Exam 3 Flashcards
(132 cards)
1
Q
upper respiratory track
A
s. pneumoniae
h. influenza
2
Q
lower respiratory track bronchitis and pneumonia
A
s. pneumoniae
h. influenza
maybe mycoplasma pneumoniae
3
Q
lower respiratory track atypical pneumonia
A
legionella pneumophila
chlamydia pneumophilia
4
Q
tuberculosis
A
mycobacterium tuberculosis
5
Q
what types of airway immune cells are there & functions
A
alveolar macrophages (M1 proinflammatory, M2 anti-inflammatory) — M1 main players
dendritic cells sample antigens
Tregs reduce activation of CD4 T cells
Mucosal Associated Invariant T cells (early immune responses)
6
Q
a gram negative bacillus facultative intercellular pathogen
one flagella, motile, strict aerobe
uses amino acids (not sugars) as main carbon source and energy
(serotyoes 1 and 6 most frequently isolated)
A
legionella pneumophilia
7
Q
can be aerosolized and spread through air conditioning systems (not spread person to person)
A
l. pneumophila
8
Q
forms biofilms in water, expresses flagellum when reaching stationary phase (less oxygen/nutrients)
A
l. pneumophila
9
Q
list 2-3 mechanisms this pathogen can use to protect itself from destruction by the immune system
A
intracellular living (avoids MAC killing & neutralization/aggregation by antibodies)
inhibition of phage some lysosome fusion
mechanism to escape the cell
10
Q
Type IV membrane protein, MOMP
A
adhesion factors
11
Q
effectors inhibit phage some lysosome fusion and high jack host ribosomes for nutrients
A
survival and replication
12
Q
phosphatase, lipase, nuclease
A
kills host cells, extracellular enzymes that aid in dissemination
13
Q
how does MOMP use opsonization to its advantage
A
C3b binds MOMP, alveolar macrophages engulph
14
Q
other than human cells, what can l. pneumophila survive in
A
protozoa
15
Q
what are two types of legionellosis
A
pontiac fever (flu-like less severe) and legionnaires’ disease
16
Q
diagnosing legionnaires disease
A
urinary At test (usually serotype 1 but can test positive for up to a year)
culture of respiratory samples (L-cysteine and iron media), slow growing
immunoassays to detect Ab or Ag (usually epidemiological investigations)
17
Q
why should l. pneumophila not be treated with beta lactams
A
many strains produce beta lactamases, but macrolides and fluoroquinolones should work
18
Q
gram positive diplococcus alpha hemolytic catalase negative
gram negative coccobacillus non-hemolytic catalase positive
A
s. pneumoniae
h. influenza
19
Q
similarities between s. pneumoniae and h. influenza
A
capsules (used for typing and vaccines)
can pick up DNA from environment (naturally transformable)
20
Q
MAC complex is only relevant for what kind of bacteria
A
gram negative (inserted into outer membrane)
21
Q
a polysaccharide capsule, adhesins (pili, chlorine binding proteins), and mucus degrading enzymes are virulence factors of what cell envelope
A
s. pneumoniae
22
Q
how does natural competency work in s. pneumoniae
A
stationary phase/quorum sensing, produces lysin to kill neighboring cells
23
Q
pore forming toxin released after autolysis, damages epithelium, released after phagolysosome fusion, pro inflammatory/leads to increased transmission shedding in nasal and respirator
A
pneumolysin
24
Q
difference between septicemia and meningitis
A
into blood vs into brain
25
what do non type able h. influenzae lack
a capsule
26
LOS (shorter sugars that LPS), type IV fimbriae, adhesins, IgA protease, protein 5 (inhibits complement cascade)
virulence factors of h. influenzae
27
what does capsule protect against
MAC formation and competent cascade (opsonization)
28
binds C4b and blocks formation of C3 convertase, hides from PRRs and TLRs using sialic acid
LOS
29
explain phase variation
methylation of dna alters gene expression
upregulate to increase attachment/adherence
downregulate when exposed to immune system to hide
30
how are s. pneumoniae and h. influenzae transmitted
human to human
co colonize with other pathogens
31
common s. pneumoniae and h. influenzae diseases
sinusitis
otitis media (ear)
lower respiratory track infections (children and older adults)
invasive: meningitis and bacteremia/sepsis
32
Type B h. influenzae vs. other types
invasive (capsulated) vs. non-invasive
33
diagnosis of s. pneumoniae
gram stain of sputum cfs blood
partial (alpha) hemolysis on blood agar
optochin disc sensitivity
34
h. influenza diagnosis methods
gram stain of sputum/CSF/blood
cannot differentiate between other h
grows in chocolate agar (not blood)
need V factor for species ID
35
why can h. influenza grow with s. aureus
needs V factor and X factor that s. aureus can produce by lysing red blood cells
36
more diagnosis of s. pneumoniae
pcr for pneumolysin gene
lateral flow for capsular antigen (not children)
bile solubility testing/dissolves colonies
quellung test = swollen capsule
37
gram negative, no peptidoglycan, small bacteria, cholesterol and long chain fatty acids for growth, obligate pathogen
mycoplasma pneumoniae
38
how is m. pneumoniae transmitted
person to person vis respiratory droplets, s. pneumoniae and h. influenza two other CAP along with this pathogen
39
is it common to have invasive m. pneumoniae infections
no (upper or lower)
tracheobronchitis, pharyngitis
“walking pneumonia” slow progression of symptoms to high fever and persistent cough
40
apical organelle, CARDS toxin, production of peroxides, intracellular survival, and molecular mimicry are all virulence factors of what
m. pneumoniae
41
complex structure surrounded by P proteins adhesins, involved in attachment and gliding motility
apical organelle
42
what happens with P1 and P30 proteins
high similarity to host, antibodies can cause damage to host (molecular mimicry)
43
what are host receptors for m. pneumoniae made from
sialic acid
44
immunogenic toxin, modulates host cells to cause hyper inflammatory state (adds ADP), can cause cell death (creates vacuoles inside cell)
CARDS toxin
45
is m. pneumoniae more of an intracellular or extracellular pathogen
more extracellular but can be intracellular, inside cell protects against phagocytosis and antibiotics
46
list ways m. pneumoniae can cause direct damage to host
adhesins/membrane fusion damage, disturbance of metabolisms/nutrient depletion, toxin damage
47
how to diagnose m. pneumoniae
molecular tests (preferred), serological (ElISA, IFA, LAT), culture (not usual/may take weeks for positive culture), drug testing/typing/PPLO agar in specialized lab (need microscope to visualize)
48
antibiotics to treat m. pneumoniae
macrolides, tetracyclines (older children and adults), fluoroquinoloes
49
acid fast positive, gram variable bacilli, no spores/exotoxins, aerobic, non-motile, facultative intracellular, slow-growing
mycobacterium tuberculosis
50
why is m. tuberculosis a risk 3 pathogen
highly contagious
low infectious dose
no effective vaccine
hard to treat
51
what intrinsic mechanisms of resistance does m. tuberculosis have
thick peptidoglycan layer
thick mycolic acid/lipid layer
52
transmission of m. tuberculosis
indirect person to person (airborne aerosol particles)
53
“containment phase”
no overt signs of disease
no transmission
dormant m. tuberculosis in granulosas
latent tuberculosis
54
LAM, fibronectin binding proteins, PDIM, type 7secretion system, survival under hypoxia conditions are all virulence factors of what
m. tuberculosis
55
how to diagnose tb
tuberculin skin test (TST), interferon-gamma release assays (IGRAs)
(measure ability of immune system to recognize and respond to mycobacteria antigens)
56
culture of slow growing bacteria (solid or liquid media)
acid fast and aura,une microscopy
Pert (qPCR that detects rig resistance)
diagnostic methods for tb
57
treatment of tb
isoniazid (adverse reactions are common)
rifampin, pyrazinamide, ethambutol
58
why can’t TB be treated with just one antibiotic?
- need to prevent selection of antibiotic resistant strains
- bacteria replicate slowly
- bacteria replicate inside macrophages
59
what is drug resistance mostly due to in m. tuberculosis
mutations (HGT not described)
60
drug resistance multiple (MDR) vs. extensively (XDR)
- isoniazid and rif
- fluoroquinolones and injectable drug
61
E. coli
Shigella
Smonella
Campylobacter
Yersinia
Aeromonas
C. difficile
invasive bacteria
62
E. coli
clostridium
perfringens
Vibrio cholera
bacillus cereus
toxic bacteria
63
gram positive bacillus, obligate anaerobe, motile, spore-forming
c diff
64
flagellum, type IV pili, fibronectin binding protein, toxins, biofilms, spores are all virulence factors of what
c diff
65
what does the type IV pilus promote
biofilm formation
66
toxins A and B are needed to cause infection, internalized, acidification what ultimately happens
breakdown of tight junctions and apoptosis
67
how is c diff transmitted
endogenous (previously existing but gut overrun when normal flora are lost)
exogenous (normal flora are lost and c diff are introduced (exposure to spores)
68
excessive diarrhea
abdominal cramping
fever
white plaques on colon (dead epithelial and immune cells)
can progress to toxic mega colon, septic shock
pseuomembranous colitis
69
how to diagnose c diff
molecular tests, gram stains, enzyme immunoassay, colonoscopy
70
how to treat c diff
stop current antibiotic treatment
vancomycin or fidaxomicin
surgical management
fecal microbiota transplant
71
enteric gram negative bacillus, facultative anaerobe, motile, ferments lactose, toxigenic and facultative intracellular pathogens
e. coli
72
what is the most common cause of sepsis/CA-UTIs and HA-UTIs and most important cause of gastroenteritis
pathogenic e coli
73
what does ETEC, EPEC, EAEC, EIEC, EHEC stand for
toxigenic, pathogenic, aggregative, invasive, hemorrhagic
74
mostly acquired through HGT, endotoxin (LPS), capsule, flagella, siderophores (iron) are general virulence factors of what bacteria
e. coli
75
colonization factor antigen (fiambriae/attachment), toxins (heat stable Sta and STb —> watery diarrhea)
EnteroToxigenic
76
EAF (adherence factor BFP & LEE type three secretion system)
EnteroPathogenic
77
AAF (adherence fimbriae), stacked-brick configuration, cytotoxins and enterotoxins (shortening microvilli, cytokine release/neutrophil recruitment)
EnteroAggregative
78
plasmid encoded invasion genes (plnv), t3ss, ONLY intracellular pathogen
EnteroInvasive
79
shiga-toxin, causes colitis/bloody diarrhea, type 3 secretion system, pathology similar to EPEC
EnteroHemorragic
80
what type of toxin is a shiga toxin
AB/can allow dissemination to other organs
81
what is usually travelers diarrhea: watery vomiting cramps nausea
ETEC
82
which e. coli binds and destroys microvilli
EPEC
83
along with ETEC, what other strain is involved in travelers diarrhea
EAEC
84
what is the most common e. coli strain in developing countries
EHEC
85
kidney disease with fragmented red blood cells, reduced platelet count, acute renal failure
hemolytic uremic syndrome (HUS)
86
shiga toxin 2 most commonly responsible for causing what
HUS
87
acquired through ingestion of contaminated food or water, person to person possible, animal reservoirs, carriers possible
epidemiology of e. coli
88
immunoassay to detect ST/PCR for ST; PCR for LEE; PCR for AAC plasmid; PCR for genes modulating invasion
ETEC; EPEC; EAEC; EIEC
89
in the highest incidence of renal failure in children, what do latex agglutination tests and immunoassays detect
O and H antigens; shiga toxin or toxin genes
90
how to treat e. coli infections
fluids, no antibiotics, dialysis/renal failure, no vaccine
91
Gram-negative curved rods, motile, facultative anaerobes, can form biofilms, mostly halophilic/halotolerant
vibrio spp
92
difference between v. cholera/v. parahaemolyticus and v. vulnificus
gastroenteritis vs additionally septicemia and wound infections
93
water is inanimate reservoir (free living/biofilms/associated with shellfish and filter feeders), estuary or sea water, humans living reservoir through water/food contamination fecal oral route
v. cholerae
94
no human to human transmission, acid sensitive bacteria (reduced gastric acid leads to increased susceptibility), asymptomatic carriage in endemic areas is common
v. cholerae
95
what is serotyping determined by for v. cholerae
the O antigen
96
what cholera pandemic are we currently in
7th
97
what case fatality ratio needs to be exceeded to be considered a pandemic
1%
98
List 4 reasons why cholera has resurfaced in parts of the world
- conflict/war
- climate change
- insecurity/poverty
- COVID19 (resources diverted to the pandemic)
99
AB cholera toxin (Ctx), Toxin Co-regulated pilus (TCP), acquired by HGT from a bacteriophage and regulated by a virulence regulon
virulence mechanisms of V. cholera
100
for v. cholera infections mucus, bile salts, and osmolarity will stimulate what
production of Toxr regulon gene expression (production of Ctx toxin)
101
what does the type 2 section system secrete in v. cholera infections
GpbA adhesins (water biofilm and copepod/epithelial cell attachment), HapA protease (gain nutrients, break down mucus/remove sialic acid, cleaves A unit of toxin, degrades adhesin)
102
what does the A subunit of the cholera toxin ultimately cause
increased cAMP, which causes reflux of ions and watery diarrhea
103
Endotoxin, T6ss, and capsule are all other virulence factors of v. cholera — what does the T6ss do?
inject damaging effector proteins in host cell and gut normal flora
104
asymptomatic or self-limited, abrupt onset of white diarrhea and vomiting, death due to dehydration, electrolyte imbalance, shock, cardiac arrest, or renal failure
symptoms of cholera
105
how does TCBS media work
thiosulfate and sodium citrate inhibits growth of enterobacteria, sucrose fermentation turns media yellow
106
what color does v. cholera turn on TCBS media
yellow
107
how to treat cholera
rehydration, antibiotics not recommended (only in pregnant/immune compromised cases)
108
sari filtration and solar water disinfection are two ways of preventing what
cholera transmission or at least reducing it
109
vaxchora, dukoral, and sanchol/euvichol-plus are what
vaccines for cholerae
110
gram negative (helical or spiral), motile, urease positive, microaerophilic, slow grower (up to 10 days)
h. pylori
111
gastritis, peptic ulcers, cancer, transmitted person to person through contaminated food or water
h. pylori
112
outer membrane proteins, ureas, type 4 secretion system (CagA and Pg fragments modulate apoptosis of host cell), VacA toxin, flagellum are all virulence factors of what
h. pylori
113
increases the pH around the bacterium, produces a,momia which is toxic and disrupts tight junction integrity, produces CO2
urease
114
A T5SS autotransporter delivered toxin, present in all strains, pore-forming cytotoxin (allows for nutrient release from cell)
VacA
115
where is the VacA toxin located
the cytoplasm
116
Secreted by T4ss, an oncoprotein, short term exposure leads to apoptosis, long term leads to apoptosis resistant cells from h. pylori infection
CagA
117
how is h. pylori diagnosed
noninvasive (stool antigen test, urea breast test, serology to detect IgG
invasive (endoscopy/stomach tissue biopsy — histology staining, culture, rapid urease testing) needed for antibiotic susceptibility testing
118
what does a urea breath test detect
CO2
119
how is h. pylori treated
amoxicillin and clarithromycin (plus protein pump inhibitor)
check for eradication
120
enteric gram negative bacillus, facultative intracellular pathogens, facultative anaerobes, motile, do not ferment lactose
salmonella enterica
121
what are the effector proteins secreted by T3ss with salmonella enterica that facilitate endocytosis and polymerize host cell actin
ENTRY
SPI-1
122
what is the s. enterica T3ss that injects effector proteins into endocytic vacuole to prevent phagosome/lysosome fusion
SURVIVAL
SPI-2
123
gastroenteritis or enteric fever (the latter is systemic and is limited to humans)
salmonellosis
124
eating raw or undercooked food, incubating 6-48 hours, may be asymptomatic to diarrhea and fever, usually self-limiting
non-typhiodal salmonella gastroenteritis
125
what is associated with the typhoidal systemic disease
dissemination to liver, spleen, and lymph nodes
126
systemic disease that initially does not trigger inflammatory response (GI tract to blood back to GI tract)
typhoid fever
127
what are rose spots
spots on upper chest and abdomen that are not contagious and don’t itch before typhoid fever
128
Tyhoidal toxin is made up of what
AB: B binds host receptor
A has two parts
CdtB = DNAse — cell cycle arrest, nuclear swelling
PltA = changes gene expression in host
129
what diagnostic test must be carried out to diagnose typhoidal salmonella infection
culture
130
what is the treatment for salmonella
none for gastroenteritis
antibiotic treatment prolonged for typhoid fever
131
TCV, Ty21a, and ViPS are all vaccines for what
typhoid fever
132
what is the age cutoff for unonjugated polysaccharide vaccines
2 years old
