Bacteriology Flashcards
(441 cards)
1
Q
MacConkey agar inhibits what bacterial growth?
A
Gram positive
2
Q
mannitol salt agar selects for what growth
A
gram positive
3
Q
what are the four groups of bacteria based on virulence
A
saphrophytes, commensals, opportunists, pathogens
4
Q
what is a saphrophyte
A
a bacteria not associated with disease - free living organisms
5
Q
what is a commensal. what is an example
A
live in association with the host, but does not cause disease. Normal gut flora
6
Q
what is an opportunist. VS a pathogen?
A
a bacteria that does not typically cause disease in healthy individuals but can when the host is compromised. A pathogen can infect even healthy people
7
Q
what are the 3 main mechanisms to cause disease by bacteria
A
- bind to or invade host cells (flagella, adhesins, capsules)
- produce proteins that directly or indireclty damage host cells (toxins)
- Release of factors that result in inflammatory response (LPS, superantigens) leading to cytokine storm or autoimmune reponse
8
Q
how is the definition for a species different in eukaryotes vs prokaryotes
A
eukaryotes have a sharp natural species boundary while prokaryotes don’t - they are more defined on genetic relatedness and possession of similar physiological functions
9
Q
what is restriction fragment length polymorphism (RFLP) used for?
A
analysis of restriction endonuclease patterns of the bacterial chromosomes. Used during hospital acquired infections to determine the source of an infection
10
Q
Nosocomial
A
hospital acquired
11
Q
what does it mean when isolates of RPLP are identical or not identical between patient and personnel
A
identical - hospital acquired infection
not identical - community acquired
12
Q
what are the two metabolism pathways of glucose and what are the products/efficiency
A
glucose -> pyruvate
respiration - uses O2 to make co2 and h20. energy efficient
fermentation - makes organic end products (usually lactate). little E production
13
Q
what is a microaerophile
A
metabolize O2 but grow in low O2
14
Q
what is a facultative anaerobe
A
metabolize o2 in presence of O2; ferment in the absence
15
Q
what is aerotolerant bacteria
A
do not metabolize O2; but ferment in the presence of absence of O2
16
Q
what is the oxidase test
A
differentiates between aerobes and facultative anaerobes. Aerobes use cytochorme C as the terminal oxidase while facultative anerobes use ctyochrome D as theirs. Cytochrome C gives a positive result with a blue change in color
17
Q
pseudomonoas aeruginosa is an aerobe. What color will appear in the oxidase test
A
blue
18
Q
E. coli is a facultative anaerobe. What color will appear for the oxidase test
A
stays white
19
Q
what is the reaction for anaerobic respiration
A
NO3 -> NO2 -> N2
20
Q
what is the diagnostic test for anaerobic bacteria
A
nitrate broth to see if bacteria make nitrate
21
Q
What range of temperature do most pathogenic bacteria fall under
A
Mesophilic - 10-45 degrees with optimum at 20-40.
22
Q
what are halophilic bacteria
A
salt loving
23
Q
which bacteria are halophilic
A
gram positive
24
Q
is staph aureus gram pos or neg
A
gram positive
25
is e. coli gram pos or neg
gram negative
26
which three bacteria are spore-forming
bacillus, clostridium and sporosarcina
27
how do you inactivate spores?
wet heat, 120 degrees, 20 minutes (autoclave)
28
what is mixed acid fermentation. Which family does this?
products are a complex mix of acids including lactate, acetate, succinate and formate and water and CO2. Characteristic of the enterobacteraceae family
29
what is butanediol fermenation. What bacteria does this
2 pyruvate + NADH => 2CO2 + 2,3-butanediol. Seen en enterobacter
30
what is selective toxicity
abx exhibit toxic effect on bacteria but not on humans. Go after targets that are completely absent in humans ideally.
31
Abx vs antiseptics vs disinfectants
disinfectants - toxic to both bacteria and humans
antiseptics - toxic to bacteria, too toxic for systemic use in humans. Ok for topical use
Abx - selective toxicity
32
Bacteriostatic vs bacteriocidal
static - inhibit growth but don't kill bacteria- relies on immune system to eradicate
cidal - kill bacteria directly - important for immunocompromised patients
33
what is the adv and disadv to broad spectrum abx
adv - can be used in emergencies when you don't know the bug
| disadv - affect normal flora leading to secondary effects (diarrhea, abx resistance)
34
what is the minimum inhibitory concentration (MIC)
the lowest conc. of abx that inhibits growth
35
what is the minimum bactericidal concentration (MBC)
the lowest concentration of abx that kills a defined proportion of bacterial pop after a specified time.
36
what is the toxic side effect of tetracycline
discoloration of the teeth
37
what is the toxic side effect of streptomycin
auditory damage
38
what is the toxic side effect of chloramphenicol
anemia
39
Is c. diff gram pos or neg
gram positive
40
what are the two mechanisms in which bacteria have genotype changes leading to enhanced growth
1. horizontal gene transfer (acquisition of foreign DNA)
| 2. spontaneous mutations
41
what are the three mechanism of resistance
1. modification (inactivation) of abx molecule itself
2. modificaiton (reprogramming) of abx antibiotic target
3. reduction of abx conc./prevention of access to target
42
what are the four abx inhibit PG synthesis
b-lactams, vancomycin, bacitracin, cycloserine
43
what abx inhibits key metabolic reactions
trimethoprim/ sulfamethoxazole
44
what 2 abx inhibt cell membrane
polymixin and daptomycin
45
what abx inhibits DNA replication and repair
fluoroquinolones
46
what 4 abx inhibits ribosome and/or protein synthesis
tetracyclines, aminoglycosides, meacrolides, oxazolidinones
47
cell wall inhibitors are most effective during what phase
the growth phase
48
which bacteria (Pos or neg) has a more protective barrier? how?
gram neg has more protection in which only proes allowing entry into cell. Gram pos only has PG which abx can easily enter
49
what are the three steps of PG synthesis
1. synthesis of MurNAc precursors in the cytoplasm. D-ala-D-ala terminus
2. Lipid linkage and transport of mlc across membrane
3. polymerization of crosslinking or precursors into PG
50
what enzyme catalyzes the third step in PG synthesis (crosslinking and polymerization)
PBP - penicillin-binding proteins
51
what inhibits PBP. what's the mechanism
beta-lactam. Doesn't allow a terminus Ala strand to cross link to another ala strand
52
what are the four examples of beta lactams
penicillin, cephalosporin, carbapenem and monobactam
53
what are the two primary mechanisms of resistance of beta lactam abx
1. production of beta lactamase that inactivates the beta-lactam
2. mutation of PBPs to prevent binding of beta-lactam
54
what are extended spectrum beta lactamases (ESBLs)
broad substrate specificities that can cleave a wide range of beta-lactams. found primarily in gram neg
55
what is the most common mechanism of beta lactam resistance seen in streptococcus and MRSA
mutations in PBPs
56
clavulanic acid
beta lactamase inhibitor - no antibacterial activity. just bind to beta lactamase to inhibit it from breakdown abx beta-lactam.
57
which bacteria (gram pos or neg) is more likely to mutate PBP
gram positive
58
which bacteria (gram pos or neg) is more likely to have b-lactamase
gram negative
59
Which bacteria (gram pos or neg) has a thicker PG layer
positive
60
what are the end colors of gram pos and neg with a gram stain. Why
positive will stay purple - stain sticks to the thicker PG layer
negative will be red
61
what are the four layers of the cell envelope
cell membrane
periplasmic space
cell wall
accessory structures
62
what is in the cell wall of gram pos bacteria
peptidoglycan (thick) and teichoic acid
63
what is in the cell wall of gram neg
outer membrane of LPS and porins
| PG (thin)
64
which bacteria (gram pos or neg) has more PG cross linking
Positive - due to longer/thicker PG
65
what is teichoic acid
seen in gram positive cell envelope
crosslinked to cytoplasmic membrane and PG
recognized by TLR signaling (innate)
66
What are four important things to know about LPS
1. gram neg
2. Has O antigen that's variable. (used as diagnostic tool)
3. Has lipid A - fever inducing - aka an endotoxin
4. PAMP recognized by TLRs
67
what are the PAMPs in gram pos and neg bacteria
negative - LPS
| positive - lipoteichoic acid
68
what are the three types of duplicated flagellum. What is there overall purpose
Purpose: virulence factors
Type II - secrete protein across inner membrane
Type III - deliver toxins into host cells
Type IV - deliver DNA into host cells
69
what is the reservoir for haemophilus
only humans
70
how is Hib transmitted
respiratory tract
71
what is the primary infection of Hib
colonization in nasopharynx. Occassionaly invasion in sinus and middle ear. Life threatening when in blood stream -> meninges infection
72
what is virulence of Hib associated with
type b polysaccharide capsule (ribose and ribitol)
73
what is the first generation vaccine to Hib like
purified capsular polysaccharide of Hib (PRP). Effective but the polysaccarides are poor immunogens, stimulate T-independent ab, and are poor immunologic memory (no production of memory B cells).
74
what is the 2nd generation Hib vaccine like
PRP protein conjugate with diphtheria toxoid as the protein carrier.
75
what pathogens have polysaccharide capsules. Of those, which have conjugate vaccines
1. Strep agalactiae (group B)
2. E. coli
3. Strep pneumoniae (conjugate)
4. neisseria meningitidis - conjugate
5. Haemophilus influenzae - conjugate
76
What is the mechanism of action of vancomycin
binds to D-ala-D-ala at the end of peptide chains in PG precursors, blocking PBPs from catalyzing transpeptidation
77
what type of bacteria (gram pos or neg) is vanco effective on
positve. Can't fit through pores of negative
78
what is vancomycin especially used for?
for beta-lactam resistant infections (MRSA) and b-lactam hypersensitivity
79
what is the mechanism of resistance for vancomycin. Where is the gene for resistance found? Where is resistance seen?
change the substrate from D-Ala-D-ala to D-ala-D-lactate . Found on transposons or plasmids. Seen in enterococci in hospitals (VRE)
80
what is the MAO of cycloserine
inhibits PG crosslinking as a competitive inhibitor of D-ala. Inhibits either alanine racemase (l-ala-> d-ala) or d-alanyl-d-alanine synthetase (d-ala -> d-ala - d ala)
81
which abx is too toxic for systemic use but ok for topical use
bacitracin
82
what is the MAO of bacitracin
binds to bactoprenol-P which is the lipid carrier for PG precursors. No PG made
83
which bacteria are 10x more sensitive to bacitracin
Group A streptococci
84
what is the MAO for daptomycin. Bactericidal or bacteriostatic
bind and disrupt the cytoplasmic membrane - loss of membrane potential. Bacteriocidal
85
What bacteria does daptomycin affect
gram positive
86
What is the MAO for polymyxins. Bacteriocidal or bacteriostatic?
Binds to LPS in outer membrane - disruption of both out and cytoplasmic membranes.
87
what bacteria does polymyxin/colistin affect
gram negative
88
what is the mechanism of tetracycline
binds 30s ribosomal subunit and interferes with binding of aminoacyl tRNA to the ribosome.
89
what are the two types of resistance to tetracycline
1. efflux pump
| 2. mutation of ribosome
90
what is the main example of an aminoglycoside
gentamicin
91
what is the MAO of aminoglycosides? Bacterialcidal or bacteriostatic?
binds irreversibly to 30s ribosomal subunit and causes misreading. Bactericidal
92
What is type of bacteria are aminoglycosides mainly used for. Which especially hard to kill gram negative?
gram negative.
| Pseudomonas aeruginosa
93
what are the side effects of aminoglycosides
ototoxic and nephrotoxic
94
what is the mechanism of resistance for aminoglycosides
transferase modification of the abx to prevent binding to ribosome
95
what is the MAO of macrolides. Bacteriostatic or bacteriocidal
binds the 50s ribosomal subunit to block elongation of proteins. Bacteriostatic
96
what are the main abx of the macrolide group
erythromycin, azithromycin, clarithromycin
97
which bacteria are macrolides used against
gram positive
98
what are the two mechanisms of resistance to macrolides
1. methylation of rRNA so that abx can't bind to methylated ribosome
2. efflux pumps
99
what is the MAO of chloramphenicol. Bacteriostatic or cidal?
binds 50s ribosome subunit to inhibit elongation. Bacteriostatic
100
what is the issue with using chloramphenicol. What is its limited use
has high toxicity of aplastic anemia. Used in severe infections like typhoid fever and rocky mountain spotted fever
101
what is the mechanism of resistance for chloramphenicols
chloramphenicol acetlytransferase catalyzes addition of acetly group to drug preventing ribosome binding
102
what is the MAO of clindamycin. Bacteriostatic or cidal?
binds 50s ribosomal subunit to block elongation. Bacteriostatic
103
what can't clindamycin be used for? What is it usually used for?
gram negative aerobes. used for community-acquired MRSA and toxin-producing s. aureas
104
what is the resistance against clindamycin
Methylation of rRNA so that abx can't bind (erm methylase gene)
105
what is the connection of clindamycin with macrolides
they exhibit cross-resistance - those that are resistance to macrolies due to presence of erm methylase gene are also resistance to clindamycin
106
what is the MAO of linezolid. Bacteriostatic or cidal
binds 50s subuint to prevent formation of 70s initiation complex. Bacteriostatic
107
what is linezolid useful for? what can't it fight against?
useful for skin infections of staph aureus, strep pyogenes or strep agalactiae. NOt useful against gram neg.
108
what is the resistance to linezolid
point mutations in ribosome to prevent abx binding.
109
what is the MAO of nalidixic acid (first generation)
binds bacterial DnA gyrase or topoisomerase to inhibit DNA replication/repair -> DNA damage.
110
what are the problems with nalidixic acid
narrow spectum, rapid selection for resistant mutants
111
what is the MAO of 2nd generation fluoroquinolones. Bacteriacidal or static?
binds to DNA gyrase or topoisomerase to disrupt DNA replication and repair. Bactericidal.
112
what are the major abx of the fluoroquinolone group
norfloxacin, ciprofloxacin, ...all end in floxacin
113
what are the 2 mechanisms of resistance to fluoroquinolones
1. point mutations of DNA gyrase to prevent abx binding.
| 2. Efflux pump
114
what is the MAO of metronidazole
produces a radical in anaerobic environment leading to toxic metabolites that damage dna
115
what is metronidazole use against
anaerobic - c. diff
116
what is the MAO of rifampin (rifampicin). Bacteriocidal or static?
Binds beta subunit of RNA polymerase to inhibit RNA synthesis. Bactericidal
117
what is the mechanism of resistance for rifampicin
mutations in beta subunit of RNA poly, preventing abx binding
118
what is the mechanism of action of fidaxomicin. bacterialcidal or static
noncompet. inhib of RNA syntheisis. Bacterialcidal
119
what is the MAO of sulfonamides
metabolic analogues of p-aminobenzoic acid of the FH4 pathway. leading to no bacterial growth due to no nucleotide production
120
what is the MAO of trimethoprim
a metobolic analog for dihydrofolate -> inhibits dihydrofolate reductase. No nucleotide production , no growth.
121
what is the mechanism of resistance for trimethoprim
get another gene that encodes dihydrofoalte reductase
122
what is synergy
the action of a combination of 2 drugs is greater than the sum of individual durgs
123
is combination beta-lactams antagonistic or agonistic
antagonistic- they can induce beta lactamases that degrade the abx
124
Do bacteria have operons? Exons and introns? How many polymerases
Yes operons. No exons/introns. Only 1 RNA polymerase
125
why can bacteria undergo horizontal transmission?
there are no natural species boundaries in prokaryotes like there is in eukaryotes
126
what are the three types of horizontal transmission
transformation, conjugation and transduction
127
what is largely responsible for rapid spread of antibiotic resistance
horizontal gene transfer
128
what are the three types of elements that can undergo gene exchange
plasmids, insertion sequences/ transposons, pathogenicity islands
129
which of the three types of elements that undergo gene exchange can replicate on their own
plasmids
130
which gene exchange element has inverted terminal repeats (ITRs) at their ends? What is this important for?
Transposons/ insertion sequences. Important for transposase to recognize the sequence to cut the DNA and allow element to move to another location
131
what is the least complex transposable element? describe it
insertion sequences. Contains the inverted repeats at end with the transposase enzyme inbetween.
132
what are composite transposons
the second most complex. have insertion sequences on each end that contain the transposase gene. In between are genese that can encode for abx resistance or toxins
133
what is the TnA family transposons
third most complex. has a gene that must be expressed to turn on the transposase expression.
134
what is the most complex transposable element
Mu bacteriophage. has the insertion sequence located on a bacteriophage.
135
what is pathogenicity island
a segment of bacterial genome carried on plasmid or by bacteriophage. Can be very large and include toxin genes. Different GC content
136
what is transformation?
a cell is lysed, DNA is taken up from environment into recipient cell and integrates into recipient's DNA
137
what is conjugation
direct cell to cell contact. Forms a pilus to transfer all three types of gene elements. Donor makes a copy before transfer.
138
what is transduction
mediated by bacteriophage which contains the bacterial DNA. A cell must lyse to release the phage.
139
what is the lytic phase
phage injects DNA in to cell and causes synthesis of more phage. Cell lyses and phage is released
140
what is the lysogenic phase
Phage injects DNA and it is incorporated into host chromosome.
141
what is a transducing phage?
the lytic stage where the DNA is be replicated to make more phage.
142
what are two toxins located in a phage genome
shiga and cholera toxin
143
what is the mechanism of the cholera toxin
A5B. Binds to GM1 receptor. Subunit internalized and interacts with g proteins regulating adenylate cyclase (ADP-R-Gs alpha). Converts ATP to cAMP -> enhanced secretion of water and electrolytes in intestinal lumen
144
What is the mechanism for shiga toxin
Binds to Gb3 glycolipid. Subunit translocated into cytosol and modifies ribosome acceptor site. Blocks protein synthesis and kills host cell.
145
What is the effect of cholera toxin
increased water and electrolyte secretion
146
what is the effect of shiga toxin
diarrhea, colitis, hemolytic uremic syndrome (anemia, acute kidney failure, thrombocytopenia)
147
what is the main mechanism for extracellular pathogens to stay extracellular
they have a capsule
148
what are two ways that bacteria induce uptake into non phagocytic cells
1. trigger mechansim - effector protein causes perturbations and cytoskeleton remodeling
2. zipper mechanism - minor membrane perturbations. Minimal cytoskeletal remodeling. Bacteria is just able to slide in.
149
what are the four bacteria that escape the phagosome to replicate in the cytosol
Rickettsia, shigella, e. coli, listeria
150
what two bacteria modulate the endocytic pathway sot hat the phagosome never fuses with lysosome
mycobacterium and salmonella
151
which bacteria can alter the trafficking of a phagosome to lead to fusion of early or late endosomes or lysosomes
legionella, brucella, chlamydia
152
How are anaerobes sensitive to O2 intermediates
1. Little superoxide dismutase to remove O2 radicals.
2. Low amounts of catalase to remove H202
3. Lack cytochromes - so must use fermentation metabolism
153
what are some unique characterisitcs of anaerobes
1. infections are foul smelling due to short chain fatty acids produced during fermentation
2. Gas producing
154
what is the most common inhabitant of the bowel. Gram pos or neg?
bacteriodes fragilis. Gram neg.
155
what virulence forms do bacteriodes fragilis have
1. capsule
2. tolerate O2 - aerotolerant
3. encode catalase and superoxide dismutase
156
what agar does bacteroides fragilis grow on
bile esculin agar
157
what is a characteristic feature of bacteriodes fragilis?
gram negative, Rod shaped bacteria that form long chains
158
features of clostridia: pos/neg?, anaerobe/aerobe?
Gram positive
obligate anaerobes or aerotolerant
spore forming
159
what pathogenesis does clostridia have
exotoxin
160
what is the physiology of clostridia
saccharolytic or proteolytic
161
what are the four types of clostridia we learned
1. difficile
2. perfringens
3. tetani
4. botulinum
162
what causes the diarrhea symptoms of c. diff
toxins A and B glycosylate Rho GTPase -> actin depolymerization -> disruption of epithelial cells
163
what is the easiest way to diagnose c. diff
PCR of toxins A and B
164
what are the treatments of c. diff
Metronidazole, vancomycin or fluoroquinolines
165
what is the invasive histotoxic clostridia
C. perfringens
166
what is the characteristic sign of having c. perfringens
black tissue with gas gangrene
167
what are the steps for invasion of c. perfringens
1. a deep wound predisposes infection
2. Host protesases release nutrients that allow bacteria to grow
3. bacteria releases alpha toxin (phopholipase) that causes gangrene
168
what are the two clostridial neurotoxins. what are the physical signs of each
c. tetani and c. botulinum.
Tetanus - spastic paralysis and lock jaw
botulism - flaccid paralysis
169
what is the mechanism of action of botulinum toxin
Cleaves SNAREs and inhibit release of ACh at presynaptic membrane of peripheral neurons -> flaccid
170
what is the mechanism of action of tetanus toxin
Bacteria remains at infection site. Toxin is transported to CNS to inhibit interneuron function by cleaving SNAREs- > spastic paralysis
171
what is the physiology of c. tetani
anaerobe
| proteolytic
172
what is DTaP
diphtheria, tetanus, pertussis vaccine. Full strength DT and acellular P
173
what is the treat for tetanus
use vaccine as therapy. Td or Tdap
174
what is the most toxic toxin to humans
botulinum toxin
175
why is there no vaccine for botulinum
it is very diverse. IT has A-G serotypes.
176
what are the common serotypes of botulinum against humans
A, B, and E
177
what serotypes of botulinum are used therapeutically as Botox. How is it possible these can be used clinically
A and B. There his high specificity since the toxin has receptors that are neuron specific.
178
what is the treatment for botulinum
no licensed vaccine. Just supportive care. CDC may have some anti-serotypes.
179
Blepharospasm
abnormal contraction or twitch of eyelid neurons leading to functional blindness. Treated with botulinum toxin
180
what are the reservoirs for bordetella
only human
181
bordetalla grm pos or neg
gram negative
182
what is bordetella metabolsim. What is the structure?
strict aerobes. Coccobacilli
183
what is the mechanism of pertussis toxin
A: 5B. adp ribosyltransferase that targets Gi protein which normally inhibits adenylate cyclase
184
what is the abx of choice for pertussis
erythromycin
185
what is the pathology due to toxins produced by the bacterium. How is this different that invasive properties of bacterium.
Toxins produced by bacterium: microbe enters, colonizes, and grows in the host, typically at a specific site in the host (growth may be limited, non invasive). Invasive bacterium damage tissues due to growth
186
what is the difference between endotoxin and exotoxin
an endotoxin is like LPS (on the membrane) that could cause fever or inflammatory response. An exotoxin is released from the bacteria
187
Does an exotoxin cause a fever response?
No
188
how can an exotoxin be used therapeutically
Converted to a toxoid by formalin to generate a vaccine
189
What are the four types of toxins
1. surface-acting
2. pore-forming
3. A/B toxins
4. Type III and IV secretions
190
which part of the AB toxin is catalytic and which allows host cell binding
B for binding. A - catalytic
191
what is the mechanism for both diphtheria and pseudomonas aeruginosa exotoxin A
ADP -ribosylate EF2: inhibits proteins synthesis
192
what is the mechanism for shiga toxin?
deadenylate adenine on RNA to inhibit protein synthesis
193
what are the steps of diptheria toxin
1. c. diphtheriae colonize in upper respiratory tract and produce a localized infection.
2. A phage releases diphtheria toxin
3. toxin inhibits protein synthesis ADP -r-EF2
4. pathology within heart liver lung and nervous system.
5. Death from cardiac failure
194
what is the vaccine timing for diphtheria
5 doses of DTaP up to 6 years of age. Then Td booster every 10 years.
195
what is the MAO of toxinA/toxin B in c. diff and what is the role in diease
Glycosylate Rho GTPase (actin depolymerize)
| Disrupts epithelial cell barrier
196
what is the MAO and type of toxin seen in staph and strep superantigens
type A
Sags form complex with T cell receptor and MHC molecule.
stimulates antigen independent cytokine storm
197
Gram negative bacilli cause CNS infections in what age group
neonates
198
strep group A and B cause CNS infections in what age group the most
neonates
199
haemophilus influenzae cause CNS infections in which age group the most
Children
200
Neisseria meningitidis cause CNS infections in which age group the most
children and adults about equal
201
what are the characteristics of n. meningitidis
```
gram negative diplococci
has LOS not LPS
Capsule
Pili
Porins A and B
aerobe
```
202
which bacteria has iron uptake from the host transferrin
n. meningitidis and gonrrhea
203
what serogroups of n. meningitidis are associated with disease
A, B, C, Y, W135
204
what are the pathogensis steps of n. meningitidis
1. attach to non ciliated columnar epithelial cells of nasopharynx via pili
2. Internalized into phag. vacuoles
3. Replication and transcytosis to subepithelial spaces
4. No phagocyte destruction due to capsule
5. LOS induces vascular damage, inflammation and intravascular coagulation
205
what are the reservoirs of N. meningitdis
only humans
206
what is the epidemic location of n. meningitidis. What time periods
sub saharan africa. Dry season and cold season
207
what serotypes is common for most epidemic n. meningitidis
serogroup A
208
what are the clinical manifestations of n. meningitidis
transient bacteremia, fever, malaise
acute bacterial meningitis - abrupt and insidious onset of chills fever, headache, meningeal inflammation (cervical and thoracolumbar rigidity, exaggerated reflexes)
infants - irritability, refusal of food, seizures, coma
adults/children - altered mental status, headaches, nausea, photophobia.
minute hemorrahagic spots (petechiae) develops into a purpura rash
209
how do you diagnose n. meningitidis
gram stain of CSF
blood culture
oxidase positive
biochemical tests
210
what is the treatment for n. meningitdis
cefotaxime, cefrtiaxone, penicillin
211
what is used for treatment of prophylaxis (someone exposed to patient with disease for more than 8 hours)
rifampin, ciprofloxacin, ceftriaxone
212
what are the two types of vaccines for n. meningitidis
1. serogroup vaccine specific for A C Y and W135 (short term)
2. Long term with conjugate diphtheria toxoid
213
which of the serotypes of n. meningitidis is most associated with infection in infants and children. Is there a vaccine for this one?
serogroup B. No vaccine because it is too similar to fetal neuron tissues
214
What are the characteristics of n. gonrrhea
```
gram negative
diplococci
oxidase positive
no capsule
pili
```
215
what are the four suface antigens of gonorrhea
porins, opa proteins, receptors for human transferrin, LOS
216
What is the role of porB in gonorrhea
interferes with neutrophil degranulation, facilitates bacterial invasion and resistant to complement
217
what is the role of opa proteins in n. gonorrhea
mediate binding to epithelial cells
218
what are the steps of pathogenesis of gonorrhea
1. sexual contact with infected person
2. attachment to non ciliated epthelial cells
3. Transcytosis to subepithelial spaces
4. Replication and release of LOS
5. Inflammation, damge to urethra or vagina epi.
219
what is the reservoir for n. gonorrhea
only humans. Most of reservoir is asymptomatic
220
why doesn't gonorrhea have a vaccine
1. no capsule
| 2. highly variable. Can turn on/off pili and have many Porb B variations.
221
who has a higher risk of acquiring gonorrhea
women 50% risk, men 20% after a single exposure
222
what are the clinical signs of gonorrhea
men: discharge and painful urination. 95% will be symptomatic
women: vaginal discharge, painful urination, ab pain.
223
what is ophthalmia neonatorum
purulent ocular infection acquired by the neonate at birth. Gonorrhea infection
224
what is the diangosis for gonorrhea
gram stain - gram neg diplococci with leukocytes in men with purlent urethritis and women with cervicitis. Culture. Nucleic acid amplification.
225
what is the treamtment for gonorrhea
1st line: dual therapy of ceftrizone and either azithromycin or doxycycline for one week
2nd line - cefixime and either azithromycine or doxycycline, followed by test for cure.
226
what are the characteristics of chlamydia
gram negative
| No PG - no susceptible to beta lactams
227
What are the two developmental cycles of chlamydia
1. elementary body - infectious form - stable in environment - highly cross linked out membrane
2. reticulate body - the replicative intracellular form - not stable in environment.
228
Replication of chlamydia within the reticulate body cycle takes place in what
inclusion bodies
229
what is the main STD chlamydia
Chlamydia trachomatis
230
what is the pathogenesis of c. trachomatis
1. attaches to non ciliated cells of urethra, endocervix, endometrium, fallopian tubes.
2. Replicate within mononuclear phagocytes
3. 1-4 wks later lesion.
4. Inguinal nodes - rupture leads to fistula.
5. Untreated leads to ulcers
231
what is the most common STD in the US
Chlamydia
232
What are the clinical symptoms of chlamydia
usually asymptomatic in women (80%)
| Men tend to be symptomatic. Can get reiter syndrome
233
what is reither syndrome
young males - urethritis and conjunctivitis from chlamydia
234
what is chronic keratoconjunctivitis
caused by serovars A, B Ba and C of chlamydia. Endeimc in Africa and S america.
Progressive dieases leading to blindness
Transmitted through infected droplets. Mainly seen in children
235
how do you diagnose chlamydia
TAke endovervical specimens not vaginal.
Cytology - look for inclusion bodies
Nucleic acid amplification is the most popular
236
what is the obligate intracellular parasite
chlaymdia
237
Characteristics of strep
gram pos
cocci
arranged in pairs or chains
facultative anaerobe
238
staph and strep. which one is catalase positive
Staph
239
what are two ways to classify strep
by lancefield typing (Group A and B) and by the hemolytic patterns on the agar
240
which strep is beta hemolytic and a group A. what does it cause
s. pyogenes. Pharyngitis
241
which strep is beta hemolytic and Group B. What does it cause
s. agalactiae. neonatal disease
242
s. pneumoniae has what type of hemolysis. What does it cause
alpha/gamma. Pneumonia, otitis media
243
what is on the surface of strep pyogenes
```
group A carb
M proteins
Lipoteichoic acid
F protein
C5a peptidase
```
244
what are the types pathogenesis of strep pyogenes
1. avoidance of opsonization and phagocytosis
2. adherence to host cells
3. invasion of host cells
4. toxins - superantigens
245
where does strep pyogenes colonize
oropharynx
246
patients with what are protected against strep pyogenes
antibodies to M proteins
247
what are the clinical diseases from strep pyogenes (7) - earlier onset
1. strep pharyngitis
2. scarlet fever
3. impetigo
4. erysipelas
5. strep toxic shock
6. endocarditis
7. necrotizing fasciitis
248
what is erysipelas
infection of skin and subcutaneious tissues edema. has a distinct advancing border
249
what are the group a strep late sequelae
1. rheumatic fever
| 2. glomerulonephritis
250
what is the lab diagnostic for strep pyogenes
main: culture - gram pos cocci in chains, catalase negative, group specific carb positive, susceptible to bacitracin
2. antigen detection of group A carb from a throatswab.
251
what is the treatment for strep pyogenes
```
pharyngitis - penicillin
penicillin allergic ( cephalosporin or macrolides)
```
252
what is the structure of strep. agalactiae
has group b carbs
| has capsule to avoid phagocytosis
253
where does strep agalactiae colonize
lower GI tract and GU tract.
254
what are the clinical diseases for strep agalacitiae
neonatal - meningitis, pneumonia
pregos - endometritis, UTI, infections
other adults - infections in joints bone, pneuomnia
255
what is the diagnosis for s. agalacitiae
gram stain of CSF of meningitis, pneumonia or wound infections.
culture
PCR
256
what is the treatment for strep agalactiae
penicillin
257
what is the unique cell wall composition of strep. pneumonia
```
has capsule (not unique for strep)
specific teichoic acids - C polysaccharide (bind to crp to cause inflammation marker) and F antigen
```
258
what makes s. pyogenes and s. peumonia different with pathology
s. peumonia infection is due mostly to host response rather than expression of bacterial toxins.
259
what are the steps of pathogenesis for s. pneumonia
colonization in oropharynx
resistance to phagocytosis
release of toxic cell wall componenets to trigger inflammatory response (PG, teichoic acid)
260
what are the clinical diseases of s. pneumonia
1. pneumococcal pneumonia (fever, chill, productive cough, chest pain)
2. sinusitis and otitis media
3. meningitis
4. bacteremia
5. endocarditis
261
what is the diagnosis of strep. pneumonia
gram stain of sputum or CSF
| culture with alpha hemolysis
262
what is the treatment of strep. pneumonia? what is it resistant to?
resistant to penicillin unlike s. pyogenes. Can use vancomycin and ceftriazone for serious infections.
263
which strep. has a vaccine?
strep. pneumonia.
264
staph are found in what form
clusters
265
what part of body are staph found? what makes their residence an issue?
anterior nares. natural flora. Hard to dermine infectious from normal flora
266
which bacteria is coagulase positive
s. aureus
267
are staph catalase pos or neg?
positive.
268
what is unique on staph's surface. what is it's purpose
protein A. they are IgG moleucles with Fc prtion bound to s. aureus. It disrupts opsonization and phagocytosis
269
what are the four toxins s. aureus produes
1. hemolysins
2. leukotoxins
3. enterotoxins
4. exfoliative toxins
270
what hemolysin does s. aureus have
beta - fully clear
271
what does the leukotoxin of s. aureus do?
attacks PMNs and macrophages
272
what does the enterotoxin of s. aureus do?
superantigen. Causes diahrrea and emesis. Causes symptoms 2-6 hours after ingestion. Includes toxic shock syndrome toxin
273
what are the exfoliative toxins of s. aureus
2 forms: ETA/ETB proteases. Lysis of intracellular attachement between cells. Causes scalded skin syndrome
274
how is s. aureus transmitted
direct contact usually. Can be air borne
275
what are the six things you can get from s. aureus
1. folliculitis
2. boil
3. impetigo
4. scalded skin syndrome
5. Pneumonia (CF patients or immunosuppressed)
6. Osteomyelitis and arthritis
276
what are the abx treatment for s. aureus
1. penicillin
2. Methicillin
3. Vancomycin
277
what is different between community and hospital acquired MRSA
community spreads more easily and can cause more skin diesase
278
what staph are coagulase negative
s. epidermidis and saprophyticus
279
where are s. epidermidis found
binds to plastics
280
where are s. saprophyticus found?
urinary tract
281
what are the gut bacteria that can cause systemic disease
listeria and salmonella typhi
282
whatare the gut bacteria that invade cells/ cause inflammation/intoxicate
shigella, enterohermoorrhagic e. coli, campybacter and helicobacter
283
what are the gut bacteria whose pathology and symptoms are due to exotxin production
vibriocholerae
284
what are the three ways that infections can alter normal physiology. What bacteria causes each?
1. penetration through an intact mucosa (listeria, salmonella)
2. inflammatory or cytotoxic destruction (shigella, nontyphoidal salmonella, e. coli, campy and helico)
3. shift in bidirectional water and electrolyte fluxes (vibrio cholera)
285
what are paneth cells
epithelial cells that secrete an array of antimicrobial peptides including defensins and lysozyme that minimzes the ability of microbes to enter the body
286
what are the characteristics of listeriosis. Gram, shape, metabolism?
aerobic gram positive rod
287
what is the human pathogen of listeriosis
listeria monocytogenes
288
what people does listeria infect
1. neonates
2. elderly
3. pregos
4. Immunocompromised
289
what is the pathogenesis of listeria
1. ingest contaminated food
2. survives stomach acid
3. adherence to host cell
4. Entry into enterocytes or m cells in peyer patch
5. ph drop in phagosome. Listeriolysin O frees it.
6. replication in cytosol
7. ActA of bacteria polymerizes host actin - movement of host cell
8. bacteria pushed into uninfected cell
9. gets into reticuloendothelial system
290
can listeria survive refrigeration?
yes
291
what are the symptoms of neonatal disease of listeria
early onset in utero of abortion or still birth
granulomatosis infantiseptica
late onset can havemeningitis
292
how do you diagnose listeria
gram stain of CSF for meningitis patients.
culture - needs cold enrichment
serologic tests
293
what is listeria naturally resistant to
cephalosporin
294
what is the characteristic of salmonella
gram neg, rods, found in soul water and normal intestinal flora
295
what serotypes do salmonella have
H antigen - flagellar proteins
K of Vi - capsular antigens
o antigens
296
what can salmonella not ferment
lactose
297
what two types of salmonella are adapted to humans
typhi and paratyphi
298
what is the pathogenesis of salmonella
```
resists stomach acid
attaches to mucosa
invade M cells in peyer patches
replicate in endocytic vacuoles
Type III secretion systems make spacious vacuoles
```
299
what is the pathogenesis ofr enteric or typhoid fever
bacteria invade cells and replicate as in gastroenteritis
typhi also replicates in macrophages and streads through the reticuloendothelial system
fever starts
300
what clinical diseases can be seen with salmonella
salmonella gastroenteritis, septicemia, and enteric fever
301
what is the diagnosis for salmonella
stool culture - lactose negative, motile, makes H2S that gives black colonies.
302
what is the tratment for salmonella
ampicillin, trimethoprim-sulfamethoxazole or ciprofolaxin for systemic infections. otherwise symptomatic release.
303
is there a vaccine for salmonella
live attenuated Ty21a older than 2
| Typhim = Vi polysaccharide capsular vaccine - less than 2 years
304
what are the characterisitcs of shigella
gram negative, non motile, no lactose ferment, no capusle. easily spreadable
305
what is the pathogenesis of shigella
1. colon - invade M cells in peyer patches
2. inject type III effectors (Ipas) to cause cytoskeleton to engulf them
3. Lyses vacuole and replicates in cytoplasm
4. polymerize host actin to move to uninfected celll
5. induce apoptosis in phagocytic cells -> intense inflammatory response
306
what does shigella secrete. How does it secrete it
shiga toxin. Type II secretory pathway
307
what type of toxin is shiga. what is the physiology
A: 5B. Cleaves 28s ribosomal RNA
308
what is the human reservoir for shigella
only humans
309
what are the symptoms of shigella
ab cramps
straining to deficate
diarrhea
dysentery - pus and blood in the stools
310
what is the diagnosis for shigella
lactose negative - shows white on macconkey agar. non motile.
311
how do you treat shigella
mild infection - self limiting
| ampicillin, trimethoprim/sulfamethoxazole used for servere infection.
312
what treatments makes shigella infection worse
antidiarrheal because shiga toxin won't be flushed from system -> more cell death and inflammation
313
what distinct histopathology does EHEC cause
attaching and effacing lesions
314
What toxin does EHEC have
Shiga toxin in a bacteriophage (STx 1 and 2)
315
What clinical diseases are seen with EHEC
uncomplicated diarrhea to hemorrhagic colitis
| Hemolytic uermic syndrome (HUS)
316
what is hUS
hemolytic uremic syndrome - under 10 years of age
acute renal failure
thrombocytopenia
microangiopathic hemolytic anemia
317
what is unique with the culturing of EHEC
inability to ferment soribitol - colonies stay colorless . normal ecoli turns pink
318
what is the treatment for EHEC
only supportive care. abx can increase shiga toxin production.
319
what are the characteristics of camplobacter
gram negative. curved rod. microaerophilic. Motile. single flagellum.
320
what are the campyloacter associated with human disease
c. jejuni, upsalensis, coli, fetus
321
what does campylobacter cause
inflammation
| autoimmune disease - guillain barre and reactive arthritis
322
where is campy most likely found
chicken
323
of the food diseases, which are the most common
campy is almost doulbe of shigella and salmonella
324
what are the clinical diseases of campy
acute enteritis
diarrhea blood stools
inflammation ulcerated mucosa
chronic diarrhea in immunocompromised patients
325
what does c. fetus cause
extraintestinal infections in compromised patients
326
how do you diagnose campylobacter
micro-stool sample, s shaped organism and RBCs and WBCs in stool
culture is difficult - slow growth, microaerophilic atm, high incubation temps
327
what is the treatment for campylobacter
fluid replacement. Azithromycin and erythromycin
328
what are the characteristics of helicobacter
gram negative curved rods
microaerophilic
produce urease
difficult to culture
329
what is the pathogenesis of helicobacter
urease expression to survive gastric acid
swim through mucus using flagella.
adhrere to gastric epithelium.
330
what causes peptic ulcer with helicobacter
two genetic loci, one being a toxin VacA. The second can be a secretion system, CagA, IL8
331
what is VacA -
multifunctional for helicobacter. forms anion channels, forms large vacuoles, alters tight junctions
332
what are the symptoms of helicobacter
asymptomatic in 80% of ppl. Ulcers, can lead to gastric adenocarcinoma and gastric b cell lymphomas
333
how can you diagnose helicobacter
urea breath test. Histologic exam of gastric biopsy. stool sample. hard to culture.
334
what is the treatment for helicobacter
proton inhibitor and macrolide and beta lactam
335
what is the characteristic of vibrio
gram neg curved rod. single polar flagella. oxidase positive. needs nacl for growth
336
what is the toxin of vibrio
cholera toxin A: 5B on bacteriophage CTXphage
337
what is the MAO of the cholera toxin
binds to GM1. A subunit ADP ribosylates the Gs protein and induces cAMP which stimulates CL secretion leading to water efflux
338
other than the cholera toxin, what else is encoded on the vibrio phage
TCP - toxin coregulated pilus - used to adhere to the mucosal epithelium and used by the phage to infect the cell
339
Without the cholera toxin, what else can virbrio have have cause diarrhea
Zot - zonnula occludens toxin - disrupts tight junction
| Ace- accessory cholera enterotoxin - increases fluid secretion
340
where are vibrio found
marine and estuarine environments
341
rice water stool
cholera from vibrio cholera
342
what is the diagnosis for vibrio
stool sample curved rod gram neg.
343
what is the treatment for vibrio
electrolyte and fluid replacement
| zaithromycin or doxycycline
344
what are the vaccine for vibrio
1. formalin inactivated whole cell vaccine
| 2. dukoral - heat killed O1 classical and El Tor strains or non toxic B subunits.
345
what are the three lower respiratory tract infections
pseudomonas aeruginosa, legionella pneumophila, mycobacterium tuberculosis
346
what is characteristic about mycobacterium.
```
lipid rich cell wall
acid fast staining
slow growth
non motile
aerobic rod
```
347
what are the three disease causing mycobacteria
tuberculosis
leprosy
pulmonary disease (MAC) -
348
what is unusual about the cultures of m. tb
cord factor (trehalose dimycolate) - dry and hard to manipulate cording pattern
349
what unique things are found in the cell wall of myco
Man Lam, AG, mycolic acids
350
what is the reservoir for m. TB
only humans
351
what is the life cycle of m. TB
inhalation, uptake into phagocytes, multiplication, granulomatous lesion -> latent or active disease
352
what are the main symptoms of TB
malaise, weight loss, productive cough, night sweats
353
what can be seen in latent TB
granulomas
354
when is it most likely to see latent TB go to active TB
when patient bceomes immune compromised
355
what stage of TB can a positive PPD skin test be seen?
both active and latent
356
how can you test for TB
PPD skin test (doesn't tell you type of myco exposed to)
quantiferon (INF gamma detection)
sputum exam
culutre is gold standard
357
the culture of TB might be the gold standar but what is the problem with this
it takes 3-6 weeks for a culture to grow
358
what makes a positive TB skin test
greater than 10 mm spot of either latent or active tb
359
the acid fast staining of myco will show what
hydrophobic cell envelope due to long chain fatty acids (mycolic acids)
360
what is the treatment for acute infections of TB
2 mo isoniazid, rifampicin, ethambutol and pyrazinamide
| then 4 mo of isoniazid and rifampicin
361
what is the treatment for latent TB
9 mo of isoniazid
362
what is the vaccine for TB
BCG. live vaccine of bovis.
363
what is the transmission for m. leprae
person to person contact - inhalation of organism or direct contact with respiratory secretions
364
what are the two types of leprosy. What makes them different
tuberculoidal - strong cell mediated immune response. Few bacilli present in tissue
lepromatous leprosy - strong humoral response. Abundance of bacilli
365
what are the clinical symptoms of tuberculoidal leprosy
few erythematous plaques. Extensive peripheral nerve damage and sensory loss.
366
what are the clinical symptoms of lepromatous leprosy
many erythematous plaques. Extensive tissue destruction. Little sensory loss.
367
what arethe characteristics of legionella
gram negative, unencapsulated rod. single flagella.
| obligate aerobe.
368
what are the growth requirements for legionella
l-cysteine and ferric iron
369
what do legionelle derive most of their energy from
breakdown of a.a instead of carbs
370
what type of pathogens are legionella
opportunistic
371
what tow diseases does legionella cause
legionaires disease and pontiac fever
372
what serogroup is the major disease in humans for legionella
l. pneumophila serogroup I
373
where do legionella live
water and in ameoba
374
how is legionella transmitted
inhlation of droplet. Aspirated into the lungs
375
where does legionella replicate
in amoeba or in the phagocyte. Prevents phagosome lysosome fusion
376
what are some virulence factors of legionella
cytotoxins, hemolysins, proteases, endotoxins, type IV secretion (dna directly into cell)
377
how is legionella taken up into a phagocyte
coliling phagocytosis
378
life cycle of legionella
coiling phagocytosis
2. nutrients brought to bacteria.
3. replicates in phagosome. No lysosomal fusion.
4. once nutrients gone, grow flagella and leave cell
379
what are the clinical features of legionaire's disease
pneumonia, cough, fever ,chest pain
380
what arehte symptoms of pontiac fever
flu-like illness
381
can you see pneumonia in xray of legionaire's or pontiac fever?
only legionaire's
382
how do you diagnose legionella
differential fluorescent antibody
culture - need specialized media. buffered charcoal yeast extract (iridescent sheen and cut glass appearance)
elisa and serotyping
383
what are the treatmetns for legionella - legionaires and pontiac fever
legionaires needs abx
| pontiac - self limiting
384
what are the characteristics of pseudomonas
```
gram negative rod
polar flagella
opportunists
biofilms
resistant to chemical disinfection
```
385
what are the two pigments p. aeruginosa make. what do they do
pyoverdin and pyocanin that are virulence factors.
| also give the green color when grown on media
386
p. aeruginosa are often associated with what (in terms of prevalence)
nosocomial infections. Found on surfaces and respiratory devices.
burn victims
387
p. aeruginosa is often the cause of death in what patient
CF patients
388
what types of colony does p. aeruginosa have when taken from the lung
shiny and stikcy. mucoid
389
p. aeruginosa is very virulent. what are the virulence factors
```
adhesins
polysaccharide capsule
mucoid phenotype
endotoxin (lipid A) - septic shock
pigments pyocyanine and pyochelin - release oxygen radicals
exotoxins - ExoA. Tissue damage
proteases - damge host tissue
```
390
what is the life cycle of p. aeruginosa
1. remains outside cell.
2. release exotoxins to inhibit protein synthesis
3. III secretion
4. toxin destroys cell
391
what is the diagnosis of pseudomonas aeruginosa
culture - defining colony size, pigmentation, hemolytic activity and odor
392
what are two bacteria that used be classified uner pseudomonads and that are capable to causing diease
burkholderia cepacia and pseudomallei
393
what does burkholderia cepacia cause
respiratory infection if CF aof CFD patients. UTIs. septicemia
394
what treats burkholderia cepacia and psudomallei
sulfamethoxazole and trimethroprim
395
what does burkholderia pseudomallei cause
chronic pulmonary disase and cutaneous infections
396
what are two opportunists bacteria
legionella and pseudomonas
397
what are the five types of mechanisms used by professional multisystem bacteria
immune evasion: antigenic variation, serum resistance and cloaking
invasiveness: cell invasion and tissue invasion
398
what are the four vector borne dieases
anaplasmosis
ehrilichiosis
rocky mountain spotted fever
lyme disease
399
what is the non vector borne multi system infections
syphilis
400
what is a transtadial transmission
when a pathogen is transmitted or maintained in the different life stages of the same indivudal vector
401
what is transovarial transmission
when a pathogen is transmiteed from one vector generation to the next. (parent to offspring)
402
what types of tick can be infected
larvae have 6 legs are are not infected. adults and nymphs have 8 legs and are infected
403
which two vector borne multi systme diseases have smaller curves for peak of cases
anaplasmosis and lyme
404
where is anaplasmosis most found
Mn and WI and north east
405
what is the tick that caues anaplasmosis
ixodes scapularis
406
what are teh characteristics of anaplasma phago.
```
obligate intracellular
replicates in vacuoles
no LPS
NO pg
has IV secretion
tiny gram neg coccobacillus
```
407
where is human ehrlichiosis found
wisonsin and the belt
408
what is the tick that causes ehrlichiosis
amblyomma americanum
409
what are the characteristics of e. chaffeensis
tiny gram negative coccobacilli
obligate intracellular, replicates in vacuoles, no LPS, No pg, IV secretion
invades monocytes
410
what is the invasion difference between ehrlichiosis and anaplasmosis
ehrichiosis invades monocytes. anaplasmosis is PMNs
411
what are the most common clinical signs of anaplasmosis and ehrlichiosis
fevers, chills, headache, myalgia, anorexia, leukopenia, thrombocytopenia, increased liver aminotransferease
412
what is the diagnosis for anaplasmosis and ehrlichiosis
morulae in PMNs or monocyte of blood spmears. PCR. Serology (takes 30 days)
413
where is rocky mountain spotted fever found
the belt
414
what is the tick for rocky mountain spotted fever
brown dog tick - rhipicephalus sanguineus
415
which of the vector borne has transovarial and transstadial transmission
rickettsia rickettsii - rocky mountain spotted fever
416
what are the characteristics of rickettsia
obligate intracellular , replicates in cytoplasm, has LPS and PG and type IV secretion.
417
what does rickettsia invade
endothelial cells
418
what is the diffrence between replication of rickettsii and ehrlichiosis and anaplasmosis
e and a replicate in vacuoles, rick replicates in cytoplasm
419
which vector borne pathogen has LPS and PG
rickettsia
420
what are the clinical signs of rocky mountain spotted fever
fever malaise, severe headache, anorexia ab pain. Rash 3-5 days after onset of illness. STarts on ankles wrists and forehead. macules progress to maculopapules then to petechiae.
421
what is the diagnosis for RMSF
no test available. Use clinical judgement. Non specific lab result are TCP, pro coagulant, leukopenia
422
where is lyme disease found
WI MN and the NE coast
423
what is the tick for lyme
ixodes scapularis, blacklegged tick
424
what bacteria causes lyme
borrelia burgdorferi
425
what are the characterisitcs of b. burgdorferi
gram negative spirochete. Extracellular. NO LPS toxins or special secretions. Have flagella between out membrane and plasma membrane
426
what is the early localized symptoms of lyme
erythemia migrans - the bullseye
427
what is the early disseminated symptoms of lyms
fever, AV nodal block, facial palsy, pancarditis
428
what aret he late stages of lymes
arthritis, encephalopathy
429
what is the down fall of useing IgM and IgG for serology testing
you can have these for years after treatment so you wont know if you successfully treated
430
what is the treatment of lyme - aerly and no CNS involvement
doxycycline (amox for pregos or under 8)
431
what is the treatment for CNS involved lyme
ceftriazone
432
is it good to use cultures to diagnose vector borne
no, difficult to grow in culture.
433
what is the bacterium that causes syphilius
treponema pallidum
434
what is primary syphilius clinically
painless lesion (chancre) at site of inoculation. Highly infectious (10-90 days)
435
what is secondary syphilus
6wks- 6 mo after primary (4-12 wks)
non itchy rash - palms and soles.
fever
wart like infectious lesion. condyloma
436
what is tertiary syphilis clinically
tabes dorsalis - loss of sensory and motor neuron function leading to intense pain and personality changes. ataxia aortic aneurism aortic valve insuffiency.
437
what causes all the symptoms in tertiary syphilus
not viruelence factos but damage from host response
438
what are some diagnostics for syhphilus
RPR and VDRL - both can be positive in autoimmune disorders
| FTA-ABS and MHA TP - specific
439
what is the treatment for syphilius
long acting penicillin
440
what are the four toxins that use ADP-ribosyltransferase for the MAO
diptheria, exotxin A (pseudo aeruginosa), cholera, pertussis
441
which strep is sensitive to bacitracin and which is sensitive to optochin
s pyogense - bacitracin
| pneumoniae - optochin
