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Microbial Pathogenesis > Lecture 5 Pathogenesis, Role, Diagnosis, Drugs (E1) > Flashcards

Lecture 5 Pathogenesis, Role, Diagnosis, Drugs (E1) Flashcards

Ch 14, 15, 16, 17

1
Q

Bacterial Virulence

A

Causes disease:
Attachment
Toxins
Immune escape

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2
Q

Pathogenicity Islands

A

group of genes typically with coordinated expression that leads to disease (strains of bacteria)

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3
Q

Disease

A

Combination of bacterial virulence and host response

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4
Q

Innoculum

A

required number of bacteria to establish infection

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5
Q

Normal Flora

A

in the right place, no problem
wrong place, opportunistic

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6
Q

Microbial acquisition

A

Getting the “normal flora”
Birth canal
Food (breast, bottle)
Breathing
Natural succession
-Lactobacilli (mouth, intestines, vagina during reproductive years)
-Coliforms (mouth, intestines)
-Anaerobes (intestines)

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7
Q

Microbial impact

A

Normal flora
Biological success (their “perspective”)
Microbial antagonism (“good” bacteria compete for space and resources on the host)
Can improve host nutrition (e.g Vit-K, short chain-Fatty Acids)- Metabolism of good bacteria
Immune stimulation/regulation
Also have potential negative impacts (opportunistic infection, immune dysregulation)

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8
Q

Sterile Sites

A

heart, liver, Kidneys, Bladder, Brain, Spinal Cord, Bones, Ovaries, Testes, Sinuses (upper), Ear (Middle, inner)
Eye (Internal), Muscles, Glands (internal)

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9
Q

Opportunistic infection

A

Normal flora in the wrong place

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10
Q

Susceptibility

A

Weaken Host defenses
Old age and extreme youth
Genetic defects in immunity, and acquired defects in immunity (AIDS)
Surgery and organ transplants
Underlying disease: cancer, liver malfunction, diabetes
Chemotherapy/ immunosuppressive drugs
Physical and mental stress

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11
Q

Portals of Entry

A

Typically where something is non-moving
Skin
Gastrointestinal tract
Respiratory Tract
Urogential Tract

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12
Q

Attachment to the host

A

Fimbriae
Capsules
Receptors
Hook or by crook

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13
Q

Surviving the Host

A

Anti-Phagocytic factors
Capsules
Leukocidins
Virulence Factors (Toxins/Exozymes)

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14
Q

Disease (causing damage to host)

A

Virulence factors (Toxins/Exozymes)
Inflammation by the host

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15
Q

Portals of Exit

A

Same as portals of entry

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16
Q

Biofilms

A

Community of bacteria
Quorum sensing- What makes bacteria difficult
Dental plague
Protection from immune system, antibiotics-have trouble getting through

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17
Q

Bacterial Adhesions

A

Bacterial structures used to attach to host cell
Fimbriae (pili)- typically the tips have an adhesion molecule (sugar molecules on the end, bind to lectins)- host cell specificity
Blood group antigens
Some adhesins bind to cell oligosaccharide receptors
Some adhesins bind to cell proteins

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18
Q

Host receptors

A

Fibrinogen
Extracellular matrix components
d-Mannose
etc

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19
Q

Invasion

A

Active avoidance (our immune system) or destruction of barriers (physical, chemical, immune)
Most bacteria cannot penetrate intact skin, however, most skin has micro-abrasions so can be breached
Induce inflammation- host response, breaks its own barriers
Block phagocytosis (even though this is our go to)- Streptococci, Staphylococci
Encourage Phagocytosis- Salmonella, Yersinia (Engulfed, to avoid our immune system, able to survive)

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20
Q

Secretory Systems

A

Sec
Tat
Type I-VII
Function- getting into your cells

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21
Q

Exoenzyme

A

Proteases, Lipases, Glycosylases (secreted outside)

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22
Q

Exotoxin

A

Toxins that knock out a host enzyme
Secreted enzymes or proteins that alter function/kill a host cell (usually knockout key enzymes)
Ex: Tetanus, Clostridium, Diptheriae, Cholera

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23
Q

Type A-B Toxin

A

Heterodimeric Toxins
A- Action component
B- Receptor binding

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24
Q

Superantigen

A

T-cell activation (cytokine storms)
release of large quantities of IL-1, IL-2, IL-6, INF-y, TNF-a, Chemokines (release systemically)
Cause life threatening fever, shock, rash, autoimmunity
Staphylococcus toxic shock syndrome

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25
Q

Diptheria toxin (A-B)

A

Target Cell Receptor- Growth factor receptor precursor
Biological Effects- Inhibition of protein synthesis, cell death

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26
Q

Anthrax toxin (A-B)

A

Target Cell Receptor- Tumor endothelial marker-8 (TEM-8); capillary morphogenesis protein 2 (CMG2)
Biological Effects- EF + PA: increase in target cell cAMP level, localized edema; LF+PA: death of target cells and experimental animals

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27
Q

Tetanus toxin (A-B)

A

Target Cell Receptor- Polysialoganglio sides plus 15-kDa glycoprotein (co-receptors)
Biological Effects- Decrease in neurotransmitter release from inhibitory neurons, spastic paralysis

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28
Q

Botulism Toxin (A-B)

A

Target Cell Receptor- Polysialogangliosides plus synaptotagmin (co-receptors)
Biological Effects- Decrease in peripheral presynaptic acetycholine release, flaccid paralysis

29
Q

Cholera Toxin (A-B)

A

Target Cell Receptor- Ganglioside (GM)
Biological Effects- Activation of adenylate cyclase, increase in cAMP level, secretory diarrhea

30
Q

Lipid A Toxicity (acute response-binding events)

A

Lipopolysaccharides in Gram Negative, Induces strong acute-phase response
1. Acute phase response- fever, leukocytosis/leukopenia, disseminated (all around body) intravascular coagulation (DIC), hypotension, Shock and death
2. FDA limit
3. Binding events: Lipid binding protein (LBP, serum) Transfers to CD14 (CR, cell membrane)- MD2 associated with TLR4 which then sends signal to interior cell (acute response
Triggered Event(direct or indirect):
Production of cytokines
LPS activates macrophages to enhanced phagocytosis and cytotoxicity
Activation of the complement cascade(C3a, C5a)
Histamine, neutrophil chemotaxis (pus)
Activation of the coagulation cascade (Factor XII)

31
Q

Granuloma

A

Mycobacteria

32
Q

Autoimmunity

A

Strptococci pyogenes, anti-M-protein (during inflammation B-cells attack, but we have similar heart protein so we attack ourselfs)

33
Q

Immune Complex

A

Chlamydia, Treponema, Borrelia, Streptococci

34
Q

DIC

A

DIC thrombosis- Disseminated Intravascular coagulation (DIS)

35
Q

Antibiotics

A

Range of activity of an antimicrobial against bacteria. A broad-spectrum antibacterial drug can inhibit a variety of gram(+) and gram(-) bacteria, whereas a narrow-spectrum drug is active against a limited variety of bacteria

36
Q

Penicillins

A

Discovered by Fleming
Block cross-linking of peptidoglycan (Transpeptidase)
All have Beta-lactam ring
Different spectra of action
Resistance due to bacterial Penicillinases; (beta-lactamases)

37
Q

Macrolides

A

are a class of drugs used to manage and treat various bacterial infections. Azithromycin, clarithromycin, and erythromycin are commonly used to treat infections like pneumonia, sinusitis, pharyngitis, and tonsillitis

38
Q

Aminoglycosides

A

Binds 30S subunit of ribosome (irreversible?)
Distorts the ribosome
Errors translation
Derived from Streptomycin and Micromonospora
Neomycin (Neosporin Ointment)
Relatively broad spectrum because they inhibit protein synthesis(good, still has toxicity problems)

39
Q

Cephalosporins

A

Different ring structure and R groups than Penicillins
Derived from Fungus Acremonium
Block cross-linking of peptidoglycan
All have beta-lactam ring (less susceptible to penicillinases)
Different spectra of action (generations)
Helps against G(-) outer membrane
Broad-spectrum
Cause fewer allergic reactions (penicillinases (hapten))

40
Q

Tetracyclines

A

Binds 30S ribosome subunit
Inhibit Protein Synthesis
Blocks the A site on the ribosome (where the tRNA comes in)
Prevents tRNA entry
Reversible reaction
Bacteriostatic
Broad spectrum

41
Q

Target Proteins

A

Goal of antimicrobial drugs
-Disrupt the cell processes or structure of bacteria, fungi, and protozoa
-or Inhibit virus replication
Most interfere with the function of enzymes required to synthesize or assemble macromolecules or destroy structures already formed
Drugs should be Selectively Toxic- They kill or inhibit microbial cells without damaging host tissues (macromolecules, proteins, nucleic acid)

42
Q

Combination Therapy

A

Combinations of antibiotics that may be used to (1) broaden the antibacterial spectrum for empirical therapy or the treatment of polymicrobial infections, (2) prevent the emergence of resistant organisms during therapy, and (3) achieve a synergistic killing effect

43
Q

Antibiotic synergism

A

Combinations of two antibiotics that have enhanced bactericidal activity when tested together compared with the activity of each antibiotic alone

44
Q

Antibiotic antagonism

A

Combination of antibiotics in which the activity of one antibiotic interferes with the activity of the other (e.g. the sum of the activity is less than the activity of the most active individual drug)

45
Q

Bacteriostatic

A

Antibiotic that inhibits the growth of bacteria but does not kill

46
Q

Bactericidal antibiotic

A

Antibiotic that kills bacteria

47
Q

Minimum inhibitory concentration(MIC)

A

Determined by exposing a standardized suspension of bacteria to a series of antimicrobial dilutions. The lowest antibiotic concentration that inhibits the growth of the bacteria is the MIC- what we need to achieve

48
Q

Minimum bactericidal concentration (MBC)

A

Determined by exposing a standardized suspension of bacteria to a series of antimicrobial dilutions. The lowest antibiotic concentration that kills 99.9% of the population is referred to as the MBC

49
Q

Beta-Lactamase

A

An enzyme that hydrolyzes the beta-lactam ring in the beta-lactam class of antibiotics, thus inactivating the antibiotic. The enzymes specific for penicillins, cephalosporins, and carbapenems are the penicillinases, cephalosporinases and carbapenemases, respectively
Degrades penicillin

50
Q

Targets of Antimicrobials

A

Cell wall inhibitors- Block synthesis and repair of peptidoglycan
Cell Membrane- Cause loss of selective permeability (Polymyxins, Daptomycin)
DNA/RNA- Inhibit replication and transcription; Inhibit gyrase (unwinding enzyme) (Quinolones, Inhibit RNA polymerase, Rifampin)-Very few drugs
Protein synthesis inhibitors acting on ribosomes (site of action 50s, 30s and both)
Folic acid synthesis- Block pathways and inhibit metabolism (Sulfa drugs)

51
Q

Plasmid mediate resistance and mutations

A

Ways microbes have built drug resistance
Plasmid- Acquisition of entire new genes or sets of genes via transfer from another species (plasmids, called resistance (R) factors)
Spontaneous mutations in critical chromosomal genes

52
Q

Porins (Gram (-))

A

Porins allow for the passive diffusion of water, ions, and other small molecules. They also help maintain osmolarity, transport nutrients and salts, and contribute to virulencePorin expression is regulated by several mechanisms, including β-barrel assembly machinery and lipopolysaccharide binding.

Antibiotic resistance
Adaptations that reduce the influx of compounds through porins can contribute to the emergence of antibiotic resistance

53
Q

B-Lactam Ring

A

Crucially part of penicillin, screws up cross-linking in the cell wall

54
Q

Efflux pumps

A

are transport proteins involved in the extrusion of toxic substrates (including virtually all classes of clinically relevant antibiotics) from within cells into the external environment. These proteins are found in both Gram-positive and -negative bacteria as well as in eukaryotic organisms.

55
Q

Cephalosporin generations

A

1st Generation more gram positive
2nd
3rd
4th
5th Generation more gram negative

56
Q

Carbapenems

A

An enzyme specific the penicillinases

57
Q

Vancomycin

A

Inhibits cross-linkage of peptidoglycan layers

58
Q

MRSA

A

Methicillin-resistant Staphylococcus aureus (MRSA) infection is caused by a type of staph bacteria that’s become resistant to many of the antibiotics used to treat ordinary staph infections

59
Q

CA-MRSA

A

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is a type of MRSA infection that can affect anyone, but some people are at higher riskMRSA infections in healthy people who have not been hospitalized or had a medical procedure (such as dialysis or surgery) within the past year

60
Q

Rifampin

A

Inhibition of Nucleic Acid Synthesis
-Prevent transcription by binding DNA-Dependent RNA polymerase
This is a difficult target because the process is well conserved (similar process and enzymes for most life forms)
Specific for bacteria- favorable therapeutic index
Prevents elongation of transcript after initiation
Useful drug for tuberculosis
Resistance can develop quickly

61
Q

Amphotericin-B

A

an antifungal used to treat fungal infections in neutropenic patients, cryptococcal meningitis in HIV infection, fungal infections, and leishmaniasis
binds sterols in cell membranes with a higher affinity toward ergosterol than mammalian cholesterol. As the concentration of the drug increases in organs such as the kidney, it begins to bind cholesterol in mammalian membranes, leading to nephrotoxicity

62
Q

Flucytosine

A

may cause decreased kidney function and liver problems. In addition, this medication may decrease bone marrow function. This serious, possibly life-threatening side effect may lead to a low number of blood cells such as red cells,
white cells, and platelets.
-used in combination with other medicine (eg, amphotericin B) to treat serious fungus infections, including Candida infections (eg, septicemia, endocarditis, urinary tract infections) or Cryptococcus infections (eg, meningitis, lung infections)
enters the fungal cell via cytosine permease; thus, flucytosine is metabolized to 5-fluorouracil within fungal organisms. The 5-fluorouracil is extensively incorporated into fungal RNA and inhibits synthesis of both DNA and RNA

63
Q

Tetracycline

A

Inhibition of Protein synthesis-
Prevent polypeptide elongation at 30S ribosome
Blocks the A site on ribosome (where tRNA comes in)
Prevents tRNA entry
REVERSIBLE reaction
Bacteriostatic
Broad spectrum

64
Q

Erythromycin

A

(Some people took for allergies/no tired)
Large lactone ring with sugars attached
relatively broad-spectrum
Fairly low toxicity (heart arrythmyia with Seldane)
Blocks protein synthesis by attaching to the 50S ribosome subunit
Mycoplasma pneumonia, legionellosis, Chlamydia infections, pertussis, diphtheria

65
Q

Tuberculosis Therapy

A

Using Rifampin, Binds to bacterial RNA polymerase
mRNA sythesis

66
Q

Isoniazid

A

Disruption of cell wall-
Inhibits mycolic acid synthesis

67
Q

Sulfamethoxazole

A

Often given with Trimethoprim, One of the primary treatments for Pneumocystis (carinii) Jiroveci pneumonia (PCP) in AIDS patients

68
Q

Trimethoprim

A

Antimetabiolite-
Inhibits dihydrofolate reductase and disrupts folic acid synthesis
Sulfa drug
THF is an important co-enzyme (we need but get in food, bacteria synthesize)- folic acid

69
Q

Fluoroquinolones

A

DNA Replication-
Few clinical drugs affect polymerization
Mechanisms are conserved: lead to toxicity
DNA gyrase inhibitors (DNA unwinders)

Microbial Pathogenesis (11 decks)

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