Complications
A rare complication mainly in immunocompromised patients, because a normal immune response usually leads to rapid resolution of the infection.[66]
Cross-resistance to valaciclovir and usually famciclovir is present.
Foscarnet is recommended. As a result of multiple toxicities and availability in intravenous form only, this treatment is reserved for patients with extensive mucocutaneous ulcerations not responsive to aciclovir, valaciclovir, or famciclovir.
Usually observed in patients who are immunocompromised, most frequently in solid organ or haematopoietic stem cell transplant recipients. It is usually caused by HSV-1 and typically presents with odynophagia and/or dysphagia. Diagnosis is confirmed by histopathology obtained by endoscopy. Viral cultures of suspicious lesions should be obtained to rule out antiviral resistance, particularly in patients who are not responding to aciclovir.
Oesophagitis is generally self-limited in immunocompetent patients, therefore a short course of aciclovir may be offered if symptoms have not already begun to improve. However, longer courses are necessary for immunocompromised patients.
Patients with disseminated disease should be managed with the assistance of an infectious disease consultant.
An acute, self-limited, but often relapsing hypersensitivity reaction. Target lesions are the most characteristic presentation. Mucosal involvement may also occur.
Erythema multiforme is caused by a cell-mediated immune response directed against viral antigens. Various factors, including genetic susceptibility, may be involved.
Onset of HSV-induced erythema multiforme is typically a few days after infection. Patients who experience frequent recurrences, however, may be candidates for continuous antiviral therapy.
Characteristic dendritic corneal lesions are present. Typically unilateral, with recurrences affecting the same eye.
Co-manage patients with an ophthalmologist. Corneal scarring may lead to significant vision impairment requiring corneal transplantation.
Consider treatment with topical trifluorothymidine (trifluridine) or aciclovir.[79]
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Aseptic meningitis may occur during primary infection or may be recurrent over months to years.
Patients with CNS disease should be managed with the assistance of an infectious disease consultant.
Risk is highest if the mother acquired HSV during the third trimester.
Maternal acquisition may be asymptomatic, and clinicians must have a high index of suspicion.
Consider if neonatal fever, seizures, lethargy, sepsis, or vesicular blisters involving skin, eye, and mucous membranes are present.
Obtain cerebrospinal fluid, serum for HSV polymerase chain reaction (PCR) testing, and eye, mouth, nasopharynx, and rectal cultures for HSV.
Treat the neonate with systemic aciclovir for 21 days if disseminated/CNS disease, and for 14 days if disease is limited to skin/mucous membranes.
HSV should be in the differential diagnosis for all cases of meningoencephalitis. HSE usually presents with acute onset of fever with altered mentation or consciousness, focal neurological deficits or seizures.
An lumbar puncture should be performed, with fluid sent for HSV PCR. Temporal lobe abnormalities on MRI are more sensitive early in the course of disease than with CT.[80]
Patients should be started on intravenous aciclovir until HSV has been ruled out (negative CSF HSV PCR obtained 3-7 days after onset of symptoms and normal neuroimaging). If HSE is diagnosed, at least 3 weeks of intravenous aciclovir should be given.[81]
Patients with CNS disease should be managed with the assistance of an infectious disease consultant.
Consider if rapid onset of vision loss and iritis with HSV.
Risks include congenital exposure or immunosuppression; however, retinitis may occur in immunocompetent individuals.
Patients should be managed with an ophthalmologist.
HSV PCR of vitreous/aqueous humour may provide a diagnosis.
Treat with aciclovir depending on clinical response.[82]
Rare infection of the distal fingers or toes with HSV-1 or HSV-2 through contact with infected genital or oral secretions with a break in the skin. It presents with painful erythematous vesicles or pustules on the extremities and may have associated lymphadenitis/lymphadenopathy.[83]
It is acquired through auto-innoculation in children, typically under 2 years of age, with primary or recurrent oral or genital herpes, or from contact with infected oral/genital secretions from carers. In adolescents and adults, it is acquired through contact between HSV and cuts or fissures on extremities; it may be acquired through contact of the extremity with infected genital secretions or oral secretions. It can be an occupational hazard for those with frequent contact with oral secretions, such as anaesthesiologists or dentists.
It is diagnosed by HSV PCR of fluid from vesicles. Incision and drainage of lesions is contraindicated.
Symptomatic recurrences are typically self-limited, although antiviral therapy at doses used for genital disease may be considered. Suppressive therapy may be used for those with frequent recurrences.
Impaired immunity resulting from pregnancy, malignancy, or immunosuppression is a risk factor. Rare in immunocompetent hosts. Often associated with disseminated disease and progression to fulminant liver failure. Typically presents with fever, nausea, vomiting, abdominal pain, leukopenia, thrombocytopenia, coagulopathy, and elevated serum transaminase levels.[84] [85]
Diagnosis can be established with either liver biopsy or confirmation of HSV viraemia with serum PCR.
Patients should be started on intravenous aciclovir until HSV has been ruled out.
Patients with disseminated disease should be managed with the assistance of an infectious disease consultant.
An acute, unilateral peripheral facial nerve palsy, which may occur when reactivation of HSV-1 results in destruction of ganglion cells, infection of Schwann cells, demyelination, and neural inflammation.[86] Bell’s palsy is a clinical diagnosis of exclusion.
By 6 months, all patients with Bell’s palsy will demonstrate some degree of remission of symptoms. Oral corticosteroids within 72 hours of symptom onset may shorten the time to complete recovery in adults. With severe presentations, combination of an antiviral and corticosteroid may reduce long-term sequelae.
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