Herpes virus delay periods

Genital ulcerative disease caused by herpes makes it easier to transmit and acquire HIV infection sexually. There is an estimated 2- to 4-fold increased risk of acquiring HIV, if individuals with genital herpes infection are genitally exposed to HIV.

In persons with both HIV and genital herpes, local activation of HIV replication at the site of genital herpes infection can increase the risk that HIV will be transmitted during contact with the mouth, vagina, or rectum of an HIV-uninfected sex partner. Neonatal herpes is one of the most serious complications of genital herpes. Women should be counseled to abstain from intercourse during the third trimester with partners known to have or suspected of having genital herpes.

While women with genital herpes may be offered antiviral medication late in pregnancy through delivery to reduce the risk of a recurrent herpes outbreak, third trimester antiviral prophylaxis has not been shown to decrease the risk of herpes transmission to the neonate.

HSV nucleic acid amplification tests NAAT are the most sensitive and highly specific tests available for diagnosing herpes. However, in some settings viral culture is the only test available. The sensitivity of viral culture can be low, especially among people who have recurrent or healing lesions.

Because viral shedding is intermittent, it is possible for someone to have a genital herpes infection even though it was not detected by NAAT or culture. Type-specific virologic tests can be used for diagnosing genital herpes when a person has recurrent symptoms or lesion without a confirmatory NAAT, culture result, or has a partner with genital herpes.

Both virologic tests and type-specific serologic tests should be available in clinical settings serving patients with, or at risk for, sexually transmitted infections. If confirmatory tests are unavailable, patients should be counseled about the limitations of available testing before serologic testing. Healthcare providers should also be aware that false-positive results occur. In instances of suspected recent acquisition, serologic testing within 12 weeks after acquisition may be associated with false negative test results.

HSV-1 serologic testing does not distinguish between oral and genital infection, and typically should not be performed for diagnosing genital HSV-1 infection.

Diagnosis of genital HSV-1 infection is confirmed by virologic tests from lesions. Patients who are at higher risk of infection e. There is no cure for herpes. Antiviral medications can, however, prevent or shorten outbreaks during the period of time the person takes the medication.

There is currently no commercially available vaccine that is protective against genital herpes infection. Candidate vaccines are in clinical trials. Correct and consistent use of latex condoms can reduce, but not eliminate, the risk of transmitting or acquiring genital herpes because herpes virus shedding can occur in areas that are not covered by a condom.

The surest way to avoid transmission of STDs, including genital herpes, is to abstain from sexual contact, or to be in a long-term mutually monogamous relationship with a partner who has been tested for STDs and is known to be uninfected. Persons with herpes should abstain from sexual activity with partners when herpes lesions or other symptoms of herpes are present. It is important to know that even if a person does not have any symptoms, he or she can still infect sex partners. Sex partners of infected persons should be advised that they may become infected and they should use condoms to reduce the risk.

Sex partners can seek testing to determine if they are infected with HSV. Incubation periods How soon to test? Types of tests When do symptoms appear? Dormancy Prevention Takeaways HSV , also known as the herpes simplex virus, is the series of viruses that cause oral and genital herpes.

Herpes incubation periods. How soon can you be tested? Type of tests used to diagnose herpes. How long does it take for symptoms of herpes to appear? Can you have herpes and not know? How to prevent the spread of herpes. Key takeaways. Read this next. Herpes Simplex.

Can You Get Herpes from Kissing? And 14 Other Things to Know. Virus replicates further in epithelial cells, reproducing the lesions of the initial infection, until infection is contained through both systemic and mucosal immunity. Latency is established when herpes simplex virus reaches the dorsal root ganglia after anterograde transmission via sensory nerve pathways.

In its latent form, intracellular herpes simplex virus DNA cannot be detected routinely unless specific molecular probes are utilized. Mucocutaneous infections are the most common clinical manifestations of herpes simplex virus 1 and 2. Gingivostomatitis, which is usually caused by herpes simplex virus 1, occurs most frequently in children less than five years of age.

Gingivostomatitis is characterized by fever, sore throat, pharyngeal edema and erythema, followed by the development of vesicular or ulcerative lesions on the oral and pharyngeal mucosa.

Recurrent herpes simplex virus 1 infections of the oropharynx most frequently manifest as herpes simplex labialis cold sores , and usually appear on the vermillion border of the lip.

Intraoral lesions as a manifestation of recurrent disease are uncommon in the normal host but do occur frequently in immunocompromised individuals.

Genital herpes is most frequently caused by herpes simplex virus 2 but an ever increasing number of cases are attributed to herpes simplex virus 1. Primary infection in women usually involves the vulva, vagina, and cervix Figure In men, initial infection is most often associated with lesions on the glans penis, prepuce or penile shaft. In individuals of either sex, primary disease is associated with fever, malaise, anorexia, and bilateral inguinal adenopathy.

Women frequently have dysuria and urinary retention due to urethral involvement. It is estimated that as many as 10 per cent of individuals will develop an aseptic meningitis with primary infection. Sacral radiculomyelitis may occur in both men and women, resulting in neuralgias, urinary retention, or obstipation.

The complete healing of primary infection may take several weeks. It has been recognized that the first episode of genital infection is less severe in individuals who have had previous herpes simplex virus infections at other sites, such as herpes simplex labialis.

Recurrent genital infections in either men or women can be particularly distressing. The frequency of recurrence varies significantly from one individual to another. It has been estimated that one-third of individuals with genital herpes have virtually no recurrences, one-third have approximately three recurrences per year, and another one-third greater than three per year.

Recent seroepidemiologic studies have found that between 25 percent and 65 percent of individuals in the United States in had antibodies to herpes simplex virus 2, and that seroprevalence is dependent upon the number of sexual partners. If genital swabs from women with a history of recurrent genital herpes are subjected to polymerase chain reaction, virus DNA can be detected in the absence of culture proof of infection. This finding suggests the chronicity of genital herpes as opposed to a recurrent infection.

Herpes simplex keratitis is usually caused by herpes simplex virus 1 and is accompanied by conjunctivitis in many cases. It is considered the most common infectious cause of blindness in the United States. The characteristic lesions of herpes simplex keratoconjunctivitis are dendritic ulcers best detected by fluorescein staining.

Deep stromal involvement has also been reported and may result in visual impairment. Herpes simplex virus infections can manifest at any skin site. Common among health care workers are lesions on abraded skin of the fingers, known as herpetic whitlows Figure Similarly, wrestlers, because of physical contact may develop disseminated cutaneous lesions known as herpes gladiatorum. Neonatal herpes simplex virus infection is estimated to occur in approximately one in deliveries in the United States annually.

Approximately 70 percent of the cases are caused by herpes simplex virus 2 and usually result from contact of the fetus with infected maternal genital secretions at the time of delivery.

Manifestations of neonatal herpes simplex virus infection can be divided into three categories: 1 skin, eye and mouth disease; 2 encephalitis; and 3 disseminated infection. As the name implies, skin, eye and mouth disease consists of cutaneous lesions and does not involve other organ systems Figure Involvement of the central nervous system may occur with encephalitis or disseminated infection, and generally results in a diffuse encephalitis.

The cerebrospinal fluid formula characteristically reveals an elevated protein and a mononuclear pleocytosis. Disseminated infection involves multiple organ systems and can produce disseminated intravascular coagulation, hemorrhagic pneumonitis, encephalitis, and cutaneous lesions. Diagnosis can be particularly difficult in the absence of skin lesions. The mortality rate for each disease classification varies from zero for skin, eye and mouth disease to 15 per cent for encephalitis and 60 percent for neonates with disseminated infection.

In addition to the high mortality associated with these infections, morbidity is significant in that children with encephalitis or disseminated disease develop normally in only approximately 40 per cent of cases, even with the administration of appropriate antiviral therapy.

Herpes simplex encephalitis is characterized by hemorrhagic necrosis of the inferiomedial portion of the temporal lobe Figure Disease begins unilaterally, then spreads to the contralateral temporal lobe.

It is the most common cause of focal, sporadic encephalitis in the United States today, and occurs in approximately 1 in , individuals. Most cases are caused by herpes simplex virus 1.

The actual pathogenesis of herpes simplex encephalitis requires further clarification, although it has been speculated that primary or recurrent virus can reach the temporal lobe by ascending neural pathways, such as the trigeminal tracts or the olfactory nerves. Hemorrhagic necrosis of the temporal lobe due to HSV encephalitis. Clinical manifestations of herpes simplex encephalitis include headache, fever, altered consciousness, and abnormalities of speech and behavior.

Focal seizures may also occur. The cerebrospinal fluid formula for these patients is variable, but usually consists of a pleocytosis with both polymorphonuclear leukocytes and monocytes present. The protein concentration is characteristically elevated and glucose is usually normal. Historically, a definitive diagnosis could only be achieved by brain biopsy, since other pathogens may produce a clinically similar illness.

However, the application of polymerase chain reaction for detection of virus DNA has replaced brain biopsy as the standard for diagnosis. The mortality and morbidity are high, even when appropriate antiviral therapy is administered. At present, the mortality rate is approximately 30 per cent one year after treatment. In addition, approximately 70 per cent of survivors will have significant neurologic sequelae.

Herpes simplex virus infections in the immunocompromised host are clinically more severe, may be progressive, and require more time for healing. Manifestations of herpes simplex virus infections in this patient population include pneumonitis, esophagitis, hepatitis, colitis, and disseminated cutaneous disease. Individuals suffering from human immunodeficiency virus infection may have extensive perineal or orofacial ulcerations.

Herpes simplex virus infections are also noted to be of increased severity in individuals who are burned. Transmission of herpes simplex virus is dependent upon intimate contact. Thus, herpes simplex virus 1 is usually transmitted by kissing or other contact with saliva, while herpes simplex virus 2 is usually a consequence of sexual contact. Nosocomial spread of herpes simplex virus 2 has been documented, particularly in newborn intensive care units.

Varicella-zoster virus is one of the most common viruses encountered by humans. Varicella-zoster virus is usually transmitted by airborne routes droplet spread with initial replication in the oropharynx Figure In the susceptible or seronegative individual, replication of virus in the oropharynx leads to primary viremia, with subsequent development of a vesicular rash. The replication of varicella-zoster virus in vitro is similar to that for herpes simplex virus, although the period of replication is somewhat prolonged.

Varicella, or chickenpox, is the manifestation of primary varicella-zoster virus infection. This infection occurs most commonly in young children of preschool age and has a characteristic disseminated vesicular rash which appears after an incubation period of 14 to 17 days. The rash begins on the face and trunk and spreads to the extremities. The lesions of chickenpox are initially vesicles which become pustular, crusted, and then scabbed prior to healing.

The average duration of lesion formation is three to five days in the normal child; however, it is usually longer in adolescents and adults and certainly in the immunocompromised. At the time of primary infection, varicella-zoster virus may establish latency in dorsal root ganglia.

The recurrent form of varicella-zoster virus is herpes zoster or shingles. This form of infection, which is a reactivation of latent virus, typically manifests as a localized vesicular rash with a dermatomal distribution. The rash initially appears within the dermatome as erythema, which is soon followed by the development of vesicles Figure Some individuals will have coalescence of vesicles into bullous lesions. New vesicles may form for five to seven days, then evolve through the sequence of healing described for the lesions of varicella.

The average time to healing for individuals with shingles ranges from 10 to 21 days, depending upon the age and immune status of the individual. Characteristic of herpes zoster is the appearance of both acute neuritis and post-herpetic neuralgia.

Acute neuritis is present in most individuals with localized zoster, the exception being young children. Post-herpetic neuralgia will develop in as many as 50 per cent of adults, depending upon the age of the individual. The treatment of acute neuritis and post-herpetic neuralgia can be problematic for individual patients.

Serious complications of chickenpox in the non-immunocompromised child are rare, but secondary bacterial infection can be problematic. Adults and immunocompromised children have a higher incidence of visceral disease. It is estimated that as many as one out of three of immunocompromised children suffer visceral disease, with a mortality of 15 per cent in the absence of antiviral therapy. Herpes zoster in the immunocompromised host may be associated with cutaneous dissemination and visceral complications.

In the absence of antiviral therapy, as many as 25 per cent of individuals with lymphoproliferative malignancies will have cutaneous dissemination and 10 per cent will develop visceral complications with an overall mortality rate of approximately 8 per cent.

The spread of varicella-zoster virus depends upon airborne droplet transmission from a person who is shedding virus to a susceptible host. By adulthood, as many as 90 to 95 per cent of individuals have serologic evidence of infection with varicella-zoster virus. The epidemiology of herpes zoster is more complicated.

It does not appear that herpes zoster can be transmitted from one individual to another. However, spread of virus from the vesicles of herpes zoster may lead to the development of varicella in a susceptible host. Individuals over the age of 50 experience zoster at a frequency of approximately 1 per cent. Cytomegalovirus infection can result in one of three distinct clinical syndromes.

Congenital cytomegalovirus infection is a common occurrence in the United States today, occurring in approximately one per cent of all live births. Some children who excrete the virus at birth, but have no other symptoms, may later have impaired hearing. An additional 10 to 25 per cent of children acquire cytomegalovirus infection early in life, either through contact with infected maternal genital secretions, blood transfusions in the premature or by acquisition from breast milk.

Symptomatic congenital disease is most frequent when the mother has a primary cytomegalovirus infection during gestation and is extremely uncommon when the infection is acquired after the neonatal period. The second manifestation of cytomegalovirus infection is that of a mononucleosis syndrome. This occurs in approximately 10 per cent of primary cytomegalovirus infections in older children and adults; the remaining 90 per cent have asymptomatic primary infection.

Mononucleosis in these patients is heterophile negative, but otherwise similar to classic Epstein-Barr virus mononucleosis. Patients characteristically have fever, malaise, atypical lymphocytosis, pharyngitis and, rarely, cervical adenopathy or hepatitis. Cytomegalovirus mononucleosis can be distinguished from Epstein-Barr virus mononucleosis by the absence of specific antibodies to either nuclear or viral capsid antigens of Epstein-Barr virus.

The third clinical entity is cytomegalovirus infection in severely immunocompromised individuals. In contrast to symptomatic congenital and mononucleosis infections, which are most commonly manifestations of primary cytomegalovirus infection, immunocompromised hosts may experience life-threatening disease from either primary or reactivated cytomegalovirus infection.

In these patients, infection can involve the lungs, gastrointestinal tract, liver, retina, and central nervous system Figure Individuals at high risk for severe disease due to cytomegalovirus infection include organ transplant recipients, particularly bone marrow transplant recipients, and individuals with human immunodeficiency virus infection.

Patients with human immunodeficiency virus infection and bone marrow transplant recipients seem particularly at risk for the development of CMV pneumonia. Replication of cytomegalovirus is most prominent in cells of glandular origin, particularly in the salivary glands and the kidneys. As a result, large quantities of virus can be shed in saliva and urine. The replicative cycle of cytomegalovirus in these organs is more prolonged than that of other herpesviruses and produces characteristic multi-nucleated giant cells with Cowdry type A intranuclear inclusions.

Intracytoplasmic inclusion bodies may also be present, but are less easily demonstrated. These giant cells can be found in the parotid gland, and similar cells can be seen excreted in the urine. Cytomegalovirus can cause persistent infection in various tissues, including those of the salivary glands, breasts, kidneys, endocervix, seminal vesicles and peripheral blood leukocytes.

This persistent infection leads to chronic viral excretion by the involved organ. Evaluation Recommended Laboratory Assessments [14] [15] A direct swab of vesicular lesions within 72 hours of onset is ideal but avoid lesions that have evidence of crusting or healing.

Do not clean area with topical alcohols before acquiring material. Swab locations include: skin via unroofing vesicles with a sterile needle, urethra via sterile swab, the cervix through the vaginal speculum, urine, swabbing of the conjunctiva, and rectal swabs through proctoscopes [16].

Primary Treatment Primary infections with multiple ulcerating lesions will resolve after approximately 19 days, regardless of treatment interventions. The oral formulation has quite a poor bioavailability, which has been improved with valacyclovir see below. The benefits of acyclovir include its low side effect profile, which allows it to be tolerated for long periods. Differential Diagnosis Infectious genital ulcerative conditions Syphilis. Prognosis There is no cure for HSV-2, early identification of symptoms, and prompt institution of pharmacotherapy can lead to early suppression of viral replication.

Untreated HSV-2 can cause meningitis; however, any part of the nervous system may be affected by this virus. During the prodrome of genital herpes and herpetic eruption, as discussed above, affected individuals may experience more systemic symptoms such as headaches, neck stiffness, and low-grade fever.

Such symptoms should lead to immediate lumbar puncture with an analysis of the CSF, often revealing a lymphocytic pleocytosis. Acute retinal necrosis - presents with a unilateral or bilateral red eye s , periorbital pain, and impaired visual acuity. Examination reveals episcleritis or scleritis and necrosis with retinal detachment. May occur with HSV-2 meningoencephalitis.

Deterrence and Patient Education Condom use recommended. Consider prophylactic suppressive therapy if frequent sexual activity is likely to occur [23]. Pearls and Other Issues HSV cannot be cured, but suppressive therapy can help prevent spread to seronegative individuals.

Enhancing Healthcare Team Outcomes The primary care physician or provider will often be the first one to diagnose and treat HSV-2 infections. The interprofessional healthcare team, to include the medical assistants and nursing staff, are pivotal in providing medical education to the patient on how to prevent unnecessary spread.

This should be documented and communicated to the treating physician. Utilizing network public health officials can help dispense information as well as track STIs in the area leading to early identification in patients who may be otherwise asymptomatic.

Pharmacists review medications, verify dosing, check for interactions, inform patients about use and potential side effects. They also may be involved in the purchase of condoms and can make patient recommendations.

Review Questions Access free multiple choice questions on this topic. Comment on this article. Figure Herpes Simplex. Contributed by DermNetNZ. Figure This was an outbreak of herpes genitalis, which had manifested as blistering on the underside of the penile shaft, just proximal to the corona of the glans, which was due to the herpes simplex 2 HSV-2 virus, otherwise referred to as genital herpes.

References 1. Sexually transmitted diseases treatment guidelines, Whitley R, Baines J. Clinical management of herpes simplex virus infections: past, present, and future.

Sauerbrei A. Herpes Genitalis: Diagnosis, Treatment and Prevention. Geburtshilfe Frauenheilkd. Herpes virus type 2 infection and genital symptoms in primary care patients. Sex Transm Dis. Herpes simplex virus infection in pregnancy and in neonate: status of art of epidemiology, diagnosis, therapy and prevention.