- Email: [email protected]
The Herpetic Whitlow
IN BRIEF
The Herpetic Whitlow James H. Rubright, MD, Adam B. Shafritz, MD infection involving the hand was first reported by H. G. Adamson in 1909.1 Numerous terms for the disease have been used1–5; however, after the seminal article by Stern et al. in 1959,2 the disease became widely known as herpetic whitlow. Whitlow (a synonym of felon) is a misnomer because it implies a suppurative infection of the digital pulp.3,6 – 8 Also, viral vesicles can involve any anatomical region of the hand.2,3,7–9 The lesion is caused by herpes simplex virus (HSV). The 2 types, HSV-1 and HSV-2, have minor serologic differences and their lesions are clinically indistinguishable. Both are alpha herpesviruses: they are rapidly growing and cytolytic, and they can escape immune clearance to establish a dormant state in neural tissue.7 They are members of the larger Herpesviridae family, including varicella zoster, cytomegalovirus, EpsteinBarr, and human herpes viruses 6, 7, and 8.7 Herpes simplex virus is spread by direct contact through mucous membranes or broken epidermis.10 Human beings are the only known natural host.7 Herpes simplex virus-1 causes gingivostomatitis in children and adults. Herpes simplex virus-2 causes herpes genitalis and typically affects sexually active adults or adolescents.3,5,7,8 Herpetic whitlow in children is caused almost exclusively by HSV-1, and in adults it can be caused by HSV-1 or HSV-2.3,8 Herpes infection of the hand predominantly presents in a bimodal age distribution: children younger than 10 years of age and young adults between 20 and 30 years of age.3 Herpes simplex virus has been isolated from the saliva of about 2.5% of normal adults.8 Direct digital contact with secretions or lesions of infected individuals or secretions of asymptomatic carriers of the virus is the likely mechanism of transmission. This
H
ERPES SIMPLEX VIRUS
In Brief
From the Department of Orthopaedic Surgery, University of Vermont College of Medicine, Burlington, VT. Received for publication October 17, 2010; accepted in revised form October 17, 2010. No benefits in any form have been received or will be received related directly or indirectly to the subject of this article. Correspondingauthor:AdamB.Shafritz,MD,DepartmentofOrthopaedicSurgery,Universityof Vermont College of Medicine, 428 Stafford Hall, 95 Carrigan Drive, Burlington, VT 05405; e-mail: [email protected]. 0363-5023/11/36A02-0026$36.00/0 doi:10.1016/j.jhsa.2010.10.014
340 䉬 © Published by Elsevier, Inc. on behalf of the ASSH.
includes autoinoculation.3,10 Herpes infection of the hand in children has been associated with finger sucking in symptomless salivary carriers or children with oral manifestations of the virus.3,8 Herpetic whitlow lesions appear after an incubation period of 2 to 20 days after inoculation7,10 and are associated with intense throbbing pain.2,7 Fever and systemic symptoms are rare. Some patients report history of a flulike prodrome before formation of cutaneous lesions.2,8,11 Regional lymphadenopathy, lymphangitis, dermatomal pain, or pain radiating proximally into the forearm may be present.2,5,7–9 Classically, a single vesicle or cluster of vesicles arises on a single digit after 3 to 4 days of skin irritation or after minor trauma.2,8,10,11 Vesicles are clear or pale yellow and have an erythematous base. They are frequently located on the terminal phalanx of the thumb, index, or long finger near the nail.2,3 More vesicles appear and eventually coalesce to form a cluster or a single bulla. The lesion might resemble a felon or bacterial paronychia.2,3,8,9,11 Unlike the classic felon, however, tension in the pulp space of the affected digit is not increased unless secondary bacterial infection is present.2,7,9 Satellite lesions may spread by outcroppings of fresh vesicles during the first 2 weeks.2,9 This coincides with a window of viral shedding that lasts an average of 12 days and is the period during which patients are most infectious.7 Vesicles usually spread around the paronychial folds but may undermine the nail or spread proximally. After the spread stops, the pain abates and the existing lesions change in appearance. The clear vesicular fluid may become turbid or hemorrhagic. This should not be mistaken for purulence.5,7,8,10,12 The lesions evolve through a period of shallow ulceration, then crusting, and eventually peeling of any remaining dried skin to leave healed epidermis beneath. The natural history of the untreated, uncomplicated herpetic whitlow is complete resolution within 3 weeks.2,6,7,10 –12 Rare complications include systemic viremia, ocular infection, nail dystrophy, nail loss, scarring, and localized hyperesthesia or hypoesthesia.8,10,13
341
After resolution of infection, the herpesvirus seen in varicella zoster infections.7,8,14 This test will passes into a latency phase, inhabiting a host neuidentify 50% to 60% of culture-proven herpetic infecral ganglion. Recurrent infections are triggered by tions.10,14 Lesion fluid specimens or scrapings can be tested for general illness, fever, sun exposure, menstruation, HSV antigen content using 2 commercially available or other physiological or psychological stresrapid viral detection techniques, including direct immusors.7,8 The exact mechanism of recurrence is unknown.7 Patients often can predict episodes of nofluorescent and indirect immunoperoxidase staining. recurrence, noting a 2- to If adequate specimen is colEDUCATIONAL OBJECTIVES 3-day prodrome of mild lected, these tests are specific burning pain, itching, or ● State the different types of herpes viruses. and useful for early detecirritation at the site where ● Summarize the natural history of herpetic whitlow. tion. They correlate with via lesion will erupt.5,7 ● Describe the typical signs and symptoms of herpetic whitlow. ral culture results of speciAbout 20% to 50% of pa- ● mens taken from vesicular Discuss the events leading to a latency phase of herpetic infection. tients experience recurlesions in 70% to 80% of ● List the diagnostic tests used to confirm herpetic infection. rences.7,8,10 Subsequent cases.7 Because viral shed● Discuss the role of pharmacologic treatment and surgery in the manageattacks are usually milder ding occurs early, a less mament of herpetic whitlow. and shorter in duration ture vesicular lesion is more than the primary infec- Earn up to 2 hours of CME credit per JHS issue when you read the related likely to yield a positive test tion.2,3,7,8,12 They can oc- articles and take an online test. To pay the $20 fee and take this month’s test, result than an older lesion.14 Because the course of pricur at regular or irregular visit http://www.assh.org/professionals/jhs. mary and recurrent herpetic intervals and may erupt at whitlow infection is self-limthe site of original infecited, surgical intervention is unnecessary.2,5,7–12 Treattion or involve a new site. Herpes simplex virus-2 infections may be more likely than HSV-1 infecment is symptomatic and consists of immobilization, 3 tions to recur. Immunosuppressed patients are at a elevation, and analgesia. Dry dressings are preferred to decrease viral spread.2,8 greater risk of more frequent and more severe HSV 7 recurrences, including disseminated infection. Antiviral pharmacological therapy may be benefi12 cial. Acyclovir, an acyclic nucleoside analogue of Diagnosis of herpetic whitlow is clinical. If the guanosine,5,15 kills herpes viruses by causing irreparadiagnosis is unclear, diagnostic tests can include viral culture, serum antibody titers, Tzanck smear, and lesion ble DNA damage.5 It has been used to treat herpes virus 5,7,14 specimen antigen detection. infections since it was introduced in 1982.5,7 Acyclovir is selectively activated in infected cells and has little or Viral culture is the most sensitive diagnostic test8,14 no toxic effect on normal cells.5,7 About 10% to 15% of and allows viral typing to determine presence of HSV-1 3 14 or HSV-2. Positive cultures are noted at 1 to 4 days. the HSV population is a thymidine-kinase– deficient strain that is resistant to acyclovir.5,16 The clinical imSerum antibody titers to HSV are diagnostic but require patient blood sampling at presentation and 3 weeks portance of resistant strains is unknown.15 12 thereafter. Neither culture nor serum titers allow rapid Topical 5% acyclovir antiviral cream shortens the duration of lesions in patients with herpes labialis and confirmation of the diagnosis, and they are of limited genitalis but has not been studied specifically in herutility when timely distinction between a suppurative petic whitlow.7 process and a viral process is needed.8,12 The Tzanck smear is performed by taking scrapings Data have shown that 200 mg of acyclovir taken with a scalpel from the base of an unroofed vesicle or an orally 3 to 4 times daily prevents or greatly decreases ulceration debrided of crust.8,9,11,14 When unroofing a recurrence rates in cases of culture-proven herpetic whitlow and other nongenital manifestations of vesicle, the pulp space is avoided. A nonpurulent fluid HSV.15,16 It is well tolerated with few side effects15,16 will be released from vesicles, and the underlying tissue will have a honeycomb appearance.2,11 This observaand can be administered for up to 2 years.15,17 The 6,11 tion can be diagnostic. prophylactic effect is only present during the treatment A smear is then made by period and applies to immunocompetent patients.15,16 spreading the scrapings onto a glass slide and staining them with Toluidine blue.5,7,8,10 Presence of multinuIntermittent suppressive therapy is ineffective.17 A total cleated epithelial giant cells on light microscopy supdaily dose of 1,600 to 2,000 mg of acyclovir given ports the diagnosis.8,14 The Tzanck test is not specific orally at the outset of prodromal symptoms of recurrent disease can prevent or shorten the duration of sympfor HSV because multinucleated giant cells can also be JHS 䉬 Vol A, February
In Brief
THE HERPETIC WHITLOW
342
THE HERPETIC WHITLOW
In Brief
toms and viral shedding. The dose and duration of treatment have not been optimized.4,7,17,18 There has been some concern that acyclovir treatment could lead to bone marrow suppression7 but the adverse effects of prolonged administration is unknown.15 Intravenous acyclovir is occasionally required in cases of immunosuppression and disseminated HSV infection but is not recommended for routine use in immunocompetent patients.7 The literature contains several case reports of complications resulting from misdiagnosed herpetic whitlow treated with incision and attempted drainage.5,6,9,11 Incision will not yield drainage because the deep pulp space is not involved unless it is iatrogenically violated.2,6,12 Secondary bacterial infection, most often staphylococcal,2,9 can result in amputation, systemic infection, and viral meningoencephalitis.5,8,10,11 Several points bear repeat mention: (1) herpetic whitlow in children is caused almost exclusively by HSV-1 and in adults can be caused by HSV-1 or HSV-2. (2) The initially clear vesicular fluid may become turbid or hemorrhagic. This should not, however, be mistaken for purulence. (3) Lesion fluid specimens or scrapings can be tested for HSV antigen content using commercially direct immunofluorescent or indirect immunoperoxidase staining techniques. If adequate specimen is collected, these tests are useful for the early detection of HSV in up to 80% of cases. (4) A total daily dose of 1,600 to 2,000 mg acyclovir given orally at the outset of the prodromal symptoms of recurrence may prevent or shorten the duration of symptoms and viral shedding. (5) Primary and recurrent herpetic whit-
low is self-limited, treatment is supportive, and surgery is not indicated. REFERENCES 1. Adamson HG. Herpes febrilis attacking the fingers. Br J Dermatol 1909;21:323–324. 2. Stern H, Elek SD, Millar DM, Anderson HF. Herpetic whitlow: a form of cross-infection in hospitals. Lancet 1959;2:871– 874. 3. Gill MJ, Arlette J, Buchan K. Herpes simplex virus infection of the hand. Am J Med 1988;84:89 –93. 4. Gill MJ, Arlette J, Buchan K, Tyrell DL. Therapy for recurrent herpetic whitlow. Ann Intern Med 1986;105:631. 5. Hurst LC, Gluck R, Sampson SP, Dowd A. Herpetic whitlow with bacterial abscess. J Hand Surg 1991;16A:311–314. 6. Carter S. Herpetic whitlow: herpetic infection of the digits. Invited comments. J Hand Surg 1979;4:93–94. 7. Fowler JR. Viral infections. Hand Clin 1989;5:613– 622. 8. Feder HM, Long SS. Herpetic whitlow: clinical characteristics, diagnosis, and treatment. Am J Dis Child 1983;137:861– 863. 9. Weinstein L, Artenstein MS, Plaut ME. Herpes simplex virus infection of fingers (herpetic whitlow). BMQ 1962;13:103–106. 10. Haedicke GJ, Grossman AI, Fisher AE. Herpetic whitlow of the digits. J Hand Surg 1989;14B:443– 446. 11. Carter S, Mersheimer WL. Infections of the hand. Orthop Clin North Am 1970;3:455– 466. 12. Louis D, Silva JJ. Herpetic whitlow: herpetic infection of the digits. J Hand Surg 1979;4:90 –93. 13. Wu IB, Schwartz RA. Herpetic whitlow. Cutis 2007;79:193–196. 14. Solomon AR, Rasmussen JE, Varani J, Pierson CL. The Tzanck smear in the diagnosis of cutaneous herpes simplex. JAMA 1984; 251:633– 635. 15. Laskin OL. Acyclovir and suppression of frequently recurring herpetic whitlow. Ann Intern Med 1985;102:494 – 495. 16. Thomas RHM, Dodd HJ, Yeo JM, Kirby JDT. Oral acyclovir in the suppression of recurrent non-genital herpes simplex virus infection. Br J Dermatol 1985;113:731–735. 17. Krusinski PA. Treatment of mucocutaneous herpes simplex infections with acyclovir. J Am Acad Dermatol 1988;18:179 –181. 18. Gill MJ, Bryant HE. Oral acyclovir therapy of recurrent herpes simplex virus type 2 infection of the hand. Antimicrob Agents Chemother 1991;35:382–383.
JOURNAL CME QUESTIONS The Herpetic Whitlow Which herpes simplex virus uniformly causes herpetic whitlow in children? a. Herpes simplex virus-1 b. Herpes simplex virus-2 c. Herpes simplex virus-1 or Herpes simplex virus-2 d. Herpes simplex virus-6 e. All of the above
What is the natural history of untreated herpetic whitlow? a. Ongoing viral shedding for 3 weeks b. Complete resolution within 3 weeks c. Period of systemic viremia followed by resolution d. Nail dystrophy e. Permanent scarring
To take the online test and receive CME credit, go to http://www.assh.org/professionals/jhs.
JHS 䉬 Vol A, February
The Herpetic Whitlow James H. Rubright, MD, Adam B. Shafritz, MD infection involving the hand was first reported by H. G. Adamson in 1909.1 Numerous terms for the disease have been used1–5; however, after the seminal article by Stern et al. in 1959,2 the disease became widely known as herpetic whitlow. Whitlow (a synonym of felon) is a misnomer because it implies a suppurative infection of the digital pulp.3,6 – 8 Also, viral vesicles can involve any anatomical region of the hand.2,3,7–9 The lesion is caused by herpes simplex virus (HSV). The 2 types, HSV-1 and HSV-2, have minor serologic differences and their lesions are clinically indistinguishable. Both are alpha herpesviruses: they are rapidly growing and cytolytic, and they can escape immune clearance to establish a dormant state in neural tissue.7 They are members of the larger Herpesviridae family, including varicella zoster, cytomegalovirus, EpsteinBarr, and human herpes viruses 6, 7, and 8.7 Herpes simplex virus is spread by direct contact through mucous membranes or broken epidermis.10 Human beings are the only known natural host.7 Herpes simplex virus-1 causes gingivostomatitis in children and adults. Herpes simplex virus-2 causes herpes genitalis and typically affects sexually active adults or adolescents.3,5,7,8 Herpetic whitlow in children is caused almost exclusively by HSV-1, and in adults it can be caused by HSV-1 or HSV-2.3,8 Herpes infection of the hand predominantly presents in a bimodal age distribution: children younger than 10 years of age and young adults between 20 and 30 years of age.3 Herpes simplex virus has been isolated from the saliva of about 2.5% of normal adults.8 Direct digital contact with secretions or lesions of infected individuals or secretions of asymptomatic carriers of the virus is the likely mechanism of transmission. This
H
ERPES SIMPLEX VIRUS
In Brief
From the Department of Orthopaedic Surgery, University of Vermont College of Medicine, Burlington, VT. Received for publication October 17, 2010; accepted in revised form October 17, 2010. No benefits in any form have been received or will be received related directly or indirectly to the subject of this article. Correspondingauthor:AdamB.Shafritz,MD,DepartmentofOrthopaedicSurgery,Universityof Vermont College of Medicine, 428 Stafford Hall, 95 Carrigan Drive, Burlington, VT 05405; e-mail: [email protected]. 0363-5023/11/36A02-0026$36.00/0 doi:10.1016/j.jhsa.2010.10.014
340 䉬 © Published by Elsevier, Inc. on behalf of the ASSH.
includes autoinoculation.3,10 Herpes infection of the hand in children has been associated with finger sucking in symptomless salivary carriers or children with oral manifestations of the virus.3,8 Herpetic whitlow lesions appear after an incubation period of 2 to 20 days after inoculation7,10 and are associated with intense throbbing pain.2,7 Fever and systemic symptoms are rare. Some patients report history of a flulike prodrome before formation of cutaneous lesions.2,8,11 Regional lymphadenopathy, lymphangitis, dermatomal pain, or pain radiating proximally into the forearm may be present.2,5,7–9 Classically, a single vesicle or cluster of vesicles arises on a single digit after 3 to 4 days of skin irritation or after minor trauma.2,8,10,11 Vesicles are clear or pale yellow and have an erythematous base. They are frequently located on the terminal phalanx of the thumb, index, or long finger near the nail.2,3 More vesicles appear and eventually coalesce to form a cluster or a single bulla. The lesion might resemble a felon or bacterial paronychia.2,3,8,9,11 Unlike the classic felon, however, tension in the pulp space of the affected digit is not increased unless secondary bacterial infection is present.2,7,9 Satellite lesions may spread by outcroppings of fresh vesicles during the first 2 weeks.2,9 This coincides with a window of viral shedding that lasts an average of 12 days and is the period during which patients are most infectious.7 Vesicles usually spread around the paronychial folds but may undermine the nail or spread proximally. After the spread stops, the pain abates and the existing lesions change in appearance. The clear vesicular fluid may become turbid or hemorrhagic. This should not be mistaken for purulence.5,7,8,10,12 The lesions evolve through a period of shallow ulceration, then crusting, and eventually peeling of any remaining dried skin to leave healed epidermis beneath. The natural history of the untreated, uncomplicated herpetic whitlow is complete resolution within 3 weeks.2,6,7,10 –12 Rare complications include systemic viremia, ocular infection, nail dystrophy, nail loss, scarring, and localized hyperesthesia or hypoesthesia.8,10,13
341
After resolution of infection, the herpesvirus seen in varicella zoster infections.7,8,14 This test will passes into a latency phase, inhabiting a host neuidentify 50% to 60% of culture-proven herpetic infecral ganglion. Recurrent infections are triggered by tions.10,14 Lesion fluid specimens or scrapings can be tested for general illness, fever, sun exposure, menstruation, HSV antigen content using 2 commercially available or other physiological or psychological stresrapid viral detection techniques, including direct immusors.7,8 The exact mechanism of recurrence is unknown.7 Patients often can predict episodes of nofluorescent and indirect immunoperoxidase staining. recurrence, noting a 2- to If adequate specimen is colEDUCATIONAL OBJECTIVES 3-day prodrome of mild lected, these tests are specific burning pain, itching, or ● State the different types of herpes viruses. and useful for early detecirritation at the site where ● Summarize the natural history of herpetic whitlow. tion. They correlate with via lesion will erupt.5,7 ● Describe the typical signs and symptoms of herpetic whitlow. ral culture results of speciAbout 20% to 50% of pa- ● mens taken from vesicular Discuss the events leading to a latency phase of herpetic infection. tients experience recurlesions in 70% to 80% of ● List the diagnostic tests used to confirm herpetic infection. rences.7,8,10 Subsequent cases.7 Because viral shed● Discuss the role of pharmacologic treatment and surgery in the manageattacks are usually milder ding occurs early, a less mament of herpetic whitlow. and shorter in duration ture vesicular lesion is more than the primary infec- Earn up to 2 hours of CME credit per JHS issue when you read the related likely to yield a positive test tion.2,3,7,8,12 They can oc- articles and take an online test. To pay the $20 fee and take this month’s test, result than an older lesion.14 Because the course of pricur at regular or irregular visit http://www.assh.org/professionals/jhs. mary and recurrent herpetic intervals and may erupt at whitlow infection is self-limthe site of original infecited, surgical intervention is unnecessary.2,5,7–12 Treattion or involve a new site. Herpes simplex virus-2 infections may be more likely than HSV-1 infecment is symptomatic and consists of immobilization, 3 tions to recur. Immunosuppressed patients are at a elevation, and analgesia. Dry dressings are preferred to decrease viral spread.2,8 greater risk of more frequent and more severe HSV 7 recurrences, including disseminated infection. Antiviral pharmacological therapy may be benefi12 cial. Acyclovir, an acyclic nucleoside analogue of Diagnosis of herpetic whitlow is clinical. If the guanosine,5,15 kills herpes viruses by causing irreparadiagnosis is unclear, diagnostic tests can include viral culture, serum antibody titers, Tzanck smear, and lesion ble DNA damage.5 It has been used to treat herpes virus 5,7,14 specimen antigen detection. infections since it was introduced in 1982.5,7 Acyclovir is selectively activated in infected cells and has little or Viral culture is the most sensitive diagnostic test8,14 no toxic effect on normal cells.5,7 About 10% to 15% of and allows viral typing to determine presence of HSV-1 3 14 or HSV-2. Positive cultures are noted at 1 to 4 days. the HSV population is a thymidine-kinase– deficient strain that is resistant to acyclovir.5,16 The clinical imSerum antibody titers to HSV are diagnostic but require patient blood sampling at presentation and 3 weeks portance of resistant strains is unknown.15 12 thereafter. Neither culture nor serum titers allow rapid Topical 5% acyclovir antiviral cream shortens the duration of lesions in patients with herpes labialis and confirmation of the diagnosis, and they are of limited genitalis but has not been studied specifically in herutility when timely distinction between a suppurative petic whitlow.7 process and a viral process is needed.8,12 The Tzanck smear is performed by taking scrapings Data have shown that 200 mg of acyclovir taken with a scalpel from the base of an unroofed vesicle or an orally 3 to 4 times daily prevents or greatly decreases ulceration debrided of crust.8,9,11,14 When unroofing a recurrence rates in cases of culture-proven herpetic whitlow and other nongenital manifestations of vesicle, the pulp space is avoided. A nonpurulent fluid HSV.15,16 It is well tolerated with few side effects15,16 will be released from vesicles, and the underlying tissue will have a honeycomb appearance.2,11 This observaand can be administered for up to 2 years.15,17 The 6,11 tion can be diagnostic. prophylactic effect is only present during the treatment A smear is then made by period and applies to immunocompetent patients.15,16 spreading the scrapings onto a glass slide and staining them with Toluidine blue.5,7,8,10 Presence of multinuIntermittent suppressive therapy is ineffective.17 A total cleated epithelial giant cells on light microscopy supdaily dose of 1,600 to 2,000 mg of acyclovir given ports the diagnosis.8,14 The Tzanck test is not specific orally at the outset of prodromal symptoms of recurrent disease can prevent or shorten the duration of sympfor HSV because multinucleated giant cells can also be JHS 䉬 Vol A, February
In Brief
THE HERPETIC WHITLOW
342
THE HERPETIC WHITLOW
In Brief
toms and viral shedding. The dose and duration of treatment have not been optimized.4,7,17,18 There has been some concern that acyclovir treatment could lead to bone marrow suppression7 but the adverse effects of prolonged administration is unknown.15 Intravenous acyclovir is occasionally required in cases of immunosuppression and disseminated HSV infection but is not recommended for routine use in immunocompetent patients.7 The literature contains several case reports of complications resulting from misdiagnosed herpetic whitlow treated with incision and attempted drainage.5,6,9,11 Incision will not yield drainage because the deep pulp space is not involved unless it is iatrogenically violated.2,6,12 Secondary bacterial infection, most often staphylococcal,2,9 can result in amputation, systemic infection, and viral meningoencephalitis.5,8,10,11 Several points bear repeat mention: (1) herpetic whitlow in children is caused almost exclusively by HSV-1 and in adults can be caused by HSV-1 or HSV-2. (2) The initially clear vesicular fluid may become turbid or hemorrhagic. This should not, however, be mistaken for purulence. (3) Lesion fluid specimens or scrapings can be tested for HSV antigen content using commercially direct immunofluorescent or indirect immunoperoxidase staining techniques. If adequate specimen is collected, these tests are useful for the early detection of HSV in up to 80% of cases. (4) A total daily dose of 1,600 to 2,000 mg acyclovir given orally at the outset of the prodromal symptoms of recurrence may prevent or shorten the duration of symptoms and viral shedding. (5) Primary and recurrent herpetic whit-
low is self-limited, treatment is supportive, and surgery is not indicated. REFERENCES 1. Adamson HG. Herpes febrilis attacking the fingers. Br J Dermatol 1909;21:323–324. 2. Stern H, Elek SD, Millar DM, Anderson HF. Herpetic whitlow: a form of cross-infection in hospitals. Lancet 1959;2:871– 874. 3. Gill MJ, Arlette J, Buchan K. Herpes simplex virus infection of the hand. Am J Med 1988;84:89 –93. 4. Gill MJ, Arlette J, Buchan K, Tyrell DL. Therapy for recurrent herpetic whitlow. Ann Intern Med 1986;105:631. 5. Hurst LC, Gluck R, Sampson SP, Dowd A. Herpetic whitlow with bacterial abscess. J Hand Surg 1991;16A:311–314. 6. Carter S. Herpetic whitlow: herpetic infection of the digits. Invited comments. J Hand Surg 1979;4:93–94. 7. Fowler JR. Viral infections. Hand Clin 1989;5:613– 622. 8. Feder HM, Long SS. Herpetic whitlow: clinical characteristics, diagnosis, and treatment. Am J Dis Child 1983;137:861– 863. 9. Weinstein L, Artenstein MS, Plaut ME. Herpes simplex virus infection of fingers (herpetic whitlow). BMQ 1962;13:103–106. 10. Haedicke GJ, Grossman AI, Fisher AE. Herpetic whitlow of the digits. J Hand Surg 1989;14B:443– 446. 11. Carter S, Mersheimer WL. Infections of the hand. Orthop Clin North Am 1970;3:455– 466. 12. Louis D, Silva JJ. Herpetic whitlow: herpetic infection of the digits. J Hand Surg 1979;4:90 –93. 13. Wu IB, Schwartz RA. Herpetic whitlow. Cutis 2007;79:193–196. 14. Solomon AR, Rasmussen JE, Varani J, Pierson CL. The Tzanck smear in the diagnosis of cutaneous herpes simplex. JAMA 1984; 251:633– 635. 15. Laskin OL. Acyclovir and suppression of frequently recurring herpetic whitlow. Ann Intern Med 1985;102:494 – 495. 16. Thomas RHM, Dodd HJ, Yeo JM, Kirby JDT. Oral acyclovir in the suppression of recurrent non-genital herpes simplex virus infection. Br J Dermatol 1985;113:731–735. 17. Krusinski PA. Treatment of mucocutaneous herpes simplex infections with acyclovir. J Am Acad Dermatol 1988;18:179 –181. 18. Gill MJ, Bryant HE. Oral acyclovir therapy of recurrent herpes simplex virus type 2 infection of the hand. Antimicrob Agents Chemother 1991;35:382–383.
JOURNAL CME QUESTIONS The Herpetic Whitlow Which herpes simplex virus uniformly causes herpetic whitlow in children? a. Herpes simplex virus-1 b. Herpes simplex virus-2 c. Herpes simplex virus-1 or Herpes simplex virus-2 d. Herpes simplex virus-6 e. All of the above
What is the natural history of untreated herpetic whitlow? a. Ongoing viral shedding for 3 weeks b. Complete resolution within 3 weeks c. Period of systemic viremia followed by resolution d. Nail dystrophy e. Permanent scarring
To take the online test and receive CME credit, go to http://www.assh.org/professionals/jhs.
JHS 䉬 Vol A, February