Common Skin Infections

Primary herpes simplex infection

Clinical Tip: With Herpes Infections look for lesions in groups/clusters. Lesions are monomorphic usually (unless secondarily infected).

Primary herpes infections can cause

• Gingivostomatitis: infection may involve the buccal and gingival mucosa, tongue and fauces. Vesicles evolve into shallow painful ulcers on an erythematous base; they may coalesce if extensive. Other features include fever, submandibular lymphadenopathy, febrile convulsions in children and abnormal liver function tests. The lymphadenopathy may persist for several weeks after the ulcers have healed. Conjunctivitis, myalgia, abdominal discomfort and pharyngitis may also occur. Oral disease may be associated with lesions elsewhere, possibly caused by autoinoculation from the site of primary infection. The incubation period is 2-12 days and illness duration is usually 2-3 weeks.

Note clustered monomorphic lesions

• Genital infection: the lesions are located principally on the vulva in women and may extend to the perineum, upper thighs and buttocks. In men, vesicular lesions are seen on the glans penis or penile shaft. Secondary bacterial infections may occur, requiring antibiotic therapy. Sacral radiculitis, associated with urinary retention and neuralgia may occur. Primary genital infection is associated with fever, dysuria, urethritis, inguinal lymphadenopathy and malaise, and lasts up to 3 weeks. Recurrent genital herpes may occur with more scanty vesicular lesions associated with localised irritation rather than significant pain. New vesicles may occur after the initial lesions have crusted over, delaying healing. Complications are rare with recurrent infection.

Clinical Tip; Complex, multi-site or slow to resolve perianal or gential HSV should alert you to the possibility of underlying HIV infection

• Eczema herpeticum/ kaposi’s varicelliform eruption: a superinfection of eczematous skin, especially in young children. There are usually systemic symptoms such as fever and lymphadenopathy. As these patients are often on steroid treatment this facilitates the spread of the virus, and untreated this condition has a significant fatality rate. Patients should be advised to take care with close contact with relatives with coldsores.

Clinical Tip- Look for groups of monomorphic punched out lesions. Don't expect to see intact blisters.

• Herpetic whitlow: an inflammation at the nail fold due to direct inoculation of the virus into the fingers through a portal of infection. This is common in health care workers especially those involved with manipulation in the mouth (e.g. anaesthetists, dentists), but may also been in nail biters and workers such as laboratory personnel who sustain a traumatic injury with contaminated needles or glassware. The whitlow is extremely painful and takes about four weeks to heal.

Herpetic whitlow. Can be differentiated from dactylitis by the presence of grouped clustered vesicles

• Conjunctivitis and keratitis: both the conjunctiva and cornea may be involved and there may be visible vesicles and ulcers on the eyelids.
• Erythema multiforme (EM). Mycoplasma pneumonia and HSV are the infectious agents most commonly recognised as precipitants of EM. Erythema multiforme does not respond to aciclovir but recurrent cases can be prevented by prophylactic acyclovir. Sometime in more severe EM it may be necessary to treat with oral steroids. 

 Erythema multiforme- typical acrally distributed targetoid lesions

Typical cold sore of HSV1

Vesicles in Herpes simplex infection- note the typical clustering

 

HSV in the immunocompromised

Infection begins usually in either the oral or genital sites and can progress rapidly to extensive ulceration. Cutaneous dissemination may make the rash look like varicella. There is also a risk of visceral dissemination causing encephalitis, pneumonia and hepatitis. In patients with HIV recurrent infection may occur at multiple sites with high frequency and the lesions may be slow to resolve.

The virus establishes a latent infection of dorsal root ganglia, the trigeminal ganglia for HSV-1 and the sacral ganglia for HSV-2. Reactivation of the virus produces recurrent infection. The triggering process is not understood but a variety of stimuli have been implicated: common cold, sunlight/ ultraviolet light exposure, stress, menstruation, infection and mild trauma. Severe primary infections are associated with a higher frequency of reactivation.

As for varicella zoster, the simplest method to make a diagnosis is to send a scraping from the base of a vesicle on a slide to virology, and a swab from the base of the lesion in viral transport medium for culture. Type specific varicella antibody detection is not generally useful, but may be performed in special cases after discussion with the virology lab e.g. repeatedly culture negative lesions which appear clinically to be HSV. 

Primary HSV1 is often mild and symptomatic treatment may be all that is needed e.g. chlorhexidine mouthwashes and simple analgesia in the case of gingivostomatitis. Primary HSV2 infection may be more severe and is more likely to present with fever. In severe cases oral aciclovir, valaciclovir or famciclovir is recommended. Steroid treatment should be withheld or reduced as it increases the severity of the disease, although as mentioned earlier it is sometimes used in more widespread EM. Aciclovir cream may be useful in the treatment of recurrent infection but the most effective treatment for severe recurrent infections is a 5-day course of oral acyclovir commenced when prodromal symptoms begin. Patients with frequent recurrences should be considered for continuous suppressive therapy.

Primary infection during the first and second trimester of pregnancy is not associated with a significant risk to the foetus. Most cases of neonatal herpes occur as a result of perinatal infection. Infection in the third trimester is associated with a risk of transmission to the baby during vaginal delivery and risk is highest when infection occurs around the time of delivery. The mothers of most infants who develop neonatal herpes do not have genital lesions at delivery. Primary genital herpes poses the greatest risk but there is also a risk with recurrent infection. A few cases occur due to transfer of the virus from oral lesions to the infant post delivery. Most cases are due to HSV-2, but HSV-1 can also cause neonatal herpes. Symptoms appear 4-5 days post partum, with evidence of skin, eye and mouth infection. The infant may also develop encephalitis and disseminated disease involving lung, liver, adrenals, eyes and skin. Mortality is greater than 80% for disseminated disease, without treatment. Most babies exhibiting only skin, eye and mouth involvement will develop permanent ocular damage and eventually show some evidence of neurological impairment. All HSV infections identified in the neonatal period should be treated with an antiviral agent. Caesarian section is recommended if clinically apparent cervical infection is present at parturition; delivery by either vaginal or Caesarian should be rapid to minimise exposure.