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GMS6121 - Infectious Diseases > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

encephalitis

A

inflammation of the brain parenchyma

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2
Q

myelitis

A

infection of the spinal cord

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3
Q

Most bacterial meningitis is ____

A

nosocomial, not usually community acquired

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4
Q

defenses of CNS

A

low complement in the CSF - not lysed efficiently
micro
microglia - similar to phagocytes

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5
Q

Damage to the CNS by meningitis

A

inflammation PMNs
vasogenic edema impaired blood flow ischemia
cell death

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6
Q

Acute bacterial meningitis in newborns is usually caused by which organisms?

A

Group B strep
E. coli K1
Listeria monocytogenes

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7
Q

Acute bacterial meningitis in infants-2 year olds is usually caused by which organisms?

A

Strep pneumo
Neisseria meningitidis
Haemophilus influenzae type B

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8
Q

Acute bacterial meningitis in adults is usually caused by which organisms?

A

Strep pneumo
Neisseria meningitidis

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9
Q

Listeria monocytogenes features

A

gram pos rod
non-spore
sero-grouped by teichoic acid
motile
soil, food, genital tract of mother

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10
Q

Listeria monocytogenes Encounter

A

Environmental - soil
Foodborne outbreaks
Meat, dairy
Genital tract of mother

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11
Q

Listeria monocytogenes Entry

A

oral
transplacental

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12
Q

Listeria monocytogenes Spread

A

invade non-phagocytes (InlA-E Cadherin)
lyse the phagosome (Listeriolysin O)
escape to cytoplasm
use host actin to spread from cell to cell (ActA)
invade through mucosal surface into bloodstream
cross blood-brain barrier
inflammation can lead to leakiness

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13
Q

Listeria monocytogenes evade defenses

A

intracellular
infects macrophages
escapes vacuole
peptidoglycan deacetylation (decreases host response - peptidoglycan is normally recognized by TLR2)

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14
Q

Listeria monocytogenes damage

A

inflammation triggered by peptidoglycan
fluid accumulation
increased intracranial pressure, hydrocephalus, and brain damage

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15
Q

Listeria monocytogenes outcome

A

highly lethal if not treated
other than mother to baby, not transmitted

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16
Q

Haemophilus influenzae type B features

A

gram neg rod
encapsulated (by b antigen)
other types cause less disease
Hib was the primary cause of meningitis in children 6 mo-2 years
vaccine all but eliminated Hib cases and invasive disease

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17
Q

Haemophilus influenzae encounter

A

human ONLY
respiratory droplets or saliva
can be endogenous

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18
Q

Haemophilus influenzae entry

A

upper respiratory tract (nasopharynx)
adherence factors pili (fimbriae)
Hap (haemophilus adhesion and penetration) - autotransporter

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19
Q

Haemophilus influenzae spread

A

goes from upper resp tract into blood, crosses blood-brain barrier to CNS

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20
Q

Haemophilus influenzae multiplication

A

fastidious, requires chocolate agar

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21
Q

Haemophilus influenzae evade defenses

A

extracellular
capsule
phosphocholine decoration of LOS = anti-LOS IgG
sialylation of LOS
binds complement factor H
IgA protease

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22
Q

Haemophilus influenzae damage

A

inflammation
LPS
Protein D - kills ciliated epithelium by cleaving glycerol phosphate (glycerophosphodiesterase)

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23
Q

Hib vaccine

A

humoral IgG to capsule prevents systemic infection by opsonization
composed of type B carbohydrate coupled to protein
drastically reduced meningitis by Hib
single serologic type of capsule associated with systemic disease makes single vaccine sufficient
part of the standard infant/child regimen

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24
Q

Neisseria meningitidis features

A

gram neg diplococcus
sero-grouped by carbohydrate capsule

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25
Q

Neisseria meningitidis encounter

A

humans only (5-10%colonization - normal flora)
respiratory droplets
can cause epidemic

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26
Q

Neisseria meningitidis entry

A

upper resp tract
adherence - type IV pili
opacity proteins (opa, opc)

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27
Q

Neisseria meningitidis spread

A

through the epithelium into the blood
ciliary stasis and death
crosses blood-brain barrier
infects CNS

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28
Q

Neisseria meningitidis evasion of defenses

A

carbohydrate capsule - numerous serogroups; group B = polysialic acid (antigenic mimicry)
LOS siacylation
factor H protein binding (fhbp)
complement-deficient patients susceptible

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29
Q

Neisseria meningitidis - group B capsule

A

polysialic acid - antigenic mimicry, which means that we can’t put this capsule into a vaccine because we don’t make antibodies to sialic acid

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30
Q

Neisseria meningitidis vaccine

A

mixture of most prevalent capsular antigens EXCEPT group B
linked to protein
induce IgG to protect blood
mixture of 4 capsule types
good efficacy
shortcoming: should induce IgA

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31
Q

Neisseria meningitidis multiplication

A

it can reach really high levels in the blood

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32
Q

Upper vs lower respiratory tract

A

Upper - ciliated epithelium (everything down to the bronchi)
Lower - non-ciliated epithelium (broncho-alveoli and alveoli)
Upper can be cleared by the mucociliary escalator but lower cannot

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33
Q

Upper respiratory tract defenses

A

physical - ciliary escalator, mucus
particle exclusion - nasal hairs, coughing and sneezing, epiglottis, larynx
chemical - lysozyme (degrades peptidoglycan) and lactoferrin (binds Fe)
Alveolar macrophages (PMNs with inflammation)

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34
Q

What size organisms can make it to the lower respiratory tract?

A

<3 micrometers

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35
Q

Cell mediated immunity

A

cytotoxic lymphocytes throughout the respiratory tract
TH1-macrophages in lower respiratory tract for intracellular pathogens

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36
Q

alpha hemolytic and non typable grouping (stept)

A

partial hemolysis, green
S. pneumoniae
Commensal oral streptococci (viridans streptococci)
usually non-invasive

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37
Q

beta hemolytic group (strept)

A

complete hemolysis, clear
Group A : S. pyogenes (GAS)- >90% pharyngitis
Group B: S. agalactiae (GBS)- neonatal sepsis
Group C: Animal pathogens,
S. dysgalactiae ~5% pharyngitis

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38
Q

gamma hemolytic group (strept)

A

no hemolysis
Group D: Many species of Enterococcus, e. g.
E. faecalis

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39
Q

Strep pyogenes features

A

gram pos cocci in chains
beta hemolysis
Group A carbohydrate
M protein (fibrillar later)
>100 serotypes of M protein - cause different diseases (antigenic variety)
hyaluronic capsule
lipoteichoic acid

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40
Q

bacitracin sensitivity test

A

differentiate
sensitive beta-hemolytic Group A streptococci
(S. pyogenes)
from beta-hemolytic non-Group A streptococci
group A cause more acute pharyngitis

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41
Q

CAMP test

A

Identify presumptive for Group B strep or Streptococcus agalactiae
CAMP factor made by S. agalactiae enhances beta-hemolysis of S. aureus (synergistic effect) by binding to already damaged RBCs
As a result, an arrow of beta-hemolysis is produced between the two streaks.

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42
Q

Spe toxin (Strep pyogenes)

A

causes scarlet fever

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43
Q

diseases caused by strep pyogenes

A

pneumonia
skin infections (superficial - impetigo; deep - necrotizing fasciitis)
streptococcal toxic shock syndrome - systemic from superantigen

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44
Q

Nonsuppurative secondary complications of strep pyogenes

A

Scarlet fever (Strains expressing pyrogenic exotoxin)
rheumatic fever - damage to the heart by the immune system; certain strains
Necrotizing fasciitis
glomerulonephritis - kidneys
Erysipelas, cellulitis (deeper)
Impetigo contagiosum

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45
Q

Scarlet fever symptoms

A

caused by strep pyogenes
pharyngitis + rash (systemic toxin that strep pyogenes makes)
red diffuse rash
“strawberry tongue”
red cracked lips
circumoral pallor
red cheeks

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46
Q

Strep pyogenes entry (adherence)

A

M protein binds fibrinogen
Lipoteichoic acid
fibronectin binding protein

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47
Q

Strep pyogenes spread

A

YES
hyaluronidase - breaks down intracellular matrix
DNase B - DNA from lysed PMNs impedes movement of bacteria because it’s gooey so DNase B breaks down that DNA from PMNs so that bacteria can spread more easily
response used in diagnosis

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48
Q

Strep pyogenes evade defenses

A

M protein - binds factor H to inhibit complement
hyaluronic acid capsule - antigenic mimicry, antiphagocytic
C5a peptidase - cleaves C5a to inhibit innate defenses

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49
Q

Strep pyogenes damage

A

primarily through inflammatory response
hemolysins - lyse defense cells - streptolysin O and streptolysin S
pyrogenic exotoxins

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50
Q

Streptolysin O

A

antibody response used in diagnosis
causes beta hemolysis on blood agar
lyses defense cells

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51
Q

Streptokinase

A

prevent walling off of infection by fibrin

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52
Q

Streptolysin S

A

lyses defense cells

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53
Q

Spe

A

Pyrogenic exotoxin
causes scarlet fever rash
phage encoded
causes T cells to secrete cytokines

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54
Q

Strep pyogenes outcome

A

transmission, highly contagious
clinical - highly variable depending on strain/patient/treatment
self-limiting except for rheumatic fever and glomerulonephritis
possible pneumonia/death
simple skin infections can be self-limiting but can lead to glomerulonephritis
serious skin infections (necrotizing fasciitis) can be fatal or require surgery

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55
Q

erysipelas

A

superficial butterfly skin infection, on face
elderly and children

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56
Q

cellulitis

A

deeper skin infection in elderly and newborns, can spread deeper and become fatal
fever and leukocytosis

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57
Q

Corynebacterium diphtheriae

A

Gram positive rods
diphtheria “leather” pseudomembrane in the back of the throat
asymptomatic carriers

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58
Q

Corynebacterium diphtheriae clinical manifestations

A

85-90% sore throat
50-85% low grade fever
26-40% dysphagia
50% pseudomembrane

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59
Q

Corynebacterium diphtheriae toxin-mediated manifestations

A

2/3 carditis
neurotoxicity in severe disease
larynx: croup, asphyxia
renal tubular necrosis

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60
Q

Corynebacterium diphtheriae epidemiology

A

Leading cause of death in infants in early 1900s
Since 2000 - 0-2 cases per year in the US (immunization became available in 1945)
still endemic in many areas in the world where vaccination is low

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61
Q

Corynebacterium diphtheriae encounter

A

humans only
inhalation

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62
Q

Corynebacterium diphtheriae entry

A

restricted to upper resp tract

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63
Q

Corynebacterium diphtheriae spread

A

NONE

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64
Q

Corynebacterium diphtheriae multiplication

A

fastidious

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65
Q

Corynebacterium diphtheriae evade defenses

A

not much to deal with in upper resp tract; adhesion and stuff hasn’t been studied much because it’s been wiped out so well

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66
Q

Corynebacterium diphtheriae damage

A

diphtheria toxin

67
Q

Corynebacterium diphtheriae outcome

A

transmission to humans
can be fatal if untreated (5-10%)

68
Q

Corynebacterium diphtheriae treatment

A

antibiotics + antitoxins

69
Q

Corynebacterium diphtheriae prevention

A

toxoid vaccine

70
Q

diphtheria toxin

A

encoded on bacteriophage (lysogenic conversion)
A-B type toxin - ADP ribosylates EF-2, inhibits protein synthesis, cytptpxic, damages heart, nerve, kidneys
heparin binding epidermal growth factor receptor
death from heart/nervous system damage
this is the target for the vaccine - chemical or genetic toxoid

71
Q

Diphtheria toxin mechanism

A

inactivates EF-2
NAD + EF2 -> EF2-ADP ribose +nicotinamide
acts at diphthamide - modified amino acid residue on EF2

72
Q

Bordatella pertussis features

A

gram neg rod (or coccobaccillus)
whooping cough
pertussis - severe cough
primarily in infants and children
“cough of 100 days”

73
Q

Bordatella pertussis stages

A
  1. catarrhal (cough, rhinorrhea)
  2. paroxysmal (cough spasms, whoop, cyanosis, vomiting, episodes, OK in between)
  3. convalescent (decreasing but continuing symptoms)
74
Q

Bordatella pertussis clinical course

A

5-10 day incubation
catarrhal stage (1-2 weeks) - communicable
paroxysmal stage (1-6 weeks)
convalescent stage (weeks to months)

75
Q

What amount of pertussis infections lead to pneumonia or death?

A

pneumonia - about 5%
death - 0.2%

76
Q

Bordatella pertussis encounter

A

human only
inhalation
highly transmissible among unvaccinated (90%)
infected adolescents/adults are the source for infants and children

77
Q

Bordatella pertussis entry

A

restricted to upper resp tract
adherence to ciliated epis - filamentous hemagglutinin, pili/fimbriae, pertactin

78
Q

Bordatella pertussis spread

A

NONE

79
Q

Bordatella pertussis multiplication

A

fastidious; Bordet-Gengou plates

80
Q

Bordatella pertussis evade defenses

A

not much in upper resp tract in non-immune
ciliated epis - mucociliary escalator - pertussis attacks with trachial cytotoxin

81
Q

Bordatella pertussis damage

A

pertussis toxin
A-B toxin
ADP-ribosylates G protein increasing cAMP
localized tissue damage
systemic toxicity - hypoglycemia, leukocytosis, neurological damage

82
Q

Tracheal Cytotoxin (TCT)

A

from B. pertussis
peptidoglycan building block derivative
loss of ciliated cells
stops mucus flow

83
Q

Bordatella pertussis outcome

A

transmissible
human to human
self-limiting but can be fatal
treatment - antibiotics

84
Q

Bordatella pertussis prevention

A

vaccine - originally killed the whole cell - neurological problems
current acellular vaccine - pertussis toxoid + FHA; safe but not optimal because it causes stimulation of IgG, which isn’t as useful in the upper resp tract, want stimulation of IgA

85
Q

Community acquired pneumonia can be caused by…

A

S. pneumoniae
Legionella pneumophilia (rarer - immunocomp patients)

86
Q

S. pneumoniae causes __% of community acquired pneumonia

A

40%

87
Q

Streptococcus pneumoniae features

A

gram pos diplococcus
carb capsule - >90 serotypes, important for vaccines
alpha hemolytic

88
Q

Pneumococcal pneumonia

A

S. pneumoniae
>1,000,000 deaths worldwide
predisposed populations - young, elderly, asplenic, complement deficient, sickle cell

89
Q

S. pneumoniae encounter

A

humans only, spread by respiratory droplet
normal flora

90
Q

S. pneumoniae entry

A

colonization of oropharynx, aspiration into lung

91
Q

S. pneumoniae spread

A

pneumonia - not necessary, but frequent - can invade into the blood
meningitis - blood to CNS
otitis media and sinusitis - not necessary

92
Q

S. pneumoniae multiplication

A

grows will in serous fluid and alveoli space

93
Q

S. pneumoniae evade defenses

A

extracellular
capsule - antiphagocytic
sIgA protease

94
Q

S. pneumoniae damage

A

inflammation - peptidoglycan (binds TLR2)

95
Q

Pneumolysin

A

S. pneumoniae
toxin binds cholesterol in the host membrane

96
Q

LytA

A

encodes autolysin

97
Q

choline binding surface proteins

A

PspA and PspC
non covalently bind phosophocholine in teichoic and lipteichoic acid
induce proinflamm molecules
reduce effectiveness of complement

98
Q

Stages of pneumonia

A

serous - fluid into alveoli
early consolidation (high bact, few WBC)
late consolidation (many WBC)
resolution (effective antibody response, macrophages clear debris)
no permanent damage in pneumococcal pneumonia

99
Q

S. pneumoniae outcome

A

transmission - droplet/saliva
could be self-resolving or fatal

100
Q

S. pneumoniae prevention

A

vaccines
-IgG to opsonize
-23-valent polysaccharides
-7-valent polysaccharide conjugated vaccine
-13-valent conjugated

101
Q

Mycobacterium tuberculosis features

A

acid fast - cell wall waxes/lipids
slow growth - 15-20 hour doubling time
obligate aerobe
antibiotics: Ethambutol + isoniazid + rifampin + pyrazinamide
big problem with resistance (due to point mutations)

102
Q

Mycobacterium tuberculosis encounter

A

humans only
1/3 of world population is infected - US, mostly immigrants
aerosol-droplet nuclei from actively infected people
resistant to drying (small desiccated respiratory droplets)

103
Q

Without intervention, about ___% of people that have TB in them will develop TB disease (active infection) at some point in life

A

10%

104
Q

Mycobacterium tuberculosis entry

A

inhaled directly into alveoli
no URT colonization

105
Q

Mycobacterium tuberculosis spread

A

YES
phagocytosed by alveolar macrophages
transported to lymph nodes
Ghon complex - inflammation of hilar lymph nodes
can cause bacteremia (hematogenous dissemination)
seed about any tissue in the body
lung single most important site of infection

106
Q

Ghon complex

A

TB granulomas
inflammation of hilar lymph nodes

107
Q

Mycobacterium tuberculosis multiplication

A

slow
intracellularly in macrophages - facultative intracellular (don’t need to be in cells but can be grown in or out o cells)
lipid metabolism
in areas with high oxygen
cultured on special agar
has unusual colony morphology

108
Q

Mycobacterium tuberculosis evade defenses

A

intracellular pathogen of macrophages
cell wall inhibits phagolysosome acidification
usually limited by initial cell mediated immune response, but organisms persist for life
immunity measured by PPD skin test or interferon gamma release assay
cell-mediated immunity is required for intracellular pathogens of macrophages

109
Q

interferon gamma release assay

A

test for TB
blood test of the patient’s lymphocytes that stimulates them with microbial antigens and see if they make interferon gamma, which is a cell-mediated immune response

110
Q

IFNgamma stimulates

A

MO

111
Q

TB vaccine

A

MYcobacterium bovis strain (BCG)
mycobacterium bovis
live-attenuated
not in US
elicit Th1 cell-mediated immunity to activate macrophages to kill intracellular pathogen
ok efficacy in children, not very good in adults
shortcoming: should not be given to immunocompromised, need more effective vaccine for adults

112
Q

Mycobacterium tuberculosis damage

A

host cell mediated immune response
delayed type hypersensitivity
granulomas (tubercles)
caseous necrosis
initial symptoms mild or non-existent

113
Q

Mycobacterium tuberculosis outcome

A

reactivation in only 10% of initially infected people
reactivation in first 5 years = 5%, other 5% is remainder of life based on decreased immunity

114
Q

Who is at higher risk of developing TB?

A

HIV infected
Persons taking anti-TNF agents (such as anti-psoriasis drugs)
Recently infected
Persons with certain medical conditions

115
Q

Mycobacterium tuberculosis spread and multiplication

A

primary - alveoli
multiplication in MO, can multiply intra and extracellular
latency and endogenous reactivation
cell mediated immunity prevents active disease after infection

116
Q

Prevention of TB

A

strictly spread person-to-person
need to identify exposed individuals and prevent them from developing active disease
screening through PPD or IGRA
Vaccine NOT used in the US

117
Q

Legionella pneumophila features

A

gram neg rod - stains irregularly, use silver stain
Causes legionnaire’s disease (pneumonia of predisposed) and Pontiac fever (flu-like in anyone)

118
Q

Legionella pneumophila encounter

A

environment only
amoeba in water
natural as well as air conditioning

119
Q

Legionella pneumophila entry

A

inhalation directly into alveoli
no initial URT

120
Q

Legionella pneumophila spread

A

not usually

121
Q

Legionnaires’ disease (Legionellosis)

A

Legionella pneumophila
flu-like > Outcome depends on host imm resp, specifically cell-mediated; lymphocytes produce IFNgamma, suppressing growth within MO, in part by inducing the MO to sequester Fe

122
Q

Pontiac fever

A

Legionella pneumophila
milder resp illness w/o pneumonia, resembles acute influenza

123
Q

Legionella pneumophila treatment

A

antibiotics that can achieve high intracellular concentrations in macrophages (e. g. doxycycline, azithromycin, ciprofloxacin)

124
Q

Legionella pneumophila prevention

A

surveillance and monitoring of plumbing and water systems

125
Q

Defenses of the skin

A

shedding, dry, acidic, temperature, lysozyme and toxic lipids, resident microflora (mainly GPC)

126
Q

normal microbiota

A

gram pos cocci Diphtheroids, Micrococci, Yeasts

127
Q

Diptheriods

A

Club-shaped, Gram positive, and not usually virulent. e.g., Propionibacterium acnes

128
Q

Micrococci

A

Staphylococcus, Streptococci, and Micrococcus

129
Q

Yeasts

A

Low numbers, can cause opportunistic disease. e.g., Candida albicans, Malassezia furfur

130
Q

Methicillin-Resistant S.
aureus MRSA)

A

resistant to the beta lactam
antibiotic methicillin

131
Q

Staphylococcus aureus features

A

GPCL
many strains - causes several different diseases
Toxic Shock Syndrome
Scalded skin syndrome (infants)
abscesses
septic arthritis, osteomyelitis
sepsis
pneumonia
endocarditis
food intoxication (food poisoning, not infection)

132
Q

Staphylococcus aureus encounter

A

humans only (some animals too)
normal flora of skin and nose
direct contact or fomite
nosocomial

133
Q

Staphylococcus aureus entry

A

skin
catheters, devices
wounds
fibronectin binding proteins

134
Q

Staphylococcus aureus spread

A

YES, through tissues

135
Q

Staphylococcus aureus multiplication

A

grows quickly, especially in food

salt resistant

136
Q

Staphylococcus aureus evade defenses

A

coagulase - stimulates clotting by activating fibrinogen to make fibrin
superantigens disrupt immune response
Panton-Valentine leukocidin
capsule
catalase
Chronic Granulomatous Disease patients at risk
Protein A (binds IgG backkwards)

137
Q

Staphylococcus aureus damage

A

pyogenic inflammation
peptidoglycan, lipoteichoic acid
Toxic Shock syndrome
Staphylococcal scalded skin syndrome
hemolysins
exoenzymes

138
Q

Staphylococcal scalded skin syndrome

A

local infection - systemic effects
exfoliative skin toxin (protease - breaks down desmosomes that link the skin cells together)
dermanecrotic toxin (exfoliative toxin)
bullous exfoliative dermatitis

139
Q

Staphylococcus aureus outcome

A

usually self-limiting, but can be fatal
transmission to humans - both direct and fomite

140
Q

Staphylococcus aureus treatment

A

antibiotic resistance is problematic
MRSA - resistant penicillin-binding protein

141
Q

Pseudomonas aeruginosa features

A

gram neg rod
aerobic
green pigment
biofilms
antibiotic resistance

142
Q

Pseudomonas aeruginosa diseases

A

hot tub dermatitis
opportunistic infections of any body site, particularly skin, burns, lung, UTI, osteomyelitis, endocarditis (IDU)

143
Q

Otitis externa

A

ear infection
swimmers ear (Pseudomonas aeruginosa)

144
Q

Pseudomonas aeruginosa encounter

A

environmental - WATER, soil, food, air
catheters
endotracheal tubes

145
Q

Pseudomonas aeruginosa entry

A

lung, intestine, wound
biofilms
pili

146
Q

Pseudomonas aeruginosa spread

A

YES - immunocompromised patients or with burns/wounds

147
Q

Pseudomonas aeruginosa multiplication

A

simple
can grow on diverse substrates, even in disinfectants and cleaning materials
easy to contaminate stuff, especially in hospitals

148
Q

Pseudomonas aeruginosa evade defenses

A

usually held in check by PMNs, so serious infections are normally in neutropenic patients
no defenses at surface so it’s easy to “set up shop”
toxins can kill phagocytes
in cystic fibrosis patients - strains mutate to produce alginate polysaccharide - mucoid

149
Q

Pseudomonas aeruginosa damage

A

inflammation
exotoxins - exotoxin A, type 3 secreted toxins, extracellular enzymes

150
Q

Pseudomonas aeruginosa outcome

A

self-limiting in healthy people
can be lethal in immunocompromised and burn patients
not normally transmitted between people

151
Q

Pseudomonas aeruginosa prevention

A

no vaccine
in hospital - vigilant infection control
clean wounds
for otitis externa keep ears dry

152
Q

Pseudomonas aeruginosa treatment

A

antibiotics
highly resistant to numerous antibiotics

153
Q

Clostridium tetani

A

gram positive obligate anaerobe, spore former

154
Q

Clostridium tetani encounter

A

strictly environmental; spores in soil

155
Q

Clostridium tetani entry

A

wound contamination with spores

156
Q

Clostridium tetani spread

A

YES via soil

157
Q

Clostridium tetani multiplication

A

wound becomes anaerobic
other bacteria consume oxygen

158
Q

Clostridium tetani evade defenses

A

not really known, but does not need to for long because damage is caused by toxin

159
Q

Clostridium tetani damage

A

tetanospasmin - very toxic - lethal dose = 1ng/kg
produced during sporulation
A-B toxin
binds to nerves
retrograde transmission to CNS
also through blood

160
Q

Tetanospasmin

A

inhibits neurotransmitter release (so you say flexed)
vesicles cannot fuse in inhibitory synapses - no inhibitory signal
opposing muscles locked on
spastic paralysis

161
Q

Clostridium tetani outcome

A

death by respiratory failure
transmission = none

162
Q

Clostridium tetani treatment

A

antitoxin (does not work against toxins that are already bound to nerve cells)
antibiotics
debridement

163
Q

Clostridium tetani prevention

A

vaccine - tetanus toxoid
IgG to neutralize toxin
immune globulin it it’s too late
disease is slow, so time to boost after exposure

164
Q

what bacteria can make endospores

A

bacillus, clostridium, and sporosarcina

GMS6121 - Infectious Diseases (4 decks)

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