Download Inoculation Herpes Simplex Virus Infections in Patients with AIDS

141
Inoculation Herpes Simplex Virus Infections in Patients with AIDS: Unusual
Appearance and Location of Lesions
Gayle Weaver and Jay R. Kostman
From the Section of Infectious Diseases, Temple University Health
Sciences Center, Philadelphia, Pennsylvania
Two patients with AIDS developed protracted infection due to autoinoculation of herpes simplex
virus in the great toe and the external ear, respectively, both unusual areas for inoculation. The
appearances of the lesions were also unusual; severe hyperkeratosis was noted in both cases and a
mass lesion in the external ear in one case. Both patients' conditions responded to acyclovir, although
one patient required amputation of a digit due to intractable pain. In each case, the diagnosis was
delayed despite the presence of mucocutaneous lesions, resulting in inappropriate treatment and
prolonged discomfort. Inoculation disease due to herpes simplex virus should be suspected in patients
with AIDS who have unusual skin lesions, particularly if oral and/or perianal lesions are also
present.
Recurrent and persistent herpes simplex virus (HSV) infections are common occurrences in HIV-infected patients [1-3].
In these patients, herpetic whitlow can be atypical, with the
appearance of hyperkeratosis or gangrene [4-6]. The unusual
appearance may lead to misdiagnosis and improper treatment
resulting in prolonged discomfort and consideration of amputation. We describe two cases of severe herpetic whitlow with
atypical appearances and secondary sites of inoculation that
involved patients with AIDS.
Case Reports
Case 1
A 24-year-old male with AIDS (CD4 lymphocyte count,
15/mm3) and a history of injection drug use developed painful,
swollen, tender fingers and lesions on his left nasolabial fold
and lower lip. Incision and drainage of the digital lesions resulted only in intensified pain and swelling. Subsequently, he
noted increasingly painful swelling of his left great toe. The
patient reported biting at his fingers and picking at them with
the needles he used to inject drugs but denied rectal intercourse
and a history ofherpetic lesions. Physical examination revealed
crusting lesions on his left nasolabial fold and lower lip; hyperkeratotic, tender lesions with necrotic fissured crusts on multiple digits; a l-cm perianal ulcer; and a swollen, erythematous,
tender left great toe with purulent drainage.
Therapy with intravenous acyclovir was begun for presumed
HSV infection with herpetic whitlow. Viral cultures of the lip
and toe lesions were positive for HSV type I, whereas the
Received 13 April 1995; revised 27 July 1995.
Reprints or correspondence: Dr. Jay R. Kostman, Sectionof Infectious Diseases,TempleUniversity Hospital, Suite500,Parkinson Pavilion, Philadelphia,
Pennsylvania 19140.
Clinical Infectious Diseases 1996; 22:141-2
© 1996 by The University of Chicago. All rights reserved.
1058-4838/96/2201-0024$02.00
perianal lesion yielded HSV type 2. The facial and rectal lesions
cleared after 5 days of therapy. The finger and toe lesions were
less painful by that time, and there was visible improvement
in the hyperkeratosis by 12 days. The patient completed a 21day course of therapy with acyclovir, and 2 weeks later the
digital lesions had resolved.
Case 2
A 23-year-old HIV-seropositive man had serous drainage
from his right ear and an ulcerated hyperkeratotic lesion on
his left index finger. Over a month, an ulcerated lesion developed on the superior aspect of the pinna of the right ear and
extended to the scalp, the auditory canal, and the entire external
ear; there was decreased hearing in the right ear on a bedside
examination. The patient noted that he used his index finger
to clean his ear. There were no perianal, genital, or oral ulcers.
CT examination of the temporal bones revealed a soft-tissue
density in the external canal, with opacification of the mastoid
air cells (figure I). After no response following I week of
treatment with intravenous cefazolin, a biopsy of the right ear
lesion revealed ulcerated skin and granulation tissue and cytological changes consistent with viral infection, and a viral culture was positive for HSV type 2. After 2 weeks of therapy
with intravenous acyclovir (10 mglkg every 8 hours), the drainage had ceased, the ulceration had healed, and the external
canal had cleared. The finger lesion became increasingly painful, and the ulceration did not change with administration of
intravenous acyclovir. An amputation was performed at the
distal interphalangeal joint, and culture of the interoperative
specimen yielded HSV type 2. The patient continued to receive
oral acyclovir (400 mg twice a day) and died ofCNS toxoplasmosis 9 months later.
Discussion
Cutaneous inoculation of HSV from mucosal lesions can
occur at sites of damaged skin other than the digit [7- 9].
142
Weaver and Kostman
em
1996;22 (January)
did not occur without antiviral therapy. A course of acyclovir
should certainly be attempted prior to consideration of amputation. A longer duration of therapy may be required for resolution of digital or other cutaneous lesions as compared to that
required for resolution of oral, rectal, or genital lesions (as in
patient I). The failure of the treatment administered to patient
2 may have been due to an acyclovir-resistant virus, although
the concurrent ear lesion resolved and antiviral susceptibility
tests were not performed.
In conclusion, in HIV-infected patients inoculation of distant
cutaneous sites with HSV may result in unusual-appearing lesions in atypical sites. The diagnosis of herpetic infection
should be considered on the basis of the appearance of more
typical herpetic lesions that may also be present. In contrast to
treatment of whitlow in immunocompetent patients, antiviral
therapy appears to be necessary for resolution of the lesions.
For resolution of digital and cutaneous lesions, a longer course
of therapy may be required than for coexisting oral, genital, or
rectal lesions. Amputation should be considered only if there
is intractable pain after a prolonged course of therapy. Failure
of acyclovir therapy administered to an HIV-infected patient
with refractory herpetic whitlow may suggest acyclovir-resistant HSV infection.
Acknowledgments
The authors thank Dr. Bennett Lorber for critical review of the
manuscriptand Ms. Marilyn Selcovitzfor assistance in manuscript
preparation.
Figure 1. A CT scan of the head of patient 2 reveals extensive
soft-tissue swelling of the pinna of the right ear and mass extension
into the auditory canal (arrow).
Recurrent eruptions are usually self-limited. In our patients,
nonhealing lesions were present in unusual locations. The purulence seen in the great toe of patient 1 and the ulcerated mass
on the external ear of patient 2 resulted from inoculation of
virus from typical HSV lesions.
The diagnosis of herpetic whitlow is suggested clinically
and can be confirmed by direct fluorescent antibody staining,
viral culture, and biopsy with histologic examination. The presence of oral or genital lesions should lead to the consideration
of HSV as the causative agent of unusual cutaneous lesions in
HIV-infected patients (patient 1), although mucous membrane
lesions may not always be present (patient 2). Aspiration or
swabbing of the lesion for viral culture or antibody staining
should be considered early to obviate the need for biopsy of
this already extremely painful lesion.
In the HIV-negative patient, antiviral therapy is not required
for the resolution of whitlow. However, in our cases, resolution
References
1. Siegal FP, Lopez C, Hammer GS, et a1. Severe acquired immunodeficiency
in male homosexuals, manifested by chronic perianal ulcerative herpes
simplex lesions. N Eng1 J Med 1981;305:1439-44.
2. Chatis PA, Miller CH, Schrager LE, Crumpacker CS. Successful treatment
with foscarnet of an acyclovir-resistant mucocutaneous infection with
herpes simplex virus in a patient with acquired immunodeficiency syndrome. N Engl J Med 1989;320:297-300.
3. Erlich KS, Mills J, Chatis P, et a1. Acyclovir-resistant herpes simplex virus
infections in patients with acquired immunodeficiency syndrome. N Engl
J Med 1989;320:293-6.
4. Baden LA, Bigby M, Kwan T. Persistent necrotic digits in a patient with
the acquired immunodeficiency syndrome. Arch Dermatol1991; 127:113,
116.
5. Norris SA, Kessler HA, Fife KH. Severe, progressive herpetic whitlow
caused by an acyclovir-resistant virus in a patient with AIDS [letter]. J
Infect Dis 1988; 157:209-10.
6. Zuretti AJ, Schwartz IS. Gangrenous herpetic whitlow in a human immunodeficiency virus-positive patient. Am J Clin Patholl990;93:828-30.
7. Selling B, Kibrick S. An outbreak of herpes simplex among wrestlers
(herpes gladiatorum). N Engl J Med 1964;270:979-82.
8. White WE, Grant-Kels JM. Transmission of herpes simplex virus type 1
infection in rugby players. JAMA 1984;252:533-5.
9. Feder HM Jr, White WE. Herpes simplex virus infections [letter]. N Engl
J Med 1987;316:754-5.