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  1. Mycology is the study of..
    fungi
  2. What are the two classifications of fungi?
    Yeasts and Molds
  3. What is the yeast morphology?
    • unicellular (single, oval or spherical fungal cell)
    • "bacteria-like" in appearance
  4. How does yeast reproduce?
    asexually by budding
  5. What are the 5 steps of budding?
    • 1. Division of nucleus
    • 2. Passage of one nucleus to a bud that "balloons out" from the wall of the mother cell
    • 3. Formation of wall between the bud and mother cell
    • 4.Daughter cell – bud or blastospore
    • 5. Daughter cell initially smaller, increases in size and produces own buds
  6. What is the fungi morphology?
    filamentous (multicellular) filamentous or tubular structures.
  7. How does mold reproduce?
    asexually
  8. What are the 6 steps of mold growth.
    • 1.Germination of condium (reproductive element) – sends out a filament that grows by elongation at its tip
    • 2. Hyphae – elongated filament
    • 3. Mycelium – multiple branches of hyphae
    • 4. Many nuclei within each hyphae
    • 5.Formation of septae – "crosswalls" within hyphae
    • 6.Conidia – terminal end of hyphae – "seeds" for new colonies
  9. Hyphae
    enlongated filament
  10. mycelium
    multiple branches of hyphae
  11. How many nuclei tend to be in each hypahe?
    many
  12. What is the formation of septae?
    "crosswalls" within hyphae
  13. Conidia
    Terminal end of hyphae - "seeds: for new colonies
  14. sexual reproduction
    two reproductive bodies connect and haploid cells fuse to form diploid cells (spores)
  15. Dimorphisim
    the property of having two morphological shapes
  16. Dimorphic fungi at 37 C froms what?
    yeast
  17. dimorphism fungi at 25C forms what?
    mold or mycelial
  18. what are the four major distinguishing morphological characteristics of dimorphic fungi?
    size, presence of capsule, cell wall thickness, spores or conidia production
  19. if dimorphic fungi is aerobic, you have
    molds
  20. if dimorphic fungi is facultative anaerobes you have.....
    yeasts
  21. what is the pH range for dimorphic fungi growth?
    4 -> 6
  22. What are the three selective medias that can be used for dimorphic fungi?
    • Sabouraud's Dextrose Agar (SDA)
    • Dermatophyte Test Media (DTM)
    • Nigerseed (birdseed) agar
  23. What is the minimal media that can be used for dimorphic fungi growth?
    corn meal agar (spore formation)
  24. what kind of slide cultures is needed for the dimorphic fungi?
    undisturbed growth
  25. Molds colonial morphology
    (dry, cotton-like, masses)
  26. yeasts colonial morphology
    (moist, opaque, creamy colonies)
  27. superficial mycoses
    "Surface infections"
  28. cutaneous mycoses or dermatomycoses
    fungal infections of keratinous structures
  29. subcutaneous mycoses
    infections penetrate beneath the skin and involve that subcutaneous connective and bone tissues
  30. systemic or deep mycoses
    infections of internal organs
  31. opportunistic mycoses
    infections in compromised or immunosuppressed
  32. superficial mycoses is minor infections of the _______ or _______
    hair or skin
  33. superficial mycoses appearance
    lesion appearance - scaly or pigmented area of the skin, or nodules on shaft of hair
  34. superficial mycoses prevention
    good hygiene
  35. What is the only contagious fungal diseas in humans?
    dermatomycoses (cutaneous mycoses)
  36. dermatophytes
    fungi that invade keratinized and cutaneous areas of the body (nails, hair and skin)
  37. What are the three major genera of dermatomycoses (cutaneous mycoses)?
    • Microsporum
    • Trichophyton– T. rubrum
    • Epidermophyton
  38. what are the three modes of infection for dermatomycoses (cutaneous mycoses)?
    • 1. Hyphae of dermatophytes grows into keratinized tissue
    • 2.Growth outward from infection site in concentric circles
    • 3. Enzyme production – keritinase, elastase and collagenase
  39. What are the 6 major infections of dermatomycoses (cutaneous mycoses)?
    • Tinea Capitis (ringworm of the scalp)
    • Tinea Barbae (ringworm of the beard)
    • Tinea Pedis (ringworm of the foot)
    • Tinea Curis (ringworm of the groin)
    • Tinea Corpis (Ringworn of the body)
    • Tinea unuium (ringworm of the nails)
  40. What is the initial symptom of tinea capitis?
    inflammation and itching of scalp
  41. tinea capitis mode of infection?
    • hyphae spread into keratinized areas of scalp and hair follicle
    • fungal growth weakens hair
    • breakage at shaft
    • alopecia (hair loss) which is localized and spotty
  42. Alopecia?
    (hair loss) which is localized and spotty
  43. what is the infection site of tinea barbae?
    bearded areas
  44. what is the superficial infection of tinea barbae?
    scaly lesions
  45. what is the severe infection of tinea barbae?
    developement of deep pustules
  46. what is the result of tinea barbae?
    permnanent hair loss
  47. what are the symptoms of tinea pedis?
    foot lesions "athletes foot"
  48. tinea barbae mode of infection?
    • growth between toes of small fluid filled vesicles
    • vesicles rupture
    • development of shallow lesions that itch
  49. pre-disposing conditions for tinea pedis?
    public showers, swimming pools, failure to dry between toes.
  50. Symptoms of tinea curis?
    • lesions in groin or perianal area
    • Red, scaly, itchy and dry "jock itch"
  51. prediposing factors of tinea curis?
    moisture in groin area, wet bathing suits, athletic suporters, tight-fitting slacks, pantyhose and obesity
  52. tinea corpis infection sites?
    non-hairy areas of the body
  53. tinea corpis symptoms?
    lesions are reddened, scaly with papular eruptions
  54. tinea unguium infection sites?
    fingernails and toenails
  55. initial symptoms of tinea unguium?
    superficial thie pathced nail bed
  56. later symptoms of tinea unguium?
    thickening of nail, accumulation of cheesy debris, cracking and discoloration of nail
  57. How can dermatomycoses be diagnosed?
    Microscopic ID : (tissue scrapings) + (10% KOH or 10% NaOH) + heat -> (frees hyphae from keratinous material) + stain (gram stain, wright stain or periodic acid - schiff) -> Presence of septate hyphae

    Macroscopic ID: Cultures on (Dermatophyte Test Media (DTM) or Sabouraud's Dextrose Agar) for about 1 to 2 weeks in room temperature -> funal colonies
  58. What is the treatment for Dermatomycoses
    (Cutaneous Mycoses) ?
    • nonprescription – salves/ointments contain tolnaflate; symptomatic relief
    • good hygiene
    • oral antibiotic therapy – griseofulvin (accumulates in keratin tissue)
    • topical antifungal agents – Azoles (ketoconazole, miconazole and itraconazole)
  59. sporotrichosis is another word for....
    Subcutaneous Mycoses
  60. What is the fungal source of subcutaneous mycoses?
    normal inhabitants of soil or organic matter
  61. how is subcutaneous mycoses introduced to the host?
    wounds or abrasions of skin
  62. cutaneous sporotrichosis is also called what?
    rose gardner's disaease
  63. what is the causative agent for cutanouse sporotrichosis?
    sporothrix schenckii
  64. what is the cutaneous sporotrichosis mode of infection?
    • traumatic implantation of fungus into skin
    • painless papule at inoculation site
    • enlarge to form an ulcerated lesion
  65. Lymphocutaneous sporotrichosis
    spread of cutaneous infection to regional lymph nodes
  66. Lymphocutaneous sporotrichosis mode of infection?
    • fungus forms multiple nodules after being spread by draining lymph channels
    • nodules may ulcerate
    • untreated lesions last years
  67. what are the occupational risk groups of Lymphocutaneous sporotrichosis
    horticulturists, foresters, gardeners, farmers and basket weavers
  68. How is subcutaneous mycoses diagnosed?
    • A direct culture is taken from lesion exudate
    • Yeast (37 C) - oval, cigar shaped
    • Mycelial phase (25 C) - brown/black colonies; conidia - flower-like clusters
  69. What are the treatments for cutaneous sporotrichosis?
    • potassium iodide orally in juice or milk
    • potassium iodide – topical application on open lesions
    • fungus cannot withstand heat – heat packs
  70. what is the treament for lymphocutaneous sporotrichosis?
    antibiotic of choice – amphotericin B
  71. systemic mycoses are also called?
    true pathogens
  72. what is the mode of infection for systemic mycoses?
    • inhalation of dried yeast cells
    • colonize lower respiratory tract
    • asymptomatic or primary pulmonary infection (PPI) that parallels TB
    • disseminated to other organs due to compromised defense mechanisms
  73. What is the major infection of systemic mycoses?
    cryptococcosis
  74. what is the causative agent for cryprtococcosis?
    Cryptococcus neoformans
  75. what is the resovoir for cryptococcosis?
    soil, high association with pigeon droppings
  76. Where does the primary infection of Cryptococcosis take place?
    Lung (PPI)
  77. where does the secondary infection of Cryptococcosis take place?
    disseminated sites - (brain, meninges, CNS and mucicutaneous systems)
  78. what are the initial symptoms of Cryptococcosis?
    fever, cough, nodules of lung
  79. what are the later symptoms of Cryptococcosis?
    arise dues to tumor-like masses at secondary sites, headaches, mental changes, coma, parlysis, eye disturbances and seizures.
  80. What are the two risk groups of Cryptococcosis?
    • Occupational risk - (outbreaks associated with workers demolishing buildings where pigeons have roosted)
    • AIDS patients - highest case rate U.S - chronic meningitis (most common)
  81. How do you diagnose Systemic Mycoses?
    The presence of the capsule
  82. What are the 4 different "presence of capsule" types you can have for systemic mycoses?
    • India Ink Preparation
    • Quelling Reaction
    • Sabouraud Agar
    • Latex Agglutination Test
  83. India Ink Preparation
    wide, clear capsular halo
  84. Quelling reaction
    capsular swelling
  85. Sarbouraud Agar (SDA)
    slimy, mucoid colony
  86. Latex Agglutination Test
    presence of crptococcal capsular polysaccharide
  87. What is bird seed agar used for in spcies identification for cryptococcus?
    pigmentation
  88. What are the treatments for systemic mycoses (cryptococcosis)?
    amphotericin B and fluconazole
  89. What is the endogenous type infection of opportunistic mycoses caused by?
    normal flora
  90. Normal flora for the opportunistic mycoses is found where in the body?
    respiratory tract, mouth, intestinal tract and vagina
  91. What is the process of an opportunistic infection?
    • overgrowth of normal flora
    • inflammation of epithelial surfaces (most frequently oral cavity and vagina)
    • dissemination
    • infectivity of internal organs
  92. What is the main type of infection that is opportunistic mycoses?
    Candidiasis infections
  93. What are the two types of candidiasis infection?
    cutaneous infections and disseminated infections
  94. What is the causative agent of the candidiasis infection?
    Candida albicans
  95. What are the four types of candidiasis cutaneous infections?
    • Thrush or oral candidiasis
    • Vaginal candidiasis (VC)
    • Esophageal candidiasis
    • General candidiasis
  96. Why do candidiasis cutaneous infections arise?
    • due to host's conditions.
    • diabetes, natural immunological deficiencies, or exposure of skin to moist environment
  97. What is the mode of infection for candidiasis cutaneous infections?
    • adherence of blastoconidia to epithelial surfaces
    • fungal proliferation
    • invasion of epithelial tissue
  98. Which candidiasis is the most common?
    Thrush or Oral Candidiasis
  99. what is the symptomatic appearance of thrush or oral candidiasis
    white, adherent patches (pseudomembranes) attach to the epithelial membranes of the tongue, gums, cheeks or throat
  100. What is another term for the oral candidiasis pseudomembrane ?
    fungal mat
  101. What is the composition of the oral candidiasis pseudomembrane?
    yeast, hyphae and epithelial debris
  102. Who has increased susceptibility to oral candidiasis?
    newborns
  103. how is oral candidiasis transmitted to a newborn or child?
    mother -> child
  104. What is the most common form of vaginal infection?
    Vaginal candidiasis (VC)
  105. What are the symptoms of vaginal candidiasis?
    yellow to white milky discharge, inflammation, painful ulcerations and itching
  106. What is the candidal overgrowth associated with vaginal candidiasis related to?
    an increased glucose content of vaginal secretions
  107. who is likely to get vaginal candidiasis?
    diabetic women, pregnant women and broad spectrum of antibiotic therapy users
  108. What is Esophageal Candidiasis?
    complication of AIDS patients
  109. What are the symptoms of Esophageal Candidiasis ?
    painful bleeding, ulcerations, nausea and vomiting
  110. What is general candidiasis infections?
    infections of epidermal tissue
  111. What are examples of areas that are succeptible to general candidiasis infections?
    • folds of skin on obese people (usual sites – upper legs or underarms)
    • tissue that remains wet (occupation –dishwasher)
    • skin covered by wet diapers (diaper rash)
  112. What are the two types of disseminated infections?
    • cutaneous infection
    • Iatrogenic infections
  113. A disseminated cutaneous infection produces what kind of disease?
    a multi-system disease
  114. What is disseminated iatrogenic infections?
    (produced by physicians) – usage of catheters or prosthetic devices
  115. How can you diagnose a candidiasis infection?
    • microscopic examination : gram stain the lesions or exudates. (gram positive = budding yeasts cells)
    • Macroscopic examination: cultures on SDA– (white to cream colored colony, pasty with a yeasty odor) // clutures on corn meal agar – (chlamydospore formation)
    • Germ tube test : yeast cells + serum + (incubation for 2-4 hours) = germ tube formation
  116. What are the treatments for the candidiasis infections?
    • cutaneous - imidazoles
    • disseminated - amphotericin B
  117. Viruses are what in size?
    hetergeneous in size
  118. Viruses are obligate _________ parasitess
    intracellular
  119. what do viruses require to replicate ?
    living cells
  120. Where do viruses replicate?
    the cytoplasm or the nucelus of infectedells.
  121. what host cell machinery does the viruses use for their own replication?
    • RNA
    • DNA
    • protein synthesizing processes
  122. what is the genetic material (genome) of viruses?
    either RNA or DNA (NOT BOTH)
  123. How is viral pathogenesis inititated?
    have to enter the host and replicate in particular cells or organs.
  124. Viral pathogenisis is the study of?
    study of how viruses cause disease in their target hostsusually carried out at the molecular or cellular level.
  125. what must viruses do to produce diesease (the process)
    viruses must enter a host, come in contact with susceptible cells, replicate and produce cell injury or cell death.
  126. What are the four routes in which viruses can enter the host.
    • Fecal-oral route
    • respiratory route
    • arthropod-borne route
    • sexually transmitted route
  127. How through viruses enter the host via the fecal-oral route?
    contaminated food or water
  128. How through viruses enter the host via the respiratory route?
    through the air
  129. How through viruses enter the host via the arthropod-borne route?
    bite of insects or animals
  130. How through viruses enter the host via the sexually transmitted route?
    unprotected sex
  131. what diseases result from viruses entering via the fecal-oral route?
    poliovirus, rotavirus, hepatits A virus
  132. what diseases result from viruses entering via the respiratory route?
    influenza viruses, parainfluenza viruses, measles virus, mumps virus, respiratory syncytial virus
  133. what diseases result from viruses entering via the arthropod-borne route?
    encephalitis viruses, rabies virus
  134. what diseases result from viruses entering via the sexually transmitted route?
    herpes viruses, haptatitis B, C and D viruses, HIV
  135. What are the two different genome a viruses can have?
    DNA/RNA
  136. Capsid
    The protein shell that surrounds the genome
  137. Nucleocapsid
    the structure of the genome AND the capsid
  138. true or false, all viruses contain enzymes associated with its genome?
    false, only some
  139. virion-associated enzymes
    enzymes associated with its genome
  140. in some viruses, an ________ encloses the capsid
    envelope
  141. What is the enevelope made of?
    viral glycoproteins and lipid bilayer derived from the membrane of the infected cell
  142. In some viruses, the envelope contains glycoproteins in the form of spikes called _________.
    peplomers
  143. peplomers
    glycoproteins in the form of spikes in the envelope
  144. Viruses containing peplomers, _______________ prior to entry into the cells.
    attach to the host cell receptor
  145. Virion
    The complete, infectious virus particle
  146. capsomer
    structural subunits of the capsid
  147. What is the criteria for virus classification?
    the organization of the genome :

    • RNA or DNA
    • Single or double strandedness
    • Manner in which the genome is expressed after uncoating in cyotplasm or infected cell.
  148. Explain how the viral genome displays its expressions.
    1. After uncoating in the infected cell



    2. Synthesis of virus-specific mRNAs that

    • are translated
    • into virus-specific

    • protein(s). Use
    • virus-specific enzymes

    • or host enzymes
    • for this process



    3. All viruses use host protein synthesizing machinery to make virus-specific protein(s).
  149. How is the genome expressed?
    synthesis of virus-specific messenger (m) RNA molecules that are translated into virus-specific protein(s).
  150. What is the strandedness for most RNA?
    single stranded
  151. what is the segmentation of RNA?
    1 or more segments
  152. What are the two kinds of polarity of RNA?
    + (mRNA) or - (Anti-mRNA)
  153. What examples of RNA have a positiv3 polarity?
    polovivirus and hepatitis A virus
  154. the genome in a positive polarity is...
    messenger-sense (+)
  155. In positive polarity, the genome can directly act as an...
    messenger RNA
  156. In positive polarity the genome is translated directly to produce...
    proteins (polyproteins)
  157. Genomic RNA in infection in which polarity?
    positive polarity
  158. What is an example of a negative polarity virus?
    rabies virus
  159. the rna genome ____ directly translated into protein in negative polarity
    CANNOT
  160. the genomic RNA in not infectious in which polarity?
    negative
  161. what happens after uncoating in the negative polarity?
    virion-associated transcriptase (RNA dependent RNA polymerase)-transcribes the negative-sense (-) RNA genome into m(+)RNA molecules
  162. What is the main difference about the positive polarity genomes between class 1 and class 3?
    The genome is class 3 has TWO identical positive (+) strands of RNA.
  163. What is the viral example of the class 3 positive polarity?
    HIV
  164. The flow of infomation in the class 3 positive polarity is...
    genomic RNA to DNA to mRNA
  165. what happens after uncoating in the class 3 positive polarity?
    virus contains a virion-associated reverse transcri­ptase, which transcribes the genome (RNA) into a complementary (c) ds-DNA
  166. What happens with double stranded (ds) DNA in class 3 positive polarity?
    • it is translocated to the nucleus and integrates with host
    • genome (provirus).
  167. What is responsible for the production of mRNA in class 3 positive polarity?
    provirus
  168. The genome (DNA) is transcribed by....
    a host cell DNA-dependent RNA polymerase in the nucleus of the infected cell (few exceptions).
  169. Class 1 of DNA replication involves what kind of viruses?
    Viruses with double-stranded (ds)-DNA
  170. What is the flow of information in the Class 1 DNA replication?
    ds-DNA to mRNA (regulated) to viral proteins (classical pathway found in eukaryotic cells)
  171. Where does the DNA replication of class 1 positive polarit take place?
    the nucleus
  172. What happens in class 1 dna replication After
    uncoating and transcription of viral genome to make mRNA’s is REGULATED?
    multiple cycles resulting in expression of alpha,beta and gamma genes
  173. what kind of genes are the alpha?
    immediate early genes - trancsription regulatory genes
  174. What kind of genes are the beta?
    early genes - required for viral DNA syntheis
  175. what kind of genes are the gamma?
    the late genes - transcribed after DNA synthesis and produce viral structural proteins
  176. what is an example of a class 1 DNA replication virus?
    herpesvirus
  177. What kind of viruses are in the class 3 of DNA replications?
    viruses with partially ds-DNA
  178. The genome in dsDNA is partially ___________.
    double stranded
  179. A revers transcriptast step is involved in which replication process?
    dsDNA
  180. what is the relaxaed circuliar genome repaired and converted into a closed ciruclar form by?
    virion-associated DNA polymerase
  181. What is the genome after the RT Step transcribed into?
    (i)mRNA that is translated to produce viral proteins and (ii) genomic length RNA that serves as a template for the synthesis of genomic DNA by a virion-encoded .RNA dependent DNA polymerase (RT)
  182. what is an example of a class 3 DNA virus?
    hepatitis B virus
  183. what is the flow of information in the class 3 relpicatiom for DNA?
    Genomic DNA to RNA to Genomic DNA
  184. What happens after uncoating in the class 3 DNA replication?
    virion genome is converted to complete ds-DNA by virion associated DNA polymerase
  185. In class 3, DNA replication, what is da-DNA transcribed by?
    HOST RNA polymerase
  186. in class 3, DNA replication, ds-DNA is transcribed by HOST RNA polymerase to make....
    (i) mRNA’s and (ii) genomic length (+) RNA
  187. in class 3 in dna replication, The (+) RNA is converted to genomic DNA .....
    virion-encoded reverse transcriptase (RT)
  188. In class 3, of DNA replication is there an intergration of viral DNA in host cell DNA?
    No
  189. What is the order of the seven steps of dna/rna replication'?
    • adsorption
    • entry into cell
    • uncoating
    • synthesis of viral proteins
    • replication of viral genome
    • morphogenesis
    • release
  190. ADSORPTION:
    virion attach to an appropriate cell via virus-specific receptor
  191. ENTRY INTO CELL:
    non-enveloped viruses: receptor-mediatedendocytosis envelopedviruses: fusion of viral envelopewith host cell membrane
  192. UNCOATING:
    removal of capsidproteins in non-enveloped viruses (genome is free in the cytoplasm of cell) or release of nucleocapsid in cytoplasm (enveloped viruses)
  193. SYNTHESIS OF VIRAL PROTEINS:
    Expression of virus genome: RNA and DNAviruses have different strategies
  194. REPLICATION OF VIRAL GENOME:
    different strategies, depending on the nature of the genome(RNA or DNA).
  195. MORPHOGENESIS:

    assembly of progeny virions in thecytoplasm (poliovirus) or in the nucleus of the infected cell (herpes virus) - depends on the virus and cell involved.
  196. RELEASE:
    progeny virions (newly synthesized) arereleased from infected cells by cell lysis (lytic cycle) or by the process of budding from the host cell membrane (enveloped viruses).
  197. How many people are infected with HIV worldwide?
    65 million people
  198. How many people are living with HIV/AIDS?
    33-36 million
  199. How many aids-orphans are there?
    over 16 million
  200. Estimated, how many people die each die of AIDS?
    15,000
  201. How many people in the u.s are living with HIV/AIDS?
    1.5 million
  202. what percentage of men, and what percentage of women are living with aids in the u.s?
    • 70% - men
    • 30% - women
  203. How many people in NYS are living with HIV/AIDS?
    121,000
  204. The New York City AIDS case rate is ____ times the national average?
    three
  205. How many people in buffalo are living with HIV/AIDS?
    10/100,000
  206. Origin of HIV
    theory that simian immunodeficiency virus crossed into humans early 1900s
  207. theory that HIV came to US from _____ in _____.
    Haiti in 1969
  208. HIV is an RNA virus with two ______.
    identical strands of RNA
  209. HIV integrates into hist genome and replicates in _____
    host cell nucleus
  210. Aids patients have ________ antibodies
    anti-HIV
  211. What are the 4 high risk groups for AIDS?
    • Homosexual and bisexual men
    • Intravenous drug users
    • Children born to mothers who are HIV+
    • Hemophiliacs (blood product recipients)
  212. What is inside the capsid of HIV?
    Genome (two identical strands of RNA)
  213. What are the three virion associated enzymes present in the HIV capsid?
    • reverse transcriptase
    • integrase
    • protease
  214. Reverse transcriptase (HIV)
    RNA dependent DNA polymerase
  215. Intergrase (HIV)
    intergrates DNA into host chromosome
  216. Protease (HIV)
    cleaves certain certain proteins during replication
  217. What are the three main things that the HIV enevelope is made up of?
    • GP41
    • GP120
    • GP160
  218. GP41 (HIV)
    stalk for GP120
  219. GP120 (HIV)
    site of attachment to host cell receptors
  220. GP160 (HIV)
    combination of GP41 and GP120
  221. HIV targets cells of the immune system that have ______.
    CD4 receptors
  222. HIV kill __ Cells and also stops the production of new ones from _____.
    • T cells
    • from bone marrow and the thymus
  223. What are the five cells that HIV targets?
    • T cells
    • Macrophages
    • Monocytes
    • Dendritic Cells in lymphocytes
    • Microglial cells in brain
  224. What is the flow of info for HIV replication?
    RNA -> DNA -> mRNA
  225. HIV genomic replication occurs when?
    within hours of virus entering the system
  226. Why is HIV a very efficient replication?
    because it brings it's own enzymes
  227. Once the ______ is present, the HIV virus cannot be removed.
    provirus
  228. why might there be several strains present in the same individual (HIV)?
    HIV undergoes rapid genetic changes
  229. What are the 7 steps of HIV replication?
    • attachment of GP120 to host cell CD4 receptor
    • fusion - viral envelope and host cell plasma membrane fuse together and release viral core into cytoplasm
    • virion -associated reverse transcriptase synthesizes a complementary double stranded DNA
    • Complemenetary DNA is intergrated into host chromosome (provirus) by integrase
    • The provirus is transcribed to produce genomic RNA (genome) and mRNA (viral proteins)
    • Assembly of new viruses occurs in the cytoplasm
    • Viruses are released by budding - acquires envelope and GP120
  230. Ptahogenesis and disease of HIV is caused by....
    the destruction of immune system cells
  231. Death from HIV is usually caused by...
    a secondary or opportunistic infection
  232. What are the factors that determine the speed and severity of the disease?
    • age
    • host cell environment
    • treatment
    • nutrition
    • viral strain
    • tuberculosis (enhances pathogenesis)
  233. The course of the HIV disease is divided into ___ stages
    4
  234. Stage 1 of HIV?
    Acute or primary HIV disease stage
  235. Stage II of HIV?
    asymptomatic HIV disease stage
  236. Stage III of HIV?
    Chronic symptomatic HIV disease stage
  237. Stage IV of HIV?
    Crisis stage of AIDS
  238. Acute retorviral is in what HIV stage?
    Stage 1
  239. Stage 1 of HIV develops ________ weeks after exposure
    2-8
  240. HIV stage I lasts how long?
    2-4 weeks
  241. Stage 1 HIV is characterized like...
    mononucleosis
  242. What are the symptoms of stage 1 HIV?
    fever, sweat, lethargy, headache, diarrhea
  243. In Stage 1, the viruses spread throughout the body with no notable immune response because...
    there are high levels of the virus
  244. What is it called when the HIV virus spreads throughout the body but there is no notable immune response?
    "window of infectivity before sensitization"
  245. the window of infectivity before sensitization
    The body has not had enought ime to produce an immune response by cells are making more viruses
  246. In stage 1 a person is highly infectious but shows HIV ________.
    negative
  247. Stage II of HIV is?
    Asymptomatic HIV disease stage
  248. How long does stage II of HIV last?
    anywhere from months to 11 years
  249. in stage II of HIV, HIV level in blood drop and the bodies make....
    antibodies against HIV
  250. In stage 2 of HIV there is a balance between the level of HIV and the level of ________.
    antibodies
  251. what stage is when the proviral DNA is in laten stage - viral genome is intergrated into host genome?
    stage 2
  252. in stage 2 of HIV patient is still infectious but there are lower levels of _____
    the virus
  253. What is stage 3 of HIV?
    chronic symptomatic HIV disease stage
  254. How long can stage 3 of HIV last?
    for months or years
  255. in stage 3 of HIV, virus replication destroys....
    T4 cells
  256. in stage 3 of HIV, the t4 cell count is ____ or less per microliter of blood
    200
  257. In what stage of HIV does viremia begin?
    3
  258. Viremia
    high levels of virus in blood which can infect more host cells
  259. What are the symptoms of stage 3 of HIV?
    fever, weight loss, malaise, fatigue, night sweats, headaches, and swollen lymph glands
  260. In stage 3 of HIV, destruction of T4 cells leads to...
    the loss of immune response and the onset of opportunsitic infections and cancer
  261. What is stage 4 of HIV called?
    Crisis stage or AIDS
  262. What does the patient aquire in stage 4 of HIV?
    opportunistic infections and cancer
  263. in what stage of HIV is there a marked destruction of immune system cells leading to sever immunodeficiency?
    stage 4
  264. What are the common organism involved in opportunsitic infection in AIDS?
    cryptosporidium, toxoplasma, pneumocystis, mycobacterium, cytomegalovirus, epstein-Barr virus, herpes simplex virus, kapsi's sarcoma
  265. HIV is not transmitted casually, but AIDS is a _________ disease
    communicable
  266. HIV can be transmitted during which stages?
    all of them
  267. what stages is HIV the greatest risk?
    first and third stages
  268. Parenteral transmission (HIV)
    blood transfusions
  269. Perinatal transmission (HIV)
    infected mother to newborn
  270. What % chance is it that HIV is passed from mother to baby?
    35%
  271. How is transmisson of HIV reduced between mother and newborn?
    Giving an antiviral
  272. If an antiviral is started before birth what is the chance of prenatal HIV transmission lowered to?
    6%
  273. If an antiviral is started after 3 days of life, what is the chance of prenatal HIV transmission lowered to?
    18%
  274. ART for HIV stands for?
    Anti-retroviral therapy
  275. A cure for HIV infections would require ......
    cleansing the body of HIV
  276. to cure HIV you would need to remove....
    all cells containing the provirus while eliminating any viruses from the body
  277. why is there no vaccine available fror HIV?
    the rate of mutation of HIV
  278. What are the 5 main anti-HIV drugs?
    • Reverse transcriptase inhibiotors
    • protease inhibitors
    • CCR5 antagonist
    • Integrase inhibitors
    • Fusion inhibitors
  279. What are two types of reverse transcriptase inhibitors?
    • Nucleoside analogs
    • Non-Nucleoside compounds
  280. What are 3 nucleoside analogs?
    AZT, tenofovir, emtricitabine
  281. what are 3 kinds of non-nucleoside compounds?
    nevirapine, delavirdine, efavirenz
  282. What are 3 types of protease inhibtors?
    saquinavir, ritonair, indinavir
  283. What does a CCR5 antagonist do?
    block receptor which inhibits viral attachment
  284. what does integrase inhibitors do?
    prevent intergration would give a better chance to eliminate virus (if it is extracellular)
  285. What are the two types of combination therapies for HIV?
    • "AIDS" cocktails
    • Highly active anti-retroviral treatment (HAART)
  286. What is Highly active anti-retroviral treatment (HAART)?
    use of triple combination therapy
  287. All anti HIV drugs are highly toxic and very _______.
    expensive
  288. Currently there is research to kill cells that are (HIV) ....?
    "reservoirs or dormant HIV"
  289. What two things rapidly kill HIV infected macrophages?
    miltefosine and perifosine
  290. ELISA stands for?
    (enzyme-linked immunosorbent assay)
  291. What does ELISA test for?
    antibodies
  292. What are two rapid HIV tests?
    • Ora Quick rapid HIV-1 antibody test
    • Uni-gold recombigen HIV
  293. If a person has a positive test for HIV, they are tested .....
    a second time six months later then a confirmatory test is performed.
  294. What is the confirmatory test for HIV?
    Western blot
  295. What does a western blot test detect?
    Several virus-specific proteins
  296. What is the paramyxoviridae genome?
    Non-segmented single stranded RNA
  297. paramyxoviridae paramyxoviridae viral glycoproteins (hemagglutinin and neuramidase) locations
    present
  298. paramyxoviridae viral glycoproteins (hemagglutinin and neuramidase) locations
    on the same glycoprotein
  299. paramyxoviridae examples? (4)
    parainfluenze, RSV, Measles, Mumps
  300. orthomyxoviridae genome
    Segmented single stranded
  301. orthomyxoviridae virion-associated polymerase presence?
    present
  302. orthomyxoviridae viral glycoproteins (hemagglutinin and neuramidase) locations?
    on seperate glycoproteins
  303. orthomyxoviridae example
    influenza
  304. Both the orthomyxoviridae and paramyxoviridae groups of viruses are responsible for what in childrean and adults?
    upper and lower respiratory tract infections
  305. Both the orthomyxoviridae and paramyxoviridae groups of viruses cause what percentage range of adult colds in the U.S?
    10-15%
  306. Human parainfluenze viruses have how many serotypes?
    4
  307. What serotypes of Human parainfluenze viruses cause infections in humans?
    1,2 and 3
  308. Human parainfluenze viruses is more common in children up to ________ years old.
    3
  309. Human parainfluenze viruses transmission?
    respiratory route (inhalation of droplets)
  310. where does Human parainfluenze viruses replicate?
    in the respiratory tract
  311. is there viremia in Human parainfluenze viruses?
    no
  312. Human parainfluenze viruses types 1 and 2 cause what in children 6mo to 3yrs?
    croup
  313. what are the clinical symptoms of croup of Human parainfluenze viruses?
    • characteristic spasmodic cough
    • difficulty breathing
    • rhinarrhea (runny-nose)
  314. what diseases are cause by Human parainfluenze viruses type 3?
    bronchiolitis and pneumonia
  315. Human parainfluenze viruses immunity?
    transient (short lived); reinfiection possible
  316. Human parainfluenze viruses diagnosis?
    detect viral antigens in cells from nasal secretions
  317. Human parainfluenze viruses treatment?
    no ant-viral drugs, only symptom management
  318. is there a vaccine for Human parainfluenze viruses?
    no
  319. how many Respiratory syncytial virus (RSV) serotypes are there?
    1
  320. Respiratory syncytial virus (RSV) is prevalent in......
    infants and children
  321. Respiratory syncytial virus (RSV) transmission
    respiratory route
  322. does Respiratory syncytial virus (RSV) have viremia?
    no
  323. what is the Respiratory syncytial virus (RSV) incubation period?
    1-5 days
  324. what are the clinical symptoms of Respiratory syncytial virus (RSV)?
    • bronchiolitis and pneumonia in infants less than 6mos old
    • fever and cough
    • rinorrhea
  325. Respiratory syncytial virus (RSV) immunity?
    transient; reinfection possible
  326. Respiratory syncytial virus (RSV) diagnosis?
    detect viral antigens in cells of nasal secretion
  327. Respiratory syncytial virus (RSV) treatments
    • Isolation of infected child
    • antiviral drug, ribavirin, used if severely infected
  328. Respiratory syncytial virus (RSV) passive immunization?
    • RSV immune globulin (synagis0 - short lived, given monthly
    • palivizumab
  329. is there a vaccine for Respiratory syncytial virus (RSV)?
    no
  330. how many serotypes does mumps have?
    1
  331. mumps is a _________ disease
    childhood
  332. mumps has a high rate of _______infections
    subclinical
  333. mumps transmission
    respiratory route
  334. where does mumps replicate?
    respiratory tract and lymph nodes
  335. does viremia occur with mumps?
    yes
  336. mumps incubation period?
    12-21 days
  337. mumps clinical symptoms?
    • fever, headache, pain
    • swelling of (one or both) parotid glands
    • symptoms have sudden onset
    • complications
  338. What are the 2 complications that can occur with mumps?
    • orchitis - swelling of testes (higher chance in adults)
    • meningitis - CNS involement
  339. mumps diagnosis?
    • IgM antibodies present for a month after infection
    • IgG antibodies not present during acute infection; present during convalescent stage and for life.
  340. is there a vaccine for mumps?
    yes
  341. what are the mumps vaccines?
    Live, attenuated (non-virulent) vaccine - MMR (measles, mumps, rebeola)
  342. when are the two doses of vaccines for mumps?
    • First at 12-15 mos old
    • Second at 4-6 years or 11-12 yrs old
  343. how many serotypes does measles (rubeola) have?
    1
  344. what does measles (rubeola) cause?
    • acute febrile (fever)
    • exanthmatous (rash)
  345. is measles (rubeola) infectious?
    yes, highly
  346. What are the two reasons that measles are able to be eliminated completely?
    • Humansa are the only natural host
    • There is no carrier state
  347. measles (rubeola) transmission
    respiratory route
  348. measles (rubeola) incubation period?
    10-14 days
  349. measles (rubeola) clinical symptoms?
    • The 3 C's : cough, coryza (head cold, rinorrhea), conjunctivitis (eye infection)
    • koplik spots
    • warthin-finkeldey
    • viremia
    • maculopapular rash
  350. koplik spots
    characteristic of measles; red/yellow spots with white ceter around molars in the mouth
  351. warthin-finkeldey syncytial cells (function)
    as virus infects neighboring cells it causes them to fuse together resulting in giant, multinucleated cells, characteristics of measles
  352. Maculopapular rash
    reddish rash on the hands and face which can spread to rest of body
  353. measles (rubeola) immunity
    permanent immunity, IgG antibodies persist for life
  354. measles (rubeola) diagnosis?
    serodiagnosis (test for antibodies)
  355. is there a vaccine for measles (rubeola) ?
    yes. MMR vaccine
  356. how many serotypes does influenza have?
    3
  357. What are the three serotypes of influenza?
    A,B and C
  358. What influenza serotypes cause infections in humans?
    only A and B
  359. what is the influenza resovoir?
    Pigs and birds
  360. _____ have a receptor for human, avian and swine influenza viruses
    pigs
  361. The influenza genome is segmented into how many pieces?
    8
  362. each influenza genome segment has its own....
    transcriptase that makes mRNA
  363. the influenza viral envelope has ____ peplomers.
    2
  364. what are the two peplomers that the influenza viral envelope has?
    • H or HA - hemagglutinatinin for attachment to cell receptor
    • N or NA - neuraminidase for release from infected cells
  365. the influenza lipid bilayer is derived from the...
    host cell membrane
  366. influenza undergoes ______ changes each year
    antigenic
  367. What do we need to do to respond to antigenic changes?
    make a new vaccine each year
  368. How can the RNA for peplomers change?
    by two mechanisms
  369. point mutations
    minor antigenic shift
  370. point mutation (action)
    virion-associated transcriptase changes one or two nucleotides which slightly changes the antigenic properties of the peplomers
  371. influenza transmission
    respiratory route
  372. influenza incubation period?
    1-2 days
  373. influenza clinical symptoms
    • abrupt onset of fever which lasts 3-4days
    • severe headache
    • myalgia (muscular aches)
    • common complication - pneumonia
  374. influenza immunity
    no permananet immunity
  375. What is there no permamnent influenza immunity?
    antigenic changes in the virus
  376. influenza diagnosis
    serodiagnosis
  377. influenza treatments
    • anti-influenza drugs :inhibit uncoating
    • Neuraminidase inhibitors
  378. What are the anti-influenza drugs?
    • amantadine
    • rimantadine
  379. The anti-influenza drugs only work for which type of influenza?
    type A
  380. today, most if not all strains of influenza are resistant to....
    anti-influenza drugs
  381. What are the neuraminidase inhibtors?
    • Relenza (zanamivir) - nasal spray
    • Tamiflu (oseltamivir) - tablet
  382. What drugs work for type A and B influenza?
    neuraminidase inhibitors
  383. How do neuarminidase inhibitors work?
    prevent the release of virus from infected cells, decreases the severity and duration of infection.
  384. all influenza vaccines contain what?
    two subtypes of influenza A and one subtype of influenza B
  385. Why does influenza vaccine composition change each year?
    to respond to antigenic changes of the virus
  386. What are the two FDA approved influenza vaccines?
    • Inactivated virus vaccine given to high risk groups
    • live, attenuated intranasal vaccine (LIAV) given to healthy people (2-49yo)
  387. Who are the high risk groups for influenza?
    elederly, people with immune, cardiovascular, pulmonary or metabolic disorders, infants, people on aspirin therapy or people with asthma.
  388. in influenza, temperature sensitive mutants can grow in....
    lower temperatures
  389. influenza mutants only grow in the....
    Upper respiratory Tract (URT)
  390. What are two contradictions for LIAV (influenza vaccine)
    • vaccine is grown in chicken eggs, so shouldnt be given to someone with allergies to eggs
    • Vaccine should not be given to people who have a fever or those who are not fully healthy.
  391. North america swine influezna virus contains genes from...
    H of H1N1
  392. Asian and Europen swine influezna virus contains genes from...
    N of H1N1
  393. North American avian virus has what subunit?
    transcriptase subunit 1
  394. Human influenza virus has what subunit?
    transcriptase subunit 2
  395. Hepatits A virus has what kind of infections?
    • subclinical or asymptomatic
    • acute viral hepatitis A infection
  396. Which Hepatits A virus infection has a higher incidence than other Hepatits A virus infections?
    subclinical/asymptomatic infection
  397. which Hepatits A virus infection occurs, but shows no symptoms, having the host not even know it's infected?
    subclincial or asymptomatic infection
  398. subclinical or clincal aysmpotomatc has ______% antibodies to the virus.
    50%
  399. does acute viral hepatitis A infection have a carrier state?
    no
  400. acute viral hepatitis A infection incubation period
    15- 50 days
  401. What is the two symptom phases of acute viral hepatitis A infection?
    • preicteric
    • icteric
  402. acute viral hepatitis A infection preicteric phase
    • virus is replicating in intesitnal cells;
    • abrupt onset of fever
    • fatigue
    • anorexia (loss of appetite)
  403. acute viral hepatitis A infection preiteric phase time length?
    a few weeks to several years
  404. acute viral hepatitis A infection icteric phase
    • viremia - liver infected
    • dark urine
    • janduice
  405. acute viral hepatitis A infection icteric phase time lentgh?
    1-2 weeks
  406. The majority of individuals with acute viral hepatitis A infection __________ recover
    fully
  407. acute viral hepatitis A infection trasnmission
    fecal-oral route (contaminated food)
  408. acute viral hepatitis A infection immune response
    IgM and IgG antibodies are produced
  409. in acute viral hepatitis A infection IgM lasts for....
    a few months
  410. in acute viral hepatitis A infection IgG last for
    entire lifetime
  411. acute viral hepatitis A infection diagnosis
    test for presence of IgM and HAV antibodies
  412. acute viral hepatitis A infection treatments
    passive and active immunization
  413. acute viral hepatitis A infection passive immunization
    human gamma globulins - give person specific antibodies for immediate but short lived protection
  414. acute viral hepatitis A infection active immunization
    vaccines
  415. what are the two vaccines for acute viral hepatitis A infection?
    • inactivated hepatitis A vaccine
    • twinrix
  416. inactivated hepatits A vaccine
    used for children between 12 and 23 mos old, two doses spaced six months apart
  417. twinrix
    combined hep A and hep B vaccine - used for persons 18 years and older.
  418. Hepatits B virus is also called
    The Dane particle
  419. an estimated _____% in the U.S ifected with Hepatits B virus develop acute hepatits.
    25
  420. 10-25% of people who develop acute hepatits from Hepatits B virus will become...
    carriers of Hepatits B virus and have a higher risk of chronic liver disease.
  421. Hepatits B virus is the major cause of what 3 diseases?
    • chronic hepatits
    • cirrhosis
    • primary hepatocellular carcinoma (HCC)
  422. can Hepatits B virusbe grown in cell celtue
    no
  423. Hepatits B virus genome
    partially double stranded DNA with a virion-assoicated polymerease
  424. Hepatitis B surface antigen
    envelope protein that is specific to Hepatits B virus
  425. HBV surface antigen function
    differentitate between hap A and hep B
  426. 30 - 70% of Hepatits B virus infections are....
    asymptomatic
  427. HBsAG is present in serum for....
    1-2 months
  428. IgG and HBsAg antibodies persist for life giving.....
    lifelong immunity
  429. Acute Hepatits B virus clinical symptoms?
    similar to HAV (have iteris and preucteric phases)
  430. acute Hepatits B virus infection incubation period
    43-180 days
  431. HBsAg is transiet and is present in serum for....
    less than six months
  432. theres a theory that fulminant hepattli is caused by ...
    HBV and HDV
  433. what causes severe cirrhosis of the liver and has a high mortality rate?
    fulminant hepatitis
  434. transmission of subclinical and actue Hepatits B virus
    sexual contact or by contaminated food
  435. chronic hbv infection carrier state
    chronic carrier state
  436. persistent viral hepatitis
    one of the common long term sequela (pathological condition resulting from disease) of acute hep B.
  437. HBsAg is in seruj for life, but a _____ amount of antibodies are produced.
    small
  438. Chronic HBV transmission
    from infected mother to infants
  439. theres a 70=90% chance for infection of Chronic HBV if the mother is a....
    carrier
  440. Chronic HBV immune response
    IgG and HBsAg antibodies are produce and give lifelong immunity after infection
  441. Chronic HBV diagnosis (2)
    • perform a test to detect the presence of HBsAg (only indicates the presence of an infection, not the type)
    • perform further tests, spaced 6 months apart to determine type
  442. Chronic HBV treatment passive immunization
    • Hepatitis B immunoglobulin (HBIG) - more selective, higher amount of antibodies for the virus
    • standard immune serum globulin
    • human gamma globulin
  443. Chronic HBV activve immunization
    • Recombinant vaccines used for 0-18 year olds
    • twinrix
    • for infants born to HBsAg postive mothers
  444. Chronic HBV recombinant vaccines?
    • recombivax HB
    • energix-B
  445. how are recombinant vaccines made?
    isolating the genes for antigen production and putting them into a yeast cell which can make the antigen thich is purified and used as a vaccine
  446. infants born to HBsAg positive mother should recieve 3 or 4 doses of ______ starting at birth.
    recombivax HB
  447. What causes post-tranfusion hepatitis?
    HCV
  448. 60 - 70% of HCV infections are ....
    asymptomatic
  449. in most cases an HCV acute infection results in...
    the establishment of a persistent infection
  450. What makes it hard to remove the HCV chronic virus?
    high rate of chronic/persistent infection leading to hepatocellular carcinoma
  451. in HCV chronic infection _______ occurs serveral weeks after infection and can last for years
    viremia
  452. HCV infections are slow or fast?
    slow
  453. time takes for HCV clinical hepatitis?
    >10 years
  454. time takes for HCV liver cirrhosis?
    >10 years
  455. time takes to develop HCV HCC?
    >29 years
  456. HCV transmission
    parentally or by sexual contact
  457. HCV diagnosis
    use antibody testing to detect the presence of HCV antigens (not type)
  458. treatment of HCV chronic infections?
    combined interferon-alpha2b and ribavirin
  459. combined interferon-alpha2b and ribavirin
    combination of two has a synergistic effect; used to reduce the level of virus which prevents or slows liver cirrhosis and HCC (cant completely remove virus)
  460. HDV is also called...
    Delta agent
  461. HDV has defective...
    RNA virus that cannot replicate itself
  462. For HBV carrie that have HDV what is needed for replication?
    requires the presence of HBV for replication and trasmission
  463. HDV share similar characteristics with...
    plant viruses (viroids)
  464. HDV trasmission is similar to that of...
    HBV
  465. Coinfection of HBV and HDV may result in...
    fulminant hepatits (higher mortality rate)
  466. HDV diagnoses
    detection of anti-HDV IgG antibodies
  467. Herpesviruses are anciet and may have infected...
    dinosaurs
  468. what are the 8 known herpes viruses that infect humans?
    • HSV-1
    • HSV-2
    • Varicella Zoster Virus VZV
    • Epstein Barr Virus EBV
    • Cytomegalovirus CMV
    • HHV6
    • HHV7
    • HHV8/KHSV
  469. the herpesvirus lipid membrane is derived from....
    the host cell (w/ glycoprotein spikes)
  470. glycoprotien spikes
    proteins made by the virus that aid in attachment
  471. herpesvirus structure components?
    • lipid membrane w/ glycoprotein spikes
    • tegument
    • nucleocapsid
    • DNA core
  472. tegument
    viral proteins that help start the infectious process in cells
  473. nucleocapsid
    icosahedral shaped structure that contains genetic material
  474. DNA core
    genetic material inside the nucelocapsid; usually double stranded linear DNA .
  475. primary herpesvirus infection is usually
    asymptomatic
  476. the major feature of herpesvirus pathogensis is...
    latent phase
  477. herpesvirus reactivation (second infection) gives rise to
    symptoms
  478. herpesvirus reactivation is caused by...
    certain signals in the host when immune system is weakened
  479. a primary herpesvirus infetion causes ubiquitous.....
    infection
  480. Most people are infected with ____ out of the 8 herpesviruses, with the exceptions of what two ?
    • five
    • HSV- 2 and HHV8
  481. HSV 1 caauses
    keratitis, encephalitis
  482. HSV2 causes
    neonatal HSV2
  483. VZV causes
    varicella - chicken pox, zoster-shingles
  484. EBV causes
    Burkitt's lympohoma, nasaopharyngeal carcinoma, oral hairy leukopaka
  485. cytomegalovirus causes
    mostly mild or asymptomatic infections
  486. HHV 6 causes
    neutopic and lymphoproliferative
  487. HHV8 causes
    kapos's sacoma
  488. HSV 1 treatment
    acyclovir, valacyclovir
  489. HSV2 treatment
    acyclovir, valacyclovir
  490. VZV treament,
    acyclovir, valacyclovir
  491. Cytomegalovirus treatment
    ganacyclovir
  492. HH8 treatment
    acyclovir, ganacyclovir
  493. poliovirus family
    picomarivirdae
  494. poliovirus trasmission
    fecal - oral route
  495. poliovirus diseases?
    • abortive and nonparalytic polio (minor)
    • paralytic and bulbar poliomyelist (severe)
  496. poliovirus treatment
    trivalent, inactivated vaccine
  497. coxsackie virus family
    picornaviridae
  498. coxsackie virus genome
    small single stranded RNA
  499. coxsackie virus transmission
    fecal - oral route
  500. coxsackie virus diseases
    • herpangina and hand foot, mouth diseases
    • pleurodyna and heart infections (severe)
  501. coxsackie virus vaccine
    no vaccine
  502. rabies family
    rhabdoviridae
  503. rabies genome
    single stranded (-) RNA, cells is bullet shape
  504. rabies transmission
    zoonotic
  505. rabies disease
    rabies (highly fatal)
  506. rabies vaccine
    inactivated vaccine
  507. rotavirus family
    revoviridae
  508. rotavirus genome
    double-caspsid segmented double stranded RNA
  509. rotavirus trasnmission
    fecal - oral route
  510. rotavirus disease
    infantile diarrhea
  511. rotavirus vaccine
    rotarix and rota Teq
  512. Nipah family
    paramyxoviridae
  513. Nipah genome
    (-) RNA
  514. Nipah resovoir
    fruruit bats
  515. Nipah transmission
    requires intermedate host (pigs) then to humans
  516. Nipah vaccine
    none
  517. Nipah treatment
    Ribavirin
  518. Dengue families
    • flaviviridae
    • arbovorus
  519. Dengue genome
    single straded (+) RNA
  520. Dengue resovoir
    monkeys and humans
  521. Dengue transmission
    insect vector
  522. Dengue vaccine
    none
  523. Dengue treatment
    None
  524. West Nile Virus families
    • flaviridae
    • arbovirus
  525. West Nile Virus genome
    singles stranded (+) RNA
  526. West Nile Virus reservoir
    bird
  527. West Nile Virus transmission
    insect vector
  528. West Nile Virus treatment
    not discussed
  529. hantavirus family
    bunyaviridae
  530. hantavirus genome
    single stranded segmented RNA
  531. hantavirus resovoir
    small mammals
  532. hantavirus transmission
    respiratory route
  533. hantavirus vaccine
    Hentavax (not FDA approved)
  534. hantavirus treatment
    none
  535. herpesvirsues have what replication cycle?
    lytic replication cycles
  536. herpesvirus replication steps
    • virus bind and enters cell
    • nucleocapsid moves through cytoplasm to host nucleus
    • nucleocapsid binds to nucleus and injects DNA and tegument
    • new viruses are assembled in the nucleus
    • viruses bud off of the nucleus and move into the golgi bodies
    • viruses exit through cell membrane and evets
  537. Where does HSV replaicate ?
    epidermal cells and neurons enervating the skin
  538. when does HSV stop repilcating?
    when it reaches the neroun cell body (end) (latent)
  539. certain singals reactivate viruses and cause recurrent infecron, in this case, it travels down to where'?
    the same area where primary infection occured
  540. HSV1 and HSV2 are genetically...
    almost identically
  541. HSV1 infects....
    the face and skull
  542. HSV2 infects...
    waist and hip area
  543. Neonatal HSV2
    disseminated infection b/c of immature immune system
  544. acyclovir function
    terminates viral DNA chai growth
  545. prodrug
    has to be activated by viral eznymes to start working
  546. HSV adds a phosphate group to
    the -OH
  547. valine increases the solubility of the drug makinging it....
    more avalible to cells
  548. once it enters a cell, valine is replaced by _______.
    hydrogen
  549. Adenosine arabinosde (araA) treats
    HSV encephalitisq
  550. trifluridine and idodeoxyuridine treats what?
    HSV keratitis
  551. what are the 5 types of lymphotropic herpesviruses?
    • EBV
    • CMV
    • the three HHV types
  552. lymphotropic herpesviruses are viruses that infect...
    cells of the immune system (t cells, b cells, monocytes,macrophages and dendritic cells)
  553. EBV blunts the T cell response and infects...
    B cells where it becomes latent
  554. EBV is a causative agent of
    mono
  555. cytomegalovirus is present in all..
    body fluids
  556. cytomegalovirus is associated with..
    monocytes, polymorphonuclear leukocytes and macrophages
  557. cytomegalovirus is the major cause of deafness and hearing loss in...............
    embryo, neonates, young children
  558. HHV6A found..
    in cerbral-spinal fluid
  559. HHV6B is associated with (bone transplants)
    encephalitis, causative agent of roseas
  560. HHV7 can infect T cells but...
    not yet associated with any human disease
  561. HHV8 is associated with
    castleman's disease, primary effusion lymphoma, and body cavity lymphoma
  562. poliovirus is an ________ human virus
    obligate
  563. why is there no vaccine for the rhinovirus
    there are more than 100 types
  564. 90% of poliovirus infections are , 5% are, 1-2% are and 0.1-2 are..
    • asymptomatic
    • abortive polio (self limiting)
    • nonparalytic polio
    • paralytic poliomylitis
  565. bulbar poliomyitid has a ____% mortlity rate.
    75%
  566. Coxsackie A has self limiting, _____ infections, while coxsackie B has ________ infections
    • localized
    • systemic
  567. rabies incubation period
    weeks or month depending on the bite
  568. three stages of rabies?
    • prodome stage - virus infects nerves onset (2 - 10 days)
    • neurolgic stage - hallucination, virus to organs (2 -10 days)
    • comatose stage and death
  569. immediate washing of wound with soap and water is a treatment for...
    rabies
  570. rotaviruses are relatively ______ at a range of pH
    stable (can pass through stomacha)
  571. rabies vaccine given on what days?
    day of exposure, days 3,7,14 and 28
  572. rotavirus incubation period
    24-48 hours
  573. 75% of emerging viruses are...
    zoonotic
  574. rotarix is ____ derived monovalent and given at 2mos and 4 mos
    human
  575. rotaTeq is ____ derived pentavalnet and given at 2,4 and 6 mos.
    bovine
  576. rotavirus prevention?
    good hygiene
  577. Nipah incubation period
    3-14 days
  578. how many strains of dengue virus is there?
    4
  579. when was dengue first observed?
    asi, africa and north america in 1780's
  580. first case of west nile virus was when and where?
    uganda, africa, 1937
  581. hantaviruses incubation period
    1-5 weeks
  582. what the four corners disease?
    hantavirus
  583. hantavirus was first isolated where?
    hantaan river in south korea in 1978
  584. what are the 5 emerging viruses of 2010?
    • avian influenza
    • monkeypox
    • rift valley fever - african cattle and sheep
    • h1n1
    • XMRV
  585. symbiosis
    coexistence where neither orgainsm harms the other
  586. mutualism
    coexistence where both organisms benefit
  587. parasitism
    coexistence where one organism has the potential to harm the other
  588. definitive host
    species in which sexual reproduction occurs
  589. intermediate host
    species in thich asexual reproduction occurs
  590. incidental host
    unnatural host that parasite is not adapted to survive in
  591. ebola and marbug family
    filoviridae
  592. ebola and marbug transmission
    respiratory or fecal-oral route, (human to human)
  593. ebola marbug vaccine
    none
  594. ebola marbug treatments
    none
  595. what are the two phylums under unicellular parasites?
    • sarcomastigophora
    • apicomplexa
  596. 2 subphylums of sarcomastigophora
    • sarcodina (amoebae)
    • mastigophora (flagellates)
  597. organism in the subphylum sarcodina
    entamoeba histolytica
  598. organisms in the subphylum mastigophora
    giardia lamblia, trypanosma cruzi
  599. classes,suborders of phylum apicomplexa
    • class sporozoea, suborder eucoccidia
    • suborder haemosporina
  600. class sporozoea, suborder eucoccidia organisms
    toxoplasma gondii, cryptosporidium
  601. suborder haemosporina organism
    plasmodium
  602. entamoeba histolytica infectious stage
    cysts (can survive high temps and chloride)
  603. entamoeba histolytica excystation
    cysts change into tropozoites, occurs in small intestines
  604. entamoeba histolytica reproductive/ pathogenic stage -
    trophozoites
  605. Amabapore
    small peptides that form pores in cell membranes
  606. entamoeba histolytica encystation
    trophozoites change into cysts, occurs during passage through the gut
  607. entamoeba histolytica pathogeneisis, transmission by...
    cysts ( 1 cysts realeases 8 trophozites)

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