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    بعض اختصارات الميكروبيولوجي-3

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    بعض اختصارات الميكروبيولوجي-3

    مُساهمة من طرف admin في الإثنين أغسطس 29, 2011 11:19 pm

    of the minor bacterial pathogens are summarized in this
    section.
    Bartonella henselae

    Gram-negative rod. Causes cat-scratch fever in
    immunocompetent individuals and bacillary angiomatosis in immunocompromised,
    especially AIDS, patients. Found as normal flora in the mouth of cats.
    Transmitted to humans by cat bite or scratch and from cat to cat by
    fleas.
    Ehrlichia chaffeensis

    Member of rickettsia family. Causes human monocytic
    ehrlichiosis. Transmitted from dog reservoir to humans by ticks, especially
    Dermacentor, the dog tick. Endemic in southern states, e.g., Arkansas.
    Forms morulae in cytoplasm of monocytes. (A morula is a "mulberry-shaped"
    inclusion body composed of many E. chaffeensis
    cells.)
    Fusobacterium nucleatum

    Anaerobic gram-negative rod with pointed ends. Member of
    the normal human flora in mouth, colon, and female genital tract. Causes brain,
    lung, abdominal, and pelvic abscesses, typically in combination with other
    anaerobes and facultative bacteria.
    Gardnerella vaginalis

    Facultative gram-variable rod. Involved in bacterial
    vaginosis, along with Mobiluncus species, which are anaerobic. See "clue
    cells," which are vaginal epithelial cells covered with G. vaginalis
    cells. Positive "whiff" test found in bacterial
    vaginosis.
    Haemophilus ducreyi

    Small gram-negative rod. Causes chancroid. Sexually
    transmitted disease with painful ulcer on genitals (in contrast to syphilis,
    which is painless). To grow in culture, it requires factor X (heme) but not
    factor V (in contrast to H. influenzae, which requires
    both).
    Moraxella catarrhalis

    Small coccobacillary gram-negative rod that resembles the
    cocci of the genus Neisseria. Causes otitis media and sinusitis primarily
    in children. Also causes bronchitis and pneumonia, primarily in older people
    with chronic obstructive pulmonary disease. It is found only in humans and is
    transmitted by respiratory aerosol.
    Yersinia enterocolitica

    Gram-negative rods. Causes enterocolitis similar to that
    caused by Shigella and Salmonella. Also causes mesenteric
    adenitis, which can mimic appendicitis. Found in domestic animals and
    transmitted to humans by fecal contamination of
    food.
    Herpes Simplex Virus Type 1

    Diseases

    Herpes labialis (fever blisters or cold sores), keratitis,
    encephalitis.

    Characteristics

    Enveloped virus with icosahedral nucleocapsid and linear
    double-stranded DNA. No virion polymerase. One serotype; cross-reaction with
    HSV-2 occurs. No herpes group–specific antigen.

    Transmission

    By saliva or direct contact with virus from the
    vesicle.

    Pathogenesis

    Initial vesicular lesions occur in the mouth or on the
    face. The virus then travels up the axon and becomes latent in sensory
    (trigeminal) ganglia. Recurrences occur in skin innervated by affected sensory
    nerve and are induced by fever, sunlight, stress, etc. Dissemination to internal
    organs occurs in patients with depressed cell-mediated immunity with
    life-threatening consequences. HSV-1 encephalitis often affects the temporal
    lobe.

    Laboratory Diagnosis

    Virus causes cytopathic effect (CPE) in cell culture. It is
    identified by antibody neutralization or fluorescent-antibody test. Tzanck smear
    of cells from the base of the vesicle reveals multinucleated giant cells with
    intranuclear inclusions. These giant cells are not specific for HSV-1; they are
    seen in the vesicular lesions caused by HSV-2 and varicella-zoster virus as
    well. A rise in antibody titer can be used to diagnose a primary infection but
    not recurrences. HSV encephalitis can be diagnosed using a PCR assay to detect
    HSV-1 DNA in spinal fluid.

    Treatment

    Acyclovir for encephalitis and disseminated disease.
    Acyclovir has no effect on the latent state of the virus. Trifluorothymidine for
    keratitis. Primary infections and localized recurrences are self-limited.

    Prevention

    Recurrences can be prevented by avoiding the specific
    inciting agent such as intense sunlight. Acyclovir can reduce recurrences. No
    vaccine is available.
    Herpes Simplex Virus Type 2

    Diseases

    Herpes genitalis, aseptic meningitis, and neonatal
    infection.

    Characteristics

    Enveloped virus with icosahedral nucleocapsid and linear
    double-stranded DNA. No virion polymerase. One serotype; cross-reaction with
    HSV-1 occurs. No herpes group–specific antigen.

    Transmission

    Sexual contact in adults and during passage through the
    birth canal in neonates.

    Pathogenesis

    Initial vesicular lesions occur on genitals. The virus then
    travels up the axon and becomes latent in sensory (lumbar or sacral) ganglion
    cells. Recurrences are less severe than the primary infection. HSV-2 infections
    in neonate can be life-threatening because neonates have reduced cell-mediated
    immunity. Asymptomatic shedding of HSV-2 in the female genital tract is an
    important contributing factor to neonatal infections.

    Laboratory Diagnosis

    Virus causes CPE in cell culture. Identify by antibody
    neutralization or fluorescent-antibody test. Tzanck smear reveals multinucleated
    giant cells but is not specific for HSV-2. A rise in antibody titer can be used
    to diagnose a primary infection but not recurrences.

    Treatment

    Acyclovir is useful in the treatment of primary and
    recurrent genital infections as well as neonatal infections. It has no effect on
    the latent state.

    Prevention

    Primary disease can be prevented by protection from
    exposure to vesicular lesions. Recurrences can be reduced by the long-term use
    of oral acyclovir. Neonatal infection can be prevented by delivering the child
    by cesarean section if the mother has visible vesicular lesions in the birth
    canal. There is no vaccine.
    Varicella-Zoster Virus

    Diseases

    Varicella (chickenpox) in children and zoster (shingles) in
    adults.

    Characteristics

    Enveloped virus with icosahedral nucleocapsid and linear
    double-stranded DNA. No virion polymerase. One serotype.

    Transmission

    Varicella is transmitted primarily by respiratory droplets.
    Zoster is not transmitted; it is caused by a reactivation of latent virus.

    Pathogenesis

    Initial infection is in the oropharynx. It spreads via the
    blood to the internal organs such as the liver and then to the skin. After the
    acute episode of varicella, the virus remains latent in the sensory ganglia and
    can reactivate to cause zoster years later, especially in older and
    immunocompromised individuals.

    Laboratory Diagnosis

    Virus causes CPE in cell culture and can be identified by
    fluorescent-antibody test. Multinucleated giant cells seen in smears from the
    base of the vesicle. Intranuclear inclusions seen in infected cells. A 4-fold or
    greater rise in antibody titer in convalescent-phase serum is diagnostic.

    Treatment

    No antiviral therapy is indicated for varicella or zoster
    in the immunocompetent patient. In the immunocompromised patient, acyclovir can
    prevent dissemination.

    Prevention

    Both the varicella vaccine and the zoster vaccine contain
    live, attenuated varicella-zoster virus. Immunocompromised patients exposed to
    the virus should receive passive immunization with varicella-zoster immune
    globulin (VZIG) and acyclovir to prevent disseminated
    disease.
    Cytomegalovirus

    Diseases

    Most common cause of congenital abnormalities in the United
    States. Cytomegalic inclusion body disease in infants. Mononucleosis in
    transfusion recipients. Pneumonia and hepatitis in immunocompromised patients.
    Retinitis and enteritis, especially in AIDS patients.

    Characteristics

    Enveloped virus with icosahedral nucleocapsid and linear
    double-stranded DNA. No virion polymerase. One serotype.

    Transmission

    Virus is found in many human body fluids, including blood,
    saliva, semen, cervical mucus, breast milk, and urine. It is transmitted via
    these fluids, across the placenta, or by organ transplantation.

    Pathogenesis

    Initial infection usually in the oropharynx. In fetal
    infections, the virus spreads to many organs, e.g., central nervous system and
    kidneys. In adults, lymphocytes are frequently involved. A latent state occurs
    in leukocytes. Disseminated infection in immunocompromised patients can result
    from either a primary infection or reactivation of a latent infection.

    Laboratory Diagnosis

    The virus causes CPE in cell culture and can be identified
    by fluorescent-antibody test. "Owl's eye" nuclear inclusions are seen. A 4-fold
    or greater rise in antibody titer in convalescent-phase serum is
    diagnostic.

    Treatment

    Ganciclovir is beneficial in treating pneumonia and
    retinitis. Acyclovir is ineffective.

    Prevention

    No vaccine is available. Ganciclovir suppresses retinitis.
    Do not transfuse CMV antibody-positive blood into newborns or antibody-negative
    immunocompromised patients.
    Epstein-Barr Virus

    Diseases

    Infectious mononucleosis; associated with Burkitt's
    lymphoma in East African children.

    Characteristics

    Enveloped virus with icosahedral nucleocapsid and linear
    double-stranded DNA. No virion polymerase. One serotype.

    Transmission

    Virus found in human oropharynx and B lymphocytes. It is
    transmitted primarily by saliva.

    Pathogenesis

    Infection begins in the pharyngeal epithelium, spreads to
    the cervical lymph nodes, then travels via the blood to the liver and spleen.
    EBV establishes latency in B lymphocytes.

    Laboratory Diagnosis

    The virus is rarely isolated. Lymphocytosis, including
    atypical lymphocytes, occurs. Heterophil antibody is typically positive
    (Monospot test). Heterophil antibody agglutinates sheep or horse red blood
    cells. A significant rise in EBV-specific antibody to viral capsid antigen is
    diagnostic.

    Treatment

    No effective drug is available.

    Prevention

    There is no drug or
    vaccine.
    Human Herpesvirus 8

    Causes Kaposi's sarcoma, especially in AIDS patients.
    Transmitted sexually. Diagnosis made by pathologic examination of lesion biopsy.
    See spindle cells and extravasated red blood cells. Purple color of lesions due
    to collections of red cells. No specific antiviral treatment and no
    vaccine.
    Smallpox Virus

    Disease

    Smallpox. The disease smallpox has been eradicated by use
    of the vaccine. The last known case was in 1977 in Somalia.

    Characteristics

    Poxviruses are the largest viruses. Enveloped virus with
    linear double-stranded DNA. DNA-dependent RNA polymerase in virion. One
    serologic type.

    Transmission

    By respiratory droplets or direct contact with the virus
    from skin lesions.

    Pathogenesis

    The virus infects the mucosal cells of the upper
    respiratory tract, then spreads to the local lymph nodes and by viremia to the
    liver and spleen and later the skin. Skin lesions progress in the following
    order: macule, papule, vesicle, pustule, crust.

    Laboratory Diagnosis

    Virus identified by CPE in cell culture or "pocks" on
    chorioallantoic membrane. Electron microscopy reveals typical particles;
    cytoplasmic inclusions seen in light microscopy. Viral antigens in the vesicle
    fluid can be detected by precipitin tests. A fourfold or greater rise in
    antibody titer in the convalescent-phase serum is diagnostic.

    Treatment

    None.

    Prevention

    Vaccine contains live, attenuated vaccinia virus. Vaccine
    is no longer used except by the military, because the disease has been
    eradicated.
    Molluscum Contagiosum Virus

    Causes molluscum contagiosum. See pinkish, papular skin
    lesions with an umbilicated center. Lesions usually on the face, especially
    around the eyes. Transmitted by direct contact. Diagnosis made clinically;
    laboratory is not involved. There is no established antiviral therapy and no
    vaccine. Cidofovir may be useful in the treatment of the extensive lesions that
    occur in immunocompromised patients.
    Adenovirus

    Diseases

    Upper and lower tract respiratory disease, especially
    pharyngitis and pneumonia. Enteric strains cause diarrhea. Some strains cause
    sarcomas in certain animals but not humans.

    Characteristics

    Nonenveloped virus with icosahedral nucleocapsid and linear
    double-stranded DNA. No virion polymerase. There are 41 serotypes, some
    associated with specific diseases.

    Transmission

    Respiratory droplet primarily; iatrogenic transmission in
    eye disease; fecal–oral transmission with enteric strains.

    Pathogenesis

    Virus preferentially infects epithelium of respiratory
    tract and eyes. After acute infection, persistent, low-grade virus production
    without symptoms can occur in the pharynx.

    Laboratory Diagnosis

    Virus causes CPE in cell culture and can be identified by
    fluorescent-antibody or complement fixation test. Antibody titer rise in
    convalescent-phase serum is diagnostic.

    Treatment

    None.

    Prevention

    Live vaccine against types 3, 4, and 7 is used in the
    military to prevent pneumonia.
    Human Papillomavirus

    Diseases

    Papillomas (warts); condylomata acuminata (genital warts);
    associated with carcinoma of the cervix and penis.

    Characteristics

    Nonenveloped virus with icosahedral nucleocapsid and
    circular double-stranded DNA. No virion polymerase. There are at least 60 types,
    which are determined by DNA sequence not by antigenicity. Many types infect the
    epithelium and cause papillomas at specific body sites.

    Transmission

    Direct contact of skin or genital lesions.

    Pathogenesis

    Two early viral genes, E6 and E7, encode proteins that
    inhibit the activity of proteins encoded by tumor suppressor genes, e.g., the
    p53 gene and the retinoblastoma gene, respectively.

    Laboratory Diagnosis

    Diagnosis is made clinically by finding koilocytes in the
    lesions. DNA hybridization tests are available. Virus isolation and serologic
    tests are not done.

    Treatment

    Podophyllin or liquid nitrogen are most commonly used.
    Alpha interferon is also available.

    Prevention

    There is no drug or
    vaccine.
    Parvovirus B19

    Diseases

    Slapped cheek syndrome (erythema infectiosum), aplastic
    anemia, arthritis, and hydrops fetalis.

    Characteristics

    Nonenveloped virus with icosahedral symmetry and
    single-stranded DNA genome. Virion contains no polymerase. There is one
    serotype.

    Transmission

    Respiratory droplets and transplacental.

    Pathogenesis

    Virus preferentially infects erythroblasts, causing
    aplastic anemia in patients with hereditary anemias; immune complexes cause rash
    and arthritis. Virus can infect fetus and cause severe anemia, leading to
    congestive heart failure and edema (hydrops fetalis).

    Laboratory Diagnosis

    Serologic tests.

    Treatment

    None.

    Prevention

    There is no drug or
    vaccine.
    Influenza Virus

    Disease

    Influenza. Influenza A virus is the main cause of worldwide
    epidemics (pandemics).

    Characteristics

    Enveloped virus with a helical nucleocapsid and segmented,
    single-stranded RNA of negative polarity. RNA polymerase in virion. The two
    major antigens are the hemagglutinin (HA) and the neuraminidase (NA) on separate
    surface spikes. Antigenic shift in these proteins as a result of reassortment of
    RNA segments accounts for the epidemics of influenza caused by influenza A
    virus. Influenza A viruses of animals are the source of the new RNA segments.
    Antigenic drift due to mutations also contributes. The virus has many serotypes
    because of these antigenic shifts and drifts. The antigenicity of the internal
    nucleocapsid protein determines whether the virus is an A, B, or C influenza
    virus.

    Transmission

    Respiratory droplets.

    Pathogenesis

    Infection is limited primarily to the epithelium of the
    respiratory tract.

    Laboratory Diagnosis

    Virus grows in cell culture and embryonated eggs and can be
    detected by hemadsorption or hemagglutination. It is identified by
    hemagglutination inhibition or complement fixation. A fourfold or greater
    antibody titer rise in convalescent-phase serum is diagnostic.

    Treatment

    Amantadine or rimantadine can be used. The neuraminidase
    inhibitors zanamivir and oseltamivir are also available.

    Prevention

    Two vaccines available: a killed (subunit) vaccine
    containing HA and NA and one containing a live, temperature-sensitive mutant of
    influenza virus. Live vaccine replicates in cool nasal passages where it induces
    secretory IgA, but not in warm lower respiratory tract. Both vaccines contain
    the strains of influenza A and B virus currently causing disease. The killed
    vaccine is not a good immunogen and must be given annually. Recommended for
    people older than age 65 years and for those with chronic diseases, especially
    of the heart and lungs. Amantadine, rimantadine, zanamivir, or oseltamivir can
    be used for prophylaxis in unimmunized people who have been
    exposed.
    Measles Virus

    Disease

    Measles. Subacute sclerosing panencephalitis is a rare late
    complication.

    Characteristics

    Enveloped virus with a helical nucleocapsid and one piece
    of single-stranded, negative-polarity RNA. RNA polymerase in virion. It has a
    single serotype.

    Transmission

    Respiratory droplets.

    Pathogenesis

    Initial site of infection is the upper respiratory tract.
    Virus spreads to local lymph nodes and then via the blood to other organs,
    including the skin. Giant cell pneumonia and encephalitis can occur. The
    maculopapular rash is due to cell-mediated immune attack by cytotoxic T cells on
    virus–infected vascular endothelial cells in the skin.

    Laboratory Diagnosis

    The virus is rarely isolated. Serologic tests are used if
    necessary.

    Treatment

    No antiviral therapy is available.

    Prevention

    Vaccine contains live, attenuated virus. Usually given in
    combination with mumps and rubella vaccines.
    Mumps Virus

    Disease

    Mumps. Sterility due to bilateral orchitis is a rare
    complication.

    Characteristics

    Enveloped virus with a helical nucleocapsid and one piece
    of single-stranded, negative-polarity RNA. RNA polymerase in virion. It has a
    single serotype.

    Transmission

    Respiratory droplets.

    Pathogenesis

    The initial site of infection is the upper respiratory
    tract. The virus spreads to local lymph nodes and then via the bloodstream to
    other organs, especially the parotid glands, testes, ovaries, meninges, and
    pancreas.

    Laboratory Diagnosis

    The virus can be isolated in cell culture and detected by
    hemadsorption. Diagnosis can also be made serologically.

    Treatment

    No antiviral therapy is available.

    Prevention

    Vaccine contains live, attenuated virus. Usually given in
    combination with measles and rubella
    vaccines.
    Rubella Virus

    Disease

    Rubella. Congenital rubella syndrome is characterized by
    congenital malformations, especially affecting the cardiovascular and central
    nervous systems, and by prolonged virus excretion. The incidence of congenital
    rubella has been greatly reduced by the widespread use of the vaccine.

    Characteristics

    Enveloped virus with an icosahedral nucleocapsid and one
    piece of single-stranded positive-polarity RNA. No polymerase in virion. It has
    a single serotype.

    Transmission

    Respiratory droplets and across the placenta from mother to
    fetus.

    Pathogenesis

    The initial site of infection is the nasopharynx, from
    which it spreads to local lymph nodes. It then disseminates to the skin via the
    bloodstream. The rash is attributed to both viral replication and immune injury.
    During maternal infection, the virus replicates in the placenta and then spreads
    to fetal tissue. If infection occurs during the first trimester, a high
    frequency of congenital malformations occurs.

    Laboratory Diagnosis

    Virus growth in cell culture is detected by interference
    with plaque formation by coxsackievirus; rubella virus does not cause CPE. To
    determine whether an adult woman is immune, a single serum specimen to detect
    IgG antibody in the hemagglutination inhibition test is used. To detect whether
    recent infection has occurred, either a single serum specimen for IgM antibody
    or a set of acute- and convalescent-phase sera for IgG antibody can be
    used.

    Treatment

    No antiviral therapy is available.

    Prevention

    Vaccine contains live, attenuated virus. Usually given in
    combination with measles and mumps vaccine.
    Parainfluenza Virus

    Disease

    Bronchiolitis in infants, croup in young children, and the
    common cold in adults.

    Characteristics

    Enveloped virus with helical nucleocapsid and one piece of
    single-stranded, negative-polarity RNA. RNA polymerase in virion. Unlike
    influenza viruses, the antigenicity of its hemagglutinin and neuraminidase is
    stable. There are four serotypes.

    Transmission

    Respiratory droplets.

    Pathogenesis

    Infection and death of respiratory epithelium without
    systemic spread of the virus. Multinucleated giant cells caused by the viral
    fusion protein are a hallmark.

    Laboratory Diagnosis

    Isolation of the virus in cell culture is detected by
    hemadsorption. Immunofluorescence is used for identification. A fourfold or
    greater rise in antibody titer can also be used for diagnosis.

    Treatment

    None.

    Prevention

    No vaccine or drug is
    available.
    Respiratory Syncytial Virus

    Diseases

    Most important cause of bronchiolitis and pneumonia in
    infants. Also causes otitis media in older children.

    Characteristics

    Enveloped virus with a helical nucleocapsid and one piece
    of single-stranded, negative-polarity RNA. RNA polymerase in virion. Unlike
    other paramyxoviruses, it has only a fusion protein in its surface spikes. It
    has no hemagglutinin. It has a single serotype.

    Transmission

    Respiratory droplets.

    Pathogenesis

    Infection involves primarily the lower respiratory tract in
    infants without systemic spread. Immune response probably contributes to
    pathogenesis.

    Laboratory Diagnosis

    Enzyme immunoassay (rapid antigen test) detects RSV
    antigens in respiratory secretions. Isolation in cell culture. Multinucleated
    giant cells visible. Immunofluorescence is used for identification. Serology is
    not useful for diagnosis in infants.

    Treatment

    Aerosolized ribavirin for very sick infants.

    Prevention

    Passive immunization with palivizumab (monoclonal antibody)
    or immune globulins in infants who have been exposed is effective. Hand washing
    and the use of gloves may prevent nosocomial outbreaks in the newborn
    nursery.
    Coronavirus

    Disease

    Common cold and SARS (severe acute respiratory
    syndrome).

    Characteristics

    Enveloped virus with helical nucleocapsid and one piece of
    single-stranded, positive-polarity RNA. No virion polymerase. There are two
    serotypes.

    Transmission

    Respiratory droplets. Animal coronaviruses may be the
    source of human infection.

    Pathogenesis

    Infection is typically limited to the mucosal cells of the
    respiratory tract. At least 50% of infections are asymptomatic. Immunity is
    brief and reinfection occurs.

    Laboratory Diagnosis

    The diagnosis primarily a clinical one. Antibody-based and
    PCR-based test are available but not often done.

    Treatment

    None.

    Prevention

    No vaccine or drug
    available.
    Rabies Virus

    Disease

    Rabies. (Rabies is an encephalitis.)

    Characteristics

    Bullet-shaped enveloped virus with a helical nucleocapsid
    and one piece of single-stranded, negative-polarity RNA. RNA polymerase in
    virion. The virus has a single serotype.

    Transmission

    Main reservoir is wild animals such as skunks, raccoons,
    and bats. Transmission to humans is usually by animal bite, but the virus is
    also transmitted by aerosols of bat saliva. In the United States, dogs are
    infrequently involved because canine immunization is so common, but in
    developing countries they are often involved.

    Pathogenesis

    Viral receptor is the acetylcholine receptor. Replication
    of virus at the site of the bite, followed by axonal transport up the nerve to
    the central nervous system. After replicating in the brain, the virus migrates
    peripherally to the salivary glands, where it enters the saliva. When the animal
    is in the agitated state as a result of encephalitis, virus in the saliva can be
    transmitted via a bite.

    Laboratory Diagnosis

    Tissue can be stained with fluorescent antibody or with
    various dyes to detect cytoplasmic inclusions called Negri bodies. The virus can
    be grown in cell culture, but the process takes too long to be useful in
    determining whether a person should receive the vaccine. Serologic testing is
    useful only to make the diagnosis in the clinically ill patient. Antibody does
    not form quickly enough to help in the decision whether or not to immunize the
    person who has been bitten. Serologic testing is also used to evaluate the
    antibody response to the vaccine given before exposure to those in high-risk
    occupations.

    Treatment

    No antiviral therapy is available.

    Prevention

    Preexposure prevention of rabies consists of the vaccine
    only. Postexposure prevention consists of (1) washing the wound; (2) giving
    rabies immune globulins (passive immunization), mostly into the wound; and (3)
    giving the inactivated vaccine (active immunization) made in human cell culture.
    The decision to give the immune serum and the vaccine depends on the
    circumstances. Prevention of rabies in dogs and cats by using a killed vaccine
    has reduced human rabies significantly.
    Poliovirus

    Diseases

    Paralytic poliomyelitis and aseptic meningitis.
    Poliomyelitis has been eradicated in the Western Hemisphere and in many other
    countries.

    Characteristics

    Naked nucleocapsid with single-stranded, positive-polarity
    RNA. Genome RNA acts as mRNA and is translated into one large polypeptide, which
    is cleaved by virus–encoded protease to form functional viral proteins. No
    virion polymerase. There are three serotypes.

    Transmission

    fecal–oral route. Humans are the natural reservoir.

    Pathogenesis

    The virus replicates in the pharynx and the GI tract. It
    can spread to the local lymph nodes and then through the bloodstream to the
    central nervous system. Most infections are asymptomatic or very mild. Aseptic
    meningitis is more frequent than paralytic polio. Paralysis is the result of
    death of motor neurons, especially anterior horn cells in the spinal cord.
    Pathogenesis of postpolio syndrome is unknown.

    Laboratory Diagnosis

    Recovery of the virus from spinal fluid indicates infection
    of the central nervous system. Isolation of the virus from stools indicates
    infection but not necessarily disease. It can be found in the GI tract of
    asymptomatic carriers. The virus can be detected in cell culture by CPE and
    identified by neutralization with type-specific antiserum. A significant rise in
    antibody titer in convalescent-phase serum is also diagnostic.

    Treatment

    No antiviral therapy is available.

    Prevention

    Disease can be prevented by both the inactivated (Salk)
    vaccine and the live, attenuated (Sabin) vaccine; both induce humoral antibody
    that neutralizes the virus in the bloodstream. However, only the oral vaccine
    induces intestinal IgA, which interrupts the chain of transmission by preventing
    GI tract infection. For that reason and because it induces immunity of longer
    duration and is orally administered rather than injected, the Sabin vaccine has
    been the preferred vaccine for many years. However, there have been a few
    vaccine-associated cases of paralytic polio caused by poliovirus in the vaccine
    that reverted to virulence. In view of this, the current recommendation in the
    United States is to use the killed vaccine.
    Coxsackieviruses

    Diseases

    Aseptic meningitis, herpangina, pleurodynia, myocarditis,
    and pericarditis are the most important diseases. Also coxsackievirus B4 may
    cause juvenile diabetes, since it will do so in mice.

    Characteristics

    Naked nucleocapsid with single-stranded, positive-polarity
    RNA. No virion polymerase. Group A and B viruses are defined by their different
    pathogenicity in mice. There are multiple serotypes in each group.

    Transmission

    fecal–oral route.

    Pathogenesis

    The initial site of infection is the oropharynx, but the
    main site is the GI tract. The virus spreads through the bloodstream to various
    organs.

    Laboratory Diagnosis

    The virus can be detected by CPE in cell culture and
    identified by neutralization. A significant rise in antibody titer in
    convalescent-phase serum is diagnostic.

    Treatment

    No antiviral therapy is available.

    Prevention

    No vaccine is available.
    Rhinoviruses

    Disease

    Common cold.

    Characteristics

    Naked nucleocapsid viruses with single-stranded,
    positive-polarity RNA. No virion polymerase. There are more than 100 serotypes,
    which explains why the common cold is so common. Rhinoviruses are destroyed by
    stomach acid and therefore do not replicate in the GI tract, in contrast to
    other picornaviruses such as poliovirus, coxsackievirus, and echovirus, which
    are resistant to stomach acid.

    Transmission

    Aerosol droplets and hand-to-nose contact.

    Pathogenesis

    Infection is limited to the mucosa of the upper respiratory
    tract and conjunctiva. The virus replicates best at the low temperatures of the
    nose and less well at 37°C, which explains its failure to infect the lower
    respiratory tract.

    Laboratory Diagnosis

    Laboratory tests are rarely used clinically. The virus can
    be recovered from nose or throat washings by growth in cell culture. Serologic
    tests are not useful.

    Treatment

    No antiviral therapy is available.

    Prevention

    No vaccine is available because there are too many
    serotypes.
    Norwalk Virus (Norovirus)

    Disease

    Gastroenteritis (watery diarrhea).

    Characteristics

    Nonenveloped virus with icosahedral nucleocapsid and one
    piece of single-stranded, positive-polarity RNA. No virion polymerase. The
    number of serotypes is uncertain.

    Transmission

    fecal–oral route.

    Pathogenesis

    Infection is typically limited to the mucosal cells of the
    intestinal tract. Many infections are asymptomatic. Immunity is brief and
    reinfection occurs.

    Laboratory Diagnosis

    The diagnosis primarily a clinical one. A PCR-based test is
    available but not often done.

    Treatment

    No antiviral drugs available. Treat diarrhea with fluid and
    electrolytes.

    Prevention

    No vaccine or drug
    available.
    Rotavirus

    Disease

    Rotavirus causes gastroenteritis (diarrhea), especially in
    young children.

    Characteristics

    Naked double-layered capsid with 10 or 11 segments of
    double-stranded RNA. RNA polymerase in virion. Rotavirus is resistant to stomach
    acid and hence can reach the small intestine. There are at least six
    serotypes.

    Transmission

    Rotavirus is transmitted by the fecal–oral route.

    Pathogenesis

    Rotavirus infection is limited to the GI tract, especially
    the small intestine.

    Laboratory Diagnosis

    Detection of rotavirus in the stool by ELISA. Isolation of
    the virus is not done from clinical specimens.

    Treatment

    No antiviral drug is available.

    Prevention

    A live vaccine containing five strains of rotavirus is
    available.
    Hepatitis A Virus

    Disease

    Hepatitis A.

    Characteristics

    Naked nucleocapsid virus with a single-stranded,
    positive-polarity RNA. No virion polymerase. Virus has a single serotype.

    Transmission

    fecal–oral route. In contrast to HBV and HCV, blood-borne
    transmission of HAV is uncommon because viremia is brief and of low titer.

    Pathogenesis

    The virus replicates in the GI tract and then spreads to
    the liver during a brief viremic period. The virus is not cytopathic for the
    hepatocyte. Hepatocellular injury is caused by immune attack by cytotoxic T
    cells.

    Laboratory Diagnosis

    The most useful test to diagnose acute infection is IgM
    antibody. Isolation of the virus from clinical specimens is not done.

    Treatment

    No antiviral drug is available.

    Prevention

    Vaccine contains killed virus. Administration of immune
    globulin during the incubation period can mitigate the
    disease.
    Hepatitis B Virus

    Diseases

    Hepatitis B; implicated as a cause of hepatocellular
    carcinoma.

    Characteristics

    Enveloped virus with incomplete circular double-stranded
    DNA; i.e., one strand has about one-third missing and the other strand is
    "nicked" (not covalently bonded). DNA polymerase in virion. HBV-encoded
    polymerase acts as a reverse transcriptase by using viral mRNA as the template
    for the synthesis of progeny genome DNA. There are three important antigens: the
    surface antigen, the core antigen, and the e antigen. In the patient's serum,
    long rods and spherical forms composed solely of HBsAg predominate. HBV has one
    serotype based on the surface antigen.

    Transmission

    Transmitted by blood, during birth, and by sexual
    intercourse.

    Pathogenesis

    Hepatocellular injury due to immune attack by cytotoxic
    (CD8) T cells. Antigen–antibody complexes cause arthritis, rash, and
    glomerulonephritis. About 5% of HBV infections result in a chronic carrier
    state. Chronic hepatitis, cirrhosis, and hepatocellular carcinoma can occur.
    Hepatocellular carcinoma may be related to the integration of part of the viral
    DNA into hepatocyte DNA.

    Laboratory Diagnosis

    HBV has not been grown in cell culture. Three serologic
    tests are commonly used: surface antigen (HBsAg), surface antibody (HBsAb), and
    core antibody (HBcAb). Detection of HbsAg for more than 6 months indicates a
    chronic carrier state. The presence of e antigen indicates a chronic carrier who
    is making infectious virus. The presence of e antigen is an important indicator
    of transmissibility. An HBV-infected person who has neither detectable HBs
    antigen nor HBs antibody is said to be in the "window" phase. Diagnosis of this
    patient is made by detecting HB core antibody. See Chapter 41 for a discussion
    of the results of these tests.

    Treatment

    Alpha interferon and lamivudine, a reverse transcriptase
    inhibitor, can reduce the inflammation associated with chronic hepatitis B but
    does not cure the carrier state.

    Prevention

    There are three main approaches: (1) vaccine that contains
    HBsAg as the immunogen; (2) hyperimmune serum globulins obtained from donors
    with high titers of HBsAb; and (3) education of chronic carriers regarding
    precautions.
    Hepatitis C Virus

    Disease

    Hepatitis C; associated with hepatocellular carcinoma. HCV
    is the most prevalent blood-borne pathogen in the United States.

    Characteristics

    Enveloped virus with one piece of single-stranded,
    positive-polarity RNA. No polymerase in virion. HCV has multiple
    serotypes.

    Transmission

    Most transmission is via blood. Sexual transmission and
    transmission from mother to child probably occurs as well.

    Pathogenesis

    Hepatocellular injury probably caused by cytotoxic T cells.
    HCV replication itself does not kill cells, i.e., does not cause a cytopathic
    effect. More than 50% of infections result in the chronic carrier state. The
    chronic carrier state predisposes to chronic hepatitis and to hepatocellular
    carcinoma.

    Laboratory Diagnosis

    Serologic testing detects antibody to HCV. A PCR-based
    assay for "viral load" can be used to evaluate whether active infection is
    present.

    Treatment

    Alpha interferon plus ribavirin mitigates chronic hepatitis
    but does not eradicate the carrier state.

    Prevention

    Posttransfusion hepatitis can be prevented by detection of
    antibodies in donated blood. There is no vaccine, and hyperimmune globulins are
    not available.
    Hepatitis D Virus

    Disease

    Hepatitis D (hepatitis delta).

    Characteristics

    Defective virus that uses hepatitis B surface antigen as
    its protein coat. HDV can replicate only in cells already infected with HBV;
    i.e., HBV is a helper virus for HDV. Genome is one piece of single-stranded,
    negative-polarity, circular RNA. No polymerase in virion. HDV has one serotype
    (because HBV has only one serotype).

    Transmission

    Transmitted by blood, sexually, and from mother to
    child.

    Pathogenesis

    Hepatocellular injury probably caused by cytotoxic T cells.
    Chronic hepatitis and chronic carrier state occur.

    Laboratory Diagnosis

    Serologic testing detects either delta antigen or antibody
    to delta antigen.

    Treatment

    Alpha interferon mitigates symptoms but does not eradicate
    the carrier state.

    Prevention

    Prevention of HBV infection by using the HBV vaccine and
    the HBV hyperimmune globulins will prevent HDV infection
    also.
    Hepatitis E Virus

    Member of calicivirus family. Causes outbreaks of
    hepatitis, primarily in developing countries. Similar to hepatitis A virus in
    the following ways: transmitted by fecal–oral route, no chronic carrier state,
    no cirrhosis, and no hepatocellular carcinoma. No antiviral therapy and no
    vaccine.
    Note

    All arboviruses are transmitted by arthropods
    (arthropod-borne) such as mosquitoes and ticks from the wild
    animal reservoir to humans.
    Eastern Equine Encephalitis Virus

    Member of the togavirus family. Causes encephalitis along
    the East Coast of the United States. Encephalitis is severe but uncommon.
    Transmitted to humans (and horses) by mosquitoes from small wild birds, such as
    sparrows. Humans and horses are "dead-end" hosts because viremia is low. There
    is no antiviral therapy and no vaccine for
    humans.
    Western Equine Encephalitis Virus, St. Louis Encephalitis
    Virus, California Encephalitis Virus, and West Nile Virus

    The transmission of these encephalitis viruses are similar,
    i.e., they are transmitted to humans by mosquitoes from small wild birds.
    However, they differ in details; i.e., they belong to different virus families
    and cause disease in different geographic areas. Please consult Chapter 42 in
    the text for specific information.

      الوقت/التاريخ الآن هو الخميس ديسمبر 14, 2017 6:23 am