Herpes, Simplex, Type 1. StatPearls [Internet]. Plos One. Humanitas Research Hospital. Herpes simplex. Cold sores Inglese. Herpes labiale. Poi sulla pelle appare un piccolo punto gonfio, duro e doloroso fase infiammatoria , sulla zona delle labbra colpita dall'herpes compaiono minuscole macchie rosse che, via via, si ingrandiscono riempiendosi di un liquido giallo traslucido fino a formare delle piccole vescicole disposte a grappolo lungo il bordo esterno delle labbra.
You can add this content to your website by syndicating. HSV-1 often causes oral herpes, which can result in cold sores or fever blisters on or around the mouth. However, most people with oral herpes do not have any symptoms. Most people with oral herpes get it during childhood or young adulthood from non-sexual contact with saliva.
Oral herpes caused by HSV-1 can spread from the mouth to the genitals through oral sex. This is why some cases of genital herpes are due to HSV Genital herpes is common in the United States. In , CDC estimates show there were , new genital herpes infections in the United States among people aged 14 to You can get genital herpes by having vaginal, anal, or oral sex with someone who has the infection.
You can get herpes if you have contact with:. You also can get genital herpes from a sex partner who does not have a visible sore or is unaware of their infection. It is also possible to get genital herpes if you receive oral sex from a partner with oral herpes.
You will not get herpes from toilet seats, bedding, or swimming pools. You also will not get it from touching objects, such as silverware, soap, or towels. If you have more questions about herpes, consider discussing your concerns with a healthcare provider. Most people with genital herpes have no symptoms or have very mild symptoms. Mild symptoms may go unnoticed or be mistaken for other skin conditions like a pimple or ingrown hair. Because of this, most people do not know they have a herpes infection.
Herpes sores usually appear as one or more blisters on or around the genitals, rectum or mouth. The blisters break and leave painful sores that may take a week or more to heal. Flu-like symptoms e. People who experience an initial outbreak of herpes can have repeated outbreaks, especially if they have HSV However, repeat outbreaks are usually shorter and less severe than the first outbreak.
Although genital herpes is a lifelong infection, the number of outbreaks may decrease over time. STD symptoms can include an unusual sore, a smelly genital discharge, burning when peeing, or bleeding between periods if you have a menstrual cycle.
Effects of long-term preventive therapies Antiviral cream Despite the possible impracticality of the intervention, 2 small crossover trials 16 38 and 23 39 patients were carried out to study the long-term effects of prophylactic application of acyclovir.
Oral antiviral medication A crossover trial investigated 11 patients given mg of acyclovir 4 times daily for 12 weeks. Side effects Indifferent cream The side effects of zinc oxide and glycerin cream included a burning sensation and itching, which occurred more often in the treatment group than in the placebo group.
Antiviral cream The reported side effects of acyclovir and penciclovir creams did not differ from those cited for the placebo groups in either type or frequency. Oral antiviral medication The most frequently reported side effects of oral antiviral medication were headache and nausea, irrespective of dosage and duration of treatment. Conclusion Herpes labialis is a frequently occurring, self-limiting ailment.
Levels of evidence Level I: At least one properly conducted randomized controlled trial, systematic review, or meta-analysis Level II: Other comparison trials, non-randomized, cohort, case-control, or epidemiologic studies, and preferably more than one study Level III : Expert opinion or consensus statements.
Footnotes This article has been peer reviewed. Contributors Drs Opstelten , Knuistingh Neven , and Eekhof contributed to the concept of the article, the literature search, the review of selected articles, and preparing the manuscript for submission. Competing interests None declared.
References 1. Second national study into diseases and actions in general practice. Prevalence of recurrent herpes labialis and aphthous ulcers among young adults on six continents. Can Med Assoc J. Sparano JA, Sarta C. Infection prophylaxis and antiretroviral therapy in patients with HIV infection and malignancy. Curr Opin Oncol. Longitudinal study of genital infection by herpes simplex virus type 1 in Western Scotland over 15 years.
Recurrences after oral and genital herpes simplex virus infection. Influence of site of infection and viral type. N Engl J Med. Corey L, Handsfield HH. Genital herpes and public health: addressing a global problem. The epidemiology of herpes simplex types 1 and 2 infection of the genital tract in Edinburgh — Genitourin Med. Wheeler CE. J Am Acad Dermatol. Esmann J. The many challenges of facial herpes simplex virus infection.
J Antimicrob Chemother. NIH Conference. Herpes simplex virus infection: biology, treatment, and prevention. Ann Intern Med. Opstelten W. In: Stomatitis herpetica. Maarssen, The Netherlands: Elsevier; Altern Ther Health Med. Cassuto J. Topical local anaesthetics and herpes simplex. Topical acyclovir therapy in patients with recurrent orofacial herpes simplex infections. Acyclovir cream for treatment of herpes simplex labialis: results of two randomized, double-blind, vehicle-controlled, multicenter clinical trials.
Antimicrob Agents Chemother. Treatment of herpes simplex labialis with topical acyclovir in polyethylene glycol. J Infect Dis. Latent virus may be reactivated and enter a replicative cycle at any point in time. The reactivation of latent virus is a well-recognized biologic phenomenon, but not one that is understood from a biochemical or genetic standpoint.
It should be noted here that an anti-sense message to one of the immediate-early genes alpha-O may be involved in the maintenance of latent virus.
Stimuli that have been observed to be associated with the reactivation of latent herpes simplex virus have included stress, menstruation, and exposure to ultraviolet light. Precisely how these factors interact at the level of the ganglia remains to be defined.
It should be noted that reactivation of herpesviruses may be clinically asymptomatic, or it may produce life-threatening disease. With the exception of cytomegalovirus retinitis, the definitive diagnosis of a herpesvirus infection requires either isolation of virus or detection of viral gene products. For virus isolation, swabs of clinical specimens or other body fluids can be inoculated into susceptible cell lines and observed for the development of characteristic cytopathic effects.
This technique is most useful for the diagnosis of infection due to herpes simplex virus 1 and 2 or varicella-zoster virus because of their relatively short replicative cycles. The identification of cytomegalovirus by cell culture requires a longer period of time due to its prolonged period of replication.
Epstein-Barr virus does not induce cytopathic changes in cell culture systems and, therefore, can only be identified in culture by transformation of cord blood lymphocytes. Similarly, human herpes virus 6 and 7 have unique growth characteristics which make identification in cell culture systems difficult. Newer and more rapid diagnostic techniques involve the detection of viral gene products.
This can be done by applying fluorescence antibody directed against immediate-early or late gene products to tissue cultures after 24 to 72 hours of incubation. A positive result is the appearance of intranuclear fluorescence. A method which utilizes monoclonal antibodies to an immediate-early gene has been most useful for the identification of CMV. Alternatively, fluorescence antibodies may be applied directly to cell monolayers or scrapings of clinical lesions, with intranuclear fluorescence again indicating a positive result.
Recently developed diagnostic techniques that have clinical utility include in situ and dot-blot hybridization and, importantly, polymerase chain reaction DNA amplification. This latter technique has proved most successful in the diagnosis of herpes simplex virus infections of the central nervous system, particularly when applied to cerebrospinal fluid. Importantly, this tool has been utilized to study the natural history of genital herpes simplex virus infections as well as identify new herpesvirus infections i.
Kaposi's sarcoma herpesvirus. In addition to new tests for virus gene products and viral DNA, improved serologic assays are also becoming available, particularly the application of immunoblot technology to distinguishing herpes simplex virus 1 from 2 infections. However, these tests are only useful for making a diagnosis in retrospect.
Finally, the diagnosis of cytomegalovirus retinitis deserves special mention because it is made clinically by the presence of characteristic retinal changes. The diagnosis is further supported by the presence of cytomegalovirus viruria or viremia, but this is not an absolute requirement. Of all the herpesviruses, herpes simplex virus type 1 and herpes simplex virus type 2 are the most closely related, with nearly 70 per cent genomic homology.
These two viruses can be distinguished most reliably by DNA composition; however, differences in antigen expression and biologic properties also serve as methods for differentiation.
A critical factor for transmission of herpes simplex viruses, regardless of virus type, is the requirement for intimate contact between a person who is shedding virus and a susceptible host. After inoculation onto the skin or mucous membrane and an incubation period of four to six days, herpes simplex virus replicates in epithelial cells Figure As replication continues, cell lysis and local inflammation ensue, resulting in characteristic vesicles on an erythematous base.
Regional lymphatics and lymph nodes become involved: viremia and visceral dissemination may develop depending upon the immunologic competence of the host. In all hosts, the virus generally ascends the peripheral sensory nerves to reach the dorsal root ganglia. Replication of herpes simplex virus within neural tissue is followed by retrograde axonal spread of the virus back to other mucosal and skin surfaces via the peripheral sensory nerves.
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.
0コメント