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Block 6 > Bacteriology > Flashcards

Bacteriology Flashcards

1
Q

How does penicilin act on bacteria?

A

Inhibits bacterial cellw all biosynthesis

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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

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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

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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

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5
Q

What is the role of teichoic acid?

A

polysaccharide that is crosslinked to a cytoplasmic membrane and peptidoglycan

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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

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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

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8
Q

What is the role of Type 2 secretion factor?

A

secrete protein across the inner membrane

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9
Q

Whatis the role of type 3 secretion system?

A

deliver toxin directly into host cell

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10
Q

What is the role fo Type 4 secretion system?

A

deliver DNA into host cells

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11
Q

Where is the primary infection point of Haemophilus?

A

Colonization of nasopharynx with occasional invasion of sunus

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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

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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

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14
Q

What type of ribosome do bacteria use?

A

70S

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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

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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

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17
Q

What does formate hydrolase role in bacteria?

A

Formate to CO2+H2, in order to decrease acid and increase pH

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18
Q

What selective media is used to select for gram + bacteria?

A

mannitol salt media, 7.5 NaCl selects

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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)

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20
Q

How does one inactivate spores?

A

Wet heat, 120 degrees C 20 minutes aka autoclave

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21
Q

What is selective toxicity?

A

antibiotics exert their activity by inhibiting gene products found only in bacteria

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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

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23
Q

What are the ways we measure suscepitibility?

A

Minimal inhibitory concentration (MIC)
Minimum bactericidal concentration (MBC)
Disk diffusion test

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24
Q

What are teh toxic side effects of tetracycline, streptomycin and chloramphenicol?

A

discoloartion of teeth
audiotry damage
chloramphenicol

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25
Q

What are the three ways that antibiotic resistance occur?

A

modification of antibiotic
modification of antibiotic target
reduction of antibiotic conc/prevent access to target

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26
Q

What is the key enzyme that causes polymerization and crosslining of peptidoglycan?

A

PBP- penicillin binding protein

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27
Q

What family is involved in preventing peptidoglycan syntehsis at the PBP stage?

A

Beta-lactams

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28
Q

What is the primary mechanism of resistance to Beta-lactam antibiotics?

A

Beta-lactamase that catalyzes the enzymatic inactvation of beta-lactam antibiotics by cleaving the ring
and mutations in PBPs preventing binding of beta lactam

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29
Q

What is the most common mechansim of beta-lactam resistance found in strep and MRSA? (gram +)

A

Mutation in PBP to preven binding of beta lactam antiobiotics

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30
Q

How does a doctor prevent cleaving of Beta-lactam by the lactamase?

A

Using Clavulanic acid to inhibit the beta-lactamase along with the antibiotic

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31
Q

What is the mechanism of action of glycopeptides and what is one example of a glycopeptide?

A

Vancomycin, which binds to the D-ala-D-ala of the peptide chain blocking PBPs from catalyzing transglycosylation.

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32
Q

What is a limitation of vancomycin?

A

Red-mans disease and only effective on most gram+; therefore mianly utilized for Beta-lactam rsistant infection

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33
Q

What is the mechanism of resitance of bacteria to glycopeptides?

A

Altered peptidoglycan structure, utilize D-ala-D-lac instead of D-ala-D-ala preventing vancomycin binding; most common in enterococci

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34
Q

How do cycloserines inhibit bacterial growth?

A

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

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35
Q

What is teh mechanism of bacitracin?

A

Peptide antibiotic-too toxic for systemic use. BInds to pyrophosphate on lipid carrier for peptidoglycan precursosrs

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36
Q

What is the mechanism of action of Daptomycin?

A

Lipopeptide antibiotic; Gram+ bacteria

Binds and disrupt of cytoplasmic membrane possibly via loss of potential

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37
Q

What is the mechanism of polymyxins?

A

polymyxin B, colistin–lipopeptide (gram -)

Binds to LPS in outer membrane leading to disruption of membranes

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38
Q

What is the mechansim of Tetracyclines?

A

Bacteriostatic broad spectrum

binds to 30S ribosomal subunit

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39
Q

What is the major forms of resistance to tetracycline?

A

Ttetracycline efflux pump(most common)

mutations on the ribosome

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40
Q

What is the mechansim of action of aminoglycosides?

A

binds irreversibly to 30s robosomal subunit. Don’t penetrate gram+ well, nephrotoxic and ototoxic adverse effects

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41
Q

How does aminoglycoside resistant bacteria mechanism go?

A

enzymatic modification of antibioitic to prevent binding

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42
Q

What is teh mechanism of action of macrolides?

A

binds 50S ribosomal subunit to block elongation

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43
Q

What is the mechanism of resistance to macrolides?

A

methylation of ribosomal RNA to prevent binding

efflux pump can expel macrolides

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44
Q

What is the mechanism of action of chloramphenicol?

A

binds 50S ribosome

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45
Q

What is the mechansim of resistance to chloramphenicol?

A

catalyzes additiono f acetyl group to drug

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46
Q

What is the mechanism of action of clindamycin?

A

used to tx MRSA and Staph aureus; binds 50S subunit

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47
Q

What is the mechanism of resistance to clindamycin?

A

methylation of rRNA, cross-resistance with macrolides

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48
Q

What is the mechanism of linezolid?

A

new class; gram+; oxazolidinone class. BInds unique site on 50S subunit

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49
Q

What is the mechanism of antibiotic resistance to linezolid?

A

point mutation on ribosomal components

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50
Q

What is the mechanism of action of Nalidixic acid and 2nd generation fluoroquinolones?

A

synthetic quinolone, binds DNA gyrase or topoisomerase to inhibit DNA. Narrow spectrum

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51
Q

What is the mechanism of resistance to quinolones?

A

point mutation in DNA gyrase, efflux pumps

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52
Q

What genes are involved in mobile genetic elements-linear DNA segment.

A

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

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53
Q

Phase variation in E. Coli is responsible for what?

A

Wheter or not fimbriae is produced by promoter element in insertion element. Fimbriae promote attachment to urinary epithelaial surface

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54
Q

What are genomic pathogenicty islands?

A

G+C content different, aencode a pathogenic virulence factor

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55
Q

What are two virulence determinance that are carreid on bacteriophage?

A

cholera toxin and shiga toxin

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56
Q

Cholera toxin phage infects what type of bacteria?

A

Filamentous bacteriophage that infects vibrio cholera
dual function for choleratoxin element, phage morphogensis and enterotoxin
c

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57
Q

How does cholera toxin work?

A

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

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58
Q

Shiga toxin phage infects what?

A

both shigella dysenteriae and EHEC strain of ecoli

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59
Q

Shiga toxin induces what?

A

severe diarrhea, hemorrhagic colitis and hemolytic-uremic syndrome

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60
Q

What is the mechanism of shiga toxin acitivity?

A

A 5B toxin; B subunit binds Gb3 glycolipid
a subunit is translocated in cytosol and modifies ribisome acceptor site
blocks protein syntehsis

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61
Q

What are the strategies used by extracellular pathogens to resist getting killed?

A

avoid recognition by phagocytes
inhibit phagocyte engulfment
kill or damage phagocytes

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62
Q

What are strategies used by intracellular pathogens to resist killing?

A

inhibit phagosome-lysosome fusion
survivie inside phagolysosome
escape from phagosome

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63
Q

How does bacterial uptake occur?

A

Recognition between ligan and receptor initiates transmembrane activation cascade. Surface structure remodeled by depolymerizing and re-polymerizing acting and other cytoskeletal components

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64
Q

What cytoskeletal component allow for maturation of phagosome from periphery to perinuclear region?

A

microtubules

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65
Q

What bacteria surive and replicate in phagolysosome?

A

Coxiella

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66
Q

What bacteria escape the phagosome and replicate in cytosol?

A

Rickettsia, shigella, escherichia coli, listeria

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67
Q

What bacteria modulate endocytic pathway?

A

Mycobaccterium and salmonella

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68
Q

What bacteria cause an alternative trafficking pathway?

A

Legionella, brucella, chlamydia

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69
Q

What are the side effect and consequences of bacteria ingestion by macrophages?

A

Tissue injury, ROI, RNI and hydrolytic enzymes, TNFalpha, and iL1 lead to fever, persisten infection adn chronic inflammation, phagocytes contribute to autoimmune,

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70
Q

What is the class of bacteria not associated with disease?

A

saprophytes

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71
Q

What are the four classes of bacterial toxins?

A

surface-acting toxin
pore-forming toxins
A/B toxins
Type 3 and 4 secretion

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72
Q

What modifications do diptheria toxin and pseudomonas aeruginosa exotoxin A?

A

ADP-ribosylate EF2: inhibits protein syntehsis

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73
Q

What modification does botulinum toxin and tetanus toxin?

A

protease for SNARE proteins

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74
Q

What large clostridium difficile toxins do to cells?

A

Glucosylate Rho proteins

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75
Q

What does Shiga toxin do to cells?

A

deadenylate adenine on RNA

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76
Q

What is bacteriodes fragilis?

A

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

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77
Q

What type of bacteria are clostridia?

A

anaerobic gram +, spore forming bacilli; obligate anaerobes or aerotolerant
pathogenisis due to exotoxin

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78
Q

Antibiotic-associated diarrhea; leads to what diarrhea?

A

C. difficile

Pathology from Toxin A and Toxin B glucosylate Rho GTPases which cause actin depolymerization

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79
Q

What is the treatment used to focus c. difficile?

A

Metronidazole, vancomycin, or a subset of fluoroquinolones

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80
Q

What does histotoxic clostridia does what?

A

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)

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81
Q

What is the the pathogenicity of clostridium botulinum?

A

botulinum toxin: AB toxin, zinc protease, heat labile, inhibits nerotransmitter release

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82
Q

What are the applcations of botulinum therapy?

A

blepharospasm abnormal contraction or twitch of eyelid neurons: cleaves SNARE proteins in spastic nerves relieving spasticity
have a long half life in neurons

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83
Q

Describe neisseria meningitidis, physiology and structure?

A 
gram - diplococci
Lipooligosaccharide
posses pili
Porins A and B
Utilize host tranferrin
LOS induces the majority of the vascular and other damage
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84
Q

Most epidemics of N. meningitidis epidemics are associated with what?

A

serotype A

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85
Q

What labatory diagnosis are done to identify N. meningitidis?

A

oxidase positive, gram negative dplococci
blood culture
biochemical tests

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86
Q

What tx is doen for N. meningitidis?

A 
vaccination
antibiotics
-cefotaxime
-ceftriaxone
-penicillin G
prophylaxis
-rifampin
-ciprofloxacin
-ceftriaxone
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87
Q

Describe the key characterisitcs of neisseria gonorrhea?

A 
gram - diplococci, oxidase positivie
requires complex growth medium
sensitive to cold
doesn't posess a polysaccharide capsule
posses pili
88
Q

What are the neisseria gonococcal antigens?

A

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
Q

What are teh laboratory diagnosis of neisseria gonococcal?

A

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
Q

What is the tx for neisseria gonorrhea?

A

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
Q

What are the characteristics of chlamydia and chlamydophila?

A

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
Q

What protein is the major pathogenisis factor associated with staph. aureus?

A

Coagulase-contributes to the clotting of plasma

93
Q

What is the way that gram + cocci are differentiated when grown?

A

Staph produce catalse and strep do not

94
Q

What is protein A?

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
Q

What are the toxins produced by S. aureus?

A

hemolysins
leukotoxins
Enterotoxins (TSST)
Exfoliative toxins

96
Q

What do hemolysisn do?

A

Contribute to pathogenicity by producing tissue damage after the establishment of a focus of infection

97
Q

What do leukotoxins do?

A

Two protein toxin, attacks PMN leukocytes nad macrophages

98
Q

What do enterotoxins do?

A

Act as a superantigen

99
Q

What is an exfoliative toxin?

A

2 forms ETA/ETB-proteases, scalded skin syndrome stimulate lysis of intercellular attatchment btw cells of epidermis?

100
Q

Staph epidermidis is what?

A

Non-coagulase staph, low virulence. Hospital acquired. Tx needs antibiogram to determine local antibiotic sensitivity

101
Q

S. saprophyticus does what?

A

UTI selectively binds to cells of urinary tract

doesn’t posess any virulence factors; based solely on tropism

102
Q

What are the three hemolytic patterns?

A

Alpha-partial or greening
Beta or complete clearing
Gamma no change in RBC

103
Q

How to streptococcus pyogenes avoid opsonization and phagocytosis?

A

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
Q

How does Strep pyogenes adhere to host cells?

A

lipoteichoic acid, M proteins, F protein-mediate attachment

105
Q

How does S. pyogenes invade host cells?

A

M and F proteins

106
Q

Streptococcus pyogenes patients that are provided with what antibodies are protected?

A

Antibodies to M proteins

107
Q

What are hte differences between Strep pyogenes and Stre pneumoniae?

A

Pyogenes:
bacitracin sensitive, beta hemolytic, M proteins, hyaluronic acid capsules, Spe toxins, enzymes

Pneumoniae:
alpha hemolytic
optochin sensitive
resistance to phagocytoisis

108
Q

Listeriosis monocytogenes causes human disease in what well-defined patients?

A

neonates, elderly, pregnant women, persons with defects in cell immunity

109
Q

How do listeria adhere to host cells?

A

InlA, internalin;

entry into enteerocytes or M cells

110
Q

What is the role of ActA in listeria?

A

located on pole of bacteria, polymerizes host actin adn allows projection into neighboring cell

111
Q

How is listeria diagnosed?

A

1-2 days culture in cold enrichment
Gram stain of CSF for meningitis patients
gentamicin with penicillin or ampicillin treat it

112
Q

Salmonella is part of what family>

A

enterobacteriaceae

113
Q

What are the main antigens presented on the surface of Salmonella?

A

H antigen=flagellar protein
K or Vi=capsular antigens for E. coli and S. typhi
O antigens=lipopolysaccaride
Don’t ferment lactose

114
Q

What are the two types of salmonella exclusive to humans?

A

Typhi and paratyphi

115
Q

Where do salmonella invade the small intestine?

A

microfold cells and enteroctyes in peyer patches

116
Q

What does salmonella do in the cell?

A

Injects vaculoues with type 3 injection, and makes it a spacious vacuole to prevent destruction.

117
Q

What are the symptoms of salmonella?

A

fever, abdominal cramps, myalgia, headache, nauesa, vomitting and non-bloody diarrhea
usually self limiiting

118
Q

Is there a vaccine for salmonella?

A

Live attenuated vaccine Ty21a and another one.

119
Q

What is unique about shigella as a enterobacteriaceae?

A

One of hte few wihtout flagella and therefore non-motile

120
Q

Shigella invade what type of cells?

A

invade M cells in Peyer patches

inject type 3 effectors to cause cytoskeleton to engulf them

121
Q

What are the symptoms of shigella?

A

dysentery, abdominal cramps, diarrhea, tenesmus, neutrophils in stool

122
Q

Only treat shigella if what occurs?

A

Enteric fever, and it’s systemic otherwise leave it and let diarrhea occur

123
Q

What protein do EHEC inject to integrate into mammalian cellular membrane?

A

Tir–> allowing it to sit in place and repliciate and release shigella toxin

124
Q

What is EHEC associated with in serotypes and why?

A

O157:H7 and associated with those that are selected for in intestinal tract of cattle.

125
Q

EHEC has what type of symptoms?

A

bloody diarrhea, vomiting, no fever and may result in hemolytic uremic syndrome, resulting in kidney failure in 5-10% of children

126
Q

How should you treat EHEC?

A

Monitor for complications and provide supportive care. Don’t give antibiotics will cause expression of more Shiga toxin.

127
Q

Campylobacter is what type of structure?

A

Gram negative curved rod; spiral or comma shaped. grows at 42 degrees. microaerophilic, motile

128
Q

Campylobacter si assoicated with what other illnesses?

A

autoimmune disorders such as Guillain Barre syndrome and reactive arthritis.

129
Q

What si treatment of campylobacter?

A

Only treat sever cases with antibiotics otherwise treat with fluid replacement.

130
Q

What is heliobacter colonization occuring?

A

lifelong possible: Urease expression allows bacteria to survive in gastric juices. adhere to to gastric epithelium through mucosal

131
Q

Heliobacter related peptic ulcers are associated with what?

A

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
Q

What is the resevoir for heliobacter?

A

only humans and asymptomatic in 70-80% of infected individuals

133
Q

What is the laboratory diagnosis?

A

urea breath test, feed radioactive urea which leads to radioactive CO2 in breath

134
Q

What is the treatment for heliobacter?

A

debatable protects against GERD and adenocarcinoma of esophagaus
PPI+macrolide+B-lactam

135
Q

Vibrio requires waht for growth?

A

NaCl, oxidase positive, toxin co-regulated pili

136
Q

What serotypes of vibrio are assoicated with epidemic disease?

A

O1 and O139

137
Q

Cholera toxin is associated with what?

A

all pahtology of vibrio cholear
A:5B protein encoded by bacteriophage CTX
leads to water efflux=osmotic diarrhea

138
Q

What is the role of pili in vibrio cholera?

A

coregulated pilus that adhere to mucosal epithelium; makes other toxins other than choleera toxin

139
Q

HOw is vibrio cholear diagnosed?

A

culture or microscopy in stool

140
Q

What are the general characteristics of mycobacterium?

A

lipid-rich cell wall; resistant to disinfectants and common stains
ID by acid-fast
fastiduous and slow growing

141
Q

What is the unusual cellw all of M. tuberculosis made of?

A

complex lipids, trehalose dimycolate(cord factor involved in production of caseating granulomas)

142
Q

What is the difference between latent and active infections of M. tuberculosis?

A

bacteria stop multiplying and the lesion calcifies in latency
bcteria rapidly multipy and lesion liquifies then bacteria disseminate in active disease

143
Q

What is the reactivation rate of TB?

A

5% in first two years, 10% lifetime if remain healthy

immunocompromised individuals have a 10% annual reactivation rate

144
Q

What are the characteristics of active TB?

A

infectious, organism in sputum, dense lesions in lung readibly detectable by Xray, malaise, weight loss, productive cough, night sweats, may disseminate

145
Q

What are the dense lesions found on xray called in TB?

A

Ghon complexes

146
Q

What are characteristic of Laten TB?

A

host not infectious, no xray signs, granulomas generated which are areas of active immune cells

147
Q

What are the characteristics of reactivation of TB?

A

rapid multiplication after immune suppresion, infectious, usually occur after suppression in TNFalpha, IFNgama or iNOS

148
Q

Difference between active and latent as far as symptoms?

A

Active: infectious, feel sick positive PPD skin test, abnormal chest xray.
Latent: non-infectious, Positive PPD, chest x raya nd sputum test normal

149
Q

How do you identify TB infection?

A 
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
Q

What is a PPD and what is a postiive?

A

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
Q

Why is gram stain innefective?

A

hydrophobic cell envelope so not truly gram +

152
Q

Recommended tx of TB?

A

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
Q

MDR TB is what?

A

displays resistance to isoniazid and rifampicin, requires 2 years of antibiotics

154
Q

XDR TB is what?

A

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
Q

What is DOTS?

A

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
Q

HOw is leprosy usually transmitted?

A

perosn to perosn following inhalation or direct contact with respiratory secretions
obligate parasite and can’t be grown on medium

157
Q

What are the two clinical manfiestations of leprosy?

A

tuberculoidal and lepromatous

158
Q

What is tuberculoidal leprosy?

A

strong-cell mediated immune response; few bacilli present in tissue and results in few plaques but extesnive peripheral nerve damage not very infectious

159
Q

What is lepromatous leprosy?

A

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
Q

What is the physiology of legionella?

A

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
Q

What group of legionella is major cause of disease?

A

L. pneumophila serogroup I

162
Q

How is legionella acquired?

A

inhalation of droplet carrying organism usually by air conditioning aspiration; no person-to-person transmission. Individuals immunocompromised most at risk

163
Q

What is the host resevoir of legionella?

A

amoeba within water supplies and survives within macrophges in humans.

164
Q

What is the virulence factors associated wtih legionella?

A

cytotoxins, hemolysins, proteases, endotoxina dn lipases; tpe 4 secretion system to alter endocytic trafficking in cell to prevent phagosome-lysosme fusion

165
Q

How is legionella identified?

A

microscopy; using diffrential fluorescent antibody. ID by culture but difficult. ELISA for antigens but only for one serotype

166
Q

What is the physiology of P. auerginosa?

A

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
Q

P aeruginosa are associated with what type of infections?

A

nosocomial due to abiltty to colonize and form microcolonies.
often cause disease in burn and puncture victims

168
Q

What is a common cause of death in CF patients?

A

p. aeruginosa, becuase of their mucoid phenotypes make them difficult to eliminate

169
Q

What are common virulence factors of psuedomonas?

A

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
Q

What two pigments are virulence factors in psuedomonas aeruginosa?

A

pyocyanine and pyochelin

171
Q

What are some of the bacterial virulence factors that are required to cause mutlisystem infections?

A

antigenic variation, serum resistance, cloaking, cell invasiona nd tissue invasion

172
Q

What bacteria employ antigenic variation for immune evasion?

A

borrelia, treponema pallidum

173
Q

What bacteria have few surface proteins to avoid the immune system?

A

treponema pallidum

174
Q

What bacteria inactivate complement?

A

borrelia, leptospira through Factor H

175
Q

What bacteria preven phagocytosis?

A

bacillus anthracis and yersinia pestis

176
Q

What bacteria invade cells?

A

chlamydia, rickettsia, Ehrlichia, ANaplasma

177
Q

What bacteria are tissue invasive to avoid immune system?

A

borrelia, treponema pallidum, leptospira

178
Q

What bacteria bind fibronectin and other plasma proteins to cloak themselves from teh immune system?

A

borrelia and leptospira

179
Q

What bacteria replicate in late endosome and autophagosomes of neutrophils?

A

anaplasma phagocytophilum

180
Q

What bacteria bind to enter and replicate in early endosome of monocytic cells?

A

Ehrlichia chaffeensis

181
Q

What bacter bind to enter and replicate in cytoplasm of endothelial cells?

A

Rickettsia

182
Q

What bacteria sequester and activate host plasminogen and metalloproteinases to invade tissue?

A

borrelia, leptospira

183
Q

What bacteria utilize endogenous proteases to invade tissue?

A

Treonema pallidum

184
Q

What bacteria penetrate between cells?

A

borrelia and leptospira

185
Q

What mutlisystem bacterial infection in US is Vector-borne?

A

anaplasmosis
Ehrlichiosis
Rocky Mountain SPotted Fever
Lyme

186
Q

What multisystem is not vector borne?

A

syphilis

187
Q

What is vector competence?

A

Ability of a vector to transmit the pathogen

188
Q

What is biological tranmission?

A

when a pathogen has a specific life stage in a vector; colonizes a specific site and alters its gene expression

189
Q

What is transstadial transmission?

A

When a pathogen is transmitted or maintained in different life stages of the same inidvidual vector (lyme disease, anaplasmosis, ehrlichiosis)

190
Q

What is tranovarial transmission?

A

Whena pathogen is transmitted from one vector generation to the next; Rocky mountain spotted fever Rickettsiosis

191
Q

What is Anaplasmosis/Ehrlichiosis?

A

tick-borne, gram-negative intracellular bacilli

192
Q

What are the vectors for anaplasmosis and lyme disease?

A

ixodes scapularis, I. pacificus

193
Q

What vector transmits Ehrlichiosis?

A

A. americanum, I . Scapularis

194
Q

What vector transmits rocky mountain spotted fever?

A

D. variabilis, D andersoni, Rhipicephalus sangunineus

195
Q

What is human granulocytic anaplasmosis?

A

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
Q

Life cycles of Anaplasma and Ehrlichia

A

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
Q

How do you diagnose anaplasmosis and ehrlichiosis?

A

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
Q

What anaplasmosis and ehrlichiosis therapy exists?

A

oral doxycycline (also treats lyme disease)

199
Q

Rickettsia rickettsii physiology is what?

A

Tiny Gram negative coccobacilli; obligate intracellular replicates in cytoplasm may invade nucleus. Does have LPS and peptidoglycan has type 4 secretion

200
Q

What are the CLINICAL symptoms of rocky mountain spotted fever?

A

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
Q

What does the CDC say about the diagnosis of Rocky mountain spotted fever?

A

there is no test available at this time that can provide a conclusive result in time to make important decisions about treatment

202
Q

What is the treatment for Rocky mountain spotted fever?

A

oral doxcycline even if under 8 or pregnant, at least 3 days past defervescence or chloramphenicol if allergy to tetracyclines

203
Q

What are the characteristics of borrelia burgdorferi?

A

gram negative, spirochete, extracellular no LPS, toxins special secretion system. Requires greater than 36 hours for transmission. Considerable antigenic variation and complement invasion

204
Q

What are the early symptoms of lyme disease localized to bite site?

A

erythema migrans greater than 5 cm, and regional lymphadenopathy

205
Q

What are the early disseminated clinical signs of lyme disease?

A

fever, malaise, secondary EM, arthalgia, myalgia, polyradiculopathy, facial pasly, pancarditis, AV node blcok

206
Q

What are the late signs of lyme disease?

A

Arthritis, encephalopathy, polyradiculopathy

207
Q

Lyme disease diagnosis>

A

clear lesion, and likely tick encounter sufficient to start therapy otherwise ELISA then immunoblot to start

208
Q

IgM and IgG serology can be used to diagnose lyme disease?

A

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
Q

how do you treat lyme disease?

A

oral doxycycline for early; amoxicillin for those pregnant or under 8
If CNS involvement utilize IV ceftriaxone. Avoid anti-inflammatory therapy

210
Q

What species of syphilis is the most invasive?

A

treponema pallidum pallidum– syphillis, world-wide STD

211
Q

What are the symptoms of syphillis primary?

A

10-90 days after encounter
painless lesion(chancre) at site of inoculation
highly infectious
regional lymphadenopathy

212
Q

What is seondary syphillis clinic?

A

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
Q

What is tertiary syphillis?

A

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
Q

What is the diagnosis for syphillis?

A

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
Q

What is the therapy fo rsyphillis?

A

long acting penicilin for primary and secondary, IV for tertiary

Block 6 (3 decks)

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