Herpes virus mortality rate

Possible complications can include dehydration if drinking becomes painful due to oral blisters. If left untreated, dehydration can lead to serious problems. Another incredibly rare complication of oral herpes is encephalitis. This occurs when the viral infection travels to the brain and causes inflammation. It may only cause mild flu-like symptoms.

Minor complications of oral herpes include a skin infection if the virus comes in contact with broken skin. This can occur if you have a cut or eczema. It can sometimes be a medical emergency if cold sores cover widespread areas of skin. Children with oral herpes may develop herpes whitlow. If a child sucks their thumb, blisters can form around the finger. If the virus spreads to the eyes , swelling and inflammation can occur near the eyelid.

An infection that spreads to the cornea can lead to blindness. See a doctor if you develop signs of a skin or eye infection. These infections can also be mild and harmless.

Minor complications with genital herpes include inflammation around the bladder and rectum area. This can lead to swelling and pain.

If swelling prevents emptying the bladder, you may need a catheter. Meningitis is another possible, though unlikely, complication. It occurs when the viral infection spreads and causes inflammation of the membranes surrounding the brain and spinal cord.

Keep in mind that having genital herpes increases the risk of other STIs. Blisters can cause breaks in the skin, making it easier for certain microbes to enter the body.

Neonatal herpes is a very serious complication of genital herpes. An infection that passes to a child during pregnancy or childbirth can cause brain damage, blindness, or even death to a newborn baby. Differences by race and Hispanic origin, and the increasing prevalence with increasing age for both HSV-1 and HSV-2, have been reported previously 4 , 5.

The higher prevalence of HSV-2 among females has also been reported 6. For both virus types, a decrease in prevalence over time was seen in all race and Hispanic-origin subpopulations. Decreasing HSV-1 prevalence has been reported previously 4—7. A nonsignificant decline in overall prevalence of HSV-2 from through was reported in a previous study 5. Data for this report are from NHANES, a cross-sectional survey that uses a complex, multistage, probability design to select a sample of the civilian noninstitutionalized U.

In —, non-Hispanic black, non-Hispanic Asian, and Hispanic persons, including Mexican American-persons, were oversampled. Examination weights were used to account for differing probabilities of selection, nonresponse, and noncoverage.

Taylor series linearization was used to calculate standard errors. Age adjustment was done by the direct method to the projected Census population using age groups 14—19, 20—29, 30—39, and 40— Linear regression modeling was used to determine significance of linear and quadratic trends with time controlling for age group. Elaine W. Prevalence of herpes simplex virus type 1 and type 2 in persons aged 14— United States, — 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.

Survivors of B virus infection of the central nervous system have been left with a broad spectrum of neurologic impairment. Recurrent cutaneous disease has been noted, but generally only in patients who initially had a severe encephalitis.

Fortunately, B virus infections in humans are uncommon, because humans are not the natural reservoir of this infection. Instead, the virus is found routinely in rhesus monkey colonies. Infection is transmitted to humans by the bite of an infected animal. Virus replicates locally in a fashion very similar to that of HSV infection. An important difference, however, is that there is a predisposition for rapid neuronal transport of virus to the central nervous system, with ensuing encephalitis in most cases.

B virus is resident in rhesus monkeys, particularly those obtained from Southeast Asia and India. As is the case with human herpesvirus infections, crowding and stress of monkeys lead to virus reactivation and excretion in saliva.

Improper animal handling techniques can cause personnel to be exposed to this virus. Strict adherence to guidelines for the handling of rhesus monkeys is advised.

At present, only one vaccine is licensed for the prevention of a herpesvirus infection; it is directed against varicella-zoster virus. This live, attenuated vaccine is intended for use in the normal child, and not in immunocompromised individuals.

Experimental vaccines for herpes simplex virus 1 and 2 and cytomegalovirus are in various stages of clinical trials. Vaccines engineered for the control of Epstein-Barr virus are in early stages of development. Passive immunization with immune or hyperimmune serum, including monoclonal antibodies, has been used either to prevent infection or as an adjunct to therapy. The administration of varicella-zoster virus immune globulin to the immunocompromised child exposed to this virus is routinely used to prevent, or at least attenuate, chickenpox in these high-risk individuals.

More recently, cytomegalovirus immune globulin has been utilized along with antiviral drugs to treat life-threatening infection in immunocompromised patients, with reported success. Infections due to herpes simplex virus, varicella-zoster virus and, to a lesser extent, cytomegalovirus are the most amenable to therapy with antiviral drugs.

Acyclovir has proved useful for the management of specific infections caused by herpes simplex and varicella-zoster viruses. At present, acyclovir is the treatment of choice for mucocutaneous HSV infections in the immunocompromised host, herpes simplex encephalitis, neonatal herpes simplex virus infections, and varicella-zoster virus infections in the immunocompromised host.

Intravenous administration is preferred for therapy against life-threatening disease. Immunocompromised individuals with mucocutaneous herpes simplex virus infections that are not life-threatening may be given oral acyclovir.

Caution must be exercised when acyclovir is used intravenously, because it may crystallize in the renal tubules when given too rapidly or to dehydrated patients. Recently, two prodrugs have been licensed for the treatment of herpes zoster in the elderly. Valaciclovir, the prodrug of acyclovir, and famciclovir, the prodrug of penciclovir, provide high plasma levels of the parent compounds and offer added efficacy as well as decreased dosing frequency in the management of shingles.

Ganciclovir and foscarnet are licensed for the treatment of cytomegalovirus retinitis in immunocompromised individuals. Treatment with ganciclovir is associated with potential hematologic toxicity, notably neutropenia and thrombocytopenia.

Dose reductions are required if evidence of toxicity appears. Foscarnet is associated with electrolyte imbalances, particularly hypocalcemia. B virus infections of humans have been treated both with acyclovir and ganciclovir with some reports of success; however, no controlled studies have been performed. There is no form of therapy for infection due to Epstein-Barr virus, human herpesvirus 6 or 7 or Kaposi's sarcoma virus at this time. Turn recording back on.

National Center for Biotechnology Information , U. Show details Baron S, editor. Search term. Chapter 68 Herpesviruses Richard J. General Concepts General Biology of Human Herpesviruses Of the more than known herpesviruses, 8 routinely infect only humans: herpes simplex virus types 1 and 2, varicella-zoster virus, cytomegalovirus, Epstein-Barr virus, human herpesvirus 6 variants A and B , human herpesvirus 7, and Kaposi's sarcoma virus or human herpesvirus 8.

Structure Herpesviruses have a unique four-layered structure: a core containing the large, double-stranded DNA genome is enclosed by an icosapentahedral capsid which is composed of capsomers.

Multiplication Transcription, genome replication, and capsid assembly occur in the host cell nucleus. Diagnosis Cytomegalovirus retinitis is diagnosed clinically. Control of Herpesvirus Infections Prevention: A vaccine to prevent varicella-zoster virus infections was recently licensed in the United States. Herpes Simplex Viruses Clinical Manifestations Herpes simplex viruses 1 and 2 have only about 50 percent genomic homology. Pathogenesis The virus replicates initially in epithelial cells, producing a characteristic vesicle on an erythematous base.

Host Defenses Interferon and humoral, mucosal, and cellular immunity are important defenses. Epidemiology Herpes simplex virus 1 transmission is primarily oral, and herpes simplex virus 2 primarily genital.

Varicella-Zoster Virus Clinical Manifestations Primary varicella-zoster virus infection causes varicella chickenpox. Pathogenesis Varicella-zoster virus is usually transmitted by droplets and replicates initially in the nasopharynx. Host Defenses As with herpes simplex virus, interferon and cellular and humoral immunity are important defenses. Epidemiology Varicella-zoster virus is highly contagious; about 95 percent of adults show serologic evidence of infection. Cytomegalovirus Clinical Manifestations Cytomegalovirus causes three clinical syndromes.

Pathogenesis Cytomegalovirus replicates mainly in the salivary glands and kidneys and is shed in saliva and urine. Epidemiology Transmission is via intimate contact with infected secretions. Epidemiology Epstein Barr virus is transmitted by intimate contact, particularly via the exchange of saliva. Human Herpesvirus 6 and 7 Clinical Manifestations Human herpes viruses 6 and 7 are associated with exanthem subitem roseola and with rejection of transplanted kidneys.

Epidemiology Antibodies to this virus are present in almost everyone by age 5. Human Herpesvirus 8 Clinical Manifestations Human herpesvirus 8 has been found associated with Kaposi's sarcoma in AIDS patients as well as intra-abdominal solid tumors. Pathogenesis and Epidemiology Virtually nothing is known about the pathogenesis and epidemiology of this newly described herpesvirus. B Virus Clinical Manifestations In humans, B virus causes an encephalitis that is usually fatal; survivors have brain damage.

Pathogenesis B virus is transmitted to humans by the bite of infected rhesus monkeys and is transported up neurons to the brain. Epidemiology The reservoir for the disease is latent infection in rhesus monkeys, particularly those from Southeast Asia and India.

Introduction In nature, herpesviruses infect both vertebrate and non-vertebrate species, and over a hundred have been at least partially characterized. General Biologic Properties The human herpesviruses share four significant biologic properties. Structure Membership in the family Herpesviridae is based on the structure of the virion.

Classification The grouping of herpesviruses into sub-families serves the purpose of identifying evolutionary relatedness as well as summarizing unique properties of each member. Alpha herpesviruses The members of the alpha herpesvirus sub-family are characterized by an extremely short reproductive cycle hours , prompt destruction of the host cell, and the ability to replicate in a wide variety of host tissues. Copyright Complaints.

Exposure of mucus membrane eyes, nose, mouth. Use of safety goggles or full face shields.