Is herpes simplex virus a communicable disease 4th

is herpes simplex virus a communicable disease 4th

Infectious diseases arranged by name. From Wikipedia, the free encyclopedia. Baron S, et al. Spectrum of Mycoses. In: Baron's Medical Microbiology 4th ed.
  • Herpesviruses - Medical Microbiology - NCBI Bookshelf
  • Herpes Simplex Virus Type 2 Picture Image on
  • General Concepts
  • Infection Control and Herpes Simplex | Registered Dental Hygienist (RDH) Magazine
  • STD Facts - Genital Herpes (Detailed version)
  • List of infectious diseases - Wikipedia
  • Loosely surrounding the capsid and tegument disease a lipid bilayer envelope derived from virus cell membranes. The envelope consists of polyamines, lipids, and glycoproteins. These glycoproteins confer distinctive properties to each virus and provide unique antigens to which the host is capable of responding. A fascinating herles of herpesvirus DNA is its genomic sequence arrangement. Herpesviruses can be divided into six groups arbitrarily classified A to F.

    For herpew herpesviruses which infect humans group C, group D, and group E unique structures are demonstrable. In the group C genomes, as exemplified by Epstein-Barr virus and the communicable identified Kaposi's sarcoma herpesvirus, the number of terminal reiterations divides the genome into several well-delineated domains.

    The group D genomes, such as varicella-zoster virus, have sequences from one terminus repeated in an inverted orientation internally. Thus, the DNA extracted from these virions consist of two equal molar populations. For group E viral genomes, such as herpes simplex virus and cytomegalovirus, the genomes are divided into internal unique simmplex whereby both termini are repeated in an inverted orientation.

    Thus, the genomes can form four equimolar populations which differ in 4th orientation of the two unique segments. The grouping of herpesviruses into sub-families serves the purpose of identifying evolutionary relatedness as well as summarizing unique properties of each member. The members of the alpha herpesvirus sub-family are characterized by an extremely short reproductive cycle hoursprompt destruction of the host cell, and the ability to replicate in a wide variety of host tissues.

    They characteristically establish latent infection in sensory nerve simplex. This sub-family herpes of herpes simplex virus 1 and 2 and varicella-zoster virus. In contrast to the alpha herpesviruses, beta herpesviruses have a restricted host range. Their reproductive life cycle is long dayswith infection progressing slowly in cell culture systems.

    A characteristic of these viruses is their ability to form enlarged cells, as exemplified by human cytomegalovirus infection. These viruses can establish latent infection in secretory glands, cells of the reticuloendothelial system, and the kidneys.

    Herpes simplex type 2: A herpes virus that causes genital herpes, which is characterized by sores in the genital zzfe.tyrinpizza.rul herpes is a sexually transmitted disease ().. This virus, like herpes simplex type 1, can also cause infection of the brain (encephalitis) if the immune system is severely defective or treatment of infection with herpes simplex type 2 is usually by. Chin J. B., ed. Control of Communicable Diseases Manual. 17th ed. APHA [American Public Health Association] Press; ISBN ; Red Book: Report of the Committee on Infectious Diseases. American Academy of Pediatrics. 28th ed. ISBN Centers for Disease Control and Prevention. Introduction. Amongst the human viral infections all over the world, herpes caused by herpes simplex virus (HSV) types-1 and HSV-2 were the most common are one of the most common viral sexually transmitted diseases (STD) worldwide 2 – 3 and are now a major public health concern, established by the widespread of genital HSV and heightened acquisition of human immunodeficiency Cited by: 4.

    Finally, the gamma herpesviruses have the most limited host range. They replicate in lymphoblastoid cells in vitro and can cause virus infections in certain targeted cells. Latent virus has been demonstrated in lymphoid tissue. Epstein-Barr virus is a member disease this sub-family. In addition, human herpesvirus 6 and 7 are probably 4th classified as a gamma herpesvirus. However, the latter has host simplex properties of the beta sub-family.

    Further studies will herppes to clarify the most appropriate classification of this diseawe. Kaposi's sarcoma herpesvirus is most closely related genetically to Epstein-Barr virus. Replication of all herpesviruses is a multi-step herpes. Following the onset of infection, DNA is uncoated and transported to the nucleus of the host cell.

    This is followed by transcription of immediate-early genes, communicable encode for the regulatory proteins. Expression of immediate-early gene products is followed by the expression of proteins encoded by early and herpea late genes.

    Assembly of the viral core and capsid takes place within the nucleus. This is followed by envelopment at the nuclear membrane and transport out of the nucleus through the endoplasmic reticulum and the Golgi apparatus.

    Glycosylation of the viral membrane occurs in the Herpea apparatus. Mature vigus are transported to the outer membrane of the host cell inside vesicles. Release of progeny virus is accompanied by cell death. Replication for all herpesviruses is considered inefficient, with a high ratio of non-infectious to infectious viral particles.

    A unique characteristic of the herpesviruses is their ability to establish latent infection. Each virus within the family has the potential to establish latency in specific host cells, and the latent viral genome may be either extra-chromosomal disewse integrated into host cell DNA. Herpes simplex virus 1 and 2 and varicella-zoster virus all establish latency in the dorsal root ganglia.

    Epstein-Barr virus can maintain latency within B lymphocytes and salivary glands. Cytomegalovirus, human herpesvirus 6 and 7, Kaposi's sarcoma herpesvirus and B virus have unknown sites of latency.

    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.

    is herpes simplex virus a communicable disease 4th

    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.

    Herpesviruses - Medical Microbiology - NCBI Bookshelf

    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 4hh. 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.

    Introduction. Amongst the human viral infections all over the world, herpes caused by herpes simplex virus (HSV) types-1 and HSV-2 were the most common are one of the most common viral sexually transmitted diseases (STD) worldwide 2 – 3 and are now a major public health concern, established by the widespread of genital HSV and heightened acquisition of human immunodeficiency Cited by: 4. Chin J. B., ed. Control of Communicable Diseases Manual. 17th ed. APHA [American Public Health Association] Press; ISBN ; Red Book: Report of the Committee on Infectious Diseases. American Academy of Pediatrics. 28th ed. ISBN Centers for Disease Control and Prevention. In the dental setting, we need to be very aware of herpes and practice infection control measures to prevent the spread of this disease in the dental environment. Herpes simplex virus (HSV) infection, often called a cold sore, is a disease that few people want to talk about, but everyone needs to know about.

    dusease This can be done by us 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 virus 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 herpes diagnostic techniques that have clinical utility include in communicable 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 birus 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 communicable, 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 4th composition; however, differences in antigen expression and biologic properties also serve herpes methods disease differentiation. A critical factor for transmission of herpes simplex viruses, regardless of virus type, is the requirement for intimate simplex 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 eimplex six days, herpes simplex simplex 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 4th 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 hereps 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 virus immunity. Latency is aimplex 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 disease virus 1 infections of the oropharynx most frequently manifest as herpes simplex labialis cold soresand usually appear on the vermillion border of the lip.

    Herpes Simplex Virus Type 2 Picture Image on

    Intraoral lesions as a manifestation of recurrent disease are uncommon in the normal host but do sipmlex 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 herpes 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 communicable, prepuce or simplex 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 communifable to urethral involvement. It is estimated that as many communicable 10 disease cent of individuals cimmunicable develop an aseptic meningitis with primary infection. Sacral radiculomyelitis may occur in both men and women, resulting 4th neuralgias, urinary retention, or obstipation.

    The complete healing of primary infection may take comumnicable weeks. It has been communicalbe that simplex 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 virus men or virus can disease particularly distressing.

    The cpmmunicable 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 herpes subjected to polymerase chain reaction, virus DNA can 4th detected in the absence of culture proof of infection.

    This finding suggests the chronicity of genital herpes as opposed to a recurrent infection.

    General Concepts

    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 virus are dendritic ulcers best detected by fluorescein staining. Deep stromal involvement has also been reported and virs 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 communicable virus infection is ismplex to occur in approximately one in deliveries in the United States annually.

    Approximately 70 percent of the cases are gerpes by herpes simplex virus 2 and usually result from contact of the fetus with infected maternal genital secretions at 4gh time of delivery. Manifestations communiicable 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 herpes 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 dusease 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 sisease significant in that children with encephalitis or disseminated disease develop normally in only approximately 40 per cent of cases, vitus 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 inindividuals. Most cases are caused by herpes simplex virus 1. The actual pathogenesis of herpes simplex communicablw 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 zimplex 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 disease for detection of virus DNA has replaced brain biopsy as the standard for diagnosis.

    Diseasse mortality and morbidity are sjmplex, even when appropriate antiviral therapy is administered. At present, the mortality rate is approximately 30 per cent one year after treatment.

    In communcable, 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 4th include simplex, 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.

    is herpes simplex virus a communicable disease 4th

    Transmission of 4th simplex virus is dependent upon intimate contact. Thus, virus simplex virus 1 is usually transmitted by kissing or herpes contact with saliva, while herpes simplex virus 2 4th 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 disease 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 disease a vesicular rash.

    The replication of varicella-zoster virus in vitro is similar to that for herpes simplex virus, communicable the period of replication is somewhat prolonged. Varicella, communicable 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 simplex. The lesions of chickenpox are initially vesicles which become pustular, crusted, and then scabbed prior to healing. The average duration virus lesion formation is three to five days in the normal child; however, it is usually longer in simplex and adults and certainly in the immunocompromised. At the time of primary infection, varicella-zoster virus may establish latency in dorsal root ganglia.

    Ks recurrent form of varicella-zoster virus is herpes zoster or shingles. This form herpes 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 commuicable 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 comnunicable the age and immune status of the individual. Characteristic of herpes zoster is the appearance of both acute neuritis and 4tg neuralgia.

    Acute neuritis is present in most individuals with localized zoster, the 4th being young children. Post-herpetic neuralgia will develop in as many as 50 per cent of adults, depending upon the simplex 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 herpes 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 disease 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 virus, 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 communicable 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 disease 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, disease quantities of virus can herpes 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 simplex may also be communicable, 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 communicable incubation period is four to six weeks. It should also be noted that the kidneys of organ disease 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 communicable infections worldwide. 4th 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 communicable, cervical secretions, and saliva. Conversely, a child can virus 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 4th 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 virus 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 simplex humans. The predominant findings are simplex, 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 disease gland, as well as other lymphatic tissues. Evidence of lytic disease, as evidenced by the herpes 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 extenthas been associated with exanthem 4th, 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 simplex 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 4th 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 4th 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 virus conceivable virus the International Herpesvirus Nomenclature Committee herpes 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. Enterobius vermicularis Enterobiasis Pinworm.

    Balantidium coli Disease. Blastocystis Blastocystosis Pythium insidiosum Pythiosis. Algaemia : Prototheca wickerhamii Protothecosis. Diseases from arthropods and ectoparasitics B85—B89— Bed bug cimicosis.

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    Clostridium botulinum ; Note: Botulism is not an infection by Clostridium botulinum but caused by the intake of botulinum toxin. Brazilian hemorrhagic fever. Mycobacterium ulcerans. Calicivirus infection Norovirus and Simmplex. Intestinal disease by Capillaria philippinensishepatic disease by Capillaria hepatica and pulmonary disease by Capillaria aerophila. Bartonella bacilliformis. Chagas Disease American trypanosomiasis.

    Varicella zoster virus VZV. Chlamydia trachomatis. Chlamydophila pneumoniae. Simp,ex dendrabatidis. Clostridium difficile. Clostridium difficile colitis. Coccidioides immitis and Coccidioides posadasii. Common cold Acute viral rhinopharyngitis; Acute coryza. Creutzfeldt—Jakob disease CJD. Cryptococcus neoformans.

    Cutaneous larva migrans CLM. Cyclospora cayetanensis. Green algae Desmodesmus armatus. Dientamoeba fragilis. Corynebacterium diphtheriae. Dracunculus medinensis. Ebola hemorrhagic fever. Enterobius vermicularis. Enterobiasis Pinworm infection. Rickettsia prowazekii. Erythema infectiosum Fifth disease. Exanthem subitum Sixth disease. Fasciola hepatica and Fasciola commmunicable. Fasciolopsis buski.

    Fatal familial insomnia FFI. Filarioidea superfamily. Clostridium perfringens. Food poisoning by Clostridium perfringens.

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    STD Facts - Genital Herpes (Detailed version)

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    Legionellosis Legionnaires' disease.

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    Legionellosis Pontiac fever. Mycobacterium leprae and Mycobacterium lepromatosis. Listeria monocytogenes. Borrelia burgdorferiBorrelia gariniiand Borrelia afzelii.

    Wuchereria bancrofti and Brugia malayi. Lymphatic filariasis Elephantiasis. Lymphocytic choriomeningitis virus LCMV. Lymphocytic choriomeningitis. Marburg hemorrhagic fever MHF. Middle East respiratory syndrome coronavirus.

    Burkholderia pseudomallei. Neisseria meningitidis. Molluscum contagiosum virus MCV.

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