Herpes labialis

Published on 02/04/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 948 times

157 Herpes labialis

Instruction

Look at this patient’s mouth.

Salient features

History

• Pain, itching, burning lasting several hours

• Vesicles

• Sore mouth

• Fever

• Gum swelling

• Mouth ulcers.

Examination

• Small vesicles with an erythematous base on the lips and around the mouth (Fig. 157.1)

• Look for:

• vesicles in the mouth (gingiva, tongue, soft and hard palate) and pharynx
• tender anterior cervical lymph nodes.
image

Fig. 157.1 Clustered intact vesicles at the skin-vermilion junction.

(With permission from DeLee et al. 2009.)

Diagnosis

This patient has small vesicles around the mouth (lesion) from herpes labialis (aetiology), which is causing severe itching (functional status).

Questions

What usually causes a ‘cold sore’?

Skin manifestations include vesicular lesions on an erythematous base. Only 10–30% of new infections are symptomatic.

Herpes simplex virus (HSV) type 1 causes an asymptomatic gingivostomatitis in children.

In adults, there may be severe stomatitis with mouth ulcers, local lymph node enlargement and systemic features.

What do you know about herpes simplex virus type 2?

HSV-2 causes a genital infection called vulvovaginitis. Women with genital herpes should have cervical screening as a link is suspected with carcinoma of the cervix.

Advanced-level questions

What are the complications of herpes infections?

• Erythema multiforme

• Disseminated infection in the immunocompromised individual

• Herpes keratitis, scarring and visual impairment

• Herpes simplex encephalitis (propensity for the temporal lobe)

• Herpetic whitlow (infection of the finger) (Fig. 157.2)

• Herpes gladiatorum (infection of the skin, described among wrestlers)

• Visceral infections, especially in viraemia in HIV (oesophagitis, pneumonitis, hepatitis)

• Neonatal HSV infection (neonates <6 weeks of age); usually visceral and/or CNS infection

• CNS complicatiosn: aseptic meningitis, sacral radiculopathy, transverse myelitis and benign recurrent lymphocytic meningitis (Mollaret’s meningitis).

image

Fig. 157.2 Herpetic whitlow.

How would you confirm your clinical diagnosis?

• Scrapings of the base of the lesions stained with Wright, Giemsa (Tzanck preparation) or Papanicolaou’s stain will demonstrate characteristic giant cells or intranuclear inclusions of herpes infection (does not differentiate from zoster infection)

• Isolation of virus in tissue culture

• Demonstration of HSV antigens in scrapings from lesions

• HerpeSelect HSV-1 and HSV-2 enzyme-linked immunosorbent assays and HSV-1 and HSV-2 immunoblot tests.

How would you treat herpes labialis?

Aciclovir cream applied locally.

What drugs are available for herpes simplex infections?

• Mucocutaneous herpes: topical aciclovir, valaciclovir, famciclovir, foscarnet

• Eye infections: idoxuridine, trifluorothymidine, topical vidarabine. Prophylactic use of aciclovir can prevent recurrent ocular HSV disease (N Engl J Med 1998;339:300–6)

• Encephalitis: intravenous aciclovir

• Neonatal infections: high-dose intravenous vidarabine and aciclovir.

In a patient suspected of herpes encephalitis, which test allows early detection?

PCR of CSF to detect HSV DNA.

What is the interaction between human immunodeficiency virus and herpes simplex virus infections?

It has been argued that HSV-2 and HIV infections are synergistic, since suppression of HSV-2 decreases HIV load, while others insist that interactions between HSV-2 and HIV-1 are more complex and that HSV-2 coinfection might, in certain cases, be associated with elevated CD4 T cell counts.

What do you know about the pathogenesis of herpes simplex mucocutaneous infections?

In the initial infection, HSV enters through breaks in the skin or mucosa; it then attaches to and enters epithelial cells to replicate. It is taken up by free sensory nerve endings found at the dermis, and the nucleocapsid containing the viral genome is transported by retrograde axonal flow to the nucleus in the sensory ganglion.

After recovery from the initial infection, the virus remains latent in the sensory ganglion for the life of the host. Periodically, the virus reactivates from the latent state and travels back down the sensory nerves to the skin or mucosal surface.

Viral shedding from mucosal surfaces occurs from lesions (clinical reactivation) obut can occur with very mild or no symptoms (subclinical reactivation). Shedding leads to transmission to other sexual partners and in some cases HSV can be transmitted from mother to infant at delivery (Lancet 2007; 370:2127–37).

Related posts:

Default ThumbnailSixth cranial nerve palsy Osteoarthrosis Cataracts Ebstein’s anomaly Paget’s disease Felty’s syndrome