Herpetic Whitlow

Herpetic whitlow is an intensely painful infection of the hand involving 1 or more fingers that typically affects the terminal phalanx.[1, 2]  Herpes simplex virus 1 (HSV-1) is the cause in approximately 60% of cases of herpetic whitlow, and herpes simplex virus 2 (HSV-2) is the cause in the remaining 40%.

Adamson first described herpetic whitlow in 1909, and in 1959, it was noted to be an occupational risk among health care workers.[2, 3]

As in other mucocutaneous herpetic infections, herpetic whitlow is initiated by viral inoculation of the host through exposure to infected body fluids via a break in the skin, most commonly a torn cuticle. The virus then invades the cells of the dermis and subcutaneous tissue, and clinical infection ensues within a matter of days.[2, 4]

In children, HSV-1 is the most likely causative agent. Infection involving the finger usually is due to autoinoculation from primary oropharyngeal lesions as a result of finger-sucking or thumb-sucking behavior in patients with herpes labialis or herpetic gingivostomatitis.

Similarly, in health care workers, infection with HSV-1 is more common and usually is secondary to unprotected exposure to infected oropharyngeal secretions of patients. This easily can be prevented by use of gloves and by scrupulous observation of universal fluid precautions.

In the general adult population, herpetic whitlow is most often due to autoinoculation from genital herpes; therefore, it is most frequently secondary to infection with HSV-2.

Subsequent to the initial exposure, an incubation period of 2-20 days is common. Although a prodrome of fever and malaise may be observed, most often initial symptoms are pain and burning or tingling of the infected digit. This usually is followed by erythema, edema, and the development of 1- to 3-mm grouped vesicles on an erythematous base over the next 7-10 days. These vesicles may ulcerate or rupture and usually contain clear fluid, although the fluid may appear cloudy or bloody. Lymphangitis and epitrochlear and axillary lymphadenopathy are not uncommon. After 10-14 days, symptoms usually improve significantly and lesions crust over and heal.

Viral shedding is believed to resolve at this point. Complete resolution occurs over subsequent 5-7 days.

As is typical of other herpetic infections, herpetic whitlow is characterized by a primary infection, which may be followed by a latent period with subsequent recurrences. After the initial infection, the virus enters cutaneous nerve endings and migrates to the peripheral ganglia and Schwann cells where it lies dormant. The primary infection usually is the most symptomatic. Recurrences observed in 20-50% of cases are usually milder and shorter in duration.

Frequency

United States

Annual incidence is estimated at 2.4-5.0 cases per 100,000 population.

Mortality/Morbidity

Mortality related to herpetic whitlow can be presumed to be negligible.

Morbidity is related primarily to bacterial superinfection or to iatrogenic complications due to a misguided incision and drainage resulting from incorrect diagnosis of the infection as a bacterial paronychia. These complications may include delayed resolution, increased incidence of bacterial superinfection, and, rarely, systemic spread and the development of herpes encephalitis.

Sex

Males and females are affected equally by herpetic whitlow.

Age

Toddlers and preschool children are most likely to engage in thumb-sucking or finger-sucking behavior; therefore, they are susceptible to herpetic whitlow if they have herpes labialis or herpetic gingivostomatitis.

Patients should be advised that their prognosis for recovery is excellent and resolution should occur in 2-4 weeks. 

Viral shedding will continue until the lesions have cleared and patients should be advised to utilize gloves or other barriers to prevent exposure and potential spread to other anatomic locations or to other persons.[2]  

Patients should be advised that antiviral treatment during the initial outbreak may shorten the clinical course and may also lessen the possibility of recurrence which may be as high as 30-50%

Patients present with complaints of pain and swelling of a finger, typically with characteristic vesicular lesions. The most commonly involved digits are the thumb and index fingers.[2, 4]

History of a prodrome of fever or malaise may precede the onset of symptoms by several days.

Similar previous problems in the same digit suggest that the patient is presenting with an episode of reactivation and recurrence.

Question patients about any recent possible exposure. Considerations are as follows:

• Healthcare workers with a history of exposure to oral or genital secretions are at risk.

• Patients in the general population with a history of caring for or coming in contact with someone that has typical lesions are at risk.

• Since autoinoculation is a common route, especially in children, ask about recent episodes consistent with herpes labialis or herpetic gingivostomatitis. In adults, inquire about a history of symptoms consistent with genital herpes.

The involved finger is often exquisitely tender and quite edematous; however, in contrast to a felon, the pulp space usually is not tensely swollen.

Examination usually reveals the characteristic grouped vesicular lesions or ulcers with surrounding erythema.

Fluid within the vesicles is usually clear, although it may appear cloudy or hemorrhagic.

Extension of infectious process into subungual space may be observed.

Lymphangitic streaking and possibly adenopathy of the epitrochlear and axillary nodes may be found.

Preexisting herpetic lesions may be noted in oral cavity or genitals.

As noted, health care workers are at risk due to possibility of exposure to virus-containing secretions from their patients.

Patients with other herpetic lesions, such as herpes labialis, herpetic gingivostomatitis, or genital herpes, are at risk due to autoinoculation.

Immunocompromised patients are at risk for primary infection, reactivation, and possibly systemic complications.

Diagnosis of herpetic whitlow usually is clinical, based on presentation of the affected digit with characteristic lesions and a typical history.[2, 4]

In children, observation of concurrent gingivostomatitis is almost pathognomonic.

In adults, the presence of occupational risk factors or finding of concurrent oral or genital herpes lesions should strongly suggest the diagnosis.

Definitive diagnostic testing includes the Tzanck test, viral cultures, serum antibody titers, fluorescent antibody testing, or DNA hybridization. Ideally, specimens should be obtained from lesions that have been present less than 24 hours to maximize sensitivity, regardless of the diagnostic modality used.

Viral culture of the aspirated vesicle fluid is the most specific assay and represents the diagnostic criterion standard. This test is usually more costly and time consuming, requiring 24-48 hours, but it does provide the ability to differentiate HSV-1 and HSV-2 infections. Specificity is 100%, with sensitivity ranging from 75% with initial episodes to as low as 50% during recurrences.

Polymerase chain reaction and immunofluorescent microscopy have become more widely available and cost effective.

HSV serologic tests are available but are of limited utility owing to lifelong positivity after initial seroconversion.

The Tzanck test is less commonly performed because of its relatively low sensitivity, but it may be helpful in certain cases. Smears are obtained by scraping the base of an unroofed vesicle. The smears are Giemsa-stained, and a positive test is indicated by light microscopy findings of multinucleated giant cells, often with visible viral inclusions.

Recurrent infections, atypical presentations, or unusual locations should suggest an immunodeficient state. HIV testing should be considered in patients with such presentations.[5, 6]

Herpetic whitlow is a self-limited disease. Treatment most often is directed toward symptomatic relief.

Acyclovir may be beneficial. Studies of clinical efficacy are limited and treatment suggestions are extrapolated from data regarding response of other HSV infections. In primary infections, topical acyclovir 5% has been demonstrated to shorten the duration of symptoms and viral shedding. Oral acyclovir may prevent recurrence. Doses of 800 mg twice daily initiated during the prodrome may abort the recurrence. Alternative dosing regimens may also be effective.[7]

Famciclovir or valacyclovir may shorten the clinical manifestations of acute occurrence.

Use antibiotic treatment only in cases complicated by bacterial superinfection.

Tense vesicles may be unroofed to help ameliorate symptoms, and wedge resection of the fingernail may be used for the same purpose in cases involving the subungual space.

Deep surgical incision is contraindicated, since this may lead to delayed resolution, bacterial superinfection or systemic spread, and complications such as herpes encephalitis.

Antiviral agents may be prescribed as noted above.

Appropriate analgesic medications should be prescribed if indicated.

Do not attempt to incise and drain lesions as this may lead to worsening scarring or possible dissemination of the virus.

Virions are shed by open lesions and patients may inadvertently spread the infection to other anatomic locations, including ocular, genital or oral and rarely the infection may progress to herpetic encephalitis. 

Inappropriate attempts to incise and drain lesions may lead to subsequent scarring.

None indicated under most circumstances, but if the diagnosis is in question, consultation to Infectious Disease physician or Dermatologist may be appropriate.

Health care workers should wear gloves while providing medical and/or dental care to prevent inadvertent exposure and subsequent infection. 

The main goals of treatment are to prevent oral inoculation or transmission of infection and to provide symptomatic relief.[7]

Class Summary

These agents are used to shorten the clinical course, prevent complications, prevent the development of latency and/or subsequent recurrences, decrease transmission, and eliminate established latency.

Acyclovir (Zovirax)

Topical form shortens duration of symptoms in primary infections; acts by interfering with DNA replication within the virions.

Oral acyclovir may abort recurrences if treatment is initiated immediately upon onset of symptoms; inhibits HSV-1 and HSV-2.

Famciclovir (Famvir)

After ingestion, the drug is rapidly biotransformed into the active compound penciclovir and phosphorylated by viral thymidine kinase. By competition with deoxyguanosine triphosphate, penciclovir triphosphate inhibits viral polymerase, subsequently inhibiting viral DNA synthesis/replication.

Adjust dose in patients with renal insufficiency or hepatic disease.

Used against herpes simplex and varicella-zoster viruses.

Valacyclovir (Valtrex)

Valacyclovir is a prodrug rapidly converted to the active drug acyclovir. It is more expensive but has a more convenient dosing regimen than acyclovir.

Class Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Penciclovir (Denavir)

Inhibitor of DNA polymerase in HSV-1 and HSV-2 strains, inhibiting viral replication.

Advise routine outpatient follow-up care to ensure resolution of infection and to monitor for evidence of bacterial superinfection.

Include analgesics in the treatment of herpetic whitlow.

Topical acyclovir may be of benefit in primary infections.[7]

In cases of superinfection, use antibiotics effective against skin pathogens.

Avoidance of exposure is key to the prevention of herpetic whitlow. Health care workers should use gloves, practice strict hand washing, and scrupulously observe universal fluid precautions.[3] ​ Studies have demonstrated herpes virus in 2.5% of asymptomatic patients and in 6.5% of hospitalized patients with tracheostomies.

Caution patients with oral, labial, or genital lesions and the parents and caregivers of children with lesions against digital contact with lesions.

Complications usually are minimal provided that affected patients are immunocompetent.

Misdiagnosis as a bacterial paronychia or felon with resultant deep incision may lead to delayed resolution, increased risk of bacterial superinfection, systemic spread (rare), and possibly development of herpes encephalitis.

Hyperesthesia or numbness has been reported in 30-50% of patients between episodes of reactivation.

Other potential complications include scarring of the affected digit and ocular spread.

Prognosis is excellent in uncomplicated cases, with spontaneous resolution in 3-4 weeks.

Advise patients of the likelihood of future recurrence and warn of the possibility of disease spreading to other parts of the body and to other individuals.