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. Transmission of virus is through contact with infected secretions.
The average incubation period is four to six weeks. It should also be noted that the kidneys of organ donors can be a source of cytomegalovirus for the recipient, and that peripheral blood leukocytes have been implicated in the transmission of cytomegalovirus via blood transfusion. Cytomegalovirus infections are among the most prevalent virus infections worldwide. As with other herpesviruses, transmission is by intimate contact.
Large quantities of virus can be excreted in saliva and urine for prolonged periods of time. Transmission of virus from mother to child can occur by one of several routes, including infected breast milk, cervical secretions, and saliva.
Conversely, a child can transmit infection to the mother through infected secretions or urine. Moreover, transmission of cytomegalovirus by children in the day care environment has introduced new occupational risks, particularly for seronegative women of child-bearing age.
Hence these susceptible women are at risk for developing primary infection during gestation and delivering a child with symptomatic congenital cytomegalovirus infection. Reactivation of cytomegalovirus infection in immunosuppressed individuals can be particularly problematic, as noted above. The extent of immunosuppression is a major determinant for severity of disease.
In addition, those seronegative individuals who receive organs from persons seropositive for CMV can develop a life-threatening primary CMV infection. The most significant clinical manifestations of Epstein-Barr virus infection are those associated with classic mononucleosis.
Epstein-Barr virus mononucleosis is the most common that occurs in humans. The predominant findings are malaise, myalgia, pharyngitis, cervical adenopathy, splenomegaly, and atypical lymphocytosis.
The diagnosis is confirmed by demonstrating heterophile antibodies or type-specific antibodies to nuclear antigen and viral capsid antigen to Epstein-Barr virus. Epstein-Barr virus is trophic for B-lymphocytes.
Replication has been documented in the parotid gland, as well as other lymphatic tissues. Evidence of lytic disease, as evidenced by the formation of multinucleated giant cells, is not apparent with infection caused by Epstein-Barr virus.
Epstein-Barr virus has also been incriminated as a cause of lymphoproliferative disease in highly immunocompromised individuals. The development of lymphoproliferative malignancy in heart and bone marrow transplant recipients has been documented, and is felt to be associated with the presence of virus.
Epstein-Barr virus is transmitted by intimate contact. Exchange of saliva provides a major route for horizontal transmission of infection. Excretion of virus from other sites does occur, but does not appear to be a major vector for transmission of infection.
Human herpesvirus 6 and 7 have recently been isolated. Human herpes virus 6 as has human herpes virus 7, but to a lesser extent , has been associated with exanthem subitum, or roseola. In addition, there has been an association between human herpesvirus 6 and rejection of transplanted kidneys, fulminant hepatitis and infections of the central nervous system.
The reservoir and mode of transmission of human herpesvirus 6 and 7 are not well understood at the present time. It should be noted that high prevalence of antibodies early in life would implicate transmission within the home from oropharyngeal secretions; however, this has not yet been documented. The epidemiology of human herpesvirus 6 and 7 is poorly understood at present. Loss of transplacental antibodies, followed by acquisition of antibodies early in life, implies horizontal transmission within the home environment.
By the age of 5, antibodies are present in virtually per cent of the population to both of these viruses. Human herpesvirus 6 exists as type A and B. The type A variant was the original isolate being retrieved from an immunocompromised host. The type B variant is associated with roseola.
Some investigators suggest that the genetic differences in these two types warrant distinct names; thus, it is conceivable that the International Herpesvirus Nomenclature Committee may designate these agents as distinct. Recently, a new herpesvirus has been associated with Kaposi's sarcoma and AIDS-related lymphomas of organ cavities. This virus immortalizes B lymphocytes. Isolation of the virus has yet to be achieved. A major concern following exposure to B virus is the development of an almost uniformly fatal encephalitis in most individuals.
The total number of cases reported in the world's literature is under 30, with a mortality of approximately 75 percent. 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. Your healthcare provider may diagnose genital herpes by simply looking at any sores that are present. Providers can also take a sample from the sore s and test it.
If sores are not present, a blood test may be used to look for HSV antibodies. Please note: A herpes blood test can help determine if you have herpes infection. It cannot tell you who gave you the infection or when you got the infection. If you are sexually active, you can do the following things to lower your chances of getting genital herpes:.
Be aware that not all herpes sores occur in areas that a condom can cover. Also, the skin can release the virus shed from areas that do not have a visible herpes sore. For these reasons, condoms may not fully protect you from getting herpes.
There is no cure for genital herpes. However, there are medicines that can prevent or shorten outbreaks. A daily anti-herpes medicine can make it less likely to pass the infection on to your sex partner s. Genital herpes can cause painful genital sores and can be severe in people with suppressed immune systems.
If you touch your sores or fluids from the sores, you may transfer herpes to another body part like your eyes. Do not touch the sores or fluids to avoid spreading herpes to another part of your body. Healing usually occurs in 2 to 4 weeks, and scars may remain.
Postherpetic neuralgia is a complication of shingles where the pain associated with the infection can persist for months and even years. Most people who experience shingles once do not experience it again. It is the major cause of infectious mononucleosis, or "mono" - the "kissing disease. Coughing, sneezing, or sharing eating utensils with an infected person can pass the virus from one person to another.
CMV is also a cause of mononucleosis. In people with healthy immune systems, the virus may not even cause any symptoms. It can be sexually transmitted, can cause problems to newborns, and can cause hepatitis. CMV can be transmitted through sexual contact, breast-feeding, blood transfusions, and organ transplants. It may lead to diarrhea, severe vision problems including blindness, infections of the stomach and intestines, and even death.
For a virus that barely causes a problem in most people with healthy immune systems, it can be amazingly nasty in people with damaged immune systems, such as people with AIDS. Human herpes virus 6 HHV6 is a recently observed agent found in the blood cells of a few patients with a variety of diseases.
It causes roseola a viral disease causing high fever and a skin rash in small children and a variety of other illnesses associated with fever in that age group. This infection accounts for many of the cases of convulsions associated with fever in infancy febrile seizures.
Like other human herpes viruses, HHV6 and HHV7 are so common that most of humankind has been infected at some point, usually early in life. HHV7 can also cause roseola, but it is not clear what other clinical effects that this virus causes.
0コメント