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2010-11-14 22:12:36
microbiology SCSU three das

Microbiology Test Three: Diseases of the Limph, Cardiovas, Skin, Eyes, Nervous Systems
Show Answers:

  1. Layers of the skin include (order - surface to deep tissue):
    • Epidermis
    • Dermis
    • Subcutanious
  2. Which one is NOT a defense of the skin?
    1. Dry skin
    2. Normal Flora
    3. Fatty acids
    4. Salt
    5. A rash
    6. Peptides
    A rash is not a defense mechanism of the skin.
  3. Symptoms: blisters all over body, itch, virus becomes latent spinal ganglia and can cause a secondary infection in adults
    A. Measles
    2. Surfer's disease
    3. Chickenpox
    4. Smallpox
  4. A CHILDHOOD complication of chickenpox is:
    1. Reye's syndrome
    2. Shingles
    3. Sync disease
    4. Bovine virus
    1. Reye's syndrome
  5. Symptoms: Few days after initial infection of original disease recedes the patient vomits a lot and exhibits signs of brain dysfunction (dizneyness or bad behavior), coma and death can follow:
    1. Rabies
    2. Polio
    3. Reye's disease
    4. Cryptococcal Menengitis
    Reye's disease. (note: inital infection is chickenpox)
  6. Why would people die from chickenpox?
    Complications that can cause encephalitis or pneumonia (1/2 of these complications occur in adults)
  7. What is the cause of chickenpox?
    1. Variola virus
    2. Varicella zoster virus (VZV)
    3. Streptococci
    4. Haemophilus
    2. Varicella zoster virus (VZV)
  8. What are the two main causes for chickenpox transmission?
    1. Skin to skin contact and blood contamination
    2. Skin to skin contact and inhalation of chicken fecal matter
    3. Blood contamination and respiratory
    4. Skin to skin contact and respiratory
    Skin to skin contact and respiratory
  9. A. What are the host defenses for chickenpox?
    1. B-cells
    2. Normal Flora
    3. Macrophages
    4. T-cells

    B. What is the clinical prevention of chickenpox?
    1. Mother's inutero antibodies
    2. Avoid exposure
    3. Try to be exposed at a young age

    C. What is the clinical treatment for chickenpox?
    1. Vaccine in two doses
    2. Vaccine in three doses
    3. Topical antiseptic
    A. T-cells (cell mediated immunity - no antibodies)

    B. Avoid Exposure

    C. Vaccine in two doses
  10. What family of virus is chicken pox a part of?
  11. A reactivation of chickenpox in adults is called _______.

    Why does this happen?

    - Virus lays dormant until stress or a compromised immune system let it wreak havoc on a certain part of the body.
  12. How does shingles resurface?

    1. Travels down nerves and produces blisters.
    2. Travels through lymph system and produces localized blisters.
    3. Travels from dermis to epidermis in the form of blisters.
    Travels down nerves and produces blisters.
  13. Symptoms include: raised rash over entire body, pustuals arise deep in the skin, pustuals scab and finally scab falls off

    1. Smallpox
    2. Cowpox
    3. Chickenpox
    4. Doxpox
  14. There are two major types of the smallpox virus, what are they:
    1. Variola major and minor
    2. Varicella major and minor
    3. Herpes simplex D major and minor
    4. Arbovirus major and minor
    Variola major and mino
  15. Variola major or minor?

    1. More severe form
    2. 1% fatality rate
    3. high fever
    4. mild rash
    5. blindness
    • 1. major
    • 2. minor (30% for major)
    • 3. major
    • 4. minor
    • 5. major
  16. How is smallpox NOT transmitted?
    1. Direct contact
    2. Inhalation
    3. Contaminated food
    4. Bodily fluids
    5. Fomites
    Bodily fluid
  17. How does the host defend itself against smallpox?
    - interferons or swelling?
  18. Diagnosis and prevention of smallpox?
    Diagnosis: isolation of virus and clinical presentation of victim.

    Prevention: Vaccine
  19. MMR vaccine refers to?
    Measles, Mumps, Rubella.
  20. Synthoms include: common cold (fever, cough, runny nose), koplik spots, a rash that begins on the face and spreads over body. You have:
    1. Smallpox
    2. Rubella
    3. HSV
    4. Measles
  21. Complications of measles are:
    Brain damage caused by encephalitis, secondary bacterial infection that may lead to puenomia and death.
  22. What is subacute sclerosis panencephalitis?
    The clinical term for brain damage caused by complications with measles. Note: mostly occures in men and appears 1 - 10 years after measles infection.
  23. How is measles transmitted?
    Respiratory - note: highly contagious.
  24. Measles: host defense, diagnosis and prevention/treatment? Please give an example of each.
    • Host defense: cell mediated (meaning no antibodies).
    • Diagnosis: presence of giant cells (formed by meales virus fusing with red blood cells) and koplik spots
    • Treatment: vaccine (MMR).

    MMR vaccine has an unexpected result: viruses it protects against now has an affinity for infants because mother is no longer immune to actually contrating virus(es) but she is immune due to MMR. Vaccinated immunoal antibodies are not as strong as the real deal...especially when passed via breastmilk or inutero.
  26. What is another name for Rubella and what are the synthoms?
    a.k.a.: German measles/ three day measles

    Symptoms: rash, enlarged lymph nodes, fever, stiff joints.

    Note: milder than measles.
  27. Rubella virus causes?
  28. Rubella is NOT transmitted via:

    1. Blood
    2. Mother to fetus
    3. Respratory droplets

    Where does Rubella multiply?
    1. Blood


    respiratory tract and spreads throughout body
  29. Rubella:

    Host defenses/ Diagnosis/ Treatment/prevention
    Host defenses: cellular and humoral - lifelong immunity

    Diagnosis: basic symptoms and serology

    Prevention/ treatment: MMR, antiserum is given to pregnant women.
  30. Congeaital Rubella Syndrome:

    What is it and who gets it?
    First trimester fetus

    • If fetus contracts this or becomes exposed to rubella complications can areise such as deafness, heart defects, retardation.
    • 35 percent change.
  31. Herpes Simplex Virus 1 (HSV-1)

    Symptoms do not include:
    Fever blisters
    Cold sores
    Genital Warts

    Transmission does not include:
    Oral Contact
    Genital Contact
    Answer to both is genital. Genital is HSV-2
  32. What is herpes encephalitis?
    A complication that can arise from HSV-1 or HSV-2 where herpes virus migrates to and infects the brain. Also known as the dirty whore brain drain.
  33. HSV-1

    Where does herpes reside when it is not being active?

    How many people who have HSV-1 become active carriers?

    Latency occurs in trigeminal nerve ganglion (nerves that lie between face and central nervous system).


  34. What common mouth disorder is mistaken for HSV-1?
    Canker sores. The cause of them is unknown.
  35. Streptococcus pyogenes has three levels of seriousness:
    Streptococcal gangrene
    put them in order of least serious to most serious:
    • Impetigo
    • Erysipelas
    • Streptococcal gangrene
  36. Streptococcus pyogeneshas three levels of seriousness:
    Streptococcal gangrene

    place the description with the level (part one):

    1. Spreads rapidly through lymph
    2. Superficial skin wound
    3. Bacteria enter blood, could be fatal
    4. Most common in children
    5. Deep tissue infection
    • Impetigo
    • Superficial Skin wound
    • Most common in children

    • Erysipelas
    • Spreads rapidly through lymph

    • Streptococcal gangrene
    • Deep tissue infection
    • Bacteria enters blood, could be fatal
  37. Streptococcus pyogenes has three levels of seriousness:
    Streptococcal gangrene

    place the description with the level (part two):

    Oozes a clear fluid
    Intense inflammation that destroys blood vessels and tissues
    Forms a crust
    Infection of the dermis
    Can enter blood stream and be fatal
    • Impetigo
    • Oozes a clear fluid
    • Forms a Crust

    • Erysipelas
    • Infection of the dermis
    • Can enter blood stream and be fatal

    • Streptococcal gangrene
    • Intense inflammation that destroys blood vessels and tissue
  38. Streptococcus pyogenes

    Host Defense
    Prevention & Treatment
    • Transmission– Contact with wound secretions
    • Host Defense– Antibodies to surface proteins & toxins
    • Diagnosis– Isolation of bacteria
    • Prevention & Treatment– Antibiotics
  39. The skin disease Staphylococcus aureus has three levels of seriousness:
    Impetigo, scaled skin syndrome and Folliculitis & Cellulitis. What is the order of seriousness?
    • Impetigo
    • Folliculitis and Cellulitis
    • Scaled skin syndrome
  40. Staphylococcus aureus causes three diseases. Link the facts with the diseases:
    Folliculitits and Cellulitis
    Scaled Skin Disease

    Exfoliating Toxin
    Diffuse skin infection
    Pus filled lessions within hair follicles
    Skin peels off
    Superficial skin layers
    • Impetigo
    • Superficial skin layer

    • Folliculitits and Cellulitis
    • Diffuse skin infection
    • Pus filled lessions within hair follicles

    • Scaled Skin Disease
    • Skin peels off
    • Exfoliating toxin
  41. How is S. aureus transmitted?
    Contact with wound or fomites (any inanimate object able o carry infectious agent, such as a stethoscope)
  42. S. aureus is a skin disease. What are the:
    a. host defense(s)
    b. diagnosis procedure
    c. prevention and treatment
    • a. antibodies
    • b. isolate bacteria from t he wound
    • c. clean all wounds, good hygiene, antibiotics
  43. What is the causing agent of Toxic Schock Syndrome (TSS)?
    Strains of Staphylococcus aureus
  44. Toxic Shock Syndrome is a skin disorder caused by S. aureus. What two from the list are NOT symptoms of TSS:

    High fever with chills
    Nauesa and Vomiting
    Abnormal growth
    Red rash followed by peeling of skin
    Organ failure (kidneys and liver)
    Pussing and abnormal growth
  45. Toxic Shock Syndrome is a skin disorder caused by S. aureus. What are some risk factors of TSS?
    • contraceptives
    • tampons
    • surgery
    • open wounds
    • S. aureus infection
  46. Toxic Shock Syndrome is a skin disorder caused by S. aureus. What is the causing TOXIN of TSS?

    How would you treat TSS?
    Toxic shock syndrome toxin (TSST)

    • Treatment:
    • antibiotics
    • supprotive
    • eliminate predisposing factors
  47. Clostridium perfringens is a disease of the skin.
    What are it's symptoms?
    • – Infects deep wounds
    • – Produces alpha-toxin and gas
    • – Skin turns black, renal failure & death
  48. Clostridium perfringens is a disease of the skin.\
    What are its causes?
    • C. perfringens bacterium
    • it's a Gram+ anaerobic rod that grows in soil
  49. Clostridium perfringens is a disease of the skin

    How is it transmitted?
    Contamination of wounds with infected soil
  50. Clostridium perfringens is a disease of the skin

    what are the host defenses and how is it diagnosed?
    Host defenses: antibodies

    • Diagnosis:
    • gas under the skin
    • isolation of bacteria
  51. Clostridium perfringens is a disease of the skin

    How can it be prevented and treated?
    Antibiotics, antitoxin, hyperbaric chamber, removal of dead tissue (amputation)
  52. Does ringworm happen more in men or women and why?
    Men because they work outside more and have less sense of hygiene.
  53. What are the symptoms of ringworm?
    • infection of skin
    • skin is locally red and may ooze fluid
    • tinea pedis, capitis, cruris, unguinum, corporis
  54. What are the fungal agents that can cause ringworm?
    • Trichophyton
    • Microsporum
    • Epidermophyton
  55. How is ringworm transmitted?
    soin, formites (inanimate objects), clothing
  56. Fungal infection of the skin: Ringworm:
    Host defenses?
    Prevention and treatment?
    • Host defenses:
    • cell mediated immunity (not antibodies)
    • local inflammation

    • Diagnosis:
    • symptoms

    • Prevention and treatment:
    • topical antifungals: micronazole
    • oral: griseofulvin
  57. Candidiasis is what kind of skin infection?
    bacterium, fungal, virus, parasitic?
  58. Candidiasis>symptoms

    What is trush?
    white plaques on mucous membranes
  59. Candidiasis> symptoms

    Define diaper rash and vaginitis
    • Diaper rash - red raised rash
    • Vaginitis - women susceptible following antibiotics, contraceptives, hormonal changes
  60. Candidiasis>symptoms

    Systemic - describe
    immunocompromised, fatal
  61. What causes the fungal skin infection Candidiasis?
    The oppertunistic pathogen Candida albicans
  62. How do you prevent the fungal skin infection Candidiasis?
    Antifungus and keep skin dry
  63. The parasitic skin infection Scabies. How do you prevent it?
    • Medication kills mites
    • Note: itching stops only after the infected skin layer is shed.
  64. What are the host defenses and diagnosis of the parasitic skin infection Scabies?
    No host defenses

    Diagnosis occures when mites and eggs under skin are identified using a microscope.
  65. Symptoms of the parasitic skin infection Scabies
    Mites live in the epidermis and can cause severe itching
  66. What is the name of the parasite that causes Scabies?
    Sarcoptes scabiei or simply mite
  67. How is the parasitic skin infection Scabies transmitted?
    • Close contact
    • Fomites (inorganic objects)

    Note: found worldwide every 15 years and lasts for 15 years
  68. Meningitis is a disease of the nervous system. It can be caused by a multitude of pathogens. If caused by a bacteria, how can it be diagnosed?
    spinal tap
  69. How does meningitis physically occur?
    Inflammation of the meninges membrane
  70. Where is the meninges membrane located?
    Between the brain or spinal chord and the body.
  71. What are some common symptoms associated with meningtis?
    sudden fever, severe headache, neck rigidity
  72. What causes Haemophilus influenza meningitis?
    Gram- aerobic bacteria
  73. Haemophilus influenzae Meningitis is a bacterial disease of the nervous system.

    Whom does it ostly affect?
    Children 6 months to 4 years
  74. Haemophilus influenzae Meningitis is a bacterial disease of the nervous system.
    It is also a normal flora located where?
  75. Haemophilus influenzae Meningitis is a bacterial disease of the nervous system.
    What kind of antigen is on it's capsule?
    type b
  76. Haemophilus influenzae Meningitis is a bacterial disease of the nervous system
    How is it prevented?
    Hib vaccine
  77. Neisseria Meningitis or Meningococcal Meningitis are bacterium that infect the nervous system.

    What kind of bacteria are they?
    Gram- aerobic cocci with capsules
  78. Neisseria Meningitis or Meningococcal Meningitis are bacterium that infect the nervous system.

    What fact is NOT true:
    10% of people are healthy carriers
    Begins as throat infection or rash
    Can cause aorta rash
    Vaccine reccomended for college student
    Can cause aorta rash
  79. Neisseria Meningitis or Meningococcal Meningitis are bacterium that infect the nervous system.

    What type is most common in US?
    serotype B
  80. Besides the three main bacterium mentioned in this chapter, wht other bacteria can cause meningitis?
    E. coli
  81. Streptococcus pneumoniae Meningitis and Pneumococcal Meningitis are bacteria infections of the nervous system.

    What kind of bacteria are they?
    Gram+ diplococci
  82. Streptococcus pneumoniae Meningitis and Pneumococcal Meningitis are bacteria infections of the nervous system.

  83. Streptococcus pneumoniae Meningitis and Pneumococcal Meningitis are bacteria infections of the nervous system.

    What facts are NOT true:
    60% of people are healthy carriers
    70% of people are healthy carriers
    Most common in children
    Most common in adults
    60% and adults
  84. Streptococcus pneumoniae Meningitis and Pneumococcal Meningitis are bacteria infections of the nervous system.

    What is the mortality rate in children and elderly?
    • 30% in children
    • 80% in elderly
  85. Aseptic meningitis is caused by:
  86. Viral aseptic meningitis is the most or least common type of meningitis
    most common
  87. What is the severity of aseptic meningitis (meningitis from a virus)?
  88. What is the treatment of viral aseptic meningitis?
  89. What causes cryptococcal meningitis?

  90. Fungal cryptococcal meningitis's scientific name is?
    Cryptococcus neoformans
  91. Who usually gets cryptococcal (fungal) meningitis?

    What transmitts it?
    underlyning conditions (surgery, immunocompromised individuals)

    Transmitted via pigeon droppings and the inhalation of dried droppings.
  92. What are the mechanics behind Tetanus (how does it work/spread)?
    • certain nerves in the human body send impulses to muscles to say "contract" while the others say "relax." tetanus tells all musculear nerves to contract causing spasms.
    • First --> lockjaw
    • Then --> back and neck
    • Last --> throat
    • Patient cant swallow. Patient chokes and needs machine assistance. Finally, respiratory muscles are affected. Breathing stops and death occurs.
  93. Where is tetanus usually found?
    Soil contaminated with animal fecal waste.
  94. What does Clostridium tetani cause?
  95. How does Clostridium tetani transmit tetanus
  96. What environment does Clostridium tetani (tetanus) grow in the best?
    Anaerobic environments: deep wounds and decaying tissues.
  97. What is the pathogensis of tetanus?
    • After Clostridium tetani cell lyces, the neurotoxin tetanospasmin is released.
    • Note: C. tetani NEVER enters central nervous system (so there is no inflamation). It actually never leaves orgional infection site.
    • Also, the tetanospasmin toxin is so potent an inkdot worth can kill 30 adults.
  98. What physical response does tetanospasmin (neurotoxin of C. tetani) cause?
    • first, a condition known as "lock jaw".
    • then, spastic paralysys.
    • finally, respratory distress.
  99. What is the treatment for tetanus before and after symptoms appear?
    Before: an antitoxin known as TIG

    After: none.
  100. How can tetanus be prevented?
    • Vaccine every 5 - 10 years.
    • the vaccine is a toxoid meaning that the antibodies produced target toxin not bacterium. Bacteria is in too small of a quantity to be targeted.
  101. What is the name of the deadly toxin that causes botulism?
  102. Botulism, among other things, is a form of food poisoning caused by?
    Clostridium botulinum. A Gram+ bacterium.
  103. C. botulinum causes botulism by it's ______.
  104. Ironically, the same environment that destroys C. botulinum (botulism) causes the production of it's deadly spores. What condition about this enviroment kills the bacterium?
    low pH causes endospores to form and also release a deadly exotoxin.
  105. What is the pathogenesis of botulism?
    Endotoxin produced by spores block release of acetylcholine 9chemical necessary for transmitting nerve impulses). Flaccid paralysys (weakness) occures in 1 - 10 days. Then respiratory paralysys.
  106. Different strains of C. botulinum create different toxins and cause seperate cases of botulism. What is the most potent?
    • Type A.
    • Note: death has been recorded even in cases of food tasting without swallowing or even in absorptions via skin breaks can cause death.
  107. Where is type A botulism found?
    West of mississippi river.
  108. What is type A botulism spores most resistant to?
  109. What is the most common cause of botulism in infants and why?
    Honey consumption. Honey contains trace ammounts of C. botulinum that is normally destroyed by the normal flora of the adult stomach before it can create spores and toxin. Infants have yet to develop normal flora.
  110. If normal flora protects everybody but infants from botulism, how do adults contract it?
    Food poisoning. Normal flora usually protects from injestion of microbe but not of toxin. When food is canned, it is heat-labiled. This destroys the bacterium but also, if not done properly, can cause the creation of spores and toxin.
  111. Hansen's disease is a less common name for what?
  112. True or false: The incubation period for Leprosy is rapid.
    False. incubation can be years because the bacteria growth is slow.
  113. What are some common early symptoms of Leprosy?
    • Skin rash
    • Persistent, chronic infections
    • Peripheral nerve damage and loss of sensation
  114. Leprosy happens in two stages: tuberculoid (a.k.a. neural; less severe) and lepromatous (a.k.a. progressive or borderline; more severe). Out of the list below, what conditions belong with each:

    cell mediated response occures
    possitive skin test
    loss of fingers, toes, nose
    skin damage
    loss of sensation is discrete spots
    inmfection is usually contained
    negative skin test (no T-cell response)
    • Tuberculoid:
    • cell mediated response
    • infection is contained
    • positive skin test
    • loss of sensation in discrete spots

    • Lepromatous:
    • poor immune response
    • skin damage
    • negative skin test (no T-cell response)
    • loss of fingers, toes, nose
  115. What disease does Mycobascterium leprae cause?
  116. Where does M. leprae (leprosy) grow?
    Peripheral nervous system
  117. How is m. leprae (leprosy) transmitted?
    Direct contact and nasal secretions
  118. Both cell mediated (T-cells) and antibodies respond to an infection of M. leprae (leprosy). Which one is effective and which one is now.
    T-cells are more effective than antibodies.
  119. The treatment for leprosy is ______.

    The prevention of leprosy is ______.
    Treatment: multidrug therapy.

    Prevention: Killed M. leprosy cells in vaccine.
  120. Is rabies caused by a parasite?
    No. A virus.
  121. What virus causes rabies and what is it's morphology?
    The Rabies virus is bullet-shaped.
  122. The epidemology of rabies has a reservoir and an end when concerning humans. What are they?
    • reservoir: can be all mammals.
    • End: humans are the end of the infectious cycle.
  123. The initial symptoms for rabies are flu-like. Then the rabies virus enters a lifecycle of two phases: excitation and paralytic. Which comes first and which comes second?
    Excitation is first than paralytic.
  124. The initial symptoms for rabies are flu-like. Then the rabies virus enters a lifecycle of two phases: excitation then paralytic. A list of symptoms are below. Put the symptoms with the stage:

    Muscle noticably weak
    signs of neurological symptoms
    speech impairment
    loss of consciousness
    loss of muscle control
    • Excitation:
    • neurological symptoms
    • loss of muscle control
    • speech impairment
    • hydrophobia

    • Paralytic:
    • muscle weakness
    • loss of conscisnous
    • death
  125. What makes bats more dangerous than most other rabies carriers?
    The virus can be dormant in bats longer than any other mammal. So bats may not show symptoms so people aren't as alert around a bat as they would be, say, a raccoon that will more likely exhibit abnormal behavior.
  126. What us the best prevention for rabies in domestic animals?
  127. What is the best prevention for rabies in wild animals?
    Wild animals are an uncontrollable reservoir of rabies. Programs are in place for wild vaccination but the best prevention is avoiding or eliminating animals that show clear signs of rabies.
  128. How can rabies be prevented in humans?
  129. How can rabies be treated in humans?
    Immune globulin is given immediately after infection.
  130. What is the mode of transport of rabies from animal to human?
    Via saliva during a bite.
  131. After a bite from an animal, where does the rabies virus replicate before becoming moble?
    The virus replicates in the muscles bear the bite.
  132. After the rabies virus replicates following initial animal bite, what does it do next?
    It transports to the central nervous system via the peripheral nervous system.
  133. The progression of the rabies virus follows this path:
    bite/saliva>replication in muscle tissue>moves to central nervous system. What's next?
    Travels up the spinal chord to the brain.
  134. After the rabies virus reaches the brain, what condition does it cause?
    Fatal encephalitis
  135. After the rabies virus reaches the brain and causes encephalitis, what is it's final destination?
    Salivary glands and other organs of victim.
  136. True or false: The incubation period for rabies is 30-50 days.
  137. What virus does the genus lyssavirus contain?
  138. Poliomyelitis (caused by the Polio virus or Picornavirus) is best known as the cause of childhood paralysis. this reputation is more out of fear than good understanding, why?
    While paralysis sucks, it only occures in 1% of victims.
  139. Since the polio virus causes paralysys in only 1% of it's victims, what symptoms do most victims experience?
    Headachs, fever, nauesia.
  140. In it's initial stage, where is polio found and where does it initially multiply?
    Mouth and throat.
  141. The pathogenesis of Poliomyelitis (polio) contains four phases:

    where does primary mutiplication occur?
  142. The pathogenesis of Poliomyelitis (polio) contains four phases:

    In which phase does the virus enter the tonsols?
  143. The pathogenesis of Poliomyelitis (polio) contains four phases:

    At which phase does the virus enter the blood
  144. The pathogenesis of Poliomyelitis (polio) contains four phases:

    At which phase does the virus enter the central nervous system and extraneural tissue?
  145. What does viermic mean in reference to a viral infestation?
    It's when the virus enters the blood. See polio.
  146. Neurogical phase is the fourth and final phase of Poliomyelitis (polio).

    Is this phase common and why or why not?
    It's not common. The phase before it is the viremic phase where the virus enters the bloodstream. The viremic phase needs to happen persistently to occur and it usually does not.
  147. Neurological phase is the final phase of Poliomyelitis (polio). It is prevented by...?
    Low levels of antibodies can prevent spread.
  148. Prevention of poliomyelitis (polio) can be achieved via the use of one of two vaccines. Whatare they and what's the difference. Also, one of them comes with a low level of danger. What is it?
    • Sabin:
    • taken orally (OPV)
    • attenuated (alive, but weakened)

    • Salk:
    • injected (IPV)
    • inactivated virus (dead)

    Sabin may cause small cases of a secondary infection.

    Note: The WHO has executed an extensive erratication effort.
  149. Why does Arbovirus Encephalitis have that paticulear nomenclature?
    Arthropod borone virus. arthropod = mosquito.
  150. What is encephalitis?
    Inflammation of the brain.
  151. Out of this incomplete list of symptoms for the Arbovirus, which one does not belong?

    trouble urinating
    trouble pissing
  152. Out of this incomplete list of symptoms for the Arbovirus, which one does not belong?

  153. Out of this incomplete list of symptoms for the Arbovirus, which ones do not belong?

    stiff neck
    muscle weakness
    muscle weakness and inflammation
  154. Arbovirus Encephalitis is defined as...
    ...an Arthropod borne virus that causes encephalitis.
  155. There are four Arbovirus variants that cause encephalitis, put them in order of most severe and least severe:

    St. Louis Encephalitis (SLE)
    Eastern Equine Encephalitis (EEE)
    California Encephalitis (CE)
    Western Equine Encephalitis (WEE)
    • Eastern Equine Encephalitis (EEE)
    • Western Equine Encephalitis (WEE)
    • - these first two are most severe in humans
    • California Encephalitis (CE)
    • - can be fatal
    • St. Louis Encephalitis (SLE)
    • - seldom fatal, relativly minor
  156. There is a variant of Arbovirus Encephalitis that infects the Far East. What is it called?
    Japanese B encephalitis
  157. true or false: diagnosing Arbovirus Encephalitis is easier during an epidemic?
  158. True or false: Diagnosing Arbovirus Encephalitis is based on the region where someone lives?
    False. It's based on symptoms and case history.
  159. In refernce to arbovirus encephalitis, what does Culex and Aedes mean?
    they are the genus of mosquito that can carry it.
  160. Besides mosquitoes what other animal can carry or be a reservoir for Arbovirus Encephalitis?
    • Birds can be carriers.
    • Small mammals, birds and horses can be a reservoir.
  161. What is the difference between a vector/carrier and a reservoir of a disease?
    A vector is a carrier (mosquito, tick) that takes the disease from an infected individual to an uninfected individual. They do not have the disease themselves, they carry the infected agent such as blood. A reservoir is any thing (person, animal, arthropod, plant, soil or substance) in which a disease lives and can multiply. The disease NEEDS the reservoir in order to survive. A vector must be living but a reservoir can be a non living thing such as soil or water. Neither actually HAVE the disease but are simply transmitters.
  162. What is the treatment for Arbovirus?
    Supportive care.
  163. Does Western Equine Encephalitis (WEE) have a vaccine?
    No. Only Japanese b encephalitis has a vaccine.
  164. How can Arbo Encephalitis be prevented?
    • Japanese B encephalitis has a vaccine.
    • Also, the controlling of mosquito populations.
  165. Transmissible Spongiform Encephalitis (TSE) can affect cows. What is this called (official and unofficial name)?
    Bovine Spongiform Encephalitis (BSE). a.k.a Mad Cow
  166. What causes Transmissible Spongiform Encephalitis (TSE)?
  167. Transmissible Spongiform Encephalitis (TSE):
    What is a sign that a sheep has what's known as "sheep scrapie?"
    The sheep will scrape itself against fences/walls until it's raw.
  168. What is Creutzfeldt-Jakob disease (CJD)?
    It's a form of Transmissible Spongiform Encephalitis (TSE), a prion that infects humans. This version is believed to be hereditary.
  169. Transmissible Spongiform Encephalitis (TSE)
    Sometimes this prion is called Kuru. Where does Kuru exist?
    Kuru affects tribes of New Guinea.
  170. Transmissible Spongiform Encephalitis (TSE)
    What is a sign of Kuru?
  171. Transmissible Spongiform Encephalitis (TSE)
    How is the prion that causes Kuru transmitted?
    Via cannibalistic ritual.
  172. What is the most famous form of the prion Transmissible Spongiform Encephalitis (TSE).
    Bovine spondiform Encephalitis (BSE) because of Mad Cow Disease.
  173. Transmissible Spongiform Encephalitis (TSE)
    What are two possible causes for Mad Cow?
    Some blame a mutated version of Sheep Scrapie and some blame genetic mutation.
  174. Transmissible Spongiform Encephalitis (TSE)

    What is one way the United States tries to prevent a spread of Mad Cow (BSE)?
    The US prohibits the use of meat from "downer" cows (animals unable to walk).
  175. Transmissible Spongiform Encephalitis (TSE)

    True or false: Bovine Spongiform Encephalitis cannot be passed onto humans.
  176. Transmissible Spongiform Encephalitis (TSE)

    How can this prion disease be prevented?
    • Animal products are screened for Mad Cow and scrape.
    • Cannibalism is no longer practiced (Kuru).
    • Blood is screened before transfusion.
  177. Transmissible Spongiform Encephalitis (TSE)

    What treatments are available for this prion disease? Is it fatal?
    Very few treatments exist to fight prions and no treatments exist for Transmissible Spongiform Encephalitis (TSE). It is chronic and fatal.
  178. What type of virus is the yellow fever virus?
    Small RA virus
  179. the vectior for yellow fever is
  180. In reference to yellow fever, what does Aedes asgypti refer to?
    The mosquito vector
  181. What is the first step in yellow fever infection?
    Mosquito bite
  182. The first step in yellow fever infection is the mosquito bite. What is the next step?
    Virus travles to lymph nodes and blood
  183. The first step in yellow fever infection is the mosquito bite.
    The second step is the travel to lymph nodes and blood.
    The third step is mutiplication. Where?
    The liver.
  184. For yellow fever, there are two phases. The first is less severe than the second. What are the symptoms of each?

    Choose from this list:
    Severe fever
    Headach (x2)
    uncontrolled bleeding
    • First:
    • fever, headache, weakness

    • Second:
    • severe fever, chills, headach, jaundice, uncontrolled bleeding
  185. What is the reservoir for yellow fever?
  186. What is the host defense of yellow fever?
    immune after infection
  187. How is yellow fever diagnosed?
    Observation of symptoms
  188. How is yellow fever prevented?
    • Restrict mosquito population
    • treat standing water
  189. How is yellow fever treated?
    line attenuated vaccine for people exposed and for travelers
  190. These symptoms describe what disease?

    fever, headach, joint and muscle pain, sore throat, weakness, diarrhea, vomiting, stomach pain, rash, red eyes, internal and external bleeding.
    Ebola virus
  191. What type of virus causes ebola?
    enveloped RNA virus
  192. If left untreated and patient has a compromised immune system, what is the worst case symptom (besides death) for ebola?
    destruction of internal organs
  193. True of False: The fatality rate for ebola in untreated victims can be as high as 40%.
    False: 90%
  194. True or False: ebola is transmitted via mosquito.
    False: transmitted via animal - specifically the fruit bat.
  195. How is ebola transmitted person to person?
    Direct contact with blood or bodily fluid.
  196. Ebola can be transmitted animal to person, person to person and a third vector is ______.
  197. Formites are.
    Inanimate objects such as needles, tabletops, stethoscopes.
  198. What is the prevention and treatment for ebola?
    Supportive care.

    isolation of patient and proper disposal of infected items to prev ent spread.
  199. What is another name for the Epestein-Barr virus (EBV)?
    human Herpesvirus 4
  200. What disease does Epstein-Barr (EBV) cause?
    infectious mononucleosis (mono)
  201. EBV/mono's symptoms are:
    sore throat
    and (two more)...
    • swollen lymph notes
    • enlarged spleen (that could rupture).
  202. EBV/mono is what type of virus
    enveloped DNA virus.
  203. What does EBV/mono first infect?
    it's latent in B lymphocytes.
  204. How is EBV/mono transmitted?
    Secreted in saliva.
  205. How is EBV/mono diagnosed?
    • Clinically.
    • Look for a high number of white blood cells.
    • Also a presence of enlarged suppressor T cells (which stop proliferation of infected B cells).
  206. What is the prevention and treatment of EBV/mono?
    • None.
    • 90% of adults have it and it reactivates periodically.
  207. true or false: hantavirus infects the lower respiratory tract?
  208. How does death usually occur for someone with the hantavirus?
    Catastrophic lung failure.
  209. Symptoms for hantavirus include all of the following except:
    muscle ach
    respritory distress
    fluid in airspace
    runny bowles
  210. What is another name for the hantavirus
    • Sin nombre (spanish for no name)
    • used to be called "four corners virus" until concern over tourism was raised
  211. How is the hantavirus transmitted?
    mouse droppings aerosolized
  212. Where is the hantavirus highest occurance?
    four corners region.

    Also, places with a high rodent population and in rural clusers
  213. True or false: there are no known host defenses for the hantavirus
  214. What are good preventative and treatment measures for the hantavirus?
    • Keep areas free of rodents and avoid contact with rodents.
    • The only treatment is supportive care.
  215. Another name for Dengue fever is
    breakbone fever
  216. Symptoms of regular dengue fever are
    severe muscle and back pain ("breakbone"), fever and a rash
  217. Is dengue fever fatal and how many people are affected?
    rarely fatal. 100 million cases a year
  218. There is a strain of dengue fever that has a fatality rate of up to 90% in children. What is it called?
    Dengue Hemorrhagic Fever (DHF).
  219. What causes dengue fever, where does it grow and what is it's morphology or composition?
    Dengue Virus. Grows virus. white blood cells. It's a RNA virus.
  220. In regard to dengue fever, what does this refer to:
    Aedea aegypti
    Aedea albopictus
    The vector mosquito
  221. true or false: for dengue fever, there is no known animal reservour.
  222. How does dengue hemorrhagic fever (DHF) occur?
    The host needs subsequent infections of dengue fever. They combine with antibodies created after first infection.
  223. What are symptoms of dengue hemorrhagic fever (DHC)?
    • rash on face and extermities
    • drop in BP
    • shock
    • death
  224. What region of the world does dengue fever occur in?
    tropical region
  225. What are the host defenses against dengue fever?
    Interferon and antibodies.
  226. Diagnosis of dengue fever includes:
    virus isolation and culture.
  227. What type of preventative measures help control the spread of dengue fever?
    Mosquito control and trying to prevent mosquito bites.
  228. True or false: the vaccine for dengue fever requires three doses
    false: there is no vaccine
  229. Two main types of plague are:
    Bubonic and Pneumonic
  230. How can you catch bubonic plague?
    rat flea bite
  231. Bubonic plague
    why do the rats bite you?
    They are starving because bacteria is clogging their digestive tract with a biofilm
  232. Where do bubonic plague bacteria first concentrate in?
    lymph nodes
  233. Symptoms of bubonic plague include
    • high fever
    • swollen luymph nodes (bubo)
    • black spots
    • death
  234. true or false:
    bubonic plague is 90% of todays plague cases
  235. true or false: bacteria cells of the bubonic plague grow within red blood cells
    false: phagocytes
  236. How can you catch pneumonic plague?
    inhalation of bacteriaryl cells. they are easially airborn and very dangerous
  237. What is the 24 hour mortality rate of pneumonic plague?
  238. What kind of bacterium causes plague?
    Yersinia pestis
  239. What kind of bacteria is the plague Y. pestis?
    Gram- coccobacillus rod
  240. Can plague be cultured for diagnosis? (yes or no)
  241. What are the prevention and treatments for plague?
    antibiotics, eliminate rodents from home, vaccinate scientists working with plague.