Bacteriology Flashcards
(215 cards)
1
Q
How does penicilin act on bacteria?
A
Inhibits bacterial cellw all biosynthesis
2
Q
What are the main differences between gram + and Gram - bacteria?
A
Gram+
Thick peptidoglycan and teichoic acid binding it to membrane
Gram-
Outermembrane that is porous
thin peptidoglycan layer cross linked toutermembrane anda periplasmic space
3
Q
What is the basic subunit of peptidoglycan?
A
disaccharide that linked to a D/L pentapeptide, that forms chains and has cross linking
4
Q
What is the difference between gram+ and gram - bacteria as far as crosslinking of peptidoglycan?
A
-: little crosslinking
+highgly cross linked btw polysaccharide C aa and D aa
5
Q
What is the role of teichoic acid?
A
polysaccharide that is crosslinked to a cytoplasmic membrane and peptidoglycan
6
Q
What are teh parts of the LPS adn what type of bacteria are they unique to?
A
O-antigen:variable region
Polysaccharide core
Lipid A
unique to gram - bacteria
7
Q
What is the function of pili and fimbriae?
A
polymers of protein, that have a role in adherence to eukaryotic cells and btw bacteria
8
Q
What is the role of Type 2 secretion factor?
A
secrete protein across the inner membrane
9
Q
Whatis the role of type 3 secretion system?
A
deliver toxin directly into host cell
10
Q
What is the role fo Type 4 secretion system?
A
deliver DNA into host cells
11
Q
Where is the primary infection point of Haemophilus?
A
Colonization of nasopharynx with occasional invasion of sunus
12
Q
What is the virulence factor associated with increased danger and meningitis rates of haemophilus influenzae?
A
Capsular polysaccharide of type B haemophilus Influenzae.
Type B: Ribose and Ribitol
13
Q
What changes did they make during hte second generation of Hib vaccine to increase it’s effectiveness?
A
conjugated the PRP to a diptheria toxin, in order to produce a T cell mediated response and produce memory B cells
14
Q
What type of ribosome do bacteria use?
A
70S
15
Q
What is used to identify slow growing or non-cultivatible bacteria with rapid identification?
A
PCR, ie used to test for Clostridium dificile
16
Q
What is the role of RFLP for bacterial identification?
A
Restriction fragment length polymorphism, used to differentiate between nosocomial and community acquired infection
17
Q
What does formate hydrolase role in bacteria?
A
Formate to CO2+H2, in order to decrease acid and increase pH
18
Q
What selective media is used to select for gram + bacteria?
A
mannitol salt media, 7.5 NaCl selects
19
Q
What is sporulation and what set of bacteria is it unique to?
A
instead of death response to decrease supply of nutrients, G+ bacteria (bacillus, clostridium, sporosarcina)
20
Q
How does one inactivate spores?
A
Wet heat, 120 degrees C 20 minutes aka autoclave
21
Q
What is selective toxicity?
A
antibiotics exert their activity by inhibiting gene products found only in bacteria
22
Q
What is the difference between disinfectants, antiseptics and antibiotics?
A
disenfectant toxic to humans and bacteria
antiseptic generally toxic to bacteria but ok for tpical use
antibiotic can be administered systematically but kills bacteria
23
Q
What are the ways we measure suscepitibility?
A
Minimal inhibitory concentration (MIC)
Minimum bactericidal concentration (MBC)
Disk diffusion test
24
Q
What are teh toxic side effects of tetracycline, streptomycin and chloramphenicol?
A
discoloartion of teeth
audiotry damage
chloramphenicol
25
What are the three ways that antibiotic resistance occur?
modification of antibiotic
modification of antibiotic target
reduction of antibiotic conc/prevent access to target
26
What is the key enzyme that causes polymerization and crosslining of peptidoglycan?
PBP- penicillin binding protein
27
What family is involved in preventing peptidoglycan syntehsis at the PBP stage?
Beta-lactams
28
What is the primary mechanism of resistance to Beta-lactam antibiotics?
Beta-lactamase that catalyzes the enzymatic inactvation of beta-lactam antibiotics by cleaving the ring
and mutations in PBPs preventing binding of beta lactam
29
What is the most common mechansim of beta-lactam resistance found in strep and MRSA? (gram +)
Mutation in PBP to preven binding of beta lactam antiobiotics
30
How does a doctor prevent cleaving of Beta-lactam by the lactamase?
Using Clavulanic acid to inhibit the beta-lactamase along with the antibiotic
31
What is the mechanism of action of glycopeptides and what is one example of a glycopeptide?
Vancomycin, which binds to the D-ala-D-ala of the peptide chain blocking PBPs from catalyzing transglycosylation.
32
What is a limitation of vancomycin?
Red-mans disease and only effective on most gram+; therefore mianly utilized for Beta-lactam rsistant infection
33
What is the mechanism of resitance of bacteria to glycopeptides?
Altered peptidoglycan structure, utilize D-ala-D-lac instead of D-ala-D-ala preventing vancomycin binding; most common in enterococci
34
How do cycloserines inhibit bacterial growth?
Strucutrally similar to D-ala and acts as a competitive inhibitor in the production of the two part peptidoglycan precursor. Both at alanine racemase and D-alanyl-Dalanine synthetase. Higher affinity than D-alanine
Important for TB tx
35
What is teh mechanism of bacitracin?
Peptide antibiotic-too toxic for systemic use. BInds to pyrophosphate on lipid carrier for peptidoglycan precursosrs
36
What is the mechanism of action of Daptomycin?
Lipopeptide antibiotic; Gram+ bacteria
| Binds and disrupt of cytoplasmic membrane possibly via loss of potential
37
What is the mechanism of polymyxins?
polymyxin B, colistin--lipopeptide (gram -)
| Binds to LPS in outer membrane leading to disruption of membranes
38
What is the mechansim of Tetracyclines?
Bacteriostatic broad spectrum
| binds to 30S ribosomal subunit
39
What is the major forms of resistance to tetracycline?
Ttetracycline efflux pump(most common)
| mutations on the ribosome
40
What is the mechansim of action of aminoglycosides?
binds irreversibly to 30s robosomal subunit. Don't penetrate gram+ well, nephrotoxic and ototoxic adverse effects
41
How does aminoglycoside resistant bacteria mechanism go?
enzymatic modification of antibioitic to prevent binding
42
What is teh mechanism of action of macrolides?
binds 50S ribosomal subunit to block elongation
43
What is the mechanism of resistance to macrolides?
methylation of ribosomal RNA to prevent binding
| efflux pump can expel macrolides
44
What is the mechanism of action of chloramphenicol?
binds 50S ribosome
45
What is the mechansim of resistance to chloramphenicol?
catalyzes additiono f acetyl group to drug
46
What is the mechanism of action of clindamycin?
used to tx MRSA and Staph aureus; binds 50S subunit
47
What is the mechanism of resistance to clindamycin?
methylation of rRNA, cross-resistance with macrolides
48
What is the mechanism of linezolid?
new class; gram+; oxazolidinone class. BInds unique site on 50S subunit
49
What is the mechanism of antibiotic resistance to linezolid?
point mutation on ribosomal components
50
What is the mechanism of action of Nalidixic acid and 2nd generation fluoroquinolones?
synthetic quinolone, binds DNA gyrase or topoisomerase to inhibit DNA. Narrow spectrum
51
What is the mechanism of resistance to quinolones?
point mutation in DNA gyrase, efflux pumps
52
What genes are involved in mobile genetic elements-linear DNA segment.
All insertion sequences or trsnposons posess inverted Terminal repeats
tranposase is the enzyme that recognizes inverted terminal repeat and cuts DNA allowing transposition of element
53
Phase variation in E. Coli is responsible for what?
Wheter or not fimbriae is produced by promoter element in insertion element. Fimbriae promote attachment to urinary epithelaial surface
54
What are genomic pathogenicty islands?
G+C content different, aencode a pathogenic virulence factor
55
What are two virulence determinance that are carreid on bacteriophage?
cholera toxin and shiga toxin
56
Cholera toxin phage infects what type of bacteria?
Filamentous bacteriophage that infects vibrio cholera
dual function for choleratoxin element, phage morphogensis and enterotoxin
c
57
How does cholera toxin work?
A-5B toxin. B subunit bind ganglioside GM1
A subunit internalized and interacts with G proteins regulated adenylate cyclase
Induces conversion of ATP to cAMP results in enhaced secretion of water and electrolytes
58
Shiga toxin phage infects what?
both shigella dysenteriae and EHEC strain of ecoli
59
Shiga toxin induces what?
severe diarrhea, hemorrhagic colitis and hemolytic-uremic syndrome
60
What is the mechanism of shiga toxin acitivity?
A 5B toxin; B subunit binds Gb3 glycolipid
a subunit is translocated in cytosol and modifies ribisome acceptor site
blocks protein syntehsis
61
What are the strategies used by extracellular pathogens to resist getting killed?
avoid recognition by phagocytes
inhibit phagocyte engulfment
kill or damage phagocytes
62
What are strategies used by intracellular pathogens to resist killing?
inhibit phagosome-lysosome fusion
survivie inside phagolysosome
escape from phagosome
63
How does bacterial uptake occur?
Recognition between ligan and receptor initiates transmembrane activation cascade. Surface structure remodeled by depolymerizing and re-polymerizing acting and other cytoskeletal components
64
What cytoskeletal component allow for maturation of phagosome from periphery to perinuclear region?
microtubules
65
What bacteria surive and replicate in phagolysosome?
Coxiella
66
What bacteria escape the phagosome and replicate in cytosol?
Rickettsia, shigella, escherichia coli, listeria
67
What bacteria modulate endocytic pathway?
Mycobaccterium and salmonella
68
What bacteria cause an alternative trafficking pathway?
Legionella, brucella, chlamydia
69
What are the side effect and consequences of bacteria ingestion by macrophages?
Tissue injury, ROI, RNI and hydrolytic enzymes, TNFalpha, and iL1 lead to fever, persisten infection adn chronic inflammation, phagocytes contribute to autoimmune,
70
What is the class of bacteria not associated with disease?
saprophytes
71
What are the four classes of bacterial toxins?
surface-acting toxin
pore-forming toxins
A/B toxins
Type 3 and 4 secretion
72
What modifications do diptheria toxin and pseudomonas aeruginosa exotoxin A?
ADP-ribosylate EF2: inhibits protein syntehsis
73
What modification does botulinum toxin and tetanus toxin?
protease for SNARE proteins
74
What large clostridium difficile toxins do to cells?
Glucosylate Rho proteins
75
What does Shiga toxin do to cells?
deadenylate adenine on RNA
76
What is bacteriodes fragilis?
virulence factors:
polysaccharie capsule
bacteroides are aerotolerant anaerobes able to tolerate atmospheric conc
Bacteroides encode two major oxidative stress response genes, catalase and superoxide dismutase
facultive anaerobes often w/ peptostreptococcus in intra-abdominbal abscess
77
What type of bacteria are clostridia?
anaerobic gram +, spore forming bacilli; obligate anaerobes or aerotolerant
pathogenisis due to exotoxin
78
Antibiotic-associated diarrhea; leads to what diarrhea?
C. difficile
| Pathology from Toxin A and Toxin B glucosylate Rho GTPases which cause actin depolymerization
79
What is the treatment used to focus c. difficile?
Metronidazole, vancomycin, or a subset of fluoroquinolones
80
What does histotoxic clostridia does what?
invasive and C. perfringens and causes majority of clostridial-mediated myonecrosis: deep wound to muscle predisposes infection
alpha toxin reduction of tissue redox potential
host proteases
alpha toxin(phospholipase)
81
What is the the pathogenicity of clostridium botulinum?
botulinum toxin: AB toxin, zinc protease, heat labile, inhibits nerotransmitter release
82
What are the applcations of botulinum therapy?
blepharospasm abnormal contraction or twitch of eyelid neurons: cleaves SNARE proteins in spastic nerves relieving spasticity
have a long half life in neurons
83
Describe neisseria meningitidis, physiology and structure?
```
gram - diplococci
Lipooligosaccharide
posses pili
Porins A and B
Utilize host tranferrin
LOS induces the majority of the vascular and other damage
```
84
Most epidemics of N. meningitidis epidemics are associated with what?
serotype A
85
What labatory diagnosis are done to identify N. meningitidis?
oxidase positive, gram negative dplococci
blood culture
biochemical tests
86
What tx is doen for N. meningitidis?
```
vaccination
antibiotics
-cefotaxime
-ceftriaxone
-penicillin G
prophylaxis
-rifampin
-ciprofloxacin
-ceftriaxone
```
87
Describe the key characterisitcs of neisseria gonorrhea?
```
gram - diplococci, oxidase positivie
requires complex growth medium
sensitive to cold
doesn't posess a polysaccharide capsule
posses pili
```
88
What are the neisseria gonococcal antigens?
porins- PORb uptake of nutrients INterferes with neutrophil degranulation, facilitates invasion and resistance to complement
Opa proteins- opaque proteins bind to epithelial cells
LOS
Receptors for human transferrin
89
What are teh laboratory diagnosis of neisseria gonococcal?
gram neg diplococci within PMN in men with purulent urethritis and women with cervicitis
culture and biochemical identifaction
nucleic acid amp assay. multiplex assay
90
What is the tx for neisseria gonorrhea?
1st line: dual therapy with ceftriazone and azithromycin or doxycycline
2nd line- cefixime and either azithromycin or doxycycline followed by a test of cure
91
What are the characteristics of chlamydia and chlamydophila?
gram - envelop with lipopolysaccharide
2 forms:
elementary body=infectious form, stable in the environment bc of a highly cross-linked outer membrane structure
reticulate body=replicative intracellular form, metabolically active; replication takes within inclusion body
92
What protein is the major pathogenisis factor associated with staph. aureus?
Coagulase-contributes to the clotting of plasma
93
What is the way that gram + cocci are differentiated when grown?
Staph produce catalse and strep do not
94
What is protein A?
Unique to Staph aureus. Major protein component of cell wall that is covalently bound to peptidoglycan. IgG bound worn way disrupts oposnization and phagocytosis
95
What are the toxins produced by S. aureus?
hemolysins
leukotoxins
Enterotoxins (TSST)
Exfoliative toxins
96
What do hemolysisn do?
Contribute to pathogenicity by producing tissue damage after the establishment of a focus of infection
97
What do leukotoxins do?
Two protein toxin, attacks PMN leukocytes nad macrophages
98
What do enterotoxins do?
Act as a superantigen
99
What is an exfoliative toxin?
2 forms ETA/ETB-proteases, scalded skin syndrome stimulate lysis of intercellular attatchment btw cells of epidermis?
100
Staph epidermidis is what?
Non-coagulase staph, low virulence. Hospital acquired. Tx needs antibiogram to determine local antibiotic sensitivity
101
S. saprophyticus does what?
UTI selectively binds to cells of urinary tract
| doesn't posess any virulence factors; based solely on tropism
102
What are the three hemolytic patterns?
Alpha-partial or greening
Beta or complete clearing
Gamma no change in RBC
103
How to streptococcus pyogenes avoid opsonization and phagocytosis?
hyaluronic acid capsule
M proteins block C3b binding
M-like proteins bind the Fc fragment of antibodies which in turn reduces and blocks complement activation by the alternative pathway
C5a peptidase degrades C5a and prevents it from acting a chemo attractant
104
How does Strep pyogenes adhere to host cells?
lipoteichoic acid, M proteins, F protein-mediate attachment
105
How does S. pyogenes invade host cells?
M and F proteins
106
Streptococcus pyogenes patients that are provided with what antibodies are protected?
Antibodies to M proteins
107
What are hte differences between Strep pyogenes and Stre pneumoniae?
Pyogenes:
bacitracin sensitive, beta hemolytic, M proteins, hyaluronic acid capsules, Spe toxins, enzymes
Pneumoniae:
alpha hemolytic
optochin sensitive
resistance to phagocytoisis
108
Listeriosis monocytogenes causes human disease in what well-defined patients?
neonates, elderly, pregnant women, persons with defects in cell immunity
109
How do listeria adhere to host cells?
InlA, internalin;
| entry into enteerocytes or M cells
110
What is the role of ActA in listeria?
located on pole of bacteria, polymerizes host actin adn allows projection into neighboring cell
111
How is listeria diagnosed?
1-2 days culture in cold enrichment
Gram stain of CSF for meningitis patients
gentamicin with penicillin or ampicillin treat it
112
Salmonella is part of what family>
enterobacteriaceae
113
What are the main antigens presented on the surface of Salmonella?
H antigen=flagellar protein
K or Vi=capsular antigens for E. coli and S. typhi
O antigens=lipopolysaccaride
Don't ferment lactose
114
What are the two types of salmonella exclusive to humans?
Typhi and paratyphi
115
Where do salmonella invade the small intestine?
microfold cells and enteroctyes in peyer patches
116
What does salmonella do in the cell?
Injects vaculoues with type 3 injection, and makes it a spacious vacuole to prevent destruction.
117
What are the symptoms of salmonella?
fever, abdominal cramps, myalgia, headache, nauesa, vomitting and non-bloody diarrhea
usually self limiiting
118
Is there a vaccine for salmonella?
Live attenuated vaccine Ty21a and another one.
119
What is unique about shigella as a enterobacteriaceae?
One of hte few wihtout flagella and therefore non-motile
120
Shigella invade what type of cells?
invade M cells in Peyer patches
| inject type 3 effectors to cause cytoskeleton to engulf them
121
What are the symptoms of shigella?
dysentery, abdominal cramps, diarrhea, tenesmus, neutrophils in stool
122
Only treat shigella if what occurs?
Enteric fever, and it's systemic otherwise leave it and let diarrhea occur
123
What protein do EHEC inject to integrate into mammalian cellular membrane?
Tir--> allowing it to sit in place and repliciate and release shigella toxin
124
What is EHEC associated with in serotypes and why?
O157:H7 and associated with those that are selected for in intestinal tract of cattle.
125
EHEC has what type of symptoms?
bloody diarrhea, vomiting, no fever and may result in hemolytic uremic syndrome, resulting in kidney failure in 5-10% of children
126
How should you treat EHEC?
Monitor for complications and provide supportive care. Don't give antibiotics will cause expression of more Shiga toxin.
127
Campylobacter is what type of structure?
Gram negative curved rod; spiral or comma shaped. grows at 42 degrees. microaerophilic, motile
128
Campylobacter si assoicated with what other illnesses?
autoimmune disorders such as Guillain Barre syndrome and reactive arthritis.
129
What si treatment of campylobacter?
Only treat sever cases with antibiotics otherwise treat with fluid replacement.
130
What is heliobacter colonization occuring?
lifelong possible: Urease expression allows bacteria to survive in gastric juices. adhere to to gastric epithelium through mucosal
131
Heliobacter related peptic ulcers are associated with what?
Toxin: VacA; multifunctional toxin that laters physiology
and the type 4 secretion system that injects CagA which induces IL8 release. Induce pedestal formation
may lead to development of cancer
132
What is the resevoir for heliobacter?
only humans and asymptomatic in 70-80% of infected individuals
133
What is the laboratory diagnosis?
urea breath test, feed radioactive urea which leads to radioactive CO2 in breath
134
What is the treatment for heliobacter?
debatable protects against GERD and adenocarcinoma of esophagaus
PPI+macrolide+B-lactam
135
Vibrio requires waht for growth?
NaCl, oxidase positive, toxin co-regulated pili
136
What serotypes of vibrio are assoicated with epidemic disease?
O1 and O139
137
Cholera toxin is associated with what?
all pahtology of vibrio cholear
A:5B protein encoded by bacteriophage CTX
leads to water efflux=osmotic diarrhea
138
What is the role of pili in vibrio cholera?
coregulated pilus that adhere to mucosal epithelium; makes other toxins other than choleera toxin
139
HOw is vibrio cholear diagnosed?
culture or microscopy in stool
140
What are the general characteristics of mycobacterium?
lipid-rich cell wall; resistant to disinfectants and common stains
ID by acid-fast
fastiduous and slow growing
141
What is the unusual cellw all of M. tuberculosis made of?
complex lipids, trehalose dimycolate(cord factor involved in production of caseating granulomas)
142
What is the difference between latent and active infections of M. tuberculosis?
bacteria stop multiplying and the lesion calcifies in latency
bcteria rapidly multipy and lesion liquifies then bacteria disseminate in active disease
143
What is the reactivation rate of TB?
5% in first two years, 10% lifetime if remain healthy
| immunocompromised individuals have a 10% annual reactivation rate
144
What are the characteristics of active TB?
infectious, organism in sputum, dense lesions in lung readibly detectable by Xray, malaise, weight loss, productive cough, night sweats, may disseminate
145
What are the dense lesions found on xray called in TB?
Ghon complexes
146
What are characteristic of Laten TB?
host not infectious, no xray signs, granulomas generated which are areas of active immune cells
147
What are the characteristics of reactivation of TB?
rapid multiplication after immune suppresion, infectious, usually occur after suppression in TNFalpha, IFNgama or iNOS
148
Difference between active and latent as far as symptoms?
Active: infectious, feel sick positive PPD skin test, abnormal chest xray.
Latent: non-infectious, Positive PPD, chest x raya nd sputum test normal
149
How do you identify TB infection?
```
PPD: tells exposure
Quantiferon: ELIS that detects IFN-gamm response to TB antigen exposure
Sputum exam by microscopy
Culture is gold standard
Molecular probe and biochemical tets
```
150
What is a PPD and what is a postiive?
mixture of tuberculoproteins from cell wall given intradermally
induration of greater than 10 mm using 5 TU of PPD is considered postivie
BCG vaccine will test positive
151
Why is gram stain innefective?
hydrophobic cell envelope so not truly gram +
152
Recommended tx of TB?
2 month isoniazied, rifampcin, ethambutol and pyrazinamide followed by 4 months of isoniazid and rifampicin
Latent TB: 9 months of isoniazid alone will not always work
153
MDR TB is what?
displays resistance to isoniazid and rifampicin, requires 2 years of antibiotics
154
XDR TB is what?
resistance to isoniazid and rifampcin, any fluorquinolone and rsistance to at least one second line drug: may be more virulent and prognosis extremely grim
155
What is DOTS?
direct observational therapy-short course 5 parts (sputum smear, government commitment, regimen of 6-8 months, uninterrupted supply of TB drugs and standardized recording and resporting)
costs only abou 10 $ of drugs per persona dn greater than 95% cure reate
156
HOw is leprosy usually transmitted?
perosn to perosn following inhalation or direct contact with respiratory secretions
obligate parasite and can't be grown on medium
157
What are the two clinical manfiestations of leprosy?
tuberculoidal and lepromatous
158
What is tuberculoidal leprosy?
strong-cell mediated immune response; few bacilli present in tissue and results in few plaques but extesnive peripheral nerve damage not very infectious
159
What is lepromatous leprosy?
Strong humoral response but weak cell mediated. Abundance of bacilli in dermal macrophages and in schwann cells-- many erythematous plaqyes and extensive tissue destruction with little sensory loss. Highly infectious; not reactive to lepromin
160
What is the physiology of legionella?
obligate aerobes, infect lungs, opportunistic, gram negative unencapsulated rods with singular flagella.
require L-cysteine and ferric iron to grow
derive energy mainly from amino acids
resistant to chemical disinfectants
161
What group of legionella is major cause of disease?
L. pneumophila serogroup I
162
How is legionella acquired?
inhalation of droplet carrying organism usually by air conditioning aspiration; no person-to-person transmission. Individuals immunocompromised most at risk
163
What is the host resevoir of legionella?
amoeba within water supplies and survives within macrophges in humans.
164
What is the virulence factors associated wtih legionella?
cytotoxins, hemolysins, proteases, endotoxina dn lipases; tpe 4 secretion system to alter endocytic trafficking in cell to prevent phagosome-lysosme fusion
165
How is legionella identified?
microscopy; using diffrential fluorescent antibody. ID by culture but difficult. ELISA for antigens but only for one serotype
166
What is the physiology of P. auerginosa?
capable of growing on a variety of complex defined surfaces even at elevated temps; can oxidise wide number of carbs; strongly hemolytic
produce variety of pigments (pyoverdin and pyocanin are important virulence factors that are pigments)
167
P aeruginosa are associated with what type of infections?
nosocomial due to abiltty to colonize and form microcolonies.
often cause disease in burn and puncture victims
168
What is a common cause of death in CF patients?
p. aeruginosa, becuase of their mucoid phenotypes make them difficult to eliminate
169
What are common virulence factors of psuedomonas?
produce adhesins, promote binding; polysaccharide capsule alginate mucoid phenotype; production of endotoxin and septic shock; pyocyanine and pyochelin and releases free radicals, exotoxins that cause tissue damage; proteases
170
What two pigments are virulence factors in psuedomonas aeruginosa?
pyocyanine and pyochelin
171
What are some of the bacterial virulence factors that are required to cause mutlisystem infections?
antigenic variation, serum resistance, cloaking, cell invasiona nd tissue invasion
172
What bacteria employ antigenic variation for immune evasion?
borrelia, treponema pallidum
173
What bacteria have few surface proteins to avoid the immune system?
treponema pallidum
174
What bacteria inactivate complement?
borrelia, leptospira through Factor H
175
What bacteria preven phagocytosis?
bacillus anthracis and yersinia pestis
176
What bacteria invade cells?
chlamydia, rickettsia, Ehrlichia, ANaplasma
177
What bacteria are tissue invasive to avoid immune system?
borrelia, treponema pallidum, leptospira
178
What bacteria bind fibronectin and other plasma proteins to cloak themselves from teh immune system?
borrelia and leptospira
179
What bacteria replicate in late endosome and autophagosomes of neutrophils?
anaplasma phagocytophilum
180
What bacteria bind to enter and replicate in early endosome of monocytic cells?
Ehrlichia chaffeensis
181
What bacter bind to enter and replicate in cytoplasm of endothelial cells?
Rickettsia
182
What bacteria sequester and activate host plasminogen and metalloproteinases to invade tissue?
borrelia, leptospira
183
What bacteria utilize endogenous proteases to invade tissue?
Treonema pallidum
184
What bacteria penetrate between cells?
borrelia and leptospira
185
What mutlisystem bacterial infection in US is Vector-borne?
anaplasmosis
Ehrlichiosis
Rocky Mountain SPotted Fever
Lyme
186
What multisystem is not vector borne?
syphilis
187
What is vector competence?
Ability of a vector to transmit the pathogen
188
What is biological tranmission?
when a pathogen has a specific life stage in a vector; colonizes a specific site and alters its gene expression
189
What is transstadial transmission?
When a pathogen is transmitted or maintained in different life stages of the same inidvidual vector (lyme disease, anaplasmosis, ehrlichiosis)
190
What is tranovarial transmission?
Whena pathogen is transmitted from one vector generation to the next; Rocky mountain spotted fever Rickettsiosis
191
What is Anaplasmosis/Ehrlichiosis?
tick-borne, gram-negative intracellular bacilli
192
What are the vectors for anaplasmosis and lyme disease?
ixodes scapularis, I. pacificus
193
What vector transmits Ehrlichiosis?
A. americanum, I . Scapularis
194
What vector transmits rocky mountain spotted fever?
D. variabilis, D andersoni, Rhipicephalus sangunineus
195
What is human granulocytic anaplasmosis?
Previously known as HGE; now anaplasma, transmitted by Ixodes. TINY Gram negative coccobacillus. Obligate intracellular replicates in vaculoes has type 4 secretion.
Invade monocytes, neutrophils
196
Life cycles of Anaplasma and Ehrlichia
Incubation is 1-2 weeks; most common signs -fever, headache, anorexia, leukopenia, thrombocytopenia, increased liver aminotransferases
severity of illness is highly variable: asymptomatic to severe and life-threatening
197
How do you diagnose anaplasmosis and ehrlichiosis?
morulae in neutrophils or monocytes, respectively, may be difficult to find in sear; PCR can be used to identify organism based on temp at which amplified DNA melts
198
What anaplasmosis and ehrlichiosis therapy exists?
oral doxycycline (also treats lyme disease)
199
Rickettsia rickettsii physiology is what?
Tiny Gram negative coccobacilli; obligate intracellular replicates in cytoplasm may invade nucleus. Does have LPS and peptidoglycan has type 4 secretion
200
What are the CLINICAL symptoms of rocky mountain spotted fever?
incubation time 1 week, fever, malaise, severe headach, myalgia anorexia, abdominal pain. Rash 3-5 days after onset of illness
Thrombocytopenia pro-coagulant coagulopathy, leukopenia, elevated aminotransferases
201
What does the CDC say about the diagnosis of Rocky mountain spotted fever?
there is no test available at this time that can provide a conclusive result in time to make important decisions about treatment
202
What is the treatment for Rocky mountain spotted fever?
oral doxcycline even if under 8 or pregnant, at least 3 days past defervescence or chloramphenicol if allergy to tetracyclines
203
What are the characteristics of borrelia burgdorferi?
gram negative, spirochete, extracellular no LPS, toxins special secretion system. Requires greater than 36 hours for transmission. Considerable antigenic variation and complement invasion
204
What are the early symptoms of lyme disease localized to bite site?
erythema migrans greater than 5 cm, and regional lymphadenopathy
205
What are the early disseminated clinical signs of lyme disease?
fever, malaise, secondary EM, arthalgia, myalgia, polyradiculopathy, facial pasly, pancarditis, AV node blcok
206
What are the late signs of lyme disease?
Arthritis, encephalopathy, polyradiculopathy
207
Lyme disease diagnosis>
clear lesion, and likely tick encounter sufficient to start therapy otherwise ELISA then immunoblot to start
208
IgM and IgG serology can be used to diagnose lyme disease?
If EM rash without evidence of systemic infection. IgM and IgG positive in 2-3 weeks and 3-6 weeks; both remain positive for years so cannot be used to assess tx success
209
how do you treat lyme disease?
oral doxycycline for early; amoxicillin for those pregnant or under 8
If CNS involvement utilize IV ceftriaxone. Avoid anti-inflammatory therapy
210
What species of syphilis is the most invasive?
treponema pallidum pallidum-- syphillis, world-wide STD
211
What are the symptoms of syphillis primary?
10-90 days after encounter
painless lesion(chancre) at site of inoculation
highly infectious
regional lymphadenopathy
212
What is seondary syphillis clinic?
6 weeks-6 months after primary, lasts 4-12 weeks
diffuse non-itchy, rash all over including palm and soles
myalgias, arthralgias
fever
condylomas latum
213
What is tertiary syphillis?
tabes dorsalis loss of sensory and motor neuron function, leading to intesnse pain, personallity changes
Damage is due to host response
worsened by HIV infection
214
What is the diagnosis for syphillis?
rapid plasma reagin and veneral disease research lab
both are cardio-lipin tests inexpensive but can be positive in other patient group
aslo speicifc confirmatory serology
215
What is the therapy fo rsyphillis?
long acting penicilin for primary and secondary, IV for tertiary
