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MOD1 > Infectious Disease > Flashcards

Infectious Disease Flashcards

1
Q

Shapes of Bacteria: rods

A

Bacillus
Salmonella tiphimurium
Bacillus anthracis

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2
Q

Shapes of bacteria: spheres

A

Coccus (sphere)
Ex: Streptococcus pneumoniae

Coccobacillus (between rod/sphere)
Ex: Yersinia pestis

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3
Q

Shapes of bacteria: others

A

Spirillum (rigid spirals)

Spirochete (undulating spirals)

Vibrio (comma shape)
Vibrio cholerae

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4
Q

Bacterial arrangements: cocci

A

Single

Diplococcus (pair)
Ex. Streptococcus pneumoniae, neisseria meningitidis

Streptococcus (chain)
Ex. Streptococcus pneumoniaeNeisseria meningitidis

Tetrad
Ex. Micrococcus luteus

Staphylococcus
Ex. Staphylococcus aureus

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5
Q

Bacterial staining

A

Gram-positive: stain blue

Gram-negative: stain red

Specialized stains:
Most useful is acid-fast stain

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6
Q

Bacterial Reproduction

A

Reproduce by binary fission

One circular chromosome per cell which doubles and the bacteria then splits to produce 2 bacteria

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7
Q

Bacteria: nucleoid

A

DNA has a large amount of DNA that must be packed into the bacteria’s small body without the presence of a nucleus

Some unknown protein helps to condense DNA w/in bacteria

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8
Q

Bacterial cytoskeleton

A

Have cytoskeletal components similar to eukaryotes and some unique proteins

MreB (homolog to actin)
FtsZ (homolog to tubulin)
Crescentin (Homolg to Intermediate filaments)
MinD/ParA
RhlB / RNase E

This is important for antimicrobial design (create a drug that target these structural proteins)

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9
Q

Bacterial exoskeleton

A

Normally referred to as the murein sacculus

Other names: peptidoglycan, cell wall, or rigid layer

Function:
Giant molecule that envelopes the bacteria and protects from stress

Importance:
Environment is generally hypertonic, without exoskeleton the cell will swell –> lysis

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10
Q

Common anti-microbial targets of bacterial exoskeleton

A 
Murein synthesis (penicillin) 
Ribosomal proteins (gentamycin)
DNA gyrase (ciprofloxacin)
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11
Q

Only bacteria that doesn’t have an exoskeleton

A

Mycoplasma:

Do not have necessary proteins to form the exoskeleton and are therefore amorphous

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12
Q

Gram-positive bacteria

A

Have a much thicker murein sacculus (stain gets trapped in this layer)

Contain specific polysaccharides in envelope
Teichoic acids polysaccharide:
covalently linked to the peptidoglycan layer or to the lipids of the cytoplasmic membrane

Difference between gram positive bacteria is based on the antigenicity of the teichoic acid **

Contain wall associated exoproteins:
Varies types
Function as a type-specific antigencity and virulence (important for host defense invasion)

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13
Q

Levels of bacterial classification

A

Morphology, Metabolism, Antigenicity, Genetics

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14
Q

Bacterial classification: Morphology

A

Staining: gram stain positive vs. negative

Then,
Shape: coccus, bacillus, spirillum, coccobacillus, spirochete, vibrio

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15
Q

Bacterial classification: Metabolism

A

Anaerobic (fermentation) vs. aerobic (Respiration)
Can be facultative or obligate

Specific nutrients (e.g. fermenter of specific carbohydrates)

Production of certain metabolic products (e.g. acid, alcohols)

Specific enzymes (e.g. catalase

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16
Q

Bacterial classification: Antigenicity

A

Use of antibodies that are particular to certain bacteria

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17
Q

Bacterial classification: Genetics

A

Most commonly we use ribosomal DNA to look for highly conserved sequences particular to a family or genus

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18
Q

Virulence factors

A

Genetic traits that enhance the ability of bacteria to cause disease

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19
Q

Pathogenicity island

A

Large chromosomal regions that contain sets of genes that encode for virulence factors

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20
Q

Possible outcomes of new exposure

A

Transient colonization & clearance
Permanent Colonization
Disease

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21
Q

Strict Pathogens

A

Virulent bacteria that promote their growth at the expense of their host

Ex: mycobacterium TB
Neisseria gonorrhoeae
Plasmodium spp. (Malaria)
Rabies virus

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22
Q

Opportunistic bacteria

A

an organism capable of infecting only when host defense are breached or compromised (some commensals are opportunistic)

Ex. Staph aureus
E. coli
Pseudomonas aeruginosa
Candida albicans

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23
Q

Commensal bacteria

A

Bacteria that does not harm nor benefit their host

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24
Q

Natural defense mechanisms for bacterial entry

A

skin, mucus, ciliated epithelium, and antibacterial secretions

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25
Q

Common ports of entry for bacteria

A

Ingestion, inhalation, trauma, needle stick, arthropod, & sexual transmission

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26
Q

Examples of bacteria that enter via ingestion

A

Salmonella spp, Shigella app. , Yersinia enterocolitica

enterotoxigenic E. coli, Vibrio spp. ,camplyobacter spp.

Clostridium botulinum, Bacillus cereus, Listeria spp, Brucella spp

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27
Q

Examples of bacteria that enter via inhalation

A

Mycobacterium spp. , Nocardia spp. , mycoplasma pneumoniae

Legionella spp., Bordetella, Chlamydophila psittaci

Chlamydophila pneumoniae, streptococcus spp.

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28
Q

Examples of bacteria that enter via trauma

A

Clostridium tetani

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29
Q

Examples of bacteria that enter via needlestick

A

Staphylococcus aureus

Pseudomonas spp.

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30
Q

Examples of bacteria that enter via arthropod bites

A

Rickettsia, ehrlichia, coxiella

Francisella Borrelia spp

Yersinia pestis

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31
Q

Examples of bacteria that enter via sexual transmission

A

Neisseria gonorrhoeae

Chlamydia trachomatis

Treponema pallidum

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32
Q

Bacterial colonization

A

Bacteria colonize if environment is suitable

If they are invading a normally sterile environment, this environment must be compromised in some fashion

Ex: In CF, the function of the ciliary mucoepithelial is comprosed allowing for pathogens to enter previously sterile locations

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33
Q

Gram negative

A

Much thiner murein than gram positive (doesn’t stain purple b/c the dye doesn’t get trapped, must use safranin to get red color)

Have outer semi-permeable membrane outside the murein sacculus –> aqueous space is created between murein and outer membrane called periplasmic space

Lipoprotein: function to stabile outer membrane to murein

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34
Q

Periplasmic space

A

Unique to gram negative bacteria

Contain periplasmic proteins:
Proteins associated w/ murein: biosynthetic enzymes that create murein or immotile murein
Soluble proteins: carry nutrients across periplasmic space to the cytoplasm
Digestive enzymes: Larger molecules that enter the periplasmic must be digested into smaller ones to enter cytoplasm

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35
Q

Gram-negative bacteria: outer membrane

A

Unique to gram-negative bacteria

Specialized, asymmetric membrane, containing:
Lipopolysaccharide (all gram negative have this)
Outer membrane proteins (function as porins & adhesins)
Phospholipids is exclusively in inner leaflet and the outer leaflet is mostly LPS

Functions to:
Provide resistance to detergents & some antibiotics (you can use this to separate gram negative from gram positive)

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36
Q

Gram-negative bacteria: LPS function

A

Contribute to the virulence of gram negative bacteria in 2 ways:

Gram negative endotoxin is found exclusively in the lipid A portion

O-antigen:
Antigen properties help to differentiate between different subtypes of bacteria
Enhances virulence b/c it acts as an anti-phagocytic factor (its covers the enter cell making it difficult to phagocytose

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37
Q

Atypical cell walls

A

Some bacteria lack typical cell wall, these contain a waxy lipid (mycolic acid) bound to a thin layer of peptidoglycan

Provide for low permeability & high degree of resistance to chemicals

Stained w/ acid-fast stain

Ex: mycobacterium tuberculosis

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38
Q

Exoproteins

A

Found in both gram positive and gram negative bacteria

Made by membrane associated ribosome

Some remain w/ cell, others are released into the environment

Some of these proteins have a toxic enzyme (referred to as exotoxins)

Gram-negative bacteria have special mechanism to traverse both membrane to release exoproteins

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39
Q

Pili

A

Optional protein appendages

Function:
Some have specialized molecules that allow for adherence to host cell
Injection of bacterial protein into host cell
Virulence factor

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40
Q

Flagellum

A

Optional protein appendages

Function:
Motility
Ability to sense environment, helps to propel bacteria toward nutrients and away from toxins
H-antigen helps to identify subtypes of flagellated bacteria

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41
Q

Flagellar arrangements: nomenclature

A

Monotrichous: one flagellum found at the pole

Lophotrichous: when many flagella are found at the pole

Amphitrichous: various flagella found at both poles

Peritrichous: when flagella are found all over bacteria

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42
Q

Glycocalyx

A

Optional bacterial surface coating

Slime: if it is loosely organized & attached
Capsule: if highly organized, tightly attached

Usually made of polysaccharides

Anti-phagocytic (determines virulence)

Antigenic (antibody target)

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43
Q

Microbial differentiation

A 
Reversible changes in: 
Structure of surface macromolecules
Organelle structure (like pilli)
cell structure & organization (sporulation)
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44
Q

Sporulation

A

In normal environment, vegetative cell will undergo normal growth and multiplication

In nutrient deprivation, vegetative cell enters sporulation cycle
The cell structure changes to form endospore –> mother cell will lysis and release spore (which can live for many years)

If nutrients are introduced, then the spore will germinate and 	enter normal vegetative growth
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45
Q

Bacterial spore

A

Structural changes result in the formation of the spore coat (made from proteins) which protect the bacteria and importantly the chromosomal DNA

Coat protects against:
Drying, heat, chemicals, UV light, & mechanical stress

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46
Q

Pilus: formation

A

Gram-negative: on outer membrane there is a shaft (made of non covalent protein-protein interactions; arranged by chaperone/usher pathway

Gram-positive: The proteins are cross-linked and joined by covalent bond; organized by sortase enzyme

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47
Q

Chaperone/usher pathway

A

Pilins are exported to the periplasmic space

Chaperone proteins bind to pilins –> deliver it to usher proteins (outer membrane transmembrane protein)

Usher helps forms tip then the pilins brought by chaperone –> are assembled into a polymer in a specific order

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48
Q

Type III secretion

A

Resembles a molecular injection

Key factor in gram-negative pathogens
Expression/activity is highly regulated

Uses:
Facilitate uptake & invasion
Promote intracellular survival & replication
Lead to apoptotic death of cell

Ex: Shigella (to enter cell) Salmonella (promotion of uptake), E. coli (creates a docking system)

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49
Q

Pilus: important ones to remember

A

P pilli
assembly proteins (PapD & PapC)
adhesin (PapG)
Pilli that causes cystitis & pyelonephritis

Curli pili
assembly proteins (CsgBEG)
adhesin (CsgA)
Pilli that causes sepsis

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50
Q

Obligate intracellular pathogens

A

Chlamydia

Rickettsia

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51
Q

Facultative Intracellular Pathogens

A 
Listeria
Mycobacteria
Shigella
Salmonella
EP E. Coli
UP E. Coli
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52
Q

Exotoxins: types

A 
Cytolytic: membrane disrupting toxins
	alpha toxin (phospholipase C): degrades sphingomyelin & 		other phospholipids

Hemolysins: insert & disrupt erythrocytes

Pore-forming toxins: promote leakage of ions & water –> disrupt cell function, can lead to lysis (e.g. streptolysin O)

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53
Q

Exotoxins: structure

A

Mostly dimeric w/ an A & B subgroup

B subgroup: binds to cell surface receptor

A subgroup: transferred into the cell –> inducing toxic effect
Common targets include: ribosomes, transport proteins, & intracellular signaling

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54
Q

Superantigens

A

Special toxin that activate T cells by binding to both T cell receptor & MHC II on APC in the absence of an antigen

Results in a large release of interleukins (cytokine storm) including IL-1, IL-2, & TNF –> leading to dangerous autoimmune-like responses

Ex:
toxic shock syndrome toxin of Staphylococcus aureus, staphylococcal enterotoxins
erythrogenic A/C of Streptococcus pyogenes

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55
Q

Recognition & response of bacterial infection

A

Bacterial cell wall components acts as a signal of infection
Specifically, bacteria have PAMPs (pathogen-associated molecular patterns) that bind to TLR (toll-like receptor) –> production of cytokines –> immune response

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56
Q

Gram-positive bacterial infection: endotoxin-like response

A

Peptidoglycan & breakdown products (teichoic & lipoteichoic acid) –> released into the environment –> pyrogenic (fever) acute phase response

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57
Q

Gram-negative bacterial infection: endotoxin

A

Endotoxin is only found in gram-negative bacteria

Endotoxin binds to receptors (CD14, TLR) on macrophages & B cells –> acute phase cytokines (IL-1, IL-6, TNF)

At low concentration –> vasodilation, fever, & acute inflammatory response

At high concentration –> leukopenia followed by leukocytosis, DIC, activation of complement, thrombocytopenia, decreased peripheral circulation & perfusion, shock, or death

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58
Q

Enterobacteriaceae

A

Ubiquitous, free-living in nature
Facultative anaerobes, lactose fermentation (E. coli, Klebsiella, enterbacter, citrobacter)
Oxidase negative
Resistance to bile salts (salmonella, shigella)

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59
Q

Antigens for classification of enterobacteriacae

A

O antigen: cell wall polysaccharide (identify strain w/in species)
K antigen: cell surface antigens
H antigen: flagellar protein
Pili: protein antigen

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60
Q

Common virulence factors in enterobactericae

A 
Endotoxin
Type III secretion
Sequestration of growth factors 
Resistance to serum killing (capsule, prevention of complement binding)
Antimicrobial resistance
Adhesins
Exotoxins
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61
Q

Sepsis: overview

A

Pt has fever or low body temp
HR > 90
RR > 20 or PaCO2 < 32
WBC > 12K, <4K, left shift

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62
Q

Severe sepsis: characteristics

A

Hypoperfusion w/ associated organ dysfunction

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63
Q

Septic shock: characteristic

A

Hypotension despite adequate fluid resuscitation

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64
Q

Sources of Sepsis by gram (-) bacilli

A 
Biliary tract
GI tract (peritonitis, intestinal infarct)
GU tract
Infected pancreatitis
Skin necrotizing infection
Pneumonia
Post-surgery
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65
Q

5 stages of sepsis

A

Local injury or infection

Systemic spillover of pro- & anti- inflammatory mediators

Development of Loss of regulatory control of proinflammatory responses (SIRS)

Inappropriate compensatory antiinflammatory response (CARS)

Ultimately can lead to multiorgan dysfunction syndrome

Sepsis happens when SIRS outweighs CARS

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66
Q

Host Defense Mechanism

A 
Species, age
Hygiene
Gastric acidity
Intestinal motility
Enteric microflora
Specific/non-specific immunity
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67
Q

Noninflammatory enteric infections

A

Involve enterotoxins
Watery diarrhea
No fecal leukocytes

Ex: V. cholerae & ETEC

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68
Q

Inflammatory Enteric Infections

A

Cell invasion & cytotoxins
Fecal leukocytes might be present

Ex: Shigella & Salmonella enteritidis

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69
Q

Penetrating Enteric Infections

A

Penetrate intact intestinal mucosa & multiply in lymphatic & RE cells

Febrile systemic illness w/ or w/out diarrhea

Fecal PMN

Ex: Salmonella typhi (Typhoid fever)

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70
Q

Evasion of immune system: Bacterial capsule

A

Most important virulence factor
Made of polysaccharide which is a poor immunogen

Makes it difficult for phagocytes to adhere to bacteria

Protects bacteria from destruction within the phagolysosome

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71
Q

Evasion of immune system: intracellular pathogens

A

Intracellular growth that hides bacteria from detection

Require TH1 T helper cell to activate macrophages to kill or creat a barrier around the cell

They can avoid being killed intracellular by:
Blocking fusion of the phagolysosome
Resistance to bactericidal lysosomal enzymes
Ability to exit phagosome before coming in contact w/ lysosomal enzymes

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72
Q

Evasion of complement system

A

Masking: antigenic variations that prevent antibody action

Inhibiting activation of complement: gram negative bacteria have an O antigen that prevents the complement system from reaching the plasma membrane

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73
Q

Genome diversity in Bacteria

A

Vibrio cholera has 2 chromosomes (smaller one provides genes for toxin)

Others have linear DNA and plasmids (Borrelia)

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74
Q

Bacterial chromosome & extrachromosomal elements

A

Chromosomes:
Single circular DNA (except vibrio & borrelia)

Plasmids:
Many bacteria have plasmids, some have many copies, replicate along with chromosome

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75
Q

Bacterial gene regulation

A

Bacterial promoters will bind repressor molecules –> gene transcription

Sigma binds DNA which attracts RNAP

76
Q

2 Component Signal Transduction

A

Sensory kinase on the bacteria surface interact w/ small molecules and phophorylate downstream effectors including response regulator that can cause changes in the DNA by interacting to various sigma protiens

77
Q

Bacteriophages

A

Similar to a virus for bacteria
Insert RNA or DNA that then directly impact protein synthesis –> encapsidation and lysis

These are important for bacteriophage therapy as a potentially more potent treatment then traditional antibiotics

78
Q

Lysogenic conversion

A

Bacteriophage can carry gene for toxin and it can then inject these genes into normally non-toxigenic strands

Ex: Shiga toxin & diphtheria toxin

79
Q

Bacterial conjugation

A

Two bacteria bind via a pilus where the plasmid of one bacteria can be transferred into the other bacteria

Plasmid with the use of transposons can integrate into DNA and then also be transferred into another bacteria via same mechanism

This allows bacteria to transfer new traits to other bacteria (referred to as lateral genetic transfer)

80
Q

Transposons

A

Motile DNA elements ( from one site of a chromosome to a chromosome, plasmids, or phage genome)

Transposase: specific enzyme that mediates transposition of the cognate

81
Q

Development of bacterial resistance

A 
By mutating: 
Through errors of replication
Through DNA damage & error prone repair 
Common mutations: 
	rRNA mutation (many antibiotic)
	r-protein S12 mutation (streptomycin) 
	DNA Gyrase mutation (novobiocin, nalidixic acid)

By acquiring resistance genes
Transposon mediated: drug resistance genes produce enzymes that can alter the drug –> making them inactive

82
Q

Anaerobic bacteria

A

Many are commensal

Help w/ stabilization of bacterial flora
Guard against colonization by pathogenic organism from outside sources

Help digesting food

83
Q

Virulence factors of anaerobes

A

Adhesins (capsule & fimbriae)

Protection against phagocytosis (capsule, proteases that drgrade immunoglobulin)

Protection against oxygen toxicity:
Superoxide dismutase (inactivates superoxide)
Catalase (inactivates hydrogen peroxide)

84
Q

Characteristic of anaerobic infection

A

Polymicrobial infections

Cause disease when spread by trauma of disease from mucosal surfaces to sterile tissues or fluid

85
Q

Common type of anaerobic infection

A 
RTI
Brain abscess
Intra-abdominal infection
Gynecological infections (pelvic inflammatory disease)
Skin & soft tissue infection
Bacteremia
Gastroenteritis
86
Q

Human monocytic ehrlichiosis

A

Organism: E. charreensis
Tick vector: lone star tick
Location: mid atlantic, mid west, south central states
Disease: Leukopenia & thrombocytopenia, flu-like, fever/chills, headache, myalgias

Seen in CT

87
Q

Human Granulocytic ehrlichiosis

A 
Organism: anaplasma phagocytophilum
Location: NE & North central USA, Europe
Vector: Deer tick
Resevoir: mice, chipmunks
Disease: 
Febrile illness, Headache, myalgias, leukopenia, thrombocytopenia, rash in less than 10%

Seen commonly in CT

88
Q

Complications/Diagnosis/Treatment of Ehrlichiosis/Anaplasmosis

A

CHF, Pericardial effusion
Renal failure
Immunosupression

Diagnosis:
peripheral blood smear: inclusions seen in WBCs (morulas)

Treatment: Doxycycline

89
Q

Normal flora: mouth & URT

A 
Staphylococcus
Streptococcus
Treponemes
Enterobacteriaceae
Candida
90
Q

Normal flora: Skin

A 
Staphylococcus
Streptococcus
Priopionibacter
Candida
Malassezia
91
Q

Normal flora: Female urogenitial

A 
Candida
Enterococcus
Lactobacillus
Peptostreptococcus
Staphylococcus
Streptococcus
92
Q

Normal flora: Lower GI tract

A 
Bacteroides
Clostridium 
Peptostreptococcus
Enterobacteriaceae
Enterococcus
Pseudomonas
Candida
Blastocystis
Entmoeba
93
Q

Erysipelothrix rhusiopathiae

A

Gram + (gram variable)
Zoonotic (swine, turkey, fish) & soil
Presents w/ cellulitis (erysipeloid)
Treated w/ penicillin

94
Q

HACEK: organisms

A 
Haemophilus (parainfluenzae, aphrophilus, paraphrophilus)
Actinobacillus actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella
95
Q

HACEK organisms: what they cause & Tx

A

Endocarditis

Eikonella (found in mouth, involved in clenched fist injury)

Treated w/ Ceftriaxone, Ampicillin-sulbactam, or fluoroquinolones

96
Q

Capnocytophaga canimorsus

A 
Filamentous gram - bacillus
CO2 eating (requires high CO2 tension)

Found in human mouth & animal mouths (associated w/ bite injuries)

97
Q

Spirochetes: general features

A

Slender, helical or planar wave
Highly motile & invasive
Double membrane w/ flagella in periplasmic space
Distantly related to gram + & gram -

98
Q

Spirochete disease: general features

A

Cause widely disseminated disease (include CNS involvement)
Disease occurs in stages
Clinical manifestations are a result of host immunity

99
Q

Mycobacteria: general features

A

Obligate aerobes
Slow growth
Waxy cell wall (made of glycolipid)

100
Q

Mycobacteria cell wall

A

Above peptidoglycan layer, have arabinogalactan, mycolates, & acetyl lipids)

mycolates & acetyl lipids make up waxy coat –> makes these organisms acid-fast

101
Q

Tuberculoid response: characterized by & seen in

A

Good T cell response & activation of macrophages

Usual state of pts w/ reactivation type (pulmonary) TB & in tuberculoid leprosy

Histology: Caseous necrosis, scant mycobacteria

102
Q

Lepromatous response: characterized by & seen in

A

Defective T cell response & lack of macrophage activation

Usually seen in pts w/ lepromatous leprosy & miliary TB, disseminated mycobacterial infections in pts w/ AIDS

Histology: No necrosis, abundant mycobacteria

103
Q

Cell wall synthesis inhibitors: overall mechanism

A

Pentaglycl unit which enables cross-linking between strands & is the site where penicillin binding protein bind

Terminal D-alanine D-alanine where the antibiotics mimic or bind to prevent cross-linking by creating steric hindrance

104
Q

Beta-lactams: groups

A

Penicillin
Cephalosporins
Carbapenems
Monobactams

105
Q

Penicillin: general considerations

A

Is bactericidal
No activity against atypical pathogens (true for all beta-lactam)
Poor penetration into human cells
Common mechanism for resistance (inactivation of penicillinase/betalactamase)

106
Q

Penicillin: clinical considerations

A

Well-tolerated
GI upset, diarrhea, allergic reactions are most common adverse effects, Allergic Rash: ~10% prevalence

Removed via kidney, basically no hepatic toxicity (must adjust for renal function)

107
Q

Natural penicillins: available agents

A 
Penicillin G (iv)
Penicillin V (po)
Procaine, benzathine (im)
108
Q

Natural penicillin: spectrum of activity

A 
Narrow-limited to: 
	Gram (+) aerobes (Strept, Entero)
		Resistance in Strep pneumoniae & staph
	Some anaerobes
	Treponema pallidum 
	POOR for gram (-)
109
Q

Anti-staph penicillins

A

Agents:
Cloxacillin / Dicloxacillin: po
Nafcillin / Oxacillin: iv

Limited to Staphylococci, Streptococci
Activity decreased vs. Streptococci compared to PCN

Resistance in Staphylococci
(Methicillin-Resistant S. aureus, “MRSA”):
Change in PBP enzyme targets
Increasing in both community and hospital settings (>50% in most hospitals)

Hepatic elimination

110
Q

Aminopenicillins

A

Combined w/ beta-lactamase inhibitor
Ex: amoxicillin or ampicillin

Improves gram (+) activity (staph)
Broader gram (-) activity (Klebsiella)
Improved anaerobic activity (Bacteroids)
111
Q

Anti-pseudomonal penicillin

A

Mezlocillin / Piperacillin / Ticarcillin: iv
Combined with beta-lactamase inhibitor (Improves activity against Staphylococci, gram-negatives, and anaerobes)

Spectrum of Activity:
Less active against Gram-positive bacteria
Active against most Gram-negatives
Resistance becoming a more important issue for select strains of :
P. aeruginosa, Acinetobacter, Enterobacter spp.,
Beta-lactamase overproducing Klebsiella spp., E. coli,
Active against most anaerobes

112
Q

Cephalosporins: general considerations

A

Ring structure less strained –> reduced tendency for hydrolyze & more stable penicillinase degradation
Acid & beta-lactamase stability

113
Q

Cephalosporins: clinical considerations

A

Bactericidal
ALL cephalosporins have NO clinically reliable activity against enterococci
MOST cephalosporins have NO reliable activity against anaerobes

Well-tolerated and have minimal drug interactions
Usual adverse effects: GI-related
Approximately 2.5-5% of patients with documented penicillin hypersensitivity will also be allergic to certain cephalosporins

Most need to have doses reduced in moderate-severe renal dysfunction

114
Q

1st generation Cephalosporins

A

Agents:
Cefazolin (Ancef): iv
Cephalexin (Keflex), Cefadroxil (Duricef): po

Most Gram-positives (except enterococci, MRSA)
Limited Gram-negatives (e.g., E. coli, Haemophilus spp.)

115
Q

2nd generation Cephalosporin

A

Most important agent: Cefuroxime (Ceftin, Zinacef): po/iv
Spectrum of Activity:
Most Gram-positives (except enterococci, MRSA),
Some beta-lactamase producing Gram-negatives (e.g., Haemophilus, Moraxella, E. coli)

Cefoxitin, Cefotetan active against most anaerobes

116
Q

3rd generation Cephalosporin

A

Most common agents:
Oral:
Cefdinir (Omnicef)
Cefixime (Suprax)

Intravenous:
Ceftazidime (Fortaz)
Ceftriaxone (Rocephin)

Most gram-positives (except enterococci & MRSA)
Most gram-negatives (except Pseudomonas and certain strains of Enterobacter, Klebsiella, Citrobacter spp.)
Ceftazidime has antipseudomonal activity

117
Q

4th generation Cephalosporin

A

Cefepime

Spectrum of Activity:
Similar to 3rd Generation Cephs but:
Effective against Pseudomonas (like Ceftazidime)
Effective against some gram negative bacteria that are 3rd- generation cephalosporin-resistant

118
Q

5th generation Cephalosporin

A

Ceftaroline (Teflaro)
Spectrum of Activity:
Gram Positives: Streptococcal spp. & Staphylococcus spp. (including MRSA!)

Gram negatives: Similar to 3rd Generation Cephs like 			ceftriaxone
119
Q

Aztreonam

A

Monobactam cell wall synthesis inhibitor
Spectrum of Activity
Gram-negatives: nearly all (including highly resistant strains)
No activity against Gram-positives, anaerobes, or atypical bacteria

Used on patient’s with confirmed penicillin allergies

120
Q

Carbapenems: clinical considerations

A

IV only: Imipenem (Primaxin), Meropenem (Merrem), Ertapenem (Invanz), Doripenem (Doribax)

BROAD-SPECTRUM: Active against nearly all Gram positive, Gram-negative, and anaerobic bacteria, No atypical antibacterial activity
Fungal superinfections may occur while on carbapenems

Risk of cross-allergenicity originally thought to be much higher than Aztreonam/Cephs for patients with PCN allergies…probably only ~5-10%

121
Q

Imipenem/Cilastatin and Meropenem & Doripenem

A

Both dosed every 6-8 hours:
Cilastatin prevents enzymatic breakdown of imipenem in the kidneys (increases half-life and allows Q6-8H dosing)

Meropenem thought to have lower risk of seizures than imipenem…but controversial

Doripenem: slightly more potent than these other combination

122
Q

Important consideration for Ertapenem

A 
iv
Dosed QD (versus Q6-8H for imipenem and meropenem)
Should NOT be used if Pseudomonas spp. documented or suspected (no activity!!!)
123
Q

MSSA: implication for beta-lactam use

A

Resistance via penicillinase:
resistant to PCN, aminoPCNs, extended-spectrum PCNs
Nafcillin, oxacillin, dicloxacillin have activity
Amox/clavulanate, Amp/sulbactam, pip/tazobactam have activity
Cephalosporins, Carbapenems have activity

124
Q

MRSA: implication for beta-lactam use

A

Still has penicillinase:
resistant to PCN, aminoPCNs, extended-spectrum PCNs
Also altered PBP-2a

NO beta-lactams have activity against MRSA except Ceftaroline

125
Q

Differences between fungi & bacteria

A

Fungi: eukaryote, larger cell size (2-15 micrometer), polysaccharide cell wall (glucans, mannans, chitin) & cell membrane contains sterols

Bacteria are prokaryotes, cell wall peptidoglycan, no sterols in cell membranes

126
Q

Fungal morphology: Yeast

A

Round/oval that undergoes budding or fission; colonial growth is smooth

127
Q

Fungal Morphology: Mold

A

Tubular structure (hyphae) that undergoes longitudinal extension & branching; colonial morphology is fuzzy

128
Q

Reproduction in yeasts

A

More species go through budding

Mechanism: Initiated by localized enzymatic cell wall lysis, cell membrane bulges, nucleus divides & the 2nd nucleus moves into bud; cell wall is repaired between daughter & mother –> daughter cell breaks off

129
Q

Hyphae: characteristics

A

Can be aseptate or septate

Septae have pores that allow nutrient movement

Can be vegetative (obtain nutrients) or aerial (form conidia or sporangiospores

130
Q

Dimorphic fungi

A

Fungi that can have both fungal morphology
Yeast form at 37 C
Mold form at 30 C

Ex: Histoplasma capsulatum, Coccidioides immitis

131
Q

Reproduction in molds

A

Sexual state: teleomorph (perfect state)
Asexual state: anamorph (imperfect state)

Asexual form grows in culture & is the name we use clinically

132
Q

Human defenses against Fungi

A

Most grow poorly at body temp
Skin & mucosal surfaces are effective barriers

Innate immunity provides initial protection (TLR 2, 4, 9 & C-type lectin receptors)

Cell-mediated immunity: is critical (require Th1 & Th17 response to decrease severity & incidence of fungal infections)

Humoral immunity: not important

133
Q

Fungal culture

A

Sabouraud’s agar: 4% dextrose, at pH 5.5
Sugar & acidity discourage bacterial growth

Fungi grow very slowly in culture

134
Q

Fungal identification in culture: yeast

A

Grows suspended in broth or on plates

Use metabolic reactions for specific organism identification

135
Q

Fungal identification in culture: molds

A

Grow slowly & form conidia

Identify by conidial, hyphal, & colonial morphology

136
Q

Minimum inhibitory concentration (MIC): defined and how we determine it

A

Determined by adding bacteria to nutrient broth with serial dilutions of antibiotic, the point where there is no growth is the MIC

Can use an E test (an agar plate that has a pre-made gradient of antibiotic, the point specifically at the meniscus is the MIC)

137
Q

Minimum Bactericidal Concentration (MBC): defined and how we determine it

A

Once the MIC is determined, you take the same samples that show no growth and remove them from the antibiotic, plate the bacteria and look for growth. The concentration where there is no growth is the MBC

138
Q

Bactericidal: mathematical relationship

A

MBC less than or equal to MIC

Or 99.9% bacteria count reduction in 24 hrs

139
Q

Bacteriostatic: mathematical relationship

A

MBC > 4x MIC

140
Q

Tolerant: mathematical realtionship

A

MBC > 32x MIC

141
Q

Bactericidal medications

A 
Beta-lactams
Aminoglycosides
Vancomycin
Fluoroquinolones
Daptomycin
Metronidazole
142
Q

Bacteriostatic medications

A 
Macrolides
Tetracyclines
Sulfonamides
Clindamycin
Linezolid
Chloramphenicol
143
Q

Concentration-Dependent Killing

A

Eliminate bacteria when levels are well-above MIC in tissue
When ratio of drug to MIC increased further, greater killing occurs
Shown up to 64x MIC
Exhibits a “post-antibiotic effect”
Even when levels trail off, the bacteria are damaged and take some time to recover

Ex: Quinolones & Aminoglycosides

144
Q

Time-Dependent Killing

A

Killing occurs only when concentration is higher than MIC
Any levels >4x MIC generally do not add to the killing effect

Ex:
Penicillins
Cephalosporins
Aztreonam
Macrolides
Clindamycin
145
Q

Antibiotic combinations: indifference

A

Combination is the sum of each alone

146
Q

Antibiotic combinations: synergy

A

Combination better than the sum of each alone

Ex:
Ampicillin breaks down cell wall, allowing improved penetration of gentamicin into bacteria

147
Q

Antibiotic combination: antagonism

A

Inhibition of antimicrobial effect

Tetracycline is “static”, thus bacteria are inhibited but not
actively growing actively growing

Penicillin requires metabolically active bacteria to affect cell wall

Metabolic stasis induced by TCN protects bacterium from
killing effects of the ampicillin

148
Q

Anti-microbial resistance: Intrinsic

A

An inherent attribute of a microbe
lacks necessary target

Ex:
Resistance of Enterococcus to cephalosporins

149
Q

Anti-microbial resistance: Circumstantial

A

A difference between in vitro and in vivo effects of an antibiotic

May appear sensitive in lab, but resistance in clinical use

Ex:
Enterococcus can appear sensitive to TMP/SMX in vitro, but can take up environmental folate in vivo

Induction of a cephalosporinase in Enterobacter

150
Q

Anti-microbial resistance: Acquired

A

A change in the genetic composition of an organism so that a drug that was once effective is no longer active

151
Q

Genetics of resistance: mechanism

A

Antibiotics apply selective pressures for microbial survival
Microbes acquire traits that permit their survival

Gene modification can occur by several mechanisms:

Mutation: Spontaneous changes in the genetic code
Transformation: Acquisition of soluable DNA
Transduction: Acquisition from phage
Conjugation: Acquisition of new traits via plasmids
Transposition: Acquisition of new traits via transposons

152
Q

Mechanism for anti-microbial resistance: Decreased Antibiotic Access

A

Decrease Outer Membrane Permeability: Beta-Lactams
Decreased Cytoplasmic transport (influx): Aminoglycosides
Increased Efflux: Tetracyclines & Quinolones

153
Q

Mechanism for anti-microbial resistance: Drug Inactivation

A

Most common resistance mechanism seen
Generally acquired by exogenous genes
Enzymatic activity of bacteria alters the antibiotic to inactive state

Examples:
b-lactamase, Aminoglygcoside enzymes, Chloramphenicol Acetyl Transferase (CAT)

154
Q

Mechanism for anti-microbial resistance: Target Modification

A 
Alters the target molecule such that it does not bind or is otherwise unaffected by the antibiotic
Ex: 
Quinolones (Gyrase modification)
Rifampin (RNA polymerase mutation)
Macrolides (rRNA methylation)
β-lactams (PBP changes)
155
Q

Changes in Penicillin Binding Proteins: MRSA

A

Bacteria possess multiple transpeptidases
Function to cross-link the cell wall, Inhibition prevents cross-linking and accumulation induces autolysis

Community-acquired Methicillin-resistant Staphylococcus aureus (ca-MRSA)
Encoded on the gene complex “type IV Staphylococcalcassette chromosome” a.k.a. SCCmec gene
PBP 2’: low β-lactam affinity, even to penicillins resistant to β-
lactamases

156
Q

Mechanisms of Antimicrobial Resistance: Target Bypass

A

The bacteria no longer need the enzyme targeted by the antibiotic to survive
Examples:
Trimethoprim: Enterococcus can use folate from the environment

Glycopeptides (Vancomycin Resistant Enterococci (VRE))
Vancomycin acts by blocking peptidoglycan synthesis
VRE use a d-ala to d-lactate instead of d-ala to d-ala
Three types: Van A, Van B, Van C

157
Q

Viral reverse transcriptase

A

Found in retro viruses

Converts RNA into DNA

158
Q

Viral ds RNA transcriptase

A

Found in reo viruses

Copies dsRNA into ssRNA

159
Q

Viral NTP phosphotransferase

A

Found in many enveloped virus

Phosphate exchange

160
Q

Viral neuraminidase

A

Found in myxo & paramyxo virus

Cleaves cell surface sugars

161
Q

Viral protein kinase

A

Found in myxo, retro, paramyxo, herpes

Phosphorylates proteins

162
Q

Viral Life Cycle: components attachment

A

Attachment:
Always to specific cell surface receptors
Some receptors are highly tissue or cell specific; other receptors are present on many or even all cells

Ex: 
HIV (CD4 antigen on T cells)
Rhino (ICAM-1 on upper respiratory epithelial cells)
Polio (Immunoglobulin-like receptors)
Influenza (Sialic acid)
Herpes Simplex (Heparan sulfate proteoglycans) 
Rabies (Acetylcholine receptor)
Hepatitis B (IgA receptor)

Uncoating & penetration (Uncoating can occur at the plasma membrane, within an endosome, & at the nuclear membrane)

mRNA synthesis & translation
Viral genome replication
Virion assembly then release

163
Q

Picornaviruses: structure

A

Single-stranded linear RNA genomes3’ polyA, VPg protein at 5’ end.
After entry and uncoating, a polyprotein is made, which self-cleaves to generate all necessary viral polypeptides.

164
Q

Picornaviruses: life cycle

A 
Specific cellular receptor
RNA serves as mRNA for viral proteins
VPg must be removed by cell proteases
RNA translated into one polyprotein, which undergoes post-translational modification into multiple polypeptides
Early host shutoff
RNA replication goes through minus strand intermediate
Assembly
Cell destruction and virus release
165
Q

Orthomyxoviruses: structure

A

Single stranded RNA genome, negative polarity
Segmented 3. Enveloped virion, lipid derived from host
several surface antigens: hemagglutinin (HA), neuraminidase (N)
distinct viral proteins: Matrix, HA-2 subunits (functions in virus-cell attachment)Nucleoprotein (NP) - internal, core associated
Three RNA transcriptase proteins, internal

166
Q

Orthomyxoviruses: life cycle

A

Attachment - mediated via HA and specific cell surface receptors
Internalization by HA conformational change and membrane fusion
RNA transported to nucleus
RNA replication requires host RNA polymerase II
Assembly and release by budding through cell membranes

167
Q

Retroviruses: basic characteristics

A 
The only oncogenic class of RNA viruses - a major cause of cancers, especially 
leukemias and lymphomas, in animals.

Likely to be important in some human cancers. (Can be oncogenic in two ways: insertional mutagenesis & transduction of host proto-oncogenes)

Transmitted both horizontally and vertically

Important replication strategy, involving integration into host genome and potential to transduce cellular genes

Many are defective - grow only with “helpers”

168
Q

Retroviruses: structure

A

Enveloped, with virus-specific membrane glycoprotein spikes.
Single-strand, dimeric RNA genome
Host tRNA
Reverse Transcriptase

169
Q

Retroviruses: LIfe cycle

A

RNA genome has distinctive structure, with U3, U5, R sequences, and bound tRNA
3 genes: gag, pol, env.

RNA converted to double stranded DNA, with LTR’s at both ends

Integration of DNA into host genome (“provirus”)

LTR’s contain genetic signals for
transcription initiation and polyadenylation

Integrated provirus is transcribed, and
RNA’s processed in several ways.

Translation yields a variety of products important for virus life cycle.

170
Q

Human Retroviruses

A

Associated w/ leukemias (HTLVs) & AIDS (HIV)

HIV has a highly specific T4 lymphocytes/CD4 receptor

171
Q

Viral genetics: recombination

A

Exchange of genes between 2 chromosomes by crossing over within regions of significant base sequence homology

172
Q

Viral genetics: complementation

A

When 1 of 2 viruses that infect the cell has a mutation that results in a nonfunctional protein. The nonmutated virus complements the mutated one by maing a functional protein that serves both viruses

173
Q

VIral genetics: phenotypic mixing

A

Occurs when a cell is infected by 2 viruses; genome from virus A is partially coated with surface proteins of B & determines the infectivity of the mixed virus. Progeny of the virus will have virus A genetic material

174
Q

RNA viral genome

A

All are ss except reoviridae

175
Q

Positive stranded RNA viruses

A

retrovirus, togavirus, flavivirus, coronavirus, hepevirus, calicivirus, & picornavirus

176
Q

viral genome infectivity

A

dsDNA & + strand ssRNA are infectious (do not require polymerase –> can be directly translated)

  • strand ssRNA & dsRNA are non-infectious alone b/c they require enzymes from the host cell
177
Q

Virus ploidy

A 
All viruses are haploid
except retrovirus (2 ssRNA)
178
Q

RNA viral replication: location

A

Occurs in the cytoplasma

Except influenza & retrovirus

179
Q

Viral envelopes: origin

A

Envelope is normally obtained by plasma membrane of a cell once it exits (except herpesvirses –> comes from nuclear membrane

180
Q

Unenveloped viruses

A

Calicivirus, picornavirus, reovirus (RNA)

Parvovirus, adenovirus, papilloma, & polyoma (DNA)

181
Q

DNA viral characteristics

A

Include hepadna, herpes, adeno, pox, parvo, papilloma, polyoma
Are ds (except parvo) & linear (papilloma, polyoma, hepadna)
Are icosahedral & replicate in the nucleus (pox)

182
Q

Cyclospora cayetanensis

A

Requires maturation outside of host to become infectious
Epi: transmission via fecally contaminated water or foods
Seen in children in low income countries, travelers

Pathogenesis: Localized to upper small bowel; invades small bowel epithelium within cytoplasmic vacuoles –> asexual & sexual replication in human host –> inflammatory response & mucosal infiltrate

Clinical: incubation is 1 week; frequent watery diarrhea which may be self-limited or prolonged; symptoms: anorexia, cramping, nausea, & weight loss

Diagnosis: Wet mount, modified acid fast staining of stool, autofluoresence under UV light

Treatment: SMX/TMP

183
Q

Trichuris trichiura

A

Eggs need to mature in soil before becoming infectious; ingestion of contaminated soil

Clinical: most infections are asymptomatic, symptoms due to mechanical imbedding of worms; symptoms: abdominal pain, weight loss, & rarely rectal prolapse; occasionally presents w/ anemia; eosinophila

Diagnosis: stool (lemon-shaped eggs w/ clear, bipolar prominence

Treatment: albendazole, mebendazole, ivermectin (combination therapy mebendazole + ivermectin)

184
Q

Babesia microti

A

infection of RBCs with rupture
spleen critical in host defense; help with clearance and immune response
B cell response important for resolution of infection

Clinical:
most cases asymptomatic
splenectomy, older age, cell-mediated immune defect, HIV/AIDS,
anti-cytokine therapy defect predisposes to ↑ severity; most fatalities seen in these groups
incubation period: 1-4 weeks
malaise, chills, fever, N&V, myalgias & arthralgias
anemia, ↓ platelets, mild ↑ in liver enzymes, proteinuria

severe infection: jaundice, hemoglobinuria and renal failure
parasitemia can approach 85% in asplenic patients
can be chronic, asymptomatic parasitemia

185
Q

Babesia: diagnosis & treatment

A

Diagnosis:
blood smears: ring forms, tetrads; serology, PCR

Treatment:
most infections probably resolve spontaneously in immunologically normal hostsif recognized should be treated
treatment:
atovaquone + azithromycin
clindamycin + quinine
exchange transfusion may be needed in severe disease may need long-term therapy in immunocompromised

MOD1 (3 decks)

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