Volume 23 Number 3, Part 1 September 1990 REFERENCES 1. Faure M, Goujon C, Perrot H, et al. Accidents cutanes provoques par Iepiroxicam. A propos de troisobservations. Ann DermatolVenereol (Paris) 1982;109:255-8. 2. Fjellner BO. Photosensitivity induced by piroxicarn. Acta Derm Venereol (Stockh) 1983;63:557-8. 3. Serrano G, Bonillo J, AJiaga A, et aI. Piroxicam-induced photosensitivity. J AM ACAD DERMATOL 1984;11:113-20. 4. Braunstein D L.Dyshydrotic eczemaassociated withpiroxicam photosensitivity. Cutis 1985;35:485-6. 5. Kochevar IE, Morison WL, Lamm JL, et al. Possible mechanism of piroxicam-induced photosensitivity. Arch DermatoI1986;122:1283-7. 6. McKerrow KJ, Greig DE. Piroxieam-induced photosensitive dermatitis. J AM ACAD DERMATOL 1986;15:1237-41.
Piroxicam-induced photosensitivity 7. Figueiredo A, Fontes Ribeiro CA, Goncalo S, et al. Piroxicam-induced photosensitivity, Contact Dermatitis 1987; 17:73-9. 8. Ljunggren B.Propionic acid-derivednon-steroidal antiinflammatory drugsare phototoxic in vitro. Pbotodermatology 1985;2:3·9. 9. Ljunggren B, Lundberg K. In vivo phototoxicity of nonsteroidal anti-inflammatory drugs evaluatedby the mouse tail technique. Photodermatology 1985;2:377-82. 10. Cirne de Castro JL, Vale E, Martins M. Mechanism of photosensitive reactions induced by piroxicam. J AM ACAD DERMATOL 1989;20:706-7.
Human immunodeficiency virus exanthem Hendrik J. Hulsebosch, MD,a Frans A. P. Claessen, MD,b Cornelis J. W. van Ginkel, MD, PhD,a Guus R. R. Kuiters, MD,a Jaap Goudsmit, MD, PhD,c and Joep M. A. Lange, MD, PhDb,c Amsterdam, The Netherlands The hwnan immunodeficiency virus (HIV) exanthem can be the primary manifestation of HIV infection. Wereportthreecases ofanexanthematous skineruption associated with acute HIV infection. HIV antigen (p24coreantigen) waspresent, whereas results of the HIV antibody test were negative. (J AM ACAD DERMATOL 1990;23:483-6.)
Primary human immunodeficiency virus (HIV) infection hasbeendefined by the CentersforDisease Control as a mononucleosis-like illness, with or without asepticmeningitis, associated with seroconversion to HIV antibody.' We have seen three patientswhohad an exanthematous skin eruption, fever, and malaise. Because they were negative for HIV antibodybut positive for HIV antigen (p24 core antigen), a primaryHIV infection was diagnosed. Shortly thereafter, seroconversion to HIV antibody positivity occurred.
From the Departmentsof Dennatology,' Internal Medicine,b and the Human Retrovirus Laboratory, DepartmentofVirology," Academic Medical Centre, University of Amsterdam. Supportedbya grantfromtheHuidstichting Chanfleury vanYsselstein. Acceptedfor publication Dec. 12,1989. Reprint requests: H. J. Hulsebosch, MD, Department of Dermatology, Academic MedicalCentre, Meibergdrcef 9,1105 AZ Amsterdam, The Netherlands. 16/1/18907
CASE REPORTS
Case 1 A 36-year-old homosexual man seronegative for HIV antibody with a history of treatedsyphilis became acutely ill and developed a generalized skineruption. It consisted of round and oval, erythematous macules and papules, some with a hemorrhagic center (Figs. 1 and 2). The mouth contained an enanthem with superficial ulcerations (Fig. 3). Lymphadenopathy was not present. A provisional diagnosis of secondary syphilis was made, and the patient was treated with penicillin. However, serologic tests revealed a Treponema pallidum hemagglutination assay titer of 1:5120 and VDRL of 1:1. Theseresults were compatible with the patient's history oftreated syphilis but not withsecondary syphilis. A test forHIV antibodies (Abbott recombinant HIV-1JHIV-2 enzyme immunoassay, AbbottLaboratories, N. Chicago, Ill.) was negative, but HIV antigen (p24 core antigen) was present. Because of thesefindings, the diagnosis was changed to acute HIV infection with HIV exanthema. Duringthefirst 3days the HIV antigenconcentration increasedandthendeclined.Two weeks laterHIV antigen
483
Journal of the American Academy of Dermatology
484 Hulsebosch et al.
Fig. 1. Case 1. HIV exanthem on chest. Fig. 2. Case 1. Erythematous macules on palm. Fig. 3. Case 1. Enanthema with superficial ulcerations. Fig. 4. Case 1. Lymphocytic perivascular infiltrate in papillary dermis. Slight hydropic degeneration of basal cells with slight exocytosis is seen. (Hematoxylin-eosin stain; X200.) was not demonstrable (Table I). HIV antibodies were detectable 7 days after the first investigation. A skin biopsy specimen showed a lymphocytic perivascular infiltrate in the papillary dermis with some plasma cells. Slight hydropic degeneration of basal cells with slight exocytosis was observed (Fig. 4). Staining for Treponema organisms was negative. Three weeks later all clinical symptoms subsided and all laboratory tests (Table II) except for the HIV antibody test returned to normal.
Case 2 This patient had fever and an exanthem. He is married to a HIV-positive woman from central Africa. Recently they had had several unprotected sexual contacts. The patient had an erythematous maculopapular eruption located predominantly on the upper part of the body (Fig. 5). Some lesions were papulosquamous and had an oval shape; some had a hemorrhagic center. The mouth showed superficial mucosal erosions and a glossitis, and
ulcers were present on the corona of the glans penis. Serologic studies revealed the presence of HIV antigen, but antibodies were lacking (Table I). A skin biopsy specimen revealed lymphohistiocytic infiltrate around blood vessels and adnexae in the papillary dermis as well as extravasation of erythrocytes. The epidermis showed some exocytosis, spongiosis, and parakeratosis (Fig. 6).
Case 3 A 29-year-old homosexual man had had a fever for 1 week. Two days later skin lesions, watery stools, anorexia, and painful swallowing developed. On examination a macular to papular, erythematous eruption was seen, with peripheral desquamation and an occasional hemorrhagic crusting on the cervical region and upper part of the trunk. The palms and soleswere also involved. A marked oral enanthema and an occasional mucosal erosion were also present. His temperature was 40° C. Gastroesophagoscopy revealed a few shallow ul-
Volume 23 Number 3, Part 1 September 1990
HIVexanthem 485
Fig. 5. Case 2. HIV exanthem on chest. Note clear resemblance to secondary syphilis. Fig. 6. Case 2. Lymphohistiocytic perivascular infiltrate with extravasation of erythrocytes. Epidermis shows some exocytosis, spongiosis, and parakeratosis. (Hematoxylin-eosin stain; XI00.)
Table I. Time course of presence in patients' serum of p24 antigen and anti-HIV antibody Case 2
Case 1 AntiDay
It 2 3 4 5 6 7
8 9 10 11 12
p24
HIV
p24
antigen
antibody
antigen
ND
ND ND
+ + + + + + +
+ +
+ + +
13 14 17 23
ND ND
Table II. Main laboratory data in three patients
pa~ent
I
pa~ent
I
pa~ent
Case 3*
AntiHIV antibody
+
Anti-
p24
mv
antigen
antibody
+ ND ND
+ ND ND
ND ND
+ + + + + + + +
+
+
ND ND ND ND ND ND ND
ND ND ND ND ND ND ND
ND ND
ND
ND
+
ND ND ND
ND ND ND
ND ND ND ND ND ND ND
ND ND ND ND ND ND ND
+
ND, Not done. *Case 3 shows a "window phase" during which both tests are negative. [Day of presentation in hospital.
cers in the esophagus, HIV antigen was positive on the day of admittance, but tests for HIV antibodies were negative, HIV p24 soon disappeared, whereas HIV antibodies were demonstrated some 3 weeks later when all clinical signs had disappeared (Table I). A skin biopsy specimen showed edema and a perivascular lymphocytic infiltrate in the papillary dermis with some degeneration of the basal layer. A slight exocytosis,
Syphilis serology TPHA 1:5120; VDRL 1:1 Negative Serologic tests for other viral infections* Leukocytes 5.2 (XI0 9 jL) 0.2 Lymphocytes (XI0 9jL) 73 Thrombocytes
Negative Negative Negative Negative
3.6
2.8
2,0
0.6
40
92
(XI0 9jL) TPHA. Treponema pallidum hemagglutination assay. *Includes tests for cytomegalovirus, Epstein-Barr virus, adenovirus, measles, rubella, and hepatitis B virus.
some dilated capillaries, and some erythrocyte extravasation was observed. DISCUSSION
HIV exanthem is mentioned in many surveys of HIV-associated skin diseases and in clinical descriptions of the primary HIV infection. In these publications the diagnosis of HIV exanthem is retrospective and is based on seroconversion after the clinical manifestations. Cooper et al.,2 in a prospective immunoepidemiologic study of homosexual men, described a mononucleosis-like truncal eruption. They believedthe eruption appeared to be nonspecific, but further immunopathologic studies were needed; only 50% of their patients with primary HIV infection had a rash. In 1986 Lindskov et aI,3 described three
Journal of the American Academy of Dermatology
486 Hulsebosch et al. patients with a maculopapular, roseola-like eruption. In two patients HIV antibody seroconversion was closely related with the acute illness. In the third patient, only seropositivity could be shown, because earlier blood samples were not available. In 1986 Lange Wantzin et a1. 4 gave a more detailed description of the primary HIV infection in three patients. As in our patients, the disease started with general symptoms, followed after several days by a maculopapular, roseola-like exanthem. In one patient the palms and soles were involved. In all of them an enanthema was present; as in our patients, lymph nodes were not involved or were only slightly enlarged. Seroconversion took place about 5 weeks after the onset of the disease. Lange Wantzin did not have an opportunity to detect the presence of HIV antigen in the early stages of the disease. We were able to prove the presence of HIV antigen during the symptomatic phase of primary HIV infection, followed by seroconversion (Table I). Of special interest in case 3 is a "window phase," during which both tests are negative. From this we conclude that tests negative for HIV antibodies and antigen during a suspected symptomatic phase of primary HIV infection do not exclude the diagnosis of primary HIV infection. Tindall et a1. 5 in 1988 reported the results of a prospective study. There were 67 seroconverting patients, of whom 39were interviewed. An acute illness during the period in which they seroconverted was reported by 36 (92.3%) ofthe subjects and by 10 (40%) subjects in a control group of HIV-seronegative homosexuals. A truncal rash was reported by 11 seroconverters (28.2%) and by no one in the control group. Data about the skin eruption were not given. The overall conclusion was that primary HIV infection gives rise to a mononucleosis-like clinical picture. HIV antigen testing was not performed in this study. The authors mention that host response might be determined by dose of virus inoculation, other concomitant viral infections, history of past viral infections, and/or the efficacy of the person's immune response. In addition, the virulence of the infecting virus strain may playa role. This possibly explains w.hy not all seroconversions are accompanied by a rash. In a report of three needlestick accidents in health care workers leading to seroconversion, no skin manifestations were mentioned.f Our description of the rash in primary HIV infection includes round or oval erythematous macules and papules, with or without desquamation, sometimes with a hemorrhagic or necrotic center,
disseminated on the upper part ofthe body or on the whole body, palms and soles included, in a pattern comparable to secondary syphilis. Because of this, and because HIV infection , like syphilis, is sexually transmitted and patient histories will reveal highrisk sexual behavior, secondary syphilis is the main differential diagnosis of the HIV exanthem. The designation "mononucleosis-like" for the primary HIV infection is adequate for both the clinical symptoms and the rash, according to the description by Katz and Andima.? However, in mononucleosis the enanthema is petechial and not ulcerative as in our three patients. Besides the exanthem and enanthema, manifestations of primary HIV infection include fever, lymphadenopathy, lymphopenia, thrombocytopenia, gastrointestinal symptoms, muscle and joint pains, pneumonitis, hepatitis, electrocardiographic disturbances, and central nervous system symptoms such as meningitis, encephalitis, and neuropathy. 8 It may be possible that the HIV exanthem is the result of a primary infection of the Langerhans cells in the epidermis, As a CD4+ cell, the Langerhans cell is a target for HIV infection? and viral replication in these cells has been reported.l?
REFERENCES 1. Centers for Disease Control. Classification system for human T-Iymphotropic virus type III/lymphadenopathy-associated virus infection. MMWR 1986;35:334-9. 2. Cooper DA, Maclean P, Finlayson R, et al. Acute AIDS retrovirus infection: definition of a clinical illness with seraconversion. Lancet 1985;1:537-40. 3. Lindskov R, Orskov Lindhardt B, Weismann K, et a1.Acute HTLV-III infection with roseola-like rash [Letter]. Lancet 1986;1:447. 4. Lange Wantzin GR, OrskovLindhart B, Weismann K, et a1. Acute HTLY-III infection associated with exanthema, diagnosed by seroconversion. Br J DermatoI1986;115:601-6 . S. Tindall B, Barker S, Donovan B, et al. Characterization of the acute clinical illness associated with human imrnunodeficiency virus infection. Arch Intern Med 1988;148:945-9. 6. Marcus R , CDC Cooperative Needlestick Surveillance Group. Surveillance of health care workers exposed to blood from patients infected with human immunodeficiency virus . N Eng! J Med 1988;319:1118-23. 7. Katz BZ, Andiman W A. Infectious mononucleosis. In : Fitzpatrick TB, Eisen AZ, Wolff K , et al, eds. Dermatology in general medicine. New York: McGraw-Hill, 1987:2372-5 . 8. Claessen FAP, Goudsmit J, Hulsebosch HJ, et a!. Primaire infecties met het humane immunodeficientie virus. Med Tijdschr Geneesk [In press]. 9. Tschachler E, Groh V, Popovic M, et al. Epidermal Langerhans cells-a target for HTLY-III/LAV infection. J Invest DermatoI1987;88:233-7. 10. Rappersberger K, Gartner S, Schenk P, et a1. Langerhans' cells are an actual site of HIV-I replication. Intervirology 1988;29:185-94.
Piroxicam-induced photosensitivity 7. Figueiredo A, Fontes Ribeiro CA, Goncalo S, et al. Piroxicam-induced photosensitivity, Contact Dermatitis 1987; 17:73-9. 8. Ljunggren B.Propionic acid-derivednon-steroidal antiinflammatory drugsare phototoxic in vitro. Pbotodermatology 1985;2:3·9. 9. Ljunggren B, Lundberg K. In vivo phototoxicity of nonsteroidal anti-inflammatory drugs evaluatedby the mouse tail technique. Photodermatology 1985;2:377-82. 10. Cirne de Castro JL, Vale E, Martins M. Mechanism of photosensitive reactions induced by piroxicam. J AM ACAD DERMATOL 1989;20:706-7.
Human immunodeficiency virus exanthem Hendrik J. Hulsebosch, MD,a Frans A. P. Claessen, MD,b Cornelis J. W. van Ginkel, MD, PhD,a Guus R. R. Kuiters, MD,a Jaap Goudsmit, MD, PhD,c and Joep M. A. Lange, MD, PhDb,c Amsterdam, The Netherlands The hwnan immunodeficiency virus (HIV) exanthem can be the primary manifestation of HIV infection. Wereportthreecases ofanexanthematous skineruption associated with acute HIV infection. HIV antigen (p24coreantigen) waspresent, whereas results of the HIV antibody test were negative. (J AM ACAD DERMATOL 1990;23:483-6.)
Primary human immunodeficiency virus (HIV) infection hasbeendefined by the CentersforDisease Control as a mononucleosis-like illness, with or without asepticmeningitis, associated with seroconversion to HIV antibody.' We have seen three patientswhohad an exanthematous skin eruption, fever, and malaise. Because they were negative for HIV antibodybut positive for HIV antigen (p24 core antigen), a primaryHIV infection was diagnosed. Shortly thereafter, seroconversion to HIV antibody positivity occurred.
From the Departmentsof Dennatology,' Internal Medicine,b and the Human Retrovirus Laboratory, DepartmentofVirology," Academic Medical Centre, University of Amsterdam. Supportedbya grantfromtheHuidstichting Chanfleury vanYsselstein. Acceptedfor publication Dec. 12,1989. Reprint requests: H. J. Hulsebosch, MD, Department of Dermatology, Academic MedicalCentre, Meibergdrcef 9,1105 AZ Amsterdam, The Netherlands. 16/1/18907
CASE REPORTS
Case 1 A 36-year-old homosexual man seronegative for HIV antibody with a history of treatedsyphilis became acutely ill and developed a generalized skineruption. It consisted of round and oval, erythematous macules and papules, some with a hemorrhagic center (Figs. 1 and 2). The mouth contained an enanthem with superficial ulcerations (Fig. 3). Lymphadenopathy was not present. A provisional diagnosis of secondary syphilis was made, and the patient was treated with penicillin. However, serologic tests revealed a Treponema pallidum hemagglutination assay titer of 1:5120 and VDRL of 1:1. Theseresults were compatible with the patient's history oftreated syphilis but not withsecondary syphilis. A test forHIV antibodies (Abbott recombinant HIV-1JHIV-2 enzyme immunoassay, AbbottLaboratories, N. Chicago, Ill.) was negative, but HIV antigen (p24 core antigen) was present. Because of thesefindings, the diagnosis was changed to acute HIV infection with HIV exanthema. Duringthefirst 3days the HIV antigenconcentration increasedandthendeclined.Two weeks laterHIV antigen
483
Journal of the American Academy of Dermatology
484 Hulsebosch et al.
Fig. 1. Case 1. HIV exanthem on chest. Fig. 2. Case 1. Erythematous macules on palm. Fig. 3. Case 1. Enanthema with superficial ulcerations. Fig. 4. Case 1. Lymphocytic perivascular infiltrate in papillary dermis. Slight hydropic degeneration of basal cells with slight exocytosis is seen. (Hematoxylin-eosin stain; X200.) was not demonstrable (Table I). HIV antibodies were detectable 7 days after the first investigation. A skin biopsy specimen showed a lymphocytic perivascular infiltrate in the papillary dermis with some plasma cells. Slight hydropic degeneration of basal cells with slight exocytosis was observed (Fig. 4). Staining for Treponema organisms was negative. Three weeks later all clinical symptoms subsided and all laboratory tests (Table II) except for the HIV antibody test returned to normal.
Case 2 This patient had fever and an exanthem. He is married to a HIV-positive woman from central Africa. Recently they had had several unprotected sexual contacts. The patient had an erythematous maculopapular eruption located predominantly on the upper part of the body (Fig. 5). Some lesions were papulosquamous and had an oval shape; some had a hemorrhagic center. The mouth showed superficial mucosal erosions and a glossitis, and
ulcers were present on the corona of the glans penis. Serologic studies revealed the presence of HIV antigen, but antibodies were lacking (Table I). A skin biopsy specimen revealed lymphohistiocytic infiltrate around blood vessels and adnexae in the papillary dermis as well as extravasation of erythrocytes. The epidermis showed some exocytosis, spongiosis, and parakeratosis (Fig. 6).
Case 3 A 29-year-old homosexual man had had a fever for 1 week. Two days later skin lesions, watery stools, anorexia, and painful swallowing developed. On examination a macular to papular, erythematous eruption was seen, with peripheral desquamation and an occasional hemorrhagic crusting on the cervical region and upper part of the trunk. The palms and soleswere also involved. A marked oral enanthema and an occasional mucosal erosion were also present. His temperature was 40° C. Gastroesophagoscopy revealed a few shallow ul-
Volume 23 Number 3, Part 1 September 1990
HIVexanthem 485
Fig. 5. Case 2. HIV exanthem on chest. Note clear resemblance to secondary syphilis. Fig. 6. Case 2. Lymphohistiocytic perivascular infiltrate with extravasation of erythrocytes. Epidermis shows some exocytosis, spongiosis, and parakeratosis. (Hematoxylin-eosin stain; XI00.)
Table I. Time course of presence in patients' serum of p24 antigen and anti-HIV antibody Case 2
Case 1 AntiDay
It 2 3 4 5 6 7
8 9 10 11 12
p24
HIV
p24
antigen
antibody
antigen
ND
ND ND
+ + + + + + +
+ +
+ + +
13 14 17 23
ND ND
Table II. Main laboratory data in three patients
pa~ent
I
pa~ent
I
pa~ent
Case 3*
AntiHIV antibody
+
Anti-
p24
mv
antigen
antibody
+ ND ND
+ ND ND
ND ND
+ + + + + + + +
+
+
ND ND ND ND ND ND ND
ND ND ND ND ND ND ND
ND ND
ND
ND
+
ND ND ND
ND ND ND
ND ND ND ND ND ND ND
ND ND ND ND ND ND ND
+
ND, Not done. *Case 3 shows a "window phase" during which both tests are negative. [Day of presentation in hospital.
cers in the esophagus, HIV antigen was positive on the day of admittance, but tests for HIV antibodies were negative, HIV p24 soon disappeared, whereas HIV antibodies were demonstrated some 3 weeks later when all clinical signs had disappeared (Table I). A skin biopsy specimen showed edema and a perivascular lymphocytic infiltrate in the papillary dermis with some degeneration of the basal layer. A slight exocytosis,
Syphilis serology TPHA 1:5120; VDRL 1:1 Negative Serologic tests for other viral infections* Leukocytes 5.2 (XI0 9 jL) 0.2 Lymphocytes (XI0 9jL) 73 Thrombocytes
Negative Negative Negative Negative
3.6
2.8
2,0
0.6
40
92
(XI0 9jL) TPHA. Treponema pallidum hemagglutination assay. *Includes tests for cytomegalovirus, Epstein-Barr virus, adenovirus, measles, rubella, and hepatitis B virus.
some dilated capillaries, and some erythrocyte extravasation was observed. DISCUSSION
HIV exanthem is mentioned in many surveys of HIV-associated skin diseases and in clinical descriptions of the primary HIV infection. In these publications the diagnosis of HIV exanthem is retrospective and is based on seroconversion after the clinical manifestations. Cooper et al.,2 in a prospective immunoepidemiologic study of homosexual men, described a mononucleosis-like truncal eruption. They believedthe eruption appeared to be nonspecific, but further immunopathologic studies were needed; only 50% of their patients with primary HIV infection had a rash. In 1986 Lindskov et aI,3 described three
Journal of the American Academy of Dermatology
486 Hulsebosch et al. patients with a maculopapular, roseola-like eruption. In two patients HIV antibody seroconversion was closely related with the acute illness. In the third patient, only seropositivity could be shown, because earlier blood samples were not available. In 1986 Lange Wantzin et a1. 4 gave a more detailed description of the primary HIV infection in three patients. As in our patients, the disease started with general symptoms, followed after several days by a maculopapular, roseola-like exanthem. In one patient the palms and soles were involved. In all of them an enanthema was present; as in our patients, lymph nodes were not involved or were only slightly enlarged. Seroconversion took place about 5 weeks after the onset of the disease. Lange Wantzin did not have an opportunity to detect the presence of HIV antigen in the early stages of the disease. We were able to prove the presence of HIV antigen during the symptomatic phase of primary HIV infection, followed by seroconversion (Table I). Of special interest in case 3 is a "window phase," during which both tests are negative. From this we conclude that tests negative for HIV antibodies and antigen during a suspected symptomatic phase of primary HIV infection do not exclude the diagnosis of primary HIV infection. Tindall et a1. 5 in 1988 reported the results of a prospective study. There were 67 seroconverting patients, of whom 39were interviewed. An acute illness during the period in which they seroconverted was reported by 36 (92.3%) ofthe subjects and by 10 (40%) subjects in a control group of HIV-seronegative homosexuals. A truncal rash was reported by 11 seroconverters (28.2%) and by no one in the control group. Data about the skin eruption were not given. The overall conclusion was that primary HIV infection gives rise to a mononucleosis-like clinical picture. HIV antigen testing was not performed in this study. The authors mention that host response might be determined by dose of virus inoculation, other concomitant viral infections, history of past viral infections, and/or the efficacy of the person's immune response. In addition, the virulence of the infecting virus strain may playa role. This possibly explains w.hy not all seroconversions are accompanied by a rash. In a report of three needlestick accidents in health care workers leading to seroconversion, no skin manifestations were mentioned.f Our description of the rash in primary HIV infection includes round or oval erythematous macules and papules, with or without desquamation, sometimes with a hemorrhagic or necrotic center,
disseminated on the upper part ofthe body or on the whole body, palms and soles included, in a pattern comparable to secondary syphilis. Because of this, and because HIV infection , like syphilis, is sexually transmitted and patient histories will reveal highrisk sexual behavior, secondary syphilis is the main differential diagnosis of the HIV exanthem. The designation "mononucleosis-like" for the primary HIV infection is adequate for both the clinical symptoms and the rash, according to the description by Katz and Andima.? However, in mononucleosis the enanthema is petechial and not ulcerative as in our three patients. Besides the exanthem and enanthema, manifestations of primary HIV infection include fever, lymphadenopathy, lymphopenia, thrombocytopenia, gastrointestinal symptoms, muscle and joint pains, pneumonitis, hepatitis, electrocardiographic disturbances, and central nervous system symptoms such as meningitis, encephalitis, and neuropathy. 8 It may be possible that the HIV exanthem is the result of a primary infection of the Langerhans cells in the epidermis, As a CD4+ cell, the Langerhans cell is a target for HIV infection? and viral replication in these cells has been reported.l?
REFERENCES 1. Centers for Disease Control. Classification system for human T-Iymphotropic virus type III/lymphadenopathy-associated virus infection. MMWR 1986;35:334-9. 2. Cooper DA, Maclean P, Finlayson R, et al. Acute AIDS retrovirus infection: definition of a clinical illness with seraconversion. Lancet 1985;1:537-40. 3. Lindskov R, Orskov Lindhardt B, Weismann K, et a1.Acute HTLV-III infection with roseola-like rash [Letter]. Lancet 1986;1:447. 4. Lange Wantzin GR, OrskovLindhart B, Weismann K, et a1. Acute HTLY-III infection associated with exanthema, diagnosed by seroconversion. Br J DermatoI1986;115:601-6 . S. Tindall B, Barker S, Donovan B, et al. Characterization of the acute clinical illness associated with human imrnunodeficiency virus infection. Arch Intern Med 1988;148:945-9. 6. Marcus R , CDC Cooperative Needlestick Surveillance Group. Surveillance of health care workers exposed to blood from patients infected with human immunodeficiency virus . N Eng! J Med 1988;319:1118-23. 7. Katz BZ, Andiman W A. Infectious mononucleosis. In : Fitzpatrick TB, Eisen AZ, Wolff K , et al, eds. Dermatology in general medicine. New York: McGraw-Hill, 1987:2372-5 . 8. Claessen FAP, Goudsmit J, Hulsebosch HJ, et a!. Primaire infecties met het humane immunodeficientie virus. Med Tijdschr Geneesk [In press]. 9. Tschachler E, Groh V, Popovic M, et al. Epidermal Langerhans cells-a target for HTLY-III/LAV infection. J Invest DermatoI1987;88:233-7. 10. Rappersberger K, Gartner S, Schenk P, et a1. Langerhans' cells are an actual site of HIV-I replication. Intervirology 1988;29:185-94.
