Viral Infections

Published on 10/02/2015 by admin

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Last modified 10/02/2015

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174 Viral Infections

Deepi G. Goyal, Kristine M. Thompson, Annie T. Sadosty

Key Points

• If herpes infection of the skin, central nervous system, or other location is suspected, initiate treatment with valacyclovir or acyclovir.

• When patients have respiratory symptoms, the use of face masks, proper hand hygiene, and prudent patient isolation may help minimize the spread of infectious agents.

• Oral acyclovir should be offered to patients with chickenpox who are more than 13 years old, but treatment must be initiated within 24 hours of the onset of the rash.

• When a patient presents with a viral syndrome in the late summer or early fall and has significant muscle weakness, consider West Nile virus.

• Patients with cutaneous pain may be in the early stage of herpes zoster infection because the skin sensation may precede the rash by several days.

Pathophysiology

A virus can be viewed as genomic machinery surrounded by a structure that allows it to bind and deliver the contents to a host cell.¹ The structural envelope also determines the mode of transmission of the virus and provides the immunologic basis for host immunity and vaccines. Viral genomes may be composed of either RNA or DNA, and they may be single or double stranded and either circular or linear.

Viruses gain entry into a host organism when the host is exposed to the virus through respiratory droplets, contaminated food or water, or body fluids or tissues. Once the host is inoculated, the virus may cause infection by reproducing locally (e.g., influenza virus causing respiratory infections), or it may be disseminated to distant sites (e.g., varicella-zoster virus [VZV]). Many viruses, such as Epstein-Barr virus (EBV), cytomegalovirus, and hepatitis B and C viruses, can cause persistent infections. Although latent, these infections can be reactivated, with resulting acceleration of viral replication and subsequent acute infection.

Virulence is often mediated by the surface proteins involved in cellular attachment and entry. By producing a protein that attaches to the structural cell coat, some viruses can enhance their infectivity.

Herpes

The word herpes derives from a Greek word meaning “to creep.” This designation refers to the tendency of herpes viruses to creep along nerve pathways. Currently, at least eight identified herpesviruses cause human disease. Each has distinguishing clinical characteristics. Herpes simplex viruses (HSV-1 and HSV-2) are the agents of herpes genitalis, herpes labialis, and herpes encephalitis. VZV causes chickenpox and herpes zoster (shingles). EBV most commonly causes mononucleosis, but it has also been implicated in several lymphoproliferative syndromes. Cytomegalovirus may also manifest as mononucleosis, although it is more commonly associated with invasive disease in immunocompromised patients. Human herpesvirus 6 is the causative agent of roseola infantum. Human herpesvirus 8 has been linked to Kaposi sarcoma and Castleman disease. More recently, herpes B virus has been linked to fatal human encephalitis. Human herpesvirus 7 has been described, but it is not completely understood. As research advances, more herpes strains will likely be identified.

Herpes Simplex Virus

Epidemiology

According to the U.S. Centers for Disease Control and Prevention, one out of five of the total adolescent and adult population in the United States is infected with HSV-2. The incidence is even higher for HSV-1, which infects approximately 80% of the U.S. population. HSV-1 most commonly infects the lips and leads to lesions referred to as “cold sores,” but it can also produce genital lesions. HSV-2 is most often associated with genital herpes, but this virus can infect the mouth during oral sex. The most common locations for herpes simplex lesions are the mouth and the genitals, but infections of the eyes, brain, fingers, face, and esophagus are also seen (Table 174.1).

Table 174.1 Herpes Simplex Infections

TYPE AND CAUSE	SIGNS AND SYMPTOMS	TREATMENTS
Oral herpes (herpes labialis) Commonly HSV-1, but can also be HSV-2	Blisters on the lips or tongue, painful swallowing, often called cold sores or fever blisters	Valacyclovir for 1-2 days for severe primary infection Topical agents (penciclovir, docosanol cream, acyclovir cream) may shorten duration of symptoms if started early

Genital herpes
Equally split between HSV-1 and HSV-2 Women: flulike illness; nerve pain; itching; abdominal pain; dysuria; blisters around the vagina, buttocks, urethra, in the vagina, or on the cervix
Men: lesions on the shaft or head of the penis, buttocks, or thigh

Primary

Acyclovir or valacyclovir

Penciclovir cream, steroid ointments, or topical lidocaine jelly for pain

Secondary

Acyclovir, valacyclovir, or famciclovir for severe outbreaks

Preventive and suppressive dosing schedules available

Ocular herpes
Usually HSV-1 Keratitis, usually in one eye
May progress to stromal keratitis, which is a major cause of corneal blindness

Trifluridine drops; acyclovir or vidarabine ointments are equally effective

Artificial tears

Consult ophthalmology

HSV encephalitis
Usually HSV-1 in adults, HSV-2 in newborns Fever, headache, stiff neck, seizures, focal weakness, altered mental status, psychosis

Acyclovir IV started immediately in suspected cases

Herpetic whitlow
HSV-1 or HSV-2 Itching, pain, or swelling of infected finger followed by blisters lasting 2-3 wk
Often associated with thumb sucking in children and occupational exposure in adults (health care workers)

Topical acyclovir

Commonly acquired from oral or genital lesions, which should be identified and treated appropriately

Bell palsy Focal weakness following distribution of peripheral cranial nerve VII

Acyclovir, valacyclovir, or famciclovir in combination with a steroid taper (data regarding efficacy conflicting)*

Eye protection (topical lubricants, eye patch at night)

HSV esophagitis
Usually HSV-1 in immunocompromised patients Dysphagia

Acyclovir IV

HSV, herpes simplex virus; IV, intravenously.

^* Allen D, Dunn L. Acyclovir or valacyclovir for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2004;4:CD001869 [update of Cochrane Database Syst Rev 2001;4:CD001869]; and Salinas R. Bell’s palsy. Clin Evid 2003;10:1504–7 [update in Clin Evid 2006;15:1745–50].

Presenting Signs and Symptoms

The first time a patient experiences a herpes simplex outbreak (primary infection), he or she often notes a prodrome of symptoms such as fever, muscle aches, headache, malaise, and swollen lymph nodes up to a week before the skin eruptions appear. The first sign of infection of the skin appears 2 to 12 days after initial exposure and begins as cutaneous edema. This edema is quickly followed by the development of small, grouped vesicles on an erythematous base. The lesions typically dry out and heal within 7 to 10 days, although they can last up to 3 weeks. The symptoms almost always recur and are often heralded by a prodrome of skin itching, pain, or paresthesias at the site of infection. Recurrent outbreaks often occur at the same site as the primary infection, but they tend to be milder and have a shorter duration. These recurrences can erupt in intervals of days, weeks, or years, and the triggers vary by patient.

Diagnostic Testing

Herpes simplex is typically identified clinically by the characteristic skin lesion of a thin-walled blister on an inflamed base. Definitive testing is available, and the Tzanck smear uses scrapings from lesions to identify the giant cells with inclusion bodies indicative of HSV infection. Although this test is the most readily available, it is not very sensitive. Viral cultures can be accurate if material is collected early in the illness when intact vesicles are sampled, but the sensitivity wanes with the duration of symptoms. Polymerase chain reaction testing is available and is considered the “gold standard.” It is the fastest and most accurate for testing cerebrospinal fluid (CSF). Serum immunologic studies can be used to identify specific strains of the virus, but most of these tests are time consuming and expensive. Although one point-of-care test is available for HSV-2, it is not widely used, and treatment in the emergency department is most often based on clinical suspicion.

Treatment and Disposition

As yet, no cure for herpes simplex exists. Some of the most exciting research is in the area of vaccination. Several vaccines in clinical trials have the potential to eliminate infection.² Until then, herpes symptoms are managed using several different antiviral medications that help to reduce outbreaks and shorten the course of illness (see the “Facts and Formulas” box). The most commonly used agents are nucleosides and nucleotide analogues that block viral reproduction. They include acyclovir, valacyclovir, famciclovir, and penciclovir. Patients with a first episode of genital herpes, even with mild symptoms, should receive antiviral therapy to decrease progression to severe or prolonged symptoms.³ For acute outbreaks, valacyclovir and famciclovir are the most commonly prescribed medications, but they must be started within 1 day of lesion onset or during the prodrome that precedes some outbreaks.³ Once-daily valacyclovir can reduce the transmission rate of genital herpes by 50% to 75%.⁴ Low-dose suppressive therapy is also available for patients with frequent outbreaks. Foscarnet is a pyrophosphate analogue that can be used for treatment of HSV strains that have become resistant to the nucleosides and nucleotide analogues.

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