Micro Final

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  1. Epidemiology
    The study of the spread, control and prevention of disease in populations
  2. Communicable Diseases
    Diseases that can be transmitted from one host to another
  3. Typhoid Fever
    • Caused by Salmonella enterica strain Typhi
    • Transmission: fecal-oral
  4. Typhoid Fever Symptoms
    Diarrhea, abdominal pain, nausea, vomiting and fever
  5. Attack Rate
    # of cases in a population exposed to an infectious agent
  6. Morbidity Rate
    #cases/population at risk
  7. Mortality Rate
    # deaths/population at risk
  8. Prevalence
    # of total cases in a population at risk
  9. Incidence
    # of NEW cases in a specific time period in a population at risk
  10. Endemic
    • Constantly present
    • Cold and seasonal flu
  11. Epidemic
    • Unusual large #
    • Flu
  12. Outbreak
    • Cluster of cases
    • Ebola in Uganda, January 2001
  13. Pandemic
    • Worldwide epidemic
    • AIDS
  14. Determinants of Infections Diseases
    • Communicable Diseases:
    • Reservoir
    • Mode of transmission
    • Portal of entry
    • Portal of exit
  15. Human Reservoir
    • Symptomatic
    • Carriers-asymptomatic
  16. Animal Reservoir
    • Fleas, mosquitoes & ticks
    • Mammals (rabies)
    • Birds (flu, Salmonella)
    • Lower vertebrates (Salmonella & turtles)
  17. Transmission
    • Horizontal
    • Vertical
    • Direct contact
    • Indirect contact
    • Food and Water
    • Vector
    • Droplet
    • Air
  18. Vertical Transmission
    Mother to fetus
  19. Direct Contact Transmission
    • Nosocomial infections
    • Fecal-oral
  20. Indirect Contact Transmission
  21. Food and Water Transmission
    • Cross contamination
    • Fecal-oral
  22. Vector Transmission
    • Mechanical
    • Biological
    • •Biting
    • •Defecating
    • •Regurgitating
  23. Air Transmission
    Droplet nuclei
  24. Dose
    • < 10 cells for bacillary dysentery (Shigella spp.)
    • 1000 cells for gonorrhea
    • 1,000,000 cells for cholera
  25. Incubation Period
    Cold vs. AIDS
  26. Population Characteristics
    • Immunity – genetic or predisposed
    • Age
    • Religious or cultural practices
    • Health
    • Genetic background
  27. Nosocomial Infections
    • Hospital acquired
    • 5-6% rate in US
    • Half of all infectious diseases treated
    • One-third preventable
  28. Usual Suspects of Nosocomial Infections
    • Enterobacteriaceae
    • -Intestinal flora
    • Escherichia coli
    • -Intestinal flora
    • Pseudomonas sp.
    • -Moist, nutrient poor areas
    • Staphylococcus aureus
    • -Nose flora
    • Klebsiella pneumoniae
  29. Reservoirs of Nosocomial Infections
    • Patient’s flora
    • Health care worker
    • Other patients
  30. Transmission of Nosocomial Infections
    • Medical devices
    • Airborn
    • Lack of proper handwashing
  31. Prevention of Nosocomial Infections
    • Handwashing
    • Gloves
    • Mask, eye protection, gown, face shield
    • Patient care equipment
    • Environmental controls
    • Linens
    • Needles
    • Patient placement
  32. Infection
    • Colonization of microbe causing illness
    • Primary
    • Secondary
  33. Infectious Disease
    Impaired body function due to infection
  34. Pathogen
    Microbe capable of causing disease (can also be opportunistic)
  35. Virulence
    Degree to which pathogen can cause disease
  36. 5 Characteristics of Infectious Diseases
    • 1. Incubation period
    • 2. Incubation and illness
    • 3. Convalescence and carrier- recovery
    • 4. Duration
    • 5. Distribution
  37. Incubation Period of Infectious Diseases
    • Infectious dose
    • 10 cells for Shigella
    • 1,000,000 cells for cholera
    • Health of host
  38. Incubation and Illness of Infectious Diseases
    • Days (cold virus); weeks (Hep A)
    • Months (rabies); years (leprosy)
    • Symptomatic or asymptomatic
  39. Convalescence and Carrier-Recovery of Infectious Diseases
    Carrier- someone who is helping but shows no sign of illness
  40. Duration of Infectious Diseases
    • Acute- short (a week or 2)
    • Chronic (forever)
    • Latent (goes away and comes back)
  41. Distribution of Infectious Diseases
    • Localized- stays in one area
    • Systemic- body wide
    • HIV
    • Bacteremia- a few cells in bloodstream
    • Septicemia- massive infection in bloodstream
  42. Mechanisms of Pathogenesis
    • Production of toxins that are ingested
    • Colonization of host mucous membranes, then toxin production
    • Invasion of host tissues
    • Invasion followed with toxin production
  43. Production of Toxins that are Ingested
    • Clostridium botulinum
    • Canned foods
    • Can eat bacteria, toxin causes disease
  44. Colonization of Host Mucous Membranes, then Toxin Production
    Vibrio cholerae; Escherichia coli O157:H7
  45. Invasion of Host Tissues
    Yersinia pestis
  46. Invasion Followed with Toxin Production
    Streptococcus pyogenes
  47. Establishments of Infection
    • Adhesins or penetration
    • -Attach or enter body
    • Colonization
    • -Avoid IgA’s
    • Uptake by host cell
    • -Effector molecules
    • Avoiding host defenses
    • -Hiding
    • -Avoiding killing
    • Damage to host
  48. Establishment of Infection: Adhesion
    • Pili, capsule or cell wall proteins
    • Highly specific
    • •Can have more than one type to broaden range
  49. Establishment of Infection: Colonization
    • IgA proteases- degrades IgAs: avoiding antibodies
    • •Complement system, enhance phagocytosis
    • Antigenic variation- constantly change out proteins: avoid recognition (antibodies)
    • Siderophores – iron binding molecules
    • •Lactoferron is produced by bacteria
  50. E. coli and the Body
    • Normal E. coli in gut attach to large intestine
    • Ingestion of E. coli by cow causes infection attaches to small intestine
    • E. coli causes urinary tract infection attaches to bladder
    • Each has specific adhesions to attach to specific cells
  51. Establishment of Infection: Uptake by Host Cell
    • Utilize sampling cells of intestine (M cells)
    • •Shigella sp. causing shigellosis
    • •Avoids getting degraded
  52. Establishment of Infection: Effector Molecules
    • Yersinia pestis causing plague
    • Salmonella
    • Induce endocytosis
    • Gram negative
    • -Type III secretion system
    • -Ruffling
  53. Shigella Uptake
    • Hops from one cell to the next while damaging each cell he passes through
    • Oral transmission
  54. Determinants of Infectious Diseases: Avoiding Host Defenses
    • Hiding in host cell – Shigella sp.
    • Avoiding complement
    • Avoid phagocytes by having C5a peptidase, toxins; Streptococcus pyogenes will destroy bacteria around
    • Avoid recognition
  55. Avoiding Complement
    • Gram + not affected by MAC
    • Thick layer of peptidoglycan on outside
    • Neisseria gonorrhoeae- has proteins on surface to inactivate c3b
    • Ex. Neisseria gonorrhoeae
    • Cell wall contains a protein that binds and inactivates C3b
  56. Avoid Recognition
    • Capsules avoid complement proteins
    • Fc receptors – Staphylococcus aureus
    • Binds antibodies backwards
    • Interfere with MCH I (found on all cells)
    • Avoiding cytotoxic t cells
  57. C5a
    Inflammation cells release this (chemokine)
  58. C5a Peptidase
    Avoiding inflammation
  59. Streptococcus pyogenes
    • Strep throat, necrotizing fasciitis
    • Destroys C5a with a peptidase
    • Toxin streptolysin O damages host cell membranes
  60. Interfering with MHCI
    • Herpesviruses – ds DNA ex. Epstein Barr (mononucleosis)
    • •Block processing and movement of MHC I to host cell surface
    • Cytomegalovirus
    • •Encodes for a “counterfeit” MHC class I molecule
  61. Determinants of Infectious Diseases: Damage to Host
    Exotoxin and endotoxins
  62. Exotoxins
    • Protein
    • Neurotoxin (nervouse system), cytotoxin (cell death) and enterotoxin (intestine)
    • A-B toxins
    • Membrane damaging toxins
  63. Endotoxins
    • Lipopolysaccharides
    • Dissemination of bacterial cell components result in inflammation throughout body - shock
    • Part of bacterial cell wall breaks off lowering blood pressure not allowing blood to flow to organs, so body goes into shock
    • Gram negatives
  64. A-B Exotoxins
    • Diphtheria toxin – Corynebacterium diptheriae
    • Single molecule sufficient to kill cell
    • B portion binds receptor
    • A portion has catalytic activity
    • Stops protein synthesis
    • Causes heart failure
    • Main targets are heart and respiratory tract
  65. Lipopolysaccharides
    • Lipid A- antigenic
    • Immense innate response- inflammatory process that goes through whole body
    • Septic shock
    • Heat-stable- can add as much heat as wanted, has no effect
  66. Bubonic Plague
    • Yersinia pestis
    • Found in Africa, South America, Middle East, Russia, and SW United States
    • The bacteria multiply in the gut of the fleas
    • Fleas regurgitate infectious material into bite wound
    • Fleas transmit the disease to amplifying reservoir (rats, rabbits, etc.)
    • Massive die-offs result in humans becoming next target
  67. Vector Transmission
    From flea to human
  68. How Bubonic Plague Spreads
    • Bacteria multiply at site of flea bite
    • Enter lymph nodes; localized swelling & necrosis = bubo
    • Accompanied by fever, headache, chills, nausea, weakness, & pain
    • Swells because B and T cells are in the lymph nodes
  69. Yersinia's Mechanisms
    3 plasmids: small, medium, large
  70. Yersinia's Small Plasmid
    Protease Pla destroys C3b and C5a- avoids inflammation, opsonization
  71. Yersina's Medium Plasmid
    • Yops (Yersinia outermembrane proteins) injected by Type III secretion
    • Yop H – disables phagocytes-avoids
    • Yop M – blocks cytokine release- avoids signaling other immune responses
  72. Yersina's Large Plasmid
    • F1 capsule protein
    • Resists phagocytosis
    • Avoid complement proteins
  73. Bubonic Plague
    • Bacteria spread to blood in large numbers (septicemic plague)
    • Intravascular coagulation & hemorrhage causes darkening of skin (“Black Death”)
    • 50-80% mortality rate if untreated
    • May spread to lungs (pneumonic plague)
  74. History of HIV in US
    • 1981 report showing unusual infections (P. carinii) in young homosexual men
    • 1982 CDC had evidence cases were caused by infectious agent
    • 1983 Pasteur Institute and NIH co-discovered retrovirus
    • Both researchers created blood tests and applied for patents
    • 1987 Pres. Reagan settled dispute
  75. Central Africa in 1950's
    • Simian Immunodeficiency Virus similar to HIV, hence HIV may have originated in African primates
    • Spread from Africa to the Caribbean, and then to the US
  76. Transmission of HIV
    • Indiscriminate unprotected sexual contact, multiple partners
    • Blood contact
    • Transfusions
    • Needle sharing
    • Mother to fetus
    • 1 in 10 miscarry
    • 15-40% infants develop AIDS
  77. Progression of HIV Disease
    • Acute HIV syndrome initially
    • Clinically latent stage
    • Clinical AIDS
  78. Acute HIV Syndrome Initially
    • 1-6 weeks after exposure; virus replicates and is abundant in blood
    • Acute retroviral syndrome (ARS): fever, sore throat, pharyngitis, rashes, moodiness
  79. Clinically Latent Stage
    • May last 10 years or longer
    • Majority of transmission period
  80. Clinical AIDs
    • Lymphadenopathy syndrome (LAS)
    • AIDS-Related Complex (ARC)
    • Includes weight loss & diarrhea
    • AIDS-defining conditions occur
  81. AIDs Defining Conditions
    • Cancer of uterine cervix, invasive
    • Candidiasis of esophagus, trachea
    • Mycobacterial disease
    • Pneumonias occurring repeatedly
    • Salmonella infection of bloodstream
  82. HIV Type 1
    • 10 subgroups of major group
    • Single stranded RNA – 2 copies
    • Surface proteins on envelope for entry
    • Gp41
    • Gp120
  83. 3 Proteins of HIV
    • Reverse transcriptase
    • Protease
    • Integrase
  84. Attachment of HIV
    • Gp120 binds CD4 molecule an co-receptor on lymphocyte, macrophage, or dendritic cells
    • Gp 120 brings virus to membrane
  85. HIV Pathogenesis
    • Internalization and uncoating
    • Reverse transcriptase makes DNA copy of genome
    • Viral DNA inserts into host cell genome
    • Transcription of viral genome proceeds
    • TH cells lyse while macrophages release virus
  86. HIV Pathogenesis
    • Results in depletion of CD4+ lymphocytes particularly TH
    • Lysis
    • Attack by CD8 T cells
    • Antibody-dependent cellular cytotoxicity and natural killer cells
    • Generalized dysfunction of uninfected cells also evident
    • Steady drop of CD4+ cells over time
    • High variability when vial genome is copied:
    • Error rate in reverse transcriptase
    • Ex. variable regions in gp120
  87. Treatment of HIV
    • No vaccine approved
    • Medications to prolong asymptomatic stage:
    • HAART (highly active antiretroviral therapy)
    • Protease inhibitors
    • R. t. inhibitors: analogs (AZT) or direct inhibitors
  88. Side Effects of HIV
    Anemia, vomiting, fatigue, liver and muscle damage, rashes, ulcers, etc.
  89. Meninges
    Three membranes that cover the brain and spinal cord
  90. Meningitis
    Inflammation or infection of meninges
  91. Encephalitis
    Generalized inflammation or infection of brain
  92. Pathways to Central Nervous System
    • Bloodstream – although it is difficult to cross the blood brain barrier
    • Nerves
    • Extensions from bone
  93. Bacterial (Septic) Meningitis Symptom
    • Bacteria enter by respiratory tract, spread to blood and taken to meninges
    • Neutrophils and other inflammatory responses attempt to destroy
  94. Viral (Aseptic) Meningitis
    • Viremia occurs after infection of throat, intestine and lymphoid tissue
    • Upon entering meninges, fewer neutrophils react
  95. Viral Meningitis Infectious Agent
    • Enteroviruses
    • (ex. Echovirus and mumps virus)
  96. Viral Meningitis Transmission
    • Respiratory route
    • (shaking hands, wiping nose)
    • Fecal –oral route
  97. Viral Meningitis Treatment
    Only for symptoms
  98. Viral Meningitis Symptoms
    Stiff neck, severe headache, confusion, nausea – last 7-10 days; recovery is complete
  99. Bacterial Meningitis Infectious Agent
    • Haemophilus influenzae
    • Streptococcus pneumoniae
    • Neisseria meningitidis
  100. Bacterial Meningitis Transmission
    • Respiratory route
    • (coughing, kissing, sneezing)
  101. Bacterial Meningitis Treatment
    • Antibiotics for specific agent:
    • Penicillin
    • (preventative measure with rifampin)
  102. Bacterial Meningitis Symptoms
    • High fever, stiff neck, severe headache, nausea several hours or 1-2 days
    • Death or disability if not treated promptly – due to bacterial cell wall components leading to toxic shock
  103. Conjugate Vaccine for Meningitis
    • H. influenza type b polysaccharide bound to a bacterial protein like the diptheria toxoid
    • Administered since 1980s
  104. Leprosy
    • —Also known as Hansen’s Disease
    • —Once common in Europe and Americas
    • Now concentrated in India, Nepal, Myanmar, Madagascar, Mozambique and Brazil
    • —WHO goal of eradication by 2005
    • —Caused by infection by Mycobacterium leprae
    • Aerobic, acid-fast, rod
  105. Leprosy Symptoms
    • Onset of increased or decreased sensation on patches of skin
    • —Areas enlarge, thicken and loose hair
    • Loose all sensation
    • —Arms and legs become painful
    • —Eventual numbness in limbs with loss of fingers or toes
    • —Nose and ears also affected
  106. Leprosy Pathogenesis
    • —Spread by contact with nasal secretions or skin abrasions
    • —M. leprae invades the small nerves of the skin, preferably in cooler areas
    • —Immune response can slow growth causing tuberculoid leprosy
    • —Bacterium can grow in macrophages and eventually grow uninterrupted, lepromatous leprosy
  107. Leprosy Treatment
    • Tuberculoid leprosy
    • Rifampin and dapsone combination
    • —Lepromatous leprosy
    • Multiple drug therapy used to avoid drug resistance
  108. Staphylococcal Wound Infection Symptoms
    • Swelling, redness, pain at site
    • Fever and toxic shock
  109. Pathogenesis of S. aureus
    • –30-100% patients are carriers
    • –Coagulase to clot blood
    • –Clumping factor for colonization
    • Protein A binds Fc of IgG
    • –Alpha toxin and other superantigens
    • Can grow aerobically and anaerobically
    • Gram positive cocci
  110. Pathogenesis of S. epidermidis
    • –Adhere to medical devices then makes a glycocalyx
    • –Causes small abscesses in healthy
    • –If carried to bloodstream can cause subacute bacterial endocarditis
    • Can grow aerobically and anaerobically
    • Gram positive cocci
  111. Staphylococcal Wound Infection Treatment
    • Clean wounds or prompt closure
    • Antistaphylococcal medication immediately before surgery
    • –Cephlasporins
    • –Lipopeptide – Cubicin
    • –Linezolid – Zyvox
  112. Cat Scratch Disease Symptoms
    • Enlargement of lymph nodes in 1-7 weeks after bite or scratch
    • 22,000 annual cases mostly under age 18
  113. Cat Scratch Disease Pathogenesis
    • Bartonella henselae- gram negative bacillus
    • Zoonosis of cats and occasionally fleas
    • Bacillary angiomatosis:Skin lesions develop in AIDs patients
  114. Cat Scratch Disease Treatment
    • Clean wound
    • Ampicillin for severe infections
    • Disappears within 2-4 months
  115. Tetanus
    • Frequently fatal but rare in US
    • —Clostidium tetani
    • Anaerobic, spore forming, Gram +
    • Found in soil and sometimes gut of humans
    • Know mode of action for diseases
    • Not transmitted from person to person
  116. Tetanus Symptoms
    • Restlessness, irritability and difficulty swallowing
    • Sustained, painful and uncontrolled muscle spasms
    • Death by pneumonia or regurgitation into lungs
  117. Pathogenesis of Tetanus
    • Endospore introduced into tissue by deep wound
    • —Vegatative cells produce tetanospasmin (AB toxin) into blood
    • Enters neurons in brain
    • Prevents release of neurotransmitters by inhibitory neurons
    • Results in spastic contraction of muscles
    • —Neonatal tetanus
    • Cutting of umbilical cord by unsterile instrument
  118. Treatment of Tetanus
    • —Prevention- vaccine with tetanus toxoid
    • Booster required at school age and every 10 years
    • Can cross the placenta
    • —Tetanus immune globulin (TIG)
    • —Wound cleaned of dead tissue
    • —Antibacterial - metronidazole
  119. Bacterial Cystitis Symptoms
    • Frequent and painful urination
    • -Because of inflammation
    • Cloudy and/or red urine
    • -Cloudy-white blood cells/pus killing off cells that are infected or bacteria
    • -Red-capillaries are broken during the process of infection
    • Complication: pyelonephritis
  120. Bacterial Cystitis Pathogenesis
    • Multiple species; commonly E. coli
    • Travel up urethra to cause inflammation
  121. Bacterial Cystitis Treatment
    Antibiotics for species; usually β lactam
  122. People most Susceptible to Bacterial Cystitis
    • Sexually active women
    • Men over 50
  123. During intercourse, fecal matter gets pushed back into the anus and near the urinary tract
    Why would E. coli be the common infectious agent for bacterial cytosis?
  124. Leptospirosis Symptoms
    • Many asymptomatic
    • Headache, fever, chills, muscle pain
    • Severe: momentary relief then bleeding; heart, brain, kidney damage
    • Generally last 1-2 weeks, but small percentage still has infection although symptoms are gone (body starts shutting down)
  125. Leptospirosis Pathogenesis
    • Leptospira interrogans
    • Enters mucous membranes then multiplies in bloodstream
    • Ig’s and complement destroy most of pathogen
    • Larger immune response injures host causing blood clotting
    • Uses hook to attach to mucus membrane
    • Once attached to mucus membrane past epithelial cells wants to replicate in bloodstream not mouth/nose
    • Massive inflammatory response in vital organs ie damage to organs
  126. Leptospirosis Epidemiology
    • Exposure to urine of infected animals
    • Can hang out and be infectious for 2 or 3 days, in mud can last 2-3 weeks
  127. Leptospirosis Treatment
    • Tetracycline
    • Vaccines for domesticated animals
  128. What is the mode of action for tetracycline?
    • Blocks tRNAs from entering ribosome
    • Bacteriostatic: Keeps it from growing
    • Broad spectrum: Have a variety of organisms it can be effective against
    • Inhibiting translation
  129. Non Venereal: Bacterial Vaginosis Symptoms
    • Thin, grayish white discharge
    • Strong odor
  130. Non Venereal: Bacterial Vaginosis Pathogenesis
    • Increase in Gardnerella vaginalis and anaerobic bacteria
    • Decrease in normal vaginal flora
    • Increase in clue cells
    • Not a sexually transmitted disease, but only women who are sexually active show the symptoms
    • Deals with air, but is not aerobic
  131. Most Susceptible to Non Venereal: Bacterial Vaginosis
    • Women during childbearing years
    • Preterm birth in pregnant women, can cause miscarriage
  132. Non Venereal: Bacterial Vaginosis Treatment
  133. Clue Cells
    Epithelial cells covered in bacterial vaginosis
  134. Metronidazole
    • Antiprotoxoal and antibacterial agent
    • Disrupts DNA’s helical structure
    • Affects replication and transcription
  135. Venereal: Trichomoniasis Symptoms
    • Itching in genital area
    • Frothy, yellow-green vaginal discharge
    • Men usually asymptomatic
  136. Venereal: Trichomoniasis Pathogenesis
    • Unknown method by Trichomonas vaginalis
    • Froth produced by hydrogen gas
  137. Venereal: Trichomoniasis Treatment
    Metronidazole- anti-protazoic and anti-bacterial
  138. Venereal: Trichomoniasis Epidemiology
    • 5 million Americans acquire each year
    • Sexual transmission
    • Humans only reservoir
  139. Sexually Transmitted Diseases
    15 million Americans (3 million teenagers) annually
  140. Types of Sexually Transmitted Diseases
    • Viral STD
    • Bacterial STD
  141. Bacterial STDs
    • Chlamydia
    • Chancroid
  142. Viral STDs
    Genital warts
  143. Prevention of STDs
    • Abstinence
    • Monogamous relationship
    • Condom (decreases chance of transmission)
  144. Chlamydia Symptoms
    • Frequent and painful urination
    • Thin gray-white discharge
    • Possible abdominal pain
  145. Chlamydia Pathogenesis
    • Chlamydia trachomitis
    • Travel up urethra or vagina; can attach to sperm
    • Induces endocytosis by epithelial cells
    • Inflammation by cytokines, sends off MHC I
    • Inflammation of fallopian tubes – pelvic inflammatory disease
    • Inflammation of epidimymis – sterility
  146. Chlamydia Treatment
    • If sexually active, have yearly tests
    • Azithromycin, tetracycline and erythromycin
    • Inhibit translation
  147. Most Susceptible to Chlamydia
    One study: 14% high school and college women were carriers
  148. Inflammation of Fallopian Tubes
    Causes scars, blocking eggs to transport
  149. Inflammation of Epidimymis
    Sperm can’t move and travel outside of penis, long term effect
  150. Ectopic Pregnancy
    Egg is fertilized outside of uterus
  151. Chlamydia
    • Attaches to epithelial cells as an elementary body and induces endocytosis
    • Attaches using pili specific for epithelial cells
    • Obligate intracellular bacteria inside host cell is called reticulate body
    • Repeatedly divides to allow release of elementary bodies from host
    • Divides so fast, before immune system catches up, infection is released to other cells
  152. T-cells, t-cytotoxic
    • Much of the tissue damage results from the cell-mediated immune response”
    • Who is actually damaging tissue?
  153. Chlamydia and the Population
    • Females show more symptoms
    • Males are more likely to be carriers
  154. Chancroid Symptoms
    • Painful ulcers in genital region – soft chancres
    • Swelling of lymph nodes
  155. Chancroid Pathogenesis
    • Uncertain of method by Haemophilus ducreyi
    • Small pimple occurs then ulcer
    • Pus filled lymph nodes may rupture
  156. Chancroid Epidemiology
    • Largely unreported or undiagnosed
    • May contribute to HIV transmission
    • Men more likely to show symptoms
  157. Chancroid Treatment
  158. The epithelial cell walls have been broken down
    An ulcer is an open wound
    As with any STD that produces ulcers, HIV transmission can be enhanced during unprotected sex. Why is this the case?
  159. Genital Warts Symptoms
    • Small warts at site of infection – papillomas
    • Lesions of cervix
    • Asymptomatic
  160. Genital Warts Pathogenesis
    • Human papillomavirus; non-enveloped, ds DNA
    • -Replication is easy because of ds DNA, can rely on host
    • 30 types by sexual transmission
    • 15 types linked to cervical cancer
    • Infect deeper epithelial cells by small abrasions
    • Latent infection
    • Waits on host to die to exit body (naked or non enveloped)
  161. Genital Warts Transmission
    • Single sexual exposure – 60% chance of infection
    • Can infect mouth as well as genitalia
    • Even if you wear a condom, infection can affect outside of vagina instead of inside
  162. Genital Warts Treatment
    • Freezing or laser
    • Imiquimod
    • Yearly Pap smear
  163. Imiquimod
    Anti-viral agent to inhibit replication of virus
  164. Genital Warts
    • 20 million in US currently infected
    • Half are ages 15 through 24 years
    • 12,000 women are diagnosed with cervical cancer yearly; 4,000 women die
  165. Genital Warts Prevention
    • HPV vaccine
    • Non-infectious HPV-like particles
    • HPV 16 and 18, which cause 70% of cervical cancers, and HPV 6 and 11, which cause 90% of genital warts
    • Recommended for 11 and 12 year-old girls
    • Inactivated vaccine
    • Sub-unit vaccine
  166. Meningococcal Meningitis Symptoms
    • Mild cold, throbbing headache, fever, stiffness of neck and back, nausea and vomiting
    • Purplish spots – petchiae on skin
  167. Meningococcal Meningitis Infectious Agent
    • Neisseria meningitidis
    • –Gram negative, aerobic
    • –Polysaccharide capsule
  168. Endotoxin of Meningitis
    • N. meninigitidis releases endotoxin into bloodstream during binary fission or autolysis
    • Resulting in shock
  169. How does endotoxin cause shock?
    • Shock is the state where not enough blood pressure is circulate blood properly
    • Circulating endotoxin causes inflammatory response body-wide
  170. Tuberculoid Leprosy
    • —6 months
    • Rifampin and dapsone combination
    • Dapsone acts as a metabolite inhibitor
  171. Lepromatous Leprosy
    • —2 years
    • Multiple drug therapy used to avoid drug resistance
    • –Third drug of clofazimine which binds mycobacterial DNA
  172. Superanitgen
    • Overrides the specificity of T-cells and causing massive release of cytokines by a large number of TH cells
    • —Stimulates hundreds more T cells by binding to MHC II and T cell
    • —Results in fever, nausea, vomiting and shock
    • Toxic shock
  173. Staphylococcus
    • —Transmitted by wound or surgical site
    • —Results in
    • Delayed healing
    • Formation of abscesses
    • Spread of bacteria or their products into other tissue or blood
    • —20% of healthy adults are carriers
    • —Transfer usually by hands
  174. You’re trying to get rid of the toxin and the source so you give both
    —Would you administer both the immune globulin AND the antibiotic? If not, which one and why?
  175. Yes, you just have to be exposed to the toxin
    —Could someone have tetanus without finding bacteria in the wound?
  176. Streptococcal Pharyngitis Symptoms
    • Painful swallowing, fever
    • Red throat with white patches
    • Enlarged neck lymph nodes
    • Activate B and T cells
  177. Streptococcal Pharyngitis Epidemiology and Pathogenesis
    • Streptococcus pyogenes by inhalation of respiratory droplets
    • Gram positive coccus
    • Peak incidence among school children in winter and spring months
  178. Streptococcal Infections
    • —Group A streptococci: Streptococcus pyogenes
    • —Virulence factors
    • Hemolysins : streptolysin O and S- beta hemolysis- likes red blood cells, wants to take up as much iron as it can
    • Protein G- Fc receptor
    • Protein F for attachment
    • Capsules of hyaluronic acid- coats itself in the capsule by avoiding the immune system response
    • C5a peptidase
    • M protein: Inactivates C3b- Compliment
  179. What is the advantage of inhibiting C5a and C3b?
    • C5a- cytokine for chemotoxins
    • The “bread crumb trail” neutrophils follow to infection
    • C3b part of complement system- binds to surface of bacterial cells
    • –Opsinization
    • –Memory attack complex
    • Inflammation
    • Strep cuts off trail for neutrophils to find infection phagocytosis does not occur
    • Fc binds antibodies tail side in (opposite)
  180. Strep Throat Pathogenesis
    • —Streptococcal pyrogenic exotoxins - superantigens
    • Complications due to lack of treatment
    • –Scarlet fever – during infection, roughening of skin and red rash caused by erythrogenic toxin
    • –Acute rheumatic fever – inflammation of joints, heart, skin and brain 3 weeks after recovery
    • Results in permanent heart valve damage
  181. Strep Throat Treatment
    Penicillin or erythromycin
  182. Strep Throat Pathogenesis
    • T helper cells are activated huge immune response
    • Super antigens cause a body wide rash during strep throat infection
    • Heart valve damage- bacteria can start colonizing in the area- clot of bacteria leaves area of infection and can go to brain causing a stroke
  183. Whooping Cough (Pertussis) Symptoms
    • Runny nose then violent uncontrollable coughing
    • -Infective during this period
    • Paroxysmal coughing
    • –Infants most at risk for mortality
    • Pneumonia can inset and kill you
    • -Caused by bordetella pertussis or another infection
  184. Whooping Cough (Pertussis) Causing Agent
    • Bordetella pertussis
    • –Aerobic gram negative rod
  185. Whooping Cough (Pertussis) Pathogenesis
    • Inhalation of droplet and attachment of respiratory epithelium
    • Grow in dense masses on surface
    • –Pertussis toxin and filamentous hemagglutinin
    • Increased mucus production and sloughing of ciliated cells
    • Pneumonia or secondary bacterial infection causes death
  186. Pertussis Toxin
    • A-B toxin
    • B portion binds to host surface
    • A portion penetrates cytoplasmic membrane
    • Causes overproduction of cAMP thus increasing mucus production
  187. Pertussis Treatment
    • Acellular vaccine given with diphtheria and tetanus toxoids –DTaP
    • –5 doses before 18 months and one more at age 4
    • Erythromycin for infection
    • A-cellular vaccine- injecting parts of the cells or a protein off of the cell
    • DTaP- inactivated vaccine
  188. Respiratory Syncytial Virus (RSV) Symptoms
    • Cough wheezing and difficulty breathing
    • Causes of croup, cold with loud high-pitched cough in older infants
    • 90,000 hospitalizations yearly with 4,500 deaths
  189. Respiratory Syncytial Virus (RSV) Causative Agent
    Respiratory syncytial virus, enveloped with SS RNA genome
  190. Respiratory Syncytial Virus (RSV) Pathogenesis
    • Enters by inhalation and infects respiratory tract epithelium
    • Bronchiolitis with partial plugging by dead sloughed cells and mucus
    • Obstructed airway by dead cells
  191. Respiratory Syncytial Virus (RSV) Prevention
    Palivizumab, no vaccine
  192. Highly contagious during runny nose period
    Causes mucus productions and schlepping off ciliated cells
    Baby doesn’t have enough antibodies
    Why does the incidence of whooping cough rise promptly when pertussis immunizations are stopped?
  193. Cytotoxins
    —How would you classify the pertussis toxin?
  194. Passive active immunity
    —Palivizumab for RSV is a monoclonal antibody. What kind of immunity is acquired from it?
  195. Rotaviral Gastroenteritis Symptoms
    • Vomiting, slight fever, profuse watery diarrhea
    • Almost every child in the US is infected at some time before age of 5
  196. Rotaviral Gastroenteritis Causative Agents
    • Rotaviruses
    • –Double walled capsid- two layers of protein
    • –Double stranded, 11 segment RNA genome
  197. Rotaviral Gastroenteritis Pathology and Epidemiology
    • Infects epithelial cells of small intestine, causing death
    • Fecal–oral; fomites
    • Responsible for 25% of traveler’s diarrhea
  198. Uses his own RNA polymerase that recognizes RNA to replicate not DNA
    How does rotavirus replicate its genome in small intestine epithelial cells? What does it require to replicate?
  199. Yes
    • Would it be possible for reassortment to occur if there was a coinfection of rotaviruses?
    • Reassortment- two different viruses affect the same cell- share their genetic information
  200. Cell lysis because of virus replication using all of the body’s nutrients
    —How does cell death occur since it is a naked virus?
  201. Norovirus Gastroenteritis Symptoms
    • Nausea, vomiting and diarrhea that lasts 12-60 hours
    • Infects from age 5 to adult
  202. Norovirus Gastroenteritis Causative Agent
    • Norovirus
    • Nonenveloped, single stranded RNA genome
  203. Norovirus Gastroenteritis Pathology and Epidemiology
    • Fecal–oral, highly contagious
    • Typically infect children and adults
    • Infect upper small intestinal epthelium
  204. Norovirus Gastroenteritis Prevention
    Hand washing
  205. Hand scanners in dorms, dining halls, and gym
    What would be a likely scenario to how the students obtained the virus?
  206. Hepatitis A
    • —“Infectious hepatitis”
    • —No animal reservoir
    • —Hepatitis A virus (HAV)
    • Single stranded, +RNA, icosahedral, naked
    • Humans are the only ones who carry hepatitis A
  207. Hepatitis A Symptoms
    • Fatigue, fever, nausea, diarrhea, chills, jaundice, clay colored feces
    • Children – asymptomatic- how a lot of transmission occurs
    • Adults – 20% require hospitalization
    • Recovery within a month
  208. Hepatitis A Epidemiology and Pathogenesis
    • Fecal-oral
    • Fecal contaminated water was being used to wash green onions
    • Ingested virus replicated in intestinal epithelium
    • Once in blood, targets liver to replicate
    • Liver tissue damaged with inflammation
    • New viruses released into feces by bile secreted to small intestine
    • T-cytotoxic cells come in to kill
    • When red blood cells die, hemoglobin is being used replacing it with billyreuben cells
    • Liver can’t clear out billyreuben causing feces to be clay like color
    • In 2007- 1 in 100,000 people will get Hepatitis A
    • Termed infection hepatitis
  209. High Risk Groups for Hepatitis A
    • Crowded and poor sanitation areas
    • Day care centers, nursing homes
  210. Hepatitis A Prevention and Treatment
    • Detected by anti-hepatitis A antibody
    • Hepatitis A vaccine - inactivated virus (1990s)
    • –Routine immunization schedule for infants
  211. Vaccines
    What would account for the drop in overall incidence of Hepatitis A?
  212. CDC put out an announcement to health centers to promote Hepatitis A vaccine
    There is a typical pattern of peak incidence in the US every 10-15 years. Why would there be a second drop in incidence particularly in the West right before 2000?
  213. Hepatitis B
    • "—Serum hepatitis”
    • —40% viral hepatitis cases in US
    • 4.5 million cases for Hepatitis B and C infection
    • —Can become chronic
    • —Hepatitis B (HBV)
    • Double-stranded circular DNA, enveloped
    • Antigen: HBsAg (surface antigen); core antigen (HBcAg); e antigen (HBeAg)
    • Normally acute, but can turn chronic
    • Different virus that Hepatitis A
  214. Hepatitis B Symptoms
    • May be asymptomatic
    • Similar to HAV but more severe
    • –Death from liver failure in up to 10% of hospital cases
  215. Hepatitis B Epidemiology
    • Exposure by blood, semen, sweat, saliva, urine, feces
    • Can be passed by injection, rubbed into minor wounds or by mouth
    • Most likely passed among homosexual men
  216. Hepatitis B Pathology
    • Carried to liver by bloodstream
    • Causes liver injury by inflammation
    • HBsAg appears in blood days or weeks after infection
    • Found as small, large spherical or tubular particles
    • —1-6% become chronically infected
    • 40% die of cirrhosis or liver cancer
    • Generally don’t see jaundice
  217. Hepatitis B Virus
    When budding, virus can have envelope particles with no nucleus in it
  218. HBV Replication
    • Upon entry, DS DNA is transcribed in host nucleus
    • RNA copy of genome packaged in capsid
    • Reverse transcriptase makes copy of single DNA then double strand
    • Does not have a complete dsDNA
    • -Host polymerase completes dsDNA
  219. Hepatits B Prevention
    • Genetically engineered HBsAg vaccine
    • –Recommended for adults with multiple partners and homosexual men
    • Known exposure: hepatitis B immune globulin (HBIG)- given artificial passive immunity
  220. Hepatitis B Treatment
    • Injections of genetically engineered interferon
    • Antiviral medication – reverse transcriptase inhibitor
    • Inactivated subunit vaccine
    • -Injecting just a piece of genetically engineered HBV
    • Interferon's is the cell signal to alert other cells to come attack HBV infection
  221. Hepatitis C
    • Most common chronic blood-born infection in US
    • —Hepatitis C virus (HCV)
    • Single-stranded, +RNA, enveloped
    • Considerable genetic variation among infected individuals
    • You see subtypes- hard to find a vaccine
  222. Hepatitis C Symptoms
    None or very mild symptoms similar to HAV, HBV
  223. Hepatitis C Epidemiology
    • Blood exposure, fecal-oral, sexual, organ transplantation
    • Toothbrush, razors, towels, tattoos, needles
  224. Hepatitis C Pathogenesis
    • 80% of those infected become chronic
    • Inflammation and immune response causes scarring of liver
    • Cirrhosis and liver cancer develops in 10-20%
  225. Hepatitis C Treatment
    • —No vaccine
    • —Interferon treatment along with an antiviral nucleoside derivative helps relieve symptoms for 30 50% of those infected
  226. Yes, because they are three totally different viruses
    You will receive a booster for A and B if you have C
    —If you had chronic hepatitis B, could you still be infected by hepatitis A and C?
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