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    بعض اختصارات الميكروبيولوجي-4

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    بعض اختصارات الميكروبيولوجي-4

    مُساهمة من طرف admin في الإثنين أغسطس 29, 2011 11:21 pm

    .
    Yellow Fever Virus

    Member of the flavivirus family. Causes yellow fever in the
    tropical areas of Africa and South America. "Jungle" yellow fever is transmitted
    from monkeys to humans by mosquitoes. "Urban" yellow fever is transmitted from
    human to human by Aedes mosquitoes, i.e., humans are the reservoir in the
    urban form. Humans are not a "dead-end" host because viremia is high. There is
    no antiviral therapy. There is a live, attenuated vaccine for
    humans.
    Dengue Virus

    Member of the flavivirus family. Causes dengue fever in the
    Caribbean region and other tropical areas. Transmitted by Aedes
    mosquitoes from one human to another. A monkey reservoir is suspected. Second
    episodes may result in dengue hemorrhagic fever, a life-threatening
    complication. There is no antiviral therapy and no vaccine for
    humans.
    Human T-Cell Lymphotropic Virus (HTLV)

    Diseases

    Adult T-cell leukemia/lymphoma and HTLV-associated
    myelopathy (also known as tropical spastic paraparesis or chronic progressive
    myelopathy).

    Characteristics

    HTLV is a member of the retrovirus family. It causes
    malignant transformation of CD4-positive T cells (in contrast to HIV, which
    kills those cells). HTLV has three structural genes common to all retroviruses,
    namely, gag, pol, and env, plus two regulatory genes, tax
    and rex. The Tax protein is required for malignant transformation. It
    activates the synthesis of IL-2 (which is T-cell growth factor) and of the IL-2
    receptor. IL-2 promotes rapid T-cell growth, which predisposes to malignant
    transformation.

    Transmission

    HTLV is transmitted primarily by intravenous drug use,
    sexually, and by breast feeding. Transmission by donated blood has greatly
    decreased in the United States because donated blood that has antibodies to HTLV
    is discarded. HTLV infection is endemic in certain geographic areas, namely, the
    Caribbean region including southern Florida; eastern South America; western
    Africa; and southern Japan.

    Pathogenesis

    HTLV induces malignant transformation of CD4-positive T
    lymphocytes by activating IL-2 synthesis as described above. It also causes
    HTLV-associated myelopathy (HAM), which is a demyelinating disease of the brain
    and spinal cord caused either by an autoimmune cross-reaction in which the
    immune response against HTLV damages the neurons or by cytotoxic T cells that
    kill HTLV-infected neurons.

    Laboratory Diagnosis

    Detect anti-HTLV antibodies in the patient's serum using
    the ELISA test. Western blot assay is used to confirm a positive ELISA result.
    PCR assay can detect the presence of HTLV RNA or DNA within infected
    cells.

    Treatment and Prevention

    No specific antiviral treatment for HTLV infection and no
    antiviral drug will cure latent infections by HTLV. No vaccine against HTLV.
    Preventive measures include discarding donated blood if anti-HTLV antibodies are
    present, using condoms to prevent sexual transmission, and encouraging women
    with HTLV antibodies to refrain from breast
    feeding.
    Human Papillomavirus

    See summary in section on DNA Nonenveloped Viruses (Human
    Papillomavirus).
    JC Virus

    Member of the papovavirus family. Causes progressive
    multifocal leukoencephalopathy (PML). Infection with JC virus is widespread, but
    PML occurs only in immunocompromised patients such as those with AIDS.
    Invariably fatal. No antiviral therapy and no
    vaccine.
    Prions

    Diseases

    Creutzfeldt-Jakob disease (CJD), variant CJD, and kuru.
    These are transmissible spongiform encephalopathies. There is a hereditary form
    of CJD called Gerstmann-Sträussler-Scheinker (GSS) syndrome.

    Characteristics

    Prions are composed of protein only. They have no
    detectable nucleic acid and are highly resistant to UV light, formaldehyde, and
    heat. They are encoded by a cellular gene. The pathogenic form increases in
    amount by inducing conformational change in normal form. Normal conformation is
    alpha helix; abnormal is beta-pleated sheet. In GSS syndrome, a mutation occurs
    that enhances the probability of the conformational change to the beta-pleated
    sheet form.

    Transmission

    In most cases of CJD, mode of transmission is unknown. CJD
    has been transmitted by pituitary extracts, brain electrodes, and corneal
    transplants. Kuru was transmitted by ingestion or inoculation of human brain
    tissue. Variant CJD probably is transmitted by ingestion of cow brain tissue in
    undercooked food.

    Pathogenesis

    Aggregation of prion filaments within neurons occurs;
    vacuoles within neurons cause spongiform changes in brain; no inflammation or
    immune response occurs.

    Laboratory Diagnosis

    Brain biopsy shows spongiform changes. No serologic tests.
    Prions cannot be grown in culture.

    Treatment

    None.

    Prevention

    There is no drug or
    vaccine.
    HIV

    Disease

    Acquired immunodeficiency syndrome (AIDS).

    Characteristics

    Enveloped virus with two copies (diploid) of a
    single-stranded, positive-polarity RNA genome. RNA-dependent DNA polymerase
    (reverse transcriptase) makes a DNA copy of the genome, which integrates into
    host cell DNA. Precursor polypeptides must be cleaved by virus–encoded protease
    to produce functional viral proteins. The tat gene encodes a protein that
    activates viral transcription. Antigenicity of the gp120 protein changes
    rapidly; therefore, there are many serotypes.

    Transmission

    Transfer of body fluids, e.g., blood and semen. Also
    transplacental and perinatal transmission.

    Pathogenesis

    Two receptors are required for HIV to enter cells. One
    receptor is CD4 protein found primarily on helper T cells. HIV infects and kills
    helper T cells, which predisposes to opportunistic infections. Other cells
    bearing CD4 proteins on the surface, e.g., astrocytes, are infected also. The
    other receptor for HIV is a chemokine receptor such as CCR5. The NEF protein is
    an important virulence factor. It reduces class I MHC protein synthesis, thereby
    reducing the ability of cytotoxic T cells to kill HIV-infected cells. Cytotoxic
    T cells are the main host defense against HIV.

    Laboratory Diagnosis

    HIV can be isolated from blood or semen, but this procedure
    is not routinely available. Diagnosis is usually made by detecting antibody with
    ELISA as screening test and Western blot as confirmatory test. Determine the
    "viral load," i.e., the amount of HIV RNA in the plasma, using PCR-based assays.
    A high viral load predicts a more rapid progression to AIDS than a low viral
    load. PCR-based assays can also detect viral RNA in infected cells, which is
    useful to detect early infections before antibody is detectable.

    Treatment

    Nucleoside analogues, such as zidovudine (AZT), lamivudine
    (3TC), stavudine (d4T), didanosine (ddI), and zalcitabine (ddC), inhibit HIV
    replication by inhibiting reverse transcriptase. Non-nucleoside inhibitors of
    reverse transcriptase, such as nevirapine and efavirenz, are used also. Protease
    inhibitors, e.g., indinavir, ritonavir, and saquinavir, prevent cleavage of
    precursor polypeptides. Highly active anti-retroviral therapy (HAART) consists
    of two nucleoside inhibitors and one protease inhibitor. Clinical improvement
    occurs, but the virus persists. Treatment of the opportunistic infection depends
    on the organism.

    Prevention

    Screening of blood prior to transfusion for the presence of
    antibody. "Safe sex," including the use of condoms. AZT with or without a
    protease inhibitor should be given to HIV-infected mothers and their newborns.
    Zidovudine (AZT), lamivudine (3TC), and a protease inhibitor should be given
    after a needle-stick injury. There is no
    vaccine.
    Note

    Only the more important of the minor viral pathogens are
    summarized in this section.
    Ebola Virus

    Member of the filovirus family. Causes Ebola hemorrhagic
    fever, which has a very high mortality rate. Animal reservoir and mode of
    transmission to humans are unknown. Human-to-human transmission, especially in
    hospital setting, is by blood and other body fluids. Diagnosis is usually a
    clinical one, but serologic tests are available. In electron microscope, see
    long "thread-like" viruses. Culturing the virus is very dangerous and should be
    done only in special laboratories. There is no antiviral therapy and no
    vaccine.
    Hantavirus (Sin Nombe Virus)

    Member of the bunyavirus family. Causes hantavirus
    pulmonary syndrome. Sin Nombre virus (SNV) is a robovirus, i.e., it is
    rodent-borne. Deer mice are the reservoir, and the virus is
    acquired by inhalation of dried urine and feces. Diagnosis made by detecting
    viral RNA in lung tissue or by serologic tests. No antiviral therapy and no
    vaccine.
    Japanese Encephalitis Virus

    Member of the flavivirus family. Causes outbreaks of
    encephalitis in Asian countries. Transmitted to humans by mosquitoes from the
    reservoir hosts, birds and pigs. No antiviral therapy. An inactivated vaccine is
    available.
    Dermatophytes (e.g., Trichophyton, Microsporum,
    Epidermophyton
    Species)

    Diseases

    Dermatophytoses, e.g., tinea capitis, tinea cruris, and
    tinea pedis.

    Characteristics

    These fungi are molds that use keratin as a nutritional
    source. Not dimorphic. Habitat of most dermatophytes that cause human disease is
    human skin, with the exception of Microsporum canis, which infects dogs
    and cats also.

    Transmission

    Direct contact with skin scales.

    Pathogenesis

    These fungi grow only in the superficial keratinized layer
    of the skin. They do not invade underlying tissue. The lesions are due to the
    inflammatory response to the fungi. Frequency of infection is enhanced by
    moisture and warmth, e.g., inside shoes. An important host defense is provided
    by the fatty acids produced by sebaceous glands. The "id" reaction is a
    hypersensitivity response in one skin location, e.g., fingers, to the presence
    of the organism in another, e.g., feet.

    Laboratory Diagnosis

    Skin scales should be examined microscopically in a KOH
    preparation for the presence of hyphae. The organism is identified by the
    appearance of its mycelium and its asexual spores on Sabouraud's agar. Serologic
    tests are not useful.

    Skin Test

    Trichophytin antigen can be used to determine the
    competence of a patient's cell-mediated immunity. Not used for diagnosis of
    tinea.

    Treatment

    Topical agents, such as miconazole, clotrimazole, or
    tolnaftate, are used. Undecylenic acid is effective against tinea pedis.
    Griseofulvin is the treatment of choice for tinea unguium and tinea
    capitis.

    Prevention

    Skin should be kept dry and
    cool.
    Sporothrix schenckii

    Disease

    Sporotrichosis.

    Characteristics

    Thermally dimorphic. Mold in the soil, yeast in the body at
    37°C. Habitat is soil or vegetation.

    Transmission

    Mold spores enter skin in puncture wounds caused by rose
    thorns and other sharp objects in the garden.

    Pathogenesis

    Local abscess or ulcer with nodules in draining
    lymphatics.

    Laboratory Diagnosis

    Cigar-shaped budding yeasts visible in pus. Culture on
    Sabouraud's agar shows typical morphology.

    Skin Test

    None.

    Treatment

    Itraconazole.

    Prevention

    Skin should be protected when
    gardening.
    Histoplasma capsulatum

    Disease

    Histoplasmosis.

    Characteristics

    Thermally dimorphic, i.e., a yeast at body temperature and
    a mold in the soil at ambient temperature. The mold grows preferentially in soil
    enriched with bird droppings. Endemic in Ohio and Mississippi River valley
    areas.

    Transmission

    Inhalation of airborne asexual spores (microconidia).

    Pathogenesis

    Microconidia enter the lung and differentiate into yeast
    cells. The yeast cells are ingested by alveolar macrophages and multiply within
    them. An immune response is mounted, and granulomas form. Most infections are
    contained at this level, but suppression of cell-mediated immunity can lead to
    disseminated disease.

    Laboratory Diagnosis

    Sputum or tissue can be examined microscopically and
    cultured on Sabouraud's agar. Yeasts visible within macrophages. The presence of
    tuberculate chlamydospores in culture at 25°C is diagnostic. A rise in antibody
    titer is useful for diagnosis, but cross-reaction with other fungi (e.g.,
    Coccidioides) occurs.

    Skin Test

    Histoplasmin, a mycelial extract, is the antigen. Useful
    for epidemiologic purposes to determine the incidence of infection. A positive
    result indicates only that infection has occurred; it cannot be used to diagnose
    active disease. Because skin testing can induce antibodies, serologic tests must
    be done first.

    Treatment

    Amphotericin B for disseminated disease; itraconazole for
    pulmonary disease.

    Prevention

    No vaccine is available. Itraconazole can be used for
    chronic suppression in AIDS patients.
    Coccidioides immitis

    Disease

    Coccidioidomycosis.

    Characteristics

    Thermally dimorphic. At 37°C in the body, it forms
    spherules containing endospores. At 25°C, either in the soil or on agar in the
    laboratory, it grows as a mold. The cells at the tip of the hyphae differentiate
    into asexual spores (arthrospores). Natural habitat is the soil of arid regions,
    e.g., San Joaquin valley in California and parts of Arizona and New
    Mexico.

    Transmission

    Inhalation of airborne arthrospores.

    Pathogenesis

    Arthrospores differentiate into spherules in the lungs.
    Spherules rupture, releasing endospores that form new spherules, thereby
    disseminating the infection within the body. A cell-mediated immune response
    contains the infection in most people, but those who are immunocompromised are
    at high risk for disseminated disease.

    Laboratory Diagnosis

    Sputum or tissue should be examined microscopically for
    spherules and cultured on Sabouraud's agar. A rise in IgM (using precipitin
    test) antibodies indicates recent infection. A rising titer of IgG antibodies
    (using complement-fixation test) indicates dissemination; a decreasing titer
    indicates a response to therapy.

    Skin Test

    Either coccidioidin, a mycelial extract, or spherulin, an
    extract of spherules, is the antigen. Useful in determining whether the patient
    has been infected. A positive test indicates prior infection but not necessarily
    active disease.

    Treatment

    Amphotericin B or itraconazole for disseminated disease;
    ketoconazole for limited pulmonary disease.

    Prevention

    No vaccine or prophylactic drug is
    available.
    Blastomyces dermatitidis

    Disease

    Blastomycosis.

    Characteristics

    Thermally dimorphic. Mold in the soil, yeast in the body at
    37°C. The yeast form has a single, broad-based bud and a thick, refractile wall.
    Natural habitat is rich soil (e.g., near beaver dams), especially in the upper
    midwestern region of the United States.

    Transmission

    Inhalation of airborne spores (conidia).

    Pathogenesis

    Inhaled conidia differentiate into yeasts, which initially
    cause abscesses followed by formation of granulomas. Dissemination is rare, but
    when it occurs, skin and bone are most commonly involved.

    Laboratory Diagnosis

    Sputum or skin lesions examined microscopically for yeasts
    with a broad-based bud. Culture on Sabouraud's agar also. Serologic tests are
    not useful.

    Skin Test

    Little value.

    Treatment

    Itraconazole is the drug of choice.

    Prevention

    No vaccine or prophylactic drug is
    available.
    Paracoccidioides brasiliensis

    Disease

    Paracoccidioidomycosis.

    Characteristics

    Thermally dimorphic. Mold in the soil, yeast in the body at
    37°C. The yeast form has multiple buds (resembles the steering wheel of a
    ship).

    Transmission

    Inhalation of airborne conidia.

    Pathogenesis

    Inhaled conidia differentiate to the yeast form in lungs.
    Can disseminate to many organs.

    Laboratory Diagnosis

    Yeasts with multiple buds visible in pus or tissues.
    Culture on Sabouraud's agar shows typical morphology.

    Skin Test

    Not useful.

    Treatment

    Itraconazole.

    Prevention

    No vaccine or prophylactic drug is
    available.
    Candida albicans

    Diseases

    Thrush, disseminated candidiasis, and chronic mucocutaneous
    candidiasis.

    Characteristics

    Candida albicans is a yeast when part of the normal
    flora of mucous membranes but forms pseudohyphae and hyphae when it invades
    tissue. The yeast form produces germ tubes when incubated in serum at 37°C. Not
    thermally dimorphic.

    Transmission

    Part of the normal flora of skin, mucous membranes, and GI
    tract. No person-to-person transmission.

    Pathogenesis

    Opportunistic pathogen. Predisposing factors include
    reduced cell-mediated immunity, altered skin and mucous membrane, suppression of
    normal flora, and presence of foreign bodies. Thrush is most common in infants,
    immunosuppressed patients, and persons receiving antibiotic therapy. Skin
    lesions occur frequently on moisture-damaged skin. Disseminated infections, such
    as endocarditis and endophthalmitis, occur in immunosuppressed patients and
    intravenous drug users. Chronic mucocutaneous candidiasis occurs in children
    with a T-cell defect in immunity to Candida.

    Laboratory Diagnosis

    Microscopic examination of tissue reveals yeasts and
    pseudohyphae. If only yeasts are found, colonization is suggested. The yeast is
    gram-positive. Forms colonies of yeasts on Sabouraud's agar. Germ tube formation
    and production of chlamydospores distinguish C. albicans from virtually
    all other species of Candida. Serologic tests not useful.

    Skin Test

    Used to determine competency of cell-mediated immunity
    rather than to diagnose candidal disease.

    Treatment

    Skin and mucous membrane disease can be treated with oral
    or topical antifungal agents such as nystatin or miconazole. Disseminated
    disease requires amphotericin B. Chronic mucocutaneous candidiasis is treatable
    with ketoconazole.

    Prevention

    Predisposing factors should be reduced or eliminated. Oral
    thrush can be prevented by using clotrimazole troches or nystatin "swish and
    swallow." There is no vaccine.
    Cryptococcus neoformans

    Disease

    Cryptococcosis, especially cryptococcal meningitis.

    Characteristics

    Heavily encapsulated yeast. Not dimorphic. Habitat is soil,
    especially where enriched by pigeon droppings.

    Transmission

    Inhalation of airborne yeast cells.

    Pathogenesis

    Organisms cause influenzalike syndrome or pneumonia. They
    spread via the bloodstream to the meninges. Reduced cell-mediated immunity
    predisposes to severe disease, but some cases of cryptococcal meningitis occur
    in immunocompetent people.

    Laboratory Diagnosis

    Visualization of the encapsulated yeast in India ink
    preparations of spinal fluid. Culture of sputum or spinal fluid on Sabouraud's
    agar produces colonies of yeasts. Latex agglutination test detects
    polysaccharide capsular antigen in spinal fluid.

    Skin Test

    Not available.

    Treatment

    Amphotericin B plus flucytosine for meningitis.

    Prevention

    Cryptococcal meningitis can be prevented in AIDS patients
    by using oral fluconazole. There is no
    vaccine.
    Aspergillus fumigatus

    Diseases

    Invasive aspergillosis is the major disease. Allergic
    bronchopulmonary aspergillosis and aspergilloma (fungus ball) are important
    also.

    Characteristics

    Mold with septate hyphae that branch at a V-shaped
    angle (low-angle branching). Not dimorphic. Habitat is the soil.

    Transmission

    Inhalation of airborne spores (conidia).

    Pathogenesis

    Opportunistic pathogen. In immunocompromised patients,
    invasive disease occurs. The organism invades blood vessels, causing thrombosis
    and infarction. A person with a lung cavity, e.g., from tuberculosis, may
    develop a "fungal ball" (aspergilloma). An allergic person, e.g., one with
    asthma, can develop allergic bronchopulmonary aspergillosis mediated by IgE
    antibody.

    Laboratory Diagnosis

    Septate hyphae invading tissue are visible microscopically.
    Invasion distinguishes disease from colonization. Forms characteristic mycelium
    when cultured on Sabouraud's agar. See chains of conidia radiating from a
    central stalk. Serologic tests detect IgG precipitins in patients with
    aspergillomas and IgE antibodies in patients with allergic bronchopulmonary
    aspergillosis.

    Skin Test

    None available.

    Treatment

    Amphotericin B for invasive aspergillosis. Some lesions
    (e.g., fungus balls) can be surgically removed. Steroid therapy is recommended
    for allergic bronchopulmonary aspergillosis.

    Prevention

    No vaccine or prophylactic drug is
    available.
    Mucor & Rhizopus Species

    Disease

    Mucormycosis.

    Characteristics

    Molds with nonseptate hyphae that typically branch at a
    90-degree angle (wide-angle branching). Not dimorphic. Habitat is the
    soil.

    Transmission

    Inhalation of airborne spores.

    Pathogenesis

    Opportunistic pathogens. They cause disease primarily in
    ketoacidotic diabetic and leukemic patients. The sinuses and surrounding tissue
    are typically involved. Hyphae invade the mucosa and progress into underlying
    tissue and vessels, leading to necrosis and infarction.

    Laboratory Diagnosis

    Microscopic examination of tissue for the presence of
    non-septate hyphae that branch at wide angles. Forms characteristic mycelium
    when cultured on Sabouraud's agar. See spores contained within a sac called a
    sporangium. Serologic tests are not available.

    Skin Test

    None.

    Treatment

    Amphotericin B and surgical debridement.

    Prevention

    No vaccine or prophylactic drug is available. Control of
    underlying disease, e.g., diabetes, tends to prevent
    mucormycosis.
    Pneumocystis carinii

    Although there is molecular evidence that Pneumocystis
    carinii
    is a fungus, it is described in this book in the section on protozoa
    that cause blood and tissue infections (see
    Pneumocystis).
    Entamoeba histolytica

    Diseases

    Amebic dysentery and liver abscess.

    Characteristics

    Intestinal protozoan. Motile ameba (trophozoite); forms
    cysts with four nuclei. Life cycle: Humans ingest cysts, which form trophozoites
    in small intestine. Trophozoites pass to the colon and multiply. Cysts form in
    the colon, which then pass in the feces.

    Transmission and Epidemiology

    fecal–oral transmission of cysts. Human reservoir. Occurs
    worldwide, especially in tropics.

    Pathogenesis

    Trophozoites invade colon epithelium and produce
    flask-shaped ulcer. Can spread to liver and cause amebic abscess.

    Laboratory Diagnosis

    Trophozoites or cysts visible in stool. Serologic testing
    (indirect hemagglutination test) positive with invasive (e.g., liver)
    disease.

    Treatment

    Metronidazole or tinidazole for symptomatic disease.
    Iodoquinol or paromomycin for asymptomatic cyst carriers.

    Prevention

    Proper disposal of human waste. Water purification. Hand
    washing.
    Giardia lamblia

    Disease

    Giardiasis, especially diarrhea.

    Characteristics

    Intestinal protozoan. Pear-shaped, flagellated trophozoite,
    forms cyst with four nuclei. Life cycle: Humans ingest cysts, which form
    trophozoites in duodenum. Trophozoites encyst and are passed in feces.

    Transmission and Epidemiology

    Fecal–oral transmission of cysts. Human and animal
    reservoir. Occurs worldwide.

    Pathogenesis

    Trophozoites attach to wall but do not invade. They
    interfere with absorption of fat and protein.

    Laboratory Diagnosis

    Trophozoites or cysts visible in stool. String test used if
    necessary.

    Treatment

    Metronidazole.

    Prevention

    Water purification. Hand
    washing.
    Cryptosporidium parvum

    Disease

    Cryptosporidiosis, especially diarrhea.

    Characteristics

    Intestinal protozoan. Life cycle: Oocysts release
    sporozoites; they form trophozoites. After schizonts and merozoites form,
    microgametes and macrogametes are produced; they unite to form a zygote and then
    an oocyst.

    Transmission and Epidemiology

    Fecal–oral transmission of cysts. Human and animal
    reservoir. Occurs worldwide.

    Pathogenesis

    Trophozoites attach to wall of small intestine but do not
    invade.

    Laboratory Diagnosis

    Oocysts visible in stool with acid-fast stain.

    Treatment

    No effective therapy; however, paromomycin may reduce
    symptoms.

    Prevention

    None.
    Trichomonas vaginalis

    Disease

    Trichomoniasis.

    Characteristics

    Urogenital protozoan. Pear-shaped, flagellated
    trophozoites. No cysts or other forms.

    Transmission and Epidemiology

    Transmitted sexually. Human reservoir. Occurs
    worldwide.

    Pathogenesis

    Trophozoites attach to wall of vagina and cause
    inflammation and discharge.

    Laboratory Diagnosis

    Trophozoites visible in secretions.

    Treatment

    Metronidazole for both sexual partners.

    Prevention

    Condoms limit
    transmission.
    Plasmodium Species (P. vivax, P. ovale, P.
    malariae, & P. falciparum)


    Disease

    Malaria.

    Characteristics

    Protozoan that infects red blood cells and tissue, e.g.,
    liver, kidney, and brain. Life cycle: Sexual cycle consists of gametogony
    (production of gametes) in humans and sporogony (production of sporozoites) in
    mosquitoes; asexual cycle (schizogony) occurs in humans. Sporozoites in saliva
    of female Anopheles mosquito enter the human bloodstream and rapidly
    invade hepatocytes (exoerythrocytic phase). There they multiply and form
    merozoites (Plasmodium vivax and Plasmodium ovale also form
    hypnozoites, a latent form). Merozoites leave the hepatocytes and infect red
    cells (erythrocytic phase). There they form schizonts that release more
    merozoites, which infect other red cells in a synchronous pattern (3 days for
    Plasmodium malariae; 2 days for the others). Some merozoites become male
    and female gametocytes, which, when ingested by female Anopheles, release
    male and female gametes. These unite to produce a zygote, which forms an oocyst
    containing many sporozoites. These are released and migrate to salivary
    glands.

    Transmission and Epidemiology

    Transmitted by female Anopheles mosquitoes. Occurs
    primarily in the tropical areas of Asia, Africa, and Latin America.

    Pathogenesis

    Merozoites destroy red cells, resulting in anemia. Cyclic
    fever pattern is due to periodic release of merozoites. Plasmodium
    falciparum
    can infect red cells of all ages and cause aggregates of red
    cells that occlude capillaries. This can cause tissue anoxia, especially in the
    brain (cerebral malaria) and the kidney (blackwater fever). Hypnozoites can
    cause relapses.

    Laboratory Diagnosis

    Organisms visible in blood smear. Thick smear is used to
    detect presence of organism and thin smear to speciate.

    Treatment

    Chloroquine if sensitive. For chloroquine-resistant P.
    falciparum,
    use mefloquine or quinine plus doxycycline. Primaquine for
    hypnozoites of P. vivax and P. ovale. In severe cases, use
    parenteral quinidine or quinine.

    Prevention

    Chloroquine in areas where organisms are sensitive. For
    those in areas with a high risk of chloroquine resistance, mefloquine or
    doxycycline. Primaquine to prevent relapses. Protection from bites. Control
    mosquitoes by using insecticides and by draining water from breeding
    areas.
    Toxoplasma gondii

    Disease

    Toxoplasmosis, including congenital toxoplasmosis.

    Characteristics

    Tissue protozoan. Life cycle: Cysts in cat feces or in meat
    are ingested by humans and differentiate in the gut into forms that invade the
    gut wall. They infect macrophages and form trophozoites (tachyzoites) that
    multiply rapidly, kill cells, and infect other cells. Cysts containing
    bradyzoites form later. Cat ingests cysts in raw meat, and bradyzoites excyst,
    multiply, and form male and female gametocytes. These fuse to form oocysts in
    cat gut, which are excreted in cat feces.

    Transmission and Epidemiology

    Transmitted by ingestion of cysts in raw meat and in food
    contaminated with cat feces. Also by passage of trophozoites transplacentally
    from mother to fetus. Infection of fetus occurs only when mother is infected
    during pregnancy and when she is infected for the first time, i.e., she has no
    protective antibody. Cat is definitive host; humans and other mammals are
    intermediate hosts. Occurs worldwide.

    Pathogenesis

    Trophozoites infect many organs, especially brain, eyes,
    and liver. Cysts persist in tissue, enlarge, and cause symptoms. Severe disease
    in patients with deficient cell-mediated immunity, e.g., encephalitis in AIDS
    patients.

    Laboratory Diagnosis

    Serologic tests for IgM and IgG antibodies are usually
    used. Trophozoites or cysts visible in tissue.

    Treatment

    Sulfadiazine plus pyrimethamine for congenital or
    disseminated disease.

    Prevention

    Meat should be cooked. Pregnant women should not handle
    cats, cat litter boxes, or raw meat.
    Pneumocystis carinii

    Disease

    Pneumonia.

    Characteristics

    Respiratory pathogen. Reclassified in 1988 as a yeast based
    on molecular evidence but medically has several attributes of a protozoan. Life
    cycle: uncertain.

    Transmission and Epidemiology

    Transmitted by inhalation. Humans are reservoir. Occurs
    worldwide. Most infections asymptomatic.

    Pathogenesis

    Organisms in alveoli cause inflammation. Immunosuppression
    predisposes to disease.

    Laboratory Diagnosis

    Organisms visible in silver stain of lung tissue or lavage
    fluid.

    Treatment

    Trimethoprim-sulfamethoxazole, pentamidine.

    Prevention

    Trimethoprim-sulfamethoxazole or aerosolized pentamidine in
    immunosuppressed individuals.
    Trypanosoma cruzi

    Disease

    Chagas' disease.

    Characteristics

    Blood and tissue protozoan. Life cycle: Trypomastigotes in
    blood of reservoir host are ingested by reduviid bug and form epimastigotes and
    then trypomastigotes in the gut. When the bug bites, it defecates and feces
    containing trypomastigotes contaminate the wound. Organisms enter the blood and
    form amastigotes within cells; these then become trypomastigotes.

    Transmission and Epidemiology

    Transmitted by reduviid bugs. Humans and many animals are
    reservoirs. Occurs in rural Latin America.

    Pathogenesis

    Amastigotes kill cells, especially cardiac muscle leading
    to myocarditis. Also neuronal damage leading to megacolon and
    megaesophagus.

    Laboratory Diagnosis

    Trypomastigotes visible in blood, but bone marrow biopsy,
    culture in vitro, xenodiagnosis, or serologic tests may be required.

    Treatment

    Nifurtimox or benznidazole for acute disease. No effective
    drug for chronic disease.

    Prevention

    Protection from bite. Insect
    control.
    Trypanosoma gambiense & Trypanosoma
    rhodesiense


    Disease

    Sleeping sickness (African trypanosomiasis).

    Characteristics

    Blood and tissue protozoan. Life cycle: Trypomastigotes in
    blood of human or animal reservoir are ingested by tsetse fly. They
    differentiate in the gut to form epimastigotes and then metacyclic
    trypomastigotes in salivary glands. When fly bites, trypomastigotes enter the
    blood. Repeated variation of surface antigen occurs, which allows the organism
    to evade the immune response.

    Transmission and Epidemiology

    Transmitted by tsetse flies. Trypanosoma gambiense
    has a human reservoir and occurs primarily in west Africa. Trypanosoma
    rhodesiense
    has an animal reservoir (especially wild antelope) and occurs
    primarily in east Africa.

    Pathogenesis

    Trypomastigotes infect brain, causing encephalitis.

    Laboratory Diagnosis

    Trypomastigotes visible in blood in early stages and in
    cerebrospinal fluid in late stages. Serologic tests useful.

    Treatment

    Suramin in early disease. Suramin plus melarsoprol if
    central nervous system symptoms exist.

    Prevention

    Protection from bite. Insect
    control.
    Leishmania donovani

    Disease

    Kala-azar (visceral leishmaniasis).

    Characteristics

    Blood and tissue protozoan. Life cycle: Human macrophages
    containing amastigotes are ingested by sandfly. Amastigotes differentiate in fly
    gut to promastigotes, which migrate to pharynx. When fly bites, promastigotes
    enter blood macrophages and form amastigotes. These can infect other
    reticuloendothelial cells, especially in spleen and liver.

    Transmission and Epidemiology

    Transmitted by sandflies (Phlebotomus or
    Lutzomyia). Animal reservoir (chiefly dogs, small carnivores, and
    rodents) in Africa, Middle East, and parts of China. Human reservoir in
    India.

    Pathogenesis

    Amastigotes kill reticuloendothelial cells, especially in
    liver, spleen, and bone marrow.

    Laboratory Diagnosis

    Amastigotes visible in bone marrow smear. Serologic tests
    useful. Skin test indicates prior infection.

    Treatment

    Sodium stibogluconate.

    Prevention

    Protection from bite. Insect control.

      الوقت/التاريخ الآن هو الخميس ديسمبر 14, 2017 6:25 am