-induced pemphigus are reviewed, and the incidence of this complication in scleroderma patients is examined. (J Am Acad Dermatol2000;42:297-9.)
P
emphigus induced by o-penicillamine is a rare skin disorder, with only about 100 cases described. Approximately 7% of patients experience this complication, usually after receiving
From the Department of Medicine, Pennsylvania Hospital,a the Department of Rheumatology, Jefferson University,b and the Department of Dermatology & Medicine, University of Pennsylvania Medical Center &Veterans Affairs Medical Center.C Reprint requests: Victoria R Werth, MD, University of Pennsylvania, 36th and Spruce, Philadelphia, PA 19104. 16/54/l
02644
the drug for rheumatoid arthritis.l We report a case of o-penicillamine-induced pemphigus vulgaris (PV) in a patient treated with o-penicillamine for systemic sclerosis. High-dose prednisone in combination with plasmapheresis and azathioprine were required to terminate disease progression.
CASE REPORT A 71-year-old woman with systemic sclerosis experienced erythematous flaccid blisters on her face, arms, trunk, and legs 3 months after starting Dpenicillamine treatment. A drug reaction to
298
Brief reports
J AM ACAD DERMATOL FEBRUARY 2000
Fig 1. Early suprabasalar acantholysis.
Fig 2. Confluent erosions with Tareflaccid pustular bullae on lateral face and neck.
furosemide was suspected and the agent was discontinued. The cutaneous eruption abated with methylprednisolone dose pack therapy. Two weeks later, new blisters, erythematous patches, and superficial erosions with turbid, flaccid bullae arose on her face, scalp, and chest. Dicloxacillin and topical 2% mupirocin were administered for probable bullous impetigo. Dicloxacillin was replaced with ciprofloxacin after skin cultures grew Pseudomonas aeruginosa . The patient continued to experience new blisters, and on re-examination 7 weeks later Nikolsky’s sign was positive. Routine histologic examination revealed early suprabasalar acantholysis with a perivascular lymphoid infiltrate with eosinophils (Fig 1). Direct immunofluorescence demonstrated IgG and C3 staining along epidermal cell surface membranes. Indirect immunofluorescence, performed by reacting serial dilutions of the patient’s serum with sections of monkey esophagus, revealed 1:64 antibody titers. PV was diagnosed and the patient was started on a regimen of prednisone, 100 mg daily. New blisters continued to appear so the dose of prednisone was increased to 140 mg/day and azathioprine 50 mg twice daily was added. DPenicillamine was discontinued because of a suspicion that it was responsible for the PV On admission, confluent erosions were present on the face, buccal mucosa of the oral cavity, neck, upper chest, and upper back (Fig 2). Crusted lesions on an erythematous base were seen on her scalp, face, arms, and hands. Despite daily intravenous methylprednisolone sodium succinate (1 g/day for 5 days), new blisters continued to appear. The progression of the cutaneous eruptions was terminated over the new week by continued steroids, azathioprine, and 3 courses of plasmapheresis. She has not
been taking any therapy and has been in remission for the past 18 months.
DISCUSSION n-Penicillamine-induced pemphigus begins as an urticarial, annular, or morbilliform erythematous prodrome. Subsequently, scaly crusted patches, vesicles, and bullae occur. Nikolsky’s sign as well as the pathologic and direct immunofluorescence findings in our patient all suggest the diagnosis.2 Before the advent of steroid therapy, most patients died of sepsis and electrolyte imbalances resulting from generalized skin failure. Currently, fatal cases are rare.3 The discontinuation of o-penicillamine therapy frequently fails to stop disease progression, as was the case with our patient. Oral steroids, steroid-sparing agents, and plasmapheresis may then be used.415 Treatment needs to be initiated early because extensive disease is significantly more resistant to treatment.6 o-Penicillamine precipitates autoantibody production through a cross-reaction phenomenon by disrupting normal T-cell function or by directly altering the antigenicity of cell surface molecules. Autoantibody binding to desmoglein 3 then results in acantholysis.7~9 Certain individuals may be predisposed to the disease because they possess HLA antigens associated with idiopathic pemphigus. Additionally, some HLA antigens are more prevalent in this set of patients.3J0J1 The coexistence of scleroderma and pemphigus is exceedingly rare. To our knowledge, only 3 cases of idiopathic PV arising in patients with scleroderma have been described.12~13 Ten cases of D-penicillamine-induced pemphigus have been reported in patients with scleroderma. The incidence of this complication appears to be between 1.5% and 2.9% in patients with scleroderma who are treated with D-
J AM ACAD DERMATOL VOLUME 42, NUMBER
Brief
penicillamine.3)14-19 Most reports of D-penicillamineinduced pemphigus are in patients with rheumatoid arthritis. REFERENCES 1. Brenner
5, Wolf
299
reports
2, PART 1
R, Ruocco
V. Drug-induced
pemphigus
I: a sur-
vey. Clin Dermatol 1993;11:501-4. 2. Levy RS, Fisher M, Alter JN.Penicillamine: review and cutaneous manifestations. J Am Acad Dermatol 1983;8:548-58. 3. McGovern TW, Bennion SD. Diffuse patient with limited scleroderma.Arch
blisters and erossions in a Dermatol 1997;133:499-
504. 4. Piamphongsant T, Ophaswongse Int J Dermatol 1991;30:139-46. 5. Walton 5, Keczkes K, Robinson
S.Treatment AE. A case
of pemphigus. of penicillamine-
induced pemphigus, successfully treated by plasma exchange. Clin Exp Dermatol 1987;12:275-6. 6. Ahmed AR,Graham J,Jordon RE,ProvostTT.Pemphigus:current concepts. Ann Intern Med 1980;92:396-405.
10. Ho VC, Stein
HB, Ongley
RC, McLeod
A. Penicillamine
induced
pemphigus. J Rheumatol 1985;12:583-6. 11. Zone J, Ward J, Boyce E, Schupbach C. Penicillamine-induced pemphigus. JAMA 1982;247:2705-7. 12. Katz AL, Nashel DJ, Goard CP, Bauer H. Pemphigus vulgaris lymphoma
in a patient
with
scleroderma.South
and
Med J 1979;72:
1463-6. 13. Woscoff EA, Remondino G, Jaimovich L, Berengust G, Rios A. Progressive systemic sclerosis and pemphigus vulgaris. J Am Acad Dermatol 1989;21:142-4. 14. Asboe-Hansen G.Treatment of generalized scleroderma with inhibitors of connective tissue formation. Acta Derm Venereol (Stockh) 1975;55:461-5. 15. Davies MG, Holt P Pemphigus in a patient lamine for a generalized morphea. Arch
treated with penicilDermatol 1976;112:
1308-g. 16. From E, Frederiksen P. Pemphigus vulgaris following o-penicillamine. Dermatologica 1976;152:358-62. 17. Kristensen JK, Wadskov 5. Penicillamine-induced pemphigus
7. Korman NJ, Eyre RW, Zone J, Stanley JR. Drug-induced pemphigus: autoantibodies directed against the pemphigus antigen complexes are present in penicillamine and captopril-induced
foliaceus. Acta Derm Venereol (Stockh) 1977;57:69-71. 18. PeAas PF, Buezo GF, Carvajal I, Dauden E, Lopez A, Diaz LA. DPenicillamine-induced pemphigus foliaceus with autoantibodies to desmoglein-1 in a patient with mixed connective tissue
pemphigus.J Invest Dermatol 1991;96:273-6. 8. Mobinin N, Ahmed AR. Immunogenetics of drug-induced bullous diseases.Clin Dermatol 1993;11:449-60. 9. Mutasim DF, Pelt NJ, Anhalt GJ. Drug-induced pemphigus.
disease. J Am Acad Dermatol 1997;37:121-3. 19. Steen VD, Blair 5, Medsger TA.The toxicity of o-penicillamine systemic sclerosis. Ann Intern Med 1986;104:699-705.
Dermatol
in
Clin 1993;11:463-71.
Bacillary
angiomatosis by Bartonella in an HIV-infected patient
quintana
Raquel Santos,a Orlando Cardoso,b Paulo Rodrigues,b Jorge Cardoso,a Jo50 Machado,b Ana Afonso,C FAtima Bacellar,d Eric Marston,e and Rui Proenc;ab Lisbon, Portugal, and Atlanta, Georgia Bacillary angiomatosis and bacillaty peliosns are opportunistic infections caused by Bartonella henselae and quintana, which occur in patients with late-stage infection. We report a case of bacillary angiomatosis in an HIV-infected patient with skin, bone, and probably liver involvement, The identification of the agent (B quintana) was done by polymerase chain reaction in the skin specimen. The patient had complete regression of all lesions after a 6-month regimen of oral erythromycin. c’JAm Acad Dermatol
Bartonella
2000;42:299-301.)
From the Departments of Dermatology and Venereology,a Infectious Diseases,b and Pathology,c Hospital Curry Cabral, Lisbon, Centro de Estudos de Vectores e Doencas Infecciosas/lnstituto National de Salide Dr Ricardo Jorge,Aguas de Moura,d and Division ofViral and Rickettsial Diseases,Centers for Disease Control and Prevention,Atlanta.e Reprint requests: Raquel Santos, Service de Dermatologia, Hospital de Curry Cabral, Rua da Beneficiencia, 1069-I 66 Lisboa, Portugal. Copyright 0 2000 by the American Academy of Dermatology, Inc. 0190-9622/2000/$12.00
+ 0
16/54/l
02645
B
acillary angiomatosis and bacillary peliosis are opportunistic infections that were first recognized in 1983 by Stoler et al,l at the beginning of the AIDS epidemic. The causative organisms are Bartonella henselae and B quintana, and the infection occurs in severely immunocompromised patients with late stage HIV infection. The manifestations of Bartonella infection in the
ACAD DERMATOL VOLUME 42, NUMBER
Brief reports 2,
297
PART 3
based on in vitro susceptibility studies using infected HL cell lines in which antituberculotic drugs, the fluoroquinolones, and the penicillins have proven efficacious (unpublished data). Isoniazid shows activity against the persistent, nonreplicating cryptic body. Levofloxacin, through its inhibition of the bacterial gyrase enzyme, interferes with the metabolically active reticulate body n-Penicillamine, a metabolite of penicillin, can reduce disulfide bonds on the surface of the elementary body eliminating its infectious capability Negative PCR and reduced antibody titers in our patient after 6 months of combination therapy validate the in vivo efficacy of this regimen. This case suggests a possible pathogenic role for C pneumoniae in the evolution or chronicity of PGlike skin ulcers. REFERENCES 1. Powell FC, Su WPD, Perry HO. Pyoderma cation and management. J Am Acad 409.
2. Huang W, McNeely MC. Neutrophilic tissue reactions. Adv Dermatol 1997;13:33-64. 3. Lear JT, Atherton MT, Byrne JPH. Neutrophilic dermatoses: pyoderma gangrenosum and Sweet’s syndrome. Postgrad Med J 1997;73:65-8. 4. Kuo C-C, Jackson LA, Campbell L, Grayston JT. Chlamydia pneumoniae (TWAR). Clin Microbial Rev 1995;8:451-61. 5. Muldowney JAS. Cblamydia pneumoniae: A treatable cause of atherosclerosis? Antimicrob Infect Dis Newsletter 1997;16:1-8. 6. Stratton CW, Mitchell WM. The pathogenesis of systemic chlamydial infections: theoretical considerations of host cell energy depletion and its metabolic consequences. Antimicrob Infect Dis Newsletter 1997;16:33-8. 7. Gupta S, Camm AJ. Chronic infection in the etiology of atherosclerosis: the case for Chlamydia pneumoniae. Clin Cardiol 1997;20:829-36. 8. Hurwitz RM, Haseman JH. The evolution of pyoderma gangrenosum: a clinicopathologic correlation. Am J Dermatopathol 1993;15:28-33. 9. Stratton CW, Mitchell WM. The pathogenesis of Chlamydia species. Antimicrob Infect Dis Newsletter 1996;15:83-90.
gangrenosum: classifiDermatol 1996;34:395-
Pemphigus vulgaris induced by D-penicillamine therapy in a patient with systemic sclerosis Michael Shapiro, MD,a Sergio Jimenez, MD,b and Victoria I! Werth, MDC Philadelphia, Pennsylvania n-Penicillamine-induced pemphigus occurs infrequently, typically in patients with rheumatoid arthritis. We describe a patient with systemic sclerosis who experienced this complication 3 months after starting Dpenicillamine therapy. Nikolsky’s sign, histopathologic findings, and direct immunofluorescence all confirmed the diagnosis. Termination of disease progression required intravenous pulse glucocorticoids, azathioprine, and 3 courses of plasmapheresis. The presentation, treatment, and etiology of Dpenicillamine-induced pemphigus are reviewed, and the incidence of this complication in scleroderma patients is examined. (J Am Acad Dermatol2000;42:297-9.)
P
emphigus induced by o-penicillamine is a rare skin disorder, with only about 100 cases described. Approximately 7% of patients experience this complication, usually after receiving
From the Department of Medicine, Pennsylvania Hospital,a the Department of Rheumatology, Jefferson University,b and the Department of Dermatology & Medicine, University of Pennsylvania Medical Center &Veterans Affairs Medical Center.C Reprint requests: Victoria R Werth, MD, University of Pennsylvania, 36th and Spruce, Philadelphia, PA 19104. 16/54/l
02644
the drug for rheumatoid arthritis.l We report a case of o-penicillamine-induced pemphigus vulgaris (PV) in a patient treated with o-penicillamine for systemic sclerosis. High-dose prednisone in combination with plasmapheresis and azathioprine were required to terminate disease progression.
CASE REPORT A 71-year-old woman with systemic sclerosis experienced erythematous flaccid blisters on her face, arms, trunk, and legs 3 months after starting Dpenicillamine treatment. A drug reaction to
298
Brief reports
J AM ACAD DERMATOL FEBRUARY 2000
Fig 1. Early suprabasalar acantholysis.
Fig 2. Confluent erosions with Tareflaccid pustular bullae on lateral face and neck.
furosemide was suspected and the agent was discontinued. The cutaneous eruption abated with methylprednisolone dose pack therapy. Two weeks later, new blisters, erythematous patches, and superficial erosions with turbid, flaccid bullae arose on her face, scalp, and chest. Dicloxacillin and topical 2% mupirocin were administered for probable bullous impetigo. Dicloxacillin was replaced with ciprofloxacin after skin cultures grew Pseudomonas aeruginosa . The patient continued to experience new blisters, and on re-examination 7 weeks later Nikolsky’s sign was positive. Routine histologic examination revealed early suprabasalar acantholysis with a perivascular lymphoid infiltrate with eosinophils (Fig 1). Direct immunofluorescence demonstrated IgG and C3 staining along epidermal cell surface membranes. Indirect immunofluorescence, performed by reacting serial dilutions of the patient’s serum with sections of monkey esophagus, revealed 1:64 antibody titers. PV was diagnosed and the patient was started on a regimen of prednisone, 100 mg daily. New blisters continued to appear so the dose of prednisone was increased to 140 mg/day and azathioprine 50 mg twice daily was added. DPenicillamine was discontinued because of a suspicion that it was responsible for the PV On admission, confluent erosions were present on the face, buccal mucosa of the oral cavity, neck, upper chest, and upper back (Fig 2). Crusted lesions on an erythematous base were seen on her scalp, face, arms, and hands. Despite daily intravenous methylprednisolone sodium succinate (1 g/day for 5 days), new blisters continued to appear. The progression of the cutaneous eruptions was terminated over the new week by continued steroids, azathioprine, and 3 courses of plasmapheresis. She has not
been taking any therapy and has been in remission for the past 18 months.
DISCUSSION n-Penicillamine-induced pemphigus begins as an urticarial, annular, or morbilliform erythematous prodrome. Subsequently, scaly crusted patches, vesicles, and bullae occur. Nikolsky’s sign as well as the pathologic and direct immunofluorescence findings in our patient all suggest the diagnosis.2 Before the advent of steroid therapy, most patients died of sepsis and electrolyte imbalances resulting from generalized skin failure. Currently, fatal cases are rare.3 The discontinuation of o-penicillamine therapy frequently fails to stop disease progression, as was the case with our patient. Oral steroids, steroid-sparing agents, and plasmapheresis may then be used.415 Treatment needs to be initiated early because extensive disease is significantly more resistant to treatment.6 o-Penicillamine precipitates autoantibody production through a cross-reaction phenomenon by disrupting normal T-cell function or by directly altering the antigenicity of cell surface molecules. Autoantibody binding to desmoglein 3 then results in acantholysis.7~9 Certain individuals may be predisposed to the disease because they possess HLA antigens associated with idiopathic pemphigus. Additionally, some HLA antigens are more prevalent in this set of patients.3J0J1 The coexistence of scleroderma and pemphigus is exceedingly rare. To our knowledge, only 3 cases of idiopathic PV arising in patients with scleroderma have been described.12~13 Ten cases of D-penicillamine-induced pemphigus have been reported in patients with scleroderma. The incidence of this complication appears to be between 1.5% and 2.9% in patients with scleroderma who are treated with D-
J AM ACAD DERMATOL VOLUME 42, NUMBER
Brief
penicillamine.3)14-19 Most reports of D-penicillamineinduced pemphigus are in patients with rheumatoid arthritis. REFERENCES 1. Brenner
5, Wolf
299
reports
2, PART 1
R, Ruocco
V. Drug-induced
pemphigus
I: a sur-
vey. Clin Dermatol 1993;11:501-4. 2. Levy RS, Fisher M, Alter JN.Penicillamine: review and cutaneous manifestations. J Am Acad Dermatol 1983;8:548-58. 3. McGovern TW, Bennion SD. Diffuse patient with limited scleroderma.Arch
blisters and erossions in a Dermatol 1997;133:499-
504. 4. Piamphongsant T, Ophaswongse Int J Dermatol 1991;30:139-46. 5. Walton 5, Keczkes K, Robinson
S.Treatment AE. A case
of pemphigus. of penicillamine-
induced pemphigus, successfully treated by plasma exchange. Clin Exp Dermatol 1987;12:275-6. 6. Ahmed AR,Graham J,Jordon RE,ProvostTT.Pemphigus:current concepts. Ann Intern Med 1980;92:396-405.
10. Ho VC, Stein
HB, Ongley
RC, McLeod
A. Penicillamine
induced
pemphigus. J Rheumatol 1985;12:583-6. 11. Zone J, Ward J, Boyce E, Schupbach C. Penicillamine-induced pemphigus. JAMA 1982;247:2705-7. 12. Katz AL, Nashel DJ, Goard CP, Bauer H. Pemphigus vulgaris lymphoma
in a patient
with
scleroderma.South
and
Med J 1979;72:
1463-6. 13. Woscoff EA, Remondino G, Jaimovich L, Berengust G, Rios A. Progressive systemic sclerosis and pemphigus vulgaris. J Am Acad Dermatol 1989;21:142-4. 14. Asboe-Hansen G.Treatment of generalized scleroderma with inhibitors of connective tissue formation. Acta Derm Venereol (Stockh) 1975;55:461-5. 15. Davies MG, Holt P Pemphigus in a patient lamine for a generalized morphea. Arch
treated with penicilDermatol 1976;112:
1308-g. 16. From E, Frederiksen P. Pemphigus vulgaris following o-penicillamine. Dermatologica 1976;152:358-62. 17. Kristensen JK, Wadskov 5. Penicillamine-induced pemphigus
7. Korman NJ, Eyre RW, Zone J, Stanley JR. Drug-induced pemphigus: autoantibodies directed against the pemphigus antigen complexes are present in penicillamine and captopril-induced
foliaceus. Acta Derm Venereol (Stockh) 1977;57:69-71. 18. PeAas PF, Buezo GF, Carvajal I, Dauden E, Lopez A, Diaz LA. DPenicillamine-induced pemphigus foliaceus with autoantibodies to desmoglein-1 in a patient with mixed connective tissue
pemphigus.J Invest Dermatol 1991;96:273-6. 8. Mobinin N, Ahmed AR. Immunogenetics of drug-induced bullous diseases.Clin Dermatol 1993;11:449-60. 9. Mutasim DF, Pelt NJ, Anhalt GJ. Drug-induced pemphigus.
disease. J Am Acad Dermatol 1997;37:121-3. 19. Steen VD, Blair 5, Medsger TA.The toxicity of o-penicillamine systemic sclerosis. Ann Intern Med 1986;104:699-705.
Dermatol
in
Clin 1993;11:463-71.
Bacillary
angiomatosis by Bartonella in an HIV-infected patient
quintana
Raquel Santos,a Orlando Cardoso,b Paulo Rodrigues,b Jorge Cardoso,a Jo50 Machado,b Ana Afonso,C FAtima Bacellar,d Eric Marston,e and Rui Proenc;ab Lisbon, Portugal, and Atlanta, Georgia Bacillary angiomatosis and bacillaty peliosns are opportunistic infections caused by Bartonella henselae and quintana, which occur in patients with late-stage infection. We report a case of bacillary angiomatosis in an HIV-infected patient with skin, bone, and probably liver involvement, The identification of the agent (B quintana) was done by polymerase chain reaction in the skin specimen. The patient had complete regression of all lesions after a 6-month regimen of oral erythromycin. c’JAm Acad Dermatol
Bartonella
2000;42:299-301.)
From the Departments of Dermatology and Venereology,a Infectious Diseases,b and Pathology,c Hospital Curry Cabral, Lisbon, Centro de Estudos de Vectores e Doencas Infecciosas/lnstituto National de Salide Dr Ricardo Jorge,Aguas de Moura,d and Division ofViral and Rickettsial Diseases,Centers for Disease Control and Prevention,Atlanta.e Reprint requests: Raquel Santos, Service de Dermatologia, Hospital de Curry Cabral, Rua da Beneficiencia, 1069-I 66 Lisboa, Portugal. Copyright 0 2000 by the American Academy of Dermatology, Inc. 0190-9622/2000/$12.00
+ 0
16/54/l
02645
B
acillary angiomatosis and bacillary peliosis are opportunistic infections that were first recognized in 1983 by Stoler et al,l at the beginning of the AIDS epidemic. The causative organisms are Bartonella henselae and B quintana, and the infection occurs in severely immunocompromised patients with late stage HIV infection. The manifestations of Bartonella infection in the