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Patho 2 > Chap 8- Infectious diseases > Flashcards

Chap 8- Infectious diseases Flashcards

(116 cards)

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1
Q

types of physical barriers

A
  • skin defenses
  • GI tract defenses
  • respiratory tract defenses
  • urogenital tract defenses
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2
Q

skin barriers

A
  • keratinized outer layer
  • low pH
  • fatty acids
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3
Q

GI tract defenses

A
  • gastric acid
  • pancreatic enzymes
  • bile detergents
  • peyer patches
  • defensins
  • peristalsis
  • protective flora
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4
Q

respiratory tract defenses

A
  • bronchial epithelium ciliary activity
  • mucous layer
  • defensins
  • IgA
  • alveolar macrophages
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5
Q

urogenital tract defenses

A
  • frequent bladder flushing with urine
  • low vaginal pH
  • intact epidermal/ epithelial barrier
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6
Q

what factors influence consequences of infectious disease?

A
  • virulence of organism
  • magnitude of infection
  • pattern of seeding
  • host factorts
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7
Q

how are most pathogens transmitted?

A
  • respiratory
  • fecal oral
  • sexual
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8
Q

stages of infection

A
  • host encounter
  • gain entry
  • multiply and spread
  • direct or indirect tissue inury
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9
Q

what are possible outcomes of infection

A
  • resolution
  • chronic active infection
  • prolonged asymptomatic excretion of agent
  • latency
  • host death
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10
Q

what are some mechanisms of immune evasion?

A
  • antigenic variation
  • resistance to antimicrobial peptides
  • resistance to phagocytes
  • evasion of apoptosis and maniupation of host cell metabolism
  • resistance to cytokine and complement sys
  • evasion of recognition by CD4 and CD8 cells
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11
Q

viral mechanism of injury

A
  • prevent synthesis of macromolecules in host
  • production of degradative enzymes and toxic proteins
  • antiviral immune responses
  • transformation of infected cells
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12
Q

tropism

A
  • ability for virus to infect certain cells only

- match for receptors on the body human body and the virus

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13
Q

mechanisms of bacterial injury

A
  • bacterial virulence
  • bacterial adherence to host cells via adhesions and pili
  • toxins
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14
Q

what factors impact bacterial virulence

A
  • ability to adhere to host cells
  • ability to invade cells/ tissues
  • ability to deliver toxins
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15
Q

what are adhesins

A
  • bacterial surface proteins

- allow bacteria to bind to host cells or ECM

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16
Q

pili

A
  • proteins in surface of bacteria

- act as adhesins

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17
Q

what are bacterial endotoxins

A
  • lipopolysaccharide in outer membrane

- stimulates host immune response and injuries of host

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18
Q

what type of bacteria produce endotoxins

A

gram-negative bacteria

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19
Q

what are exotoxins

A
  • produced during normal growth and metabolism of bacteria

- secreted or released following lysis

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20
Q

what type of bacteria produce exotoxins

A

gram positive bacteria

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21
Q

examples of acute viral infections

A
  • measles
  • mumps
  • poliovirus
  • viral hemorrhagic fevers
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22
Q

examples of chronic productive viral infections

A
  • HBV

- HIV

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23
Q

examples of chronic latent viral infections

A
  • HSV
  • VZV
  • CMV
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24
Q

examples of transforming viral infections

A
  • EBV

- produce cancers

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25
measles
- affects multiple organs - severity ranges from self limited to severe - leading cause of vaccine preventable death and illness worldwide
26
how is measles transmitted?
respiratory droplets
27
pathogenesis of measles
- replication of virus in respiratory tract/ lymphatic tissue - viremia and systemic dissemination - T cell mediated - antibody mediated immunity to protect against reinfection
28
what is responsible for the measles rash
T cell mediated response
29
what is another name for measles
rubeola
30
mumps
- acute systemic viral infection - pain and swelling of salivary glands - vaccine has reduced incidence greatly in US
31
what are clinical symptoms of mumps
- pain and swelling of salivary glands - aseptic meningitis - orchitis - pancreatitis
32
what type of virus are the measles and mumps viruses
paramyxovirus family
33
pathogenesis of mumps
- upper respiratory tract infection - lymph node infection and dissemination into blood stream - salivary gland swelling and pain
34
how is polio transmitted
fecal oral route (enterovirus)
35
poliovirus pathogenesis
- ingested - replicates in mucosa of pharynx and gut - moves through lymphatics to lymph nodes then blood - causes viremia and fever - antibodies control disease in most cases
36
poliovirus symptoms
- mostly asymptomatic - 1% of pts it invades CNS and replicates in motor neurons - can cause spinal polioyelitis or bulbar poliomyelitis
37
spinal poliomyelitis
- paralysis of limb muscles | - especially affects kids
38
what disease does polio mimc
guillian barre syndrome
39
viral hemorrhagic fever pathogenesis
- life threatening multisystem syndrome -> vascular dysregulation and damage -> shock - infect endothelial cells, macrophages and dendritic cells -> cytokine released - reduced ability of dendritic cells to present antigen - damage to BV -> hemorrhage
40
how are viral hemorrhagic fevers transmitted?
through infected insects or animals
41
what viruses cause viral hemorrhagic fevers
- enveloped RNA viruses - arenavirus - filovirus - bunyavirus - flavivirus
42
mild symptoms of viral hemorrhagic fevers
- fever - HA - rash - myalgia - neutropenia - thrombocytopenia
43
severe sx of viral hemorrhagic fevers
- life threatening hemodynamic deterioration | - shock
44
what type of virus is the herpes virus
- dna virus | - establishes latent infection
45
classifications of HSV
- alpha herpesvirinae - beta herpesvirinae - gamma herpesvirinae
46
what are examples of alpha herpesvirinae
- HSV type 1 - HSV type 2 - varicella zoster
47
what are examples of beta herpesvirinae
- cytomegalovirus - human herpes virus type 6 - hyman herpes virus type 7
48
what are examples of gamma herpesvirinae
epstein barr virus
49
HSV pathogenesis
- replicate in skin and mucosa membrane - viral multiplication - lysis of epithelial cells -> ulcers
50
where do HSV and varicella reside
- usually trigeminal nerve
51
where does cytomegalovirus usually reside
monocytes
52
where does EBV usually reside
b cells
53
HSV 1
- cold sores - gingivostomatitis - major cause of corneal blindness and fatal encephalitis
54
HSV 2
- genital sores | - can lead to life threatening disseminated visceral infections and encephalitis
55
how is varicella zoster virus transmitted
- respiratory aerosols | - gets into blood and causes skin lesions
56
acute infection of VZV
chickenpox
57
reactivation of VZV
- shingles - innervated by trigeminal ganglia - see blisters in specific dermatomes
58
other manifestations of VZV
- interstitial pneumonia - encephalitis - transverse myelitis - necrotizing visceral lesions
59
cytomegalovirus
- infects monocytes and bone marrow progenitors - in healthy typically asymptomatic - in neonates and immunocompromised can cause serious systemic infection - most common opportunistic viral pathogen in AIDS
60
how is cytomegalovirus transmitted
- saliva - sexually - transplacentally from pregnant mother to unborn baby - blood transfusions or organ transplants - during childbirth
61
typical symptoms of CMV in infants
- deafness and mental retardation
62
typical symptoms of CMV in immunosuppressed
- pneumonitis - hepatitis - choriorentitis - meningoencephalitis
63
cytomegalic inclusinon disease
- caused by CMV - IUGR - hemolytic anemia - jaundice - encephalitis
64
oncogene viruses
- EBV - HPV - HBV - HTLV-1
65
EBV infection outcomes
- infectious - lymphadenopathy and splenomegaly - lymphomas - infect B cells -> proliferate -> thrombocytopenia - nasopharyngeal carcinomas - resolves in most pts with in 4-6 weeks
66
lymphomas associated with EBV
- burkitt | - hodgkin
67
s. aureus infections
- skin lesions - abscesses - sepsis - osteomyelitis - pneumonia - endocarditis - food poisoning - toxic shock syndrome
68
what type of bacteria is staphylococcus
gram positive cocci
69
why can staphylococcus result in toxic shock syndrome
- contains superantigens | - superantigens cause inappropriate and excessive stimulation of T cells
70
ways staphylococcus evades infection
- surface receptors binding to endothelial cells - superantigens - surface A protein - bacterial toxins - capsule and biofilm
71
types of streptococcus
- alpha hemolytic | - beta hemolytic
72
types of alpha hemolytic streptococcus
- s. pneumoniae | - viridans streptococci
73
types of beta hemolytic streptococcus
- s. pyogenes | - s. agalactiae
74
s. pneumoniae
- alpha hemolytic streptococcus - common cause of community acquired pneumonia in elderly - causes meningitis in kids and adults
75
viridans streptococci
- alpha hemolytic streptococcus - found in normal oral flora - common cause of endocarditis
76
s. pyogenes
- beta hemolytic streptococcus - pharyngitis - scarlet fever - erysipelas - impetigo - rheumatic fever - toxic shock syndrome - glomerulonephritis
77
s. agalactiae
- beta hemolytic streptococcus - colonizes in female genital tract - causes spesis and meningitis in neonates - chorioamnionitis in pregnancy
78
ways that steptococcus evades immune response
- m protein - protein F - streptokinase - pneumolysin - hyaluronic acid capsule
79
m protein
- prevents phagocytosis | - binds fibrinogen and complement proteins
80
protein F
- mediates adhesion to fibronectin | - fibronectin is ECM protein
81
streptokinase
- cleaves plasminogen to activate plasmin | - dissolves clot
82
pneumolysin
inserts into host cell membrane and lyses cell
83
diptheria
- caused by corynebacterium diptheriae | - transmitted by respiratory droplets or skin exudate
84
ways that diptheria evades immune response
- AB toxin which blocks protein synthesis | - forms pseudomembrane
85
pseudomembrane in diptheria
- exotoxin - causes necrosis of epithelial cells - liberates serous and fibrinous material
86
types on neisserial infections
- n. meningitidis | - n. gonorrhoeae
87
n. meningitidis
- causes meningitis in adolescents and young adults - transmitted through respiratory route - most can eliminate infection - antigenic variation
88
how does n. meningitidis evade immune response
- covered in capsule | - capsule inhibits opsonization and destruction by complement system
89
n. gonorrhoeae
- 2nd most common STD - infection in urogenital tract by interacting with epithelial cells -> cellular invasion - causes PMN - arthritis, meningitis, and neonatal opthalmia
90
who is more likely to become infected by nisseria
- people who lack complement proteins that form MAC
91
pertussis
- gram negative coccobacillus - highly communicable - produces AB toxin - inhibit neutrophils and macrophages - paralyzes cilia
92
what is another name for pertussis
whooping cough
93
what are possible outcomes of severe bordetella infection
- laryngotracheobronchitis causing: - bronchial mucosal erosion - hyperemia - copious mucopurulent exudate - lymphadenopathy
94
p. aeruginosa
- gram negative bacillus - deadly in people with CF, severe burns, neutropenia - very resistant to antibiotics - common hospital acquired infection
95
possible clinical outcomes of p. aeruginosa
- corneal keratitis in contact lens wearers - endocarditis and osteomyelitis in IV drug users - external otitis
96
how does p. aeruginosa evade immune response
- excrete exotoxin A -> inhibits protein synthesis - elastase - leukocidin - hemolysins- destroys cell membranes
97
what is the evidence of infection in Tb
- fibrocalcific pulmonary nodule at site of infection | - can lay dormant for years
98
what affects outcome of Tb
- T cell mediated immunity | - causes pathologic lesions like caeseating granulomas and cavitation
99
where does Tb infection reside/ replicate
macrophages
100
what is the ghon complex
- parenchymal lung lesion | - nodal involvement
101
pathogenesis of Tb
- 3 weeks post infection IL12 released by dendritic cells - Th1 response - release IFN gamma - macrophages activated - granuloma and caseous necrosis
102
primary Tb
develops in previously unexposed person
103
secondary Tb
- develops in previously sensitized host | - usually involves apex of upper lobes of one or both lungs with cavitation
104
systemic symptoms of Tb
- related to cytokine released by activated macrophages - malaise - anorexia - weight loss - low grade fever - night sweats
105
late stages of Tb
- increasing amounts of sputum, hemoptysis, pleuritic pain
106
dx of Tb
- history - xrays - gold standard= sputum culture
107
syphilis
- chronic STD - varied clinical sx - caused by spirochete tryponema pallidium
108
primary syphilis
- 3 weeks after contact - chancre on penis, cervix, vaginal walls, or anus - heals without therapy
109
secondary syphilis
- 2-10 weeks post exposure - widespread mucocutaneous lesions in oral cavity, palms of hands, soles of feet - lymphadenopathy - mild fever - malaise - weight loss
110
tertiary syphilis
- long latent period (5 years) - CV syphilis - neurosyphilis - benign tertiary syphilis
111
CV syphilis
- aortitis | - aortic valve insufficiency
112
neurosyphilis
- meningovascular disease - diffuse brain parenchymal disease - CSF abnormalities - increased protein - decreased glucose
113
benign tertiary syphilis
- gummas in bone, skin, and mucous memrbanes | - gummas are bumps/ elevations
114
what causes lyme disease
- borrelia burgdorferi | - can be persistent or severe
115
how does lyme disease evade immune response
antigenic variation
116
what causes damage from lyme disease
- host immune response - does NOT produce toxin - T cell and cytokine release mediates immune response - antibodies made 2-4 weeks post infection - direct complement mediated phagocytosis and killing of bacteria

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