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USMLE First AID > microbiology > Flashcards

microbiology Flashcards

1
Q

Bacterial structures: function & chem composition

peptidoglycan

A
  • gives rigid support, protects against osmotic pressure

- sugar backbone with peptide side chains crosslinked by transpeptidase

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2
Q

Bacterial structures: function & chem composition

cell wall/cell membrane (gram +)

A
  • major surface antigen

- peptidoglycan for support. Lipoteichoic acid induces TNF & IL-1

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3
Q

Bacterial structures: function & chem composition

outer membrane (gram -)

A
  • site of endotoxin (lipopolysaccharide (LPS)); major surface antigen
  • lipid A induces TNF & IL-1; O polysaccharide is the antigen
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4
Q

Bacterial structures: function & chem composition

plasma membrane

A
  • site of oxidative & transport enzymes

- lipoprotein bilayer

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5
Q

Bacterial structures: function & chem composition

ribosome

A
  • protein synthesis

- 50S & 30S subunits

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6
Q

Bacterial structures: function & chem composition

periplasm

A
  • space btw cytoplasmic membrane & outer membrane in gram- bact
  • contains many hydrolytic enzymes, including beta-lactamases
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7
Q

Bacterial structures: function & chem composition

capsule

A
  • protects against phagocytosis

- polysaccharide (except Bacillus anthracis, which contains D-glutamate)

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8
Q

Bacterial structures: function & chem composition

pilus/fimbria

A
  • mediate aherence of bact to cell surface; sex pilus forms attachment btw 2 bact during conjugation
  • glycoprotein
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9
Q

Bacterial structures: function & chem composition

flagellum

A
  • motility

- protein

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10
Q

Bacterial structures: function & chem composition

spore

A
  • resistant to dehydration, heat, chemicals

- keratin-like coat; dipicolinic acid; peptidoglycan

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11
Q

Bacterial structures: function & chem composition

plasmid

A
  • contains a variety of genes for antibiotic resistance, enzymes, toxins
  • DNA
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12
Q

Bacterial structures: function & chem composition

glycocalyx

A
  • mediates adherence to surfaces, especially foreign surfaces (eg. indwelling catheters)
  • polysaccharide
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13
Q

Bacterial taxonomy morphology:

  1. gram+ eg.
  2. gram- eg.

circular (coccus)

A
  1. pos
    - Staphylococcus
    - Streptococcus
  2. neg
    - Neisseria
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14
Q

Bacterial taxonomy morphology:

  1. gram+ eg.
  2. gram- eg.

Rod (bacillus)

A
  1. pos
    - Clostridium
    - Corynebacterium
    - Bacillus
    - Listeria
    - Mycobacterium (acid fast)
    - Gardnerella (Gram variable)
  2. neg
    a) enterics
    - E. Coli
    - Shigella
    - Salmonella
    - Yersinia
    - Klebsiella
    - Proteus
    - Enterobacter
    - Serratia
    - Vibrio
    - Campylobacter
    - Helicobacter
    - Pseudomonas
    - Bacteroides
    b) respiratory
    - Haemophilus (pleomorphic)
    - Legionella (silver)
    - Bordetella
    c) Zoonotic
    - Francisella
    - Brucella
    - Pasteurella
    - Bartonella
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15
Q

Bacterial taxonomy morphology:

  1. gram+ eg.
  2. gram- eg.

branching filamentous

A
  1. pos
    - Actinomyces
    - Nocardia (weakly acid fast)
  2. neg
    - none
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16
Q

Bacterial taxonomy morphology:

  1. gram+ eg.
  2. gram- eg.

pleomorphic

A
  1. pos
    - none
  2. neg
    - Richettsiae (Giemsa)
    - Chlamydiae (Giemsa)
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17
Q

Bacterial taxonomy morphology:

  1. gram+ eg.
  2. gram- eg.

spiral

A
  1. pos
    - none
  2. neg
    a) spirochetes
    - Leptospira
    - Borrelia (Giemsa)
    - Treponema
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18
Q

Bacterial taxonomy morphology:

  1. gram+ eg.
  2. gram- eg.

no cell wall

A
  1. pos
    - Mycoplasma (does not Gram stain)
  2. neg
    - none
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19
Q

Bacteria c unusual cell membranes/walls

A
  1. mycoplasma-contains sterols and have no cell wall

2. mycobacteria-contain mycolic acid, high lipid content

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20
Q

gram stain limitations:

six bugs

A

These bugs do not Gram stain well:

  1. Treponema
  2. Rickettsia
  3. Mycobacteria
  4. Mycoplasma
  5. Legionella pneumophila
  6. Chlamydia
    * **These Rascals May Microscopically Lack Color
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21
Q

These bugs do not Gram stain well because:

Treponema-

A

too thin to be visualized

-dark-field microscopy & fluorescent antibody staining

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22
Q

These bugs do not Gram stain well because:

Rickettsia

A

intracellular parasite

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23
Q

These bugs do not Gram stain well because:

Mycobacteria

A

high lipid content in cell wall detected by cardolfuchsin in acid-fast stain

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24
Q

These bugs do not Gram stain well because:

Mycoplasma

A

no cell wall

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25
Q

These bugs do not Gram stain well because:

Legionella pneumophila

A

primarily intracellular

-stain silver

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26
Q

These bugs do not Gram stain well because:

Chlamydia

A

intracellular parasite; lacks muramic acid in cell wall

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27
Q

Stains:

  1. Giemsa
  2. PAS (periodic acid-schiff)
  3. Ziehl-Neelson (carbol fuchsin)
  4. India ink
  5. Silver stain
A
  1. Giemsa
    - Chlamydia, BOrrelia, Rickettsiae, Trypanosomes, Plasmodium
    - **Certain Bugs Really TRY my Patience
  2. PAS (periodic acid-schiff)
    - Stains glycogen, muoploysaccharides; used to dx Whipple’s dz (Trypheryma whipplei)
    - ***PAS the sugar
  3. Ziehl-Neelson (carbol fuchsin)
    - acid-fast organisms (Norcardia, Mycobacterium)
  4. India ink
    - Cryptococcus neoformans (mucicarmine can also be used to stain thick polysaccharide capsule red)
  5. Silver stain
    - fungi (eg. Pneumocystis), Legionella, Helicobacter pylori
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28
Q

Special culture requirements:
Bug & media used for isolation

H. influenzae

A

chocolate agar with factors V (NAD+) & X (hematin)

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29
Q

Special culture requirements:
Bug & media used for isolation

N. gonorrhoeae & N. meningitidis

A
  • Thayer-Martin (or VPN) media
  • Vancomycin- inhibits gram+ organisms
  • Polymyxin- inhibit gram- organisms except Neisseria
  • Nystatin- inhibit fungi
  • **to connect to Neisseria, please use your VPN client
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30
Q

Special culture requirements:
Bug & media used for isolation

B. pertussis

A
  • Bordet-Gengou (potato) agar

- **Bordet for Bordetella

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31
Q

Special culture requirements:
Bug & media used for isolation

C. diphtheriae

A

Tellurite plate, Loffler’s media

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32
Q

Special culture requirements:
Bug & media used for isolation

M. tuberculosis

A

Lowenstein-Jensen agar

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33
Q

Special culture requirements:
Bug & media used for isolation

M. pneumoniae

A

Eaton’s agar

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34
Q

Special culture requirements:
Bug & media used for isolation

Lactose-fermenting enterics

A
  • pink colonies on MacConkey’s agar-fermentation produces acid, turning colony pink
  • E. coli is also grown on eosin-methylene blue (EMB) agar as colonies with green metallic sheen
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35
Q

Special culture requirements:
Bug & media used for isolation

Legionella

A

-charcoal yeast extrac agar buffered with cysteine and iron

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36
Q

Special culture requirements:
Bug & media used for isolation

fungi

A
  • Sabouraud’s agar

- **Sab’s a fun guy

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37
Q

Obligate aerobes

A
  • use an O2-dependent system to generate ATP
  • e.g: Nocardia, Pseudomonas aeruginosa, Mycobacterium tuberculosis, Bacillus
  • **Nagging Pests Must Breathe
  • **P. aeruginosa is an aerobe seen in burn wounds, complications of diabetes, nosocomial pneumonia, and pneumonia in cystic fibrosis patients
  • reactivation of M tuberculosis-has a predilection for the apices of the lungs, which highest PO2
  • eg. after immune compromise or TNF-alpha inhibitor use
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38
Q

obligate anaerobes

A
  • eg.: Clostridium, Bacteroides, Actinomyces
  • *-anaerobes can’t breathe air
  • they lack catalase and/or superoxide dismutase and are thus susceptible to oxidative damage.
  • generally foul smelling (short chain fatty acid), are difficult to culture and produce gas in tissue (CO2 and H2)
  • anaerobes are normal flora in GI tract, pathogenic elsewhere
  • AminO2glycosides are ineffective against anaerobes bcuz these antibiotics require O2 to enter into bacterial cell
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39
Q

Intracellular bugs:

obligate intracelluar (2)

A
  • Rickettsia, Chlamydia
  • can’t make their own ATP
  • stay inside cells when it is Really Cold
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40
Q

Intracellular bugs:

facultative intracelluar

A
  • Salmonella
  • Neisseria
  • Brucella
  • Mycobacterium
  • Listeria
  • Francisella
  • Legionella
  • Yersinia pestis
  • *Some Nasty Bugs May Live FacultativeLY
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41
Q

encapsulated bacteria

A
  • positive quellung rxn- if encapsulated bug is present, capsule swells when specific anticapsular antisera are added
  • *Quellung= capsular “swellung.”
  • eg: Streptococcus pneumoniae, Haemophilus influenzae type B, Neisseria meningitidis, Escherichia coli, Salmonella, Klebsiella pneumoniae, and group B Strep.
  • **SHiNE SKiS
  • are opsonized and the cleared by spleen
  • asplenics have decreased opsonizing ability and are at risk for severe infections. Give S.pneumoniae, H. influenzae, N. menigitidis vaccines
  • their capsules serve as an antiphagocytic virulence factor.
  • capsule + protein conjugate serve as an antigen in vaccines
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42
Q

catalase-positive organisms

A
  • Catalase degrades H2O2 before it can be converted to microbicidal products by the enzyme myeloperoxidase.
  • people with chronic granulomatous disease (NADPH oxidase deficiency) have recurrent infections with these microbes because they degrade the limited H2O2
  • eg: Pseudomonas, Listeria, Aspergillus, Candida, E.Coli, S. aureus, Serratia
  • **you need PLACESS for your cats.
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43
Q

vaccines

A
  • for vaccines containing polysaccharide capsule antigen, a protein is conjugated to the polysaccharide antigen to promote T-cell activation and subsequent class switching
  • a polysaccharide antigen alone cannot be presented to T cells; therefore, only IgM antibodies would be produced.
  • pneumovax-polysaccharide vaccine with no conjugated protein
  • Prevnar-conjugated vaccine
  • H. influenzae type B- conjugated vaccine
  • meningococcal vaccines-conjugated vaccines
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44
Q

urease-positive bugs

A
  1. Crytococcus
  2. H.pylori
  3. Proteus
  4. Ureaplasma
  5. Nocardia
  6. Klebsiella
  7. S. epidermidis
  8. S. saprophyticus
    * *CHuck Norris hates PUNKSS
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45
Q

pigment-producing bacteria

A
  • actinmyces israelii-yellow “sulfur” granules, which are composed of filaments of bacteria
  • **Israel has yellow sand
  • S. aureus-yellow pigment
  • **aureus (latin)= gold
  • Pseudomonas aeruginosa-blue-green pigment
  • **Aerugula is green
  • Serratia marcescens- red pigment
  • **Serratia marcescens-think red maraschino cherries
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46
Q

bacterial virulence factors:

  1. protein A
  2. IgA protease
  3. M protein
A

these promote evasion of host immune response

  1. protein A
    - binds Fc region of Ig
    - prevents opsinization and phagocytosis.
    - expressed by S. aureus
  2. IgA protease
    - enxyme that cleaves IgA
    - secreted by S. pneumoniae, H. influencae type B, Neisseria (SHiN) in order to colonize respiratory mucosa
  3. M protein
    - helps prevent phagocytosis
    - expressed by group A streptococci
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47
Q

main features of exotoxins & endotoxins

  1. source
  2. secreted from cell
  3. chemistry
  4. location of genes
  5. toxicity
  6. clinical effects
  7. mode of action
  8. antigenicity
  9. vaccines
  10. heat stability
  11. typical dz
A 
1.source
ex-certain species of some gram+ & gram- bact
en-outer cell membrane of most gram- bact
2.secreted from cell
ex-yes
en-no
3.chemistry
ex-polypeptide
en-lipopolysaccharide, structural part of abcteria; released when lysed
4.location of genes
ex-plasmid or bacteriophage
en-bacterial chromosome
5.toxicity
ex-high, fatal dose on the order of 1 microgram
en-low, fatal dose on the oder of hundreds of micrograms
6.clinical effects
ex-various effects
en-fever, shock
7.mode of action
ex-various modes
en-induces TNF, IL-1
8.antigenicity
ex-induces high-titer antibodies called antitoxins
en-poorly antigenic
9.vaccines
ex-toxoids used as vaccines
en-no toxoids formed and no vaccin available
10.heat stability
ex-destroyed rapidly at 60C except staphylococcal enterotoxin
en-stable at 100C for 1 hr
11.typical dz
ex-tetanus, botulism, diphtheria
en-meningococcemia; sepsis by gram- rods
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48
Q

Bugs with exotoxins that inhibit protein synthesis (4)

A
  1. corynebacterium diphtheriae
  2. Pseudomonas aeruginosa
  3. Shigella spp.
  4. Enterohemorrhagic E. colo (EHEC) including 0157:H7 strain
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49
Q

Bugs with exotoxins that inhibit protein synthesis:

  1. toxin
  2. mechanism
  3. manifestation

corynebacterium diphtheriae

A
  1. toxin
    - diphtheria toxin; is an ADP ribosylating A-B toxin: -B binding component binds to host cell surface receptor, enabling endocytosis;
    - A active component attaches ADP-ribosyl to disrupt host cell proteins
  2. mechanism
    - inactivate elongation factor (EF-2)
  3. manifestation
    - pharyngitis c pseudomembranes in throat & svere lymphadenopathy (bull neck)
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50
Q

Bugs with exotoxins that inhibit protein synthesis:

  1. toxin
  2. mechanism
  3. manifestation

Pseudomonas aeruginosa

A
  1. toxin
    - exotoxin A;is an ADP ribosylating A-B toxin: -B binding component binds to host cell surface receptor, enabling endocytosis;
    - A active component attaches ADP-ribosyl to disrupt host cell proteins
  2. mechanism
    - -inactivate elongation factor (EF-2)
  3. manifestation
    - host cell death
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51
Q

Bugs with exotoxins that inhibit protein synthesis:

  1. toxin
  2. mechanism
  3. manifestation

Shigella spp.

A
  1. toxin
    - Shiga toxin (ST)
  2. mechanism
    - inactivate 60S ribosome by removing adenine from rRNA
  3. manifestation
    - GI mucosal damage–>dysentery; ST also enhances cytokine release, causing HUS
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52
Q

Bugs with exotoxins that inhibit protein synthesis:

  1. toxin
  2. mechanism
  3. manifestation

Enterohemorrhagic E. colo (EHEC) including 0157:H7 strain

A
  1. toxin
    - Shiga-like toxin (SLT)
  2. mechanism
    - -inactivate 60S ribosome by removing adenine from rRNA
  3. manifestation
    - SLT enhances cytokine release, causing HUS; unlike Shigella, EHEC does not invade host cells
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53
Q

Bugs with exotoxins that increase fluid secretion (3)

A
  1. enterotoxigenic E. Coli (ETEC)
  2. Bacillus anthracis
  3. Vibrio cholerae
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54
Q

Bugs with exotoxins that increase fluid secretion

  1. toxin
  2. mechanism
  3. manifestation

enterotoxigenic E. Coli (ETEC)

A
  1. toxin
    - heat-labile toxin (LT); is an ADP ribosylating A-B toxin: -B binding component binds to host cell surface receptor, enabling endocytosis;
    - A active component attaches ADP-ribosyl to disrupt host cell proteins
    - Heat-stable toxin (ST)
  2. mechanism
    - heat-labile: overactivates adenylate cyclase (inc cAMP) lead to inc Cl- secretion in gut & H20 efflux
    - heat-stable: overactivate guanylate cyclase (inc cGMP) lead to dec resorption of NaCl & H2O in gut
  3. manifestation
    - watery diarrhea: labile in the Air (Adenylate cyclase), stable on the Ground (Guanylate cyclase)
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55
Q

Bugs with exotoxins that increase fluid secretion

  1. toxin
  2. mechanism
  3. manifestation

Bacillus anthracis

A
  1. toxin
    - edema factor
  2. mechanism
    - mimics the adenylate cyclase enzyme (inc cAMP)
  3. manifestation
    - likely responsible for characteristic edematous borders of black eschar in cutaneous anthrax
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56
Q

Bugs with exotoxins that increase fluid secretion

  1. toxin
  2. mechanism
  3. manifestation

Vibrio cholerae

A
  1. toxin
    - cholera toxin; is an ADP ribosylating A-B toxin: -B binding component binds to host cell surface receptor, enabling endocytosis;
    - A active component attaches ADP-ribosyl to disrupt host cell proteins
  2. mechanism
    - overactivates adenylate cylcase (inc cAMP) by permanently activating Gs leading to inc Cl- secretion in gut & H2O efflux
  3. manifestation
    - voluminous “rice-water” diarrhea
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57
Q

Bugs with exotoxins that inhibit phagocytic ability (1)

  1. toxin
  2. mechanism
  3. manifestation
A

Bordetella pertussis

  1. toxin
    - pertussis toxin; is an ADP ribosylating A-B toxin: -B binding component binds to host cell surface receptor, enabling endocytosis;
    - A active component attaches ADP-ribosyl to disrupt host cell proteins
  2. mechanism
    - overactivates adenylate cyclase (inc cAMP) by disabling Gi, impairing phagocytosis to permit survival of microbe
  3. manifestation
    - Whooping cough: child coughs on expiration and whoops on inspiration; toxin may not actually be cause of cough; can cause 100-day cough in adults
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58
Q

Bugs with exotoxins that inhibit release of neurotransmitter (2)

A
  1. clostridium tetani

2. clostridium botulinum

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59
Q

Bugs with exotoxins that inhibit release of neurotransmitter:

  1. toxin
  2. mechanism
  3. manifestation

clostridium tetani

A
  1. toxin
    - tetanospasmin
  2. mechanism
    - Cleave SNARE protein required for neurotransmitter release
  3. manifestation
    - muscle rigidity and lock jaw
    - toxin prevents release of inhibitory (GABA & glycine) neurotransmitters in spinal cord
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60
Q

Bugs with exotoxins that inhibit release of neurotransmitter:

  1. toxin
  2. mechanism
  3. manifestation

clostridium botulinum

A
  1. toxin
    - botulinum toxin
  2. mechanism
    - Cleave SNARE protein required for neurotransmitter release
  3. manifestation
    - flaccid paralysis, floppy baby
    - toxin prevents release of stimulatory (ACh) signals at neuromuscular junctions–>flaccid paralysis
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61
Q

Bugs with exotoxins that lyse cell membranes (2)

A
  1. Clostridium perfringens

2. Streptococcus pyogenes

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62
Q

Bugs with exotoxins that lyse cell membranes

  1. toxin
  2. mechanism
  3. manifestation

Clostridium perfringens

A
  1. toxin
    - Alpha toxin
  2. mechanism
    - phospholipase that degrades tissue and cell membrane
  3. manifestation
    - degradation of phospholipid C–>myonecrosis (gas gangrene) and hemolysis (double zone of hemolysis on blood agar)
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63
Q

Bugs with exotoxins that lyse cell membranes

  1. toxin
  2. mechanism
  3. manifestation

Streptococcus pyogenes

A
  1. toxin
    - Streptolysin O
  2. mechanism
    - protein that degrades cell membrane
  3. manifestation
    - lyses RBCs
    - contributes to beta-hemolysis
    - host antibodies against toxin (ASO) used to dx rheumatic fever (do not confuse c immune complexes of poststreptoccocal glomerulonephritis)
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64
Q

Bugs with exotoxins that superantigens causing shock (2)

A
  1. staphylococcus aureus

2. streptococcus pyogenes

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65
Q

Bugs with exotoxins that superantigens causing shock

  1. toxin
  2. mechanism
  3. manifestation

staphylococcus aureus

A
  1. toxin
    - toxic shock syndrome toxin (TSST-1)
  2. mechanism
    - bring MHC II & TCR in proximity to outside of antigen binding site to cause overwhelming release of IFN-gamma & IL-2 leading to shock
  3. manifestation
    - toxic shock syndrome: fever, rash, shock
    - other toxins cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin)
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66
Q

Bugs with exotoxins that superantigens causing shock

  1. toxin
  2. mechanism
  3. manifestation

streptococcus pyogenes

A
  1. toxin
    - exotoxin A
  2. mechanism
    - bring MHC II & TCR in proximity to outside of antigen binding site to cause overwhelming release of IFN-gamma & IL-2 leading to shock
  3. manifestation
    - toxic shock syndrome: fever, rash, shock
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67
Q

What is endotoxin and the signs & symptoms

A

-a lipopolysaccharide found in outer membrane of gram - bact
**ENDOTOXIN
Edema
Nitric oxide
DIC/Death
Outer membrane
TNF-alpha
O-antigen
-Xtremely heat stable
-IL-1
-Neutrophil chemotaxis

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68
Q

bacterial growth curve:

  1. lag phase
  2. exponential/log phase
  3. stationary phase
  4. death
A
  1. lag phase
    - metabolic activity w/o division
  2. exponential/log phase
    - rapid cell division. penicillins and cephalosporins act here as peptidoglycan is being made
  3. stationary phase
    - nutrient depletion slows growth. Spore formation in some bacteria
  4. death
    - prolonged nutrient depletion and buildup of waste products lead to death
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69
Q

bacterial genetics: transformation

A

a-ability to take up naked DNA (ie. from cell lysis) from environment (also known as competence)

  • a feature of many bact, especially S. pneumoniae, H. influenzae type B, and Neisseria (SHiN)
  • any DNA can be used
  • adding deoxyribonuclease to environment will degrade naked DNA in medium–>no transformation seen.
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70
Q

bacterial genetics: 2 types of conjugation

A
  1. F+ x F-
    - F+ plasmid contains genes required for sex pilus and conjugation
    - bact w/o this plasmid are termed F-
    - plasmid (dsDNA) is replicated and transferred through pilus from F+ cell
    - no transfer of chromosomal genes
  2. Hfr x F-
    - F+ plasmid can become incorporated into bacterial chromosomal DNA, termed high-frequency recombination (Hfr) cell
    - replication of incorporated plasmid DNA may include some flanking chromosomal DNA
    - transfer of plasmid & chromosomal genes
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71
Q

bacterial genetics: transposition

A
  • segment of DNA that can jump (excision & reintergration) from one location to another, can transfer genes from plasmid to chromosome and vice versa
  • when excision occurs, may include some flanking chromosomal DNA, which can be incorporated into a plasmid and transferred to another bacterium
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72
Q

bacterial genetics: generalized transduction

A
  1. generalized
    - a packaging event
    - lytic phage infects bacterium, leading to cleavage of bacterial DNA
    - parts of bacterial chromosomal DNA may become packaged in viral capsid
    - phage infects another bacterium, transferring these genes
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73
Q

bacterial genetics: specialized transduction

A
  1. specialized
    - an excision event
    - lysogenic phage infects bacterium
    - viral DNA incorporates into bact chromosome
    - when phage DNA is excised, flanking bact genes may be excised with it.
    - DNA is packaged into phage viral capsid and can infect another bacterium
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74
Q

lysogeny, specialized transduction

A
  • genes for the following 5 bacterial toxins encoded in a lysogenic phage:
    1. ShigA-like toxin
    2. Botulinum toxin (certain strains)
    3. Cholera toxin
    4. Diphtheria toxin
    5. Erythrogenic toxin of Streptococcus pyogenes
  • *ABCDE
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75
Q

ID of gram+ cocci: Staphylococci

A

NOvobiocein-Saprophyticus is Resistant; Epidermidis is Sensitive
-on the office’s staph retreat, there was NO StRESs

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76
Q

ID of gram+ cocci: Streptococci

A

Optochin- Viridans is Resistant; Pneumoniae is Sensitive
**OVRPS (overpass)
Bacitracin-group B strep are Resistant; group A strep are sensitive
**B-BRAS

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77
Q

alpha-hemolytic bacteria

A
  • form green ring arpund colonies on blood agar
  • include the following organisms:
    1. streptococcus pneumoniae-catalase negative & optochin sensitive
    2. viridans streptococi-catalse negative & optochin resistant
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78
Q

Beta-hemolytic bact

A

form clear area of hemolysis on blood agar. Include:

  1. staphyloccus aureus-catalase & coagulase +
  2. streptococcus pyogenes-group A strep; catalse neg & bacitracin sensitive
  3. streptococcu agalactiae-group B strep; catalase neg & bacitracin resistant
  4. Listeria moncytogenes- tumbling motility, menigitis in newborns, unpasterurized milk
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79
Q

Staphylococcus aureu

  1. what is it
  2. what it causes
A
  1. what is it
    - gram+ cocci in clusters
    - protein A (virulence factor) binds Fc-IgG, inhibiting complement fixation and phagocytosis
  2. what it causes
    - inflammatory dz; skin infections, organ abscesses, pneumonia
    - toxin-mediated dz; toxic shock syndrome (TSST-1), scalded skin syndrome (exfoliative toxin), rapid-onset food poisoning (enterotoxins)
    - MRSA (methicillin-resistant S. aureus) infection; important causes of serious nosocomial & community acquired infections; resistant to beta-lactams becuz of altered penicillin-binding protein
    - S. aureus food poisoning is due to ingestion of preformed toxin
    - causes acute bacterial endocarditis, osteomyelitis
    - Staph make ctalse bcuz they have more staff. Bad staph (aureus) make coagulase and toxins. forms fibrin clot around self; can lead to abscess.
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80
Q

what is TSST

A
  • is a superantigen that binds to MHC II and T-cell receptor, resulting in polyclonal T-cell activation.
  • presents as fever, vomiting, rash, desquamation, shock, end-organ failure
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81
Q

staphylococcus epidermidis

A

infects prosthetic devices and intravenous catheters by producing adherent biofilms
-component of normal skin flora; contaminates blood cultures

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82
Q

Streptococcus oneumoniae

  1. what is it?
  2. causes?
A
  1. lancet-shaped, gram+ diplococci. encapsulated. IgA protease
    2.causes:
    Meningitis
    Otitis media in children
    Pneumonia
    Sinusitus
    ***S. pneumoniae MOPS are Most OPtochin Sensitive
    -Pneumococcus is associate with rusty sputum, sepsis in sickle cell anemia and splenectomy
    -no virulence w/o capsule
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83
Q

viridans group streptococci

A
  • viridans strep are alpha-hemolytic
  • they are normal flora of oropharynx and cause dental caries (strep mutans) and subacute bact endocarditis at damaged valves (S. sanguis)
  • resistant to optochin, differentiating them from S. pneumoniae, which is alpha-hemolytic but is optochin sensitive
  • sanguis=blood. lots of blood in heart, endocarditis
  • S. sanguis sticks to damaged valves by making glycocalyx
  • viridans group strep live in the mouth bcuz they are not afraid of the chin (op-to-chin) resistant)
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84
Q

streptococcus pyogenes: group A streptococci

  1. causes
  2. sensitivity
A

causes:

  1. pyogenic-pharyngitis, cellulitis, impetigo
  2. toxigenic-scarlet fever, toxic shock-like syndrome, necrotizing fasciitis
  3. mmunologic-rheumatic fever, acute glomerulonephritis
    - bacitracin sensitive
    - antibodies to M protein enhance host defenses against S. pyogenes but can give rise to rheumatic fever
    - ASO titer detects recent S. pyogenes infection
    - Pharyngitis can result in rheumatic phever and glomerulonephritis
    - impetigo more commonly precedes glomerulonephritis than pharyngitis
    - scarlet fever: scarlet rash sparing face, strawberry (scarlet) tongue, scarlet throat
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85
Q

**J<3NES criteria to dx rheumatic fever:

A

JOints-arthritis

s chorea

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86
Q

streptococcus agalactiae: group B streptococci

A
  • bacitracin resistant, beta-hemolytic, colonizes vagina; causes pneumonia, meningitis, and sepsis, mainly in babies
  • produces CAMP factor, which enlarges the area of hemolysis formed by S. aureus (CAMP is the authors’ name for the test not cyclic AMP)
  • screen pregnant XX at 35-37 wks
  • pt with positive culture receive intrapartum penicillin prophylaxis
  • *group B for Babies
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87
Q

enterococci: group D streptococci

A
  • enterocicci (enterococcus faecalis and E. faecium) are normal flora that are penicillin G resistant and cause UTI, biliary tract infections, subacute endocarditis
  • Lancefield group D includes the enterococci and the nonenterococcal group D streptpcocci
  • Lancefield grouping is based on differences in the C carbohydrate on the bacterial cell wall.
  • variable hemolysis
  • VRE (vancomycin-resistant enterococci) are an important cause of nosocomial infection
  • enterococci, hardier than nonenterococcal group D, can grow in 6.5% NaCl and bile (lab test)
  • Entero=intestine, faecalis=feces, strepto=twisted (chains), coccus=berry
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88
Q

streptococcus bovis:group D streptococci

A
  • colonizes the gut.
  • can cause bacteremia and subacute endocarditis in colon CA pts.
  • *Bovis in the Blood=CA int he Colon
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89
Q

Corynebacterium diphtheriae

A

-causes diphtheria via exotoxin encoded by beta-prophage
-potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2
-symptoms include pseudomembranous pharyngitis (grayish-white membrane) with lymphadenopathy, myocarditis, and arrhythmias
-lab dx based on gram+ rods with metachromatic (blue&red) granules and Elek’s test for toxin
-toxoid vaccine prevents diphtheria
-Coryne=club shaped
-black colonies on cysteine-tellurite agar
-***ABCDEFG
ADP-ribosylation
-Beta-prophage
-Corynebacterium
-Diphtheria
-Elongation Factor 2
-Granules

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90
Q

spores: bacterial

A
  • some bact can form spores at the end of the stationary phase when nutrients are limited
  • spores are highly resistant to heat and chemicals
  • have dipicolinic acid in their core
  • have no metabolic activity
  • must autoclave to kill spores (as is done to surgical equipment) by steaming at 121C for 15 minutes
  • spore-forming gram+ bacteria found in soil: Bacillus anthracis, Clostridium perfringens, C. tetani
  • other spore formers include B. cereus, C. botulinum, Coxiella burnetii
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91
Q

what are Clostridia with toxins?

name the four.

A
  • gram+, spore-forming, obligate anaerobic bacilli
    1. C. tetani
    2. C. botulinum
    3. C. perfringens
    4. C. difficile
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92
Q

Clostridia with toxins: C. tetani

A

-produces tetanospasmin, an exotoxin causing tetanus
-tetanus toxin (and botulinum toxin) are proteases that cleave releasing protein for neurotransmitters
-Tetanus is tetanic paralysis (blocks glycine & GABA release, which are inhibitory neurotransmitters) from Renshaw cells in spinal cord
-causes spastic paralysis, trismus (lockjaw), and risus sardonicus
-

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93
Q

Clostridia with toxins: C. botulinum

A
  • produces a preformed, heat-liable toxin that inhibits ACh release at the neuromuscular junction, causing botulism
  • in adult, dz is caused by ingestion of preformed toxin
  • in babies, ingestion of spores in honey causes dz (floppy baby syndrome)
  • **botulinum is from bad bottles of food an honey (causes a flaccid paralysis)
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94
Q

Clostridia with toxins: C. perfringens

A
  • produces alpha-toxin (lecithinase, a phospholipase) that can cause myonecrosis (gas gangrene) and hemolysis
  • **Perfringens perforates a gangrenous leg
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95
Q

Clostridia with toxins: C. difficile

A
  • produces 2 toxins
  • toxin A, enterotoxin, binds to the brush border of the gut.
  • toxin B, cytotoxin, destroys the cytoskeletal structure of enterocytes, causing pseudomembranous colitis
  • often 2’ to abx use, especially clindamycin or ampicillin
  • dx by detection of one or both toxins in stool
  • **Difficile causes diarrhea
  • tx: metronidazole or oral vancomycin
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96
Q
  1. anthrax caused by

2. 2 types

A
  • caused by Bacillus anthracis, gram +, spore-forming rod that produces anthrax toxin
  • the only bacterium with a polypeptide capsule (contains D-glutamate)
    1. cutaneous anthrax
    2. pulmonary anthrax
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97
Q

cutaneous anthrax

A

contact–> black eschar (painless ulcer); can progress to bacteremia and death
-black skin lesions-black eschar (necrosis) surrounded by edematous ring. Caused by lethal factor and edema factor

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98
Q

pulmonary anthrax

A
  • inhalation of spores–>flu-like symptoms that rapidly progress to fever, pulmonary hemorrhage, mediastinitis, shock
  • Woolsorter’s dz- inhalation of spores from contaminated wool
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99
Q

bacillus cereus

A
  • causes food poisoning
  • spores survive cooking rice
  • keep rice warm results in germination of spores nad enterotoxin formation
  • emetic type usually seen with rice and pasta
  • n/v within 1-5 hours caused by cereulide, a preformed roin
  • diarrhea type causes watery, nonbloody diarrhea and GI pain in 8-18 hrs.
  • reheated rice syndrome
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100
Q

listeria monocytogenes

A
  • facultative intracelluar microbe; acquired by ingestion of unpasteurized milk/cheese and deli meats or by vaginal transmission during birth
  • form actin rockets by which they move from cell to cell.
  • characteristic tumbling motility
  • can cause amnionitis, septicemia, spontaneous abortion in pregnant xx
  • granulomatosis infantiseptica, neonatal meningitis in immunocompromised pts
  • mild gastroenteritis in healthy indivisuals
  • tx: gastroenteritis usually self-limited; ampicillin in infants, immunocompromised pts, and the elderly in empirical tx of meningitis
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101
Q

actinomyces vs. nocardia

A

both form long, branching filaments resembling fungi
act
1.gram+ anaerobe
2.not acid fast
3.normal oral flora
4.causes oral/facial abscesses that drain through sinus tracts, forms yellow “sulfur granules.”
5.tx c penicillin

noc

  1. gram+ aerobe
  2. acid fast
  3. found in soil
  4. causes pulmonary infections in immunocompromised & cutaneous infections after trauma in immunocompetent
  5. tx c sulfonamides
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102
Q

mycobacteria

TB symtoms:

A
  • Mycobacterium tuberculosis (TB, often resistant to multiple drugs)
  • M. kansasii- pulmonary TB-like symptoms
  • M. avium-intracellulare, causes disseminated non TB dz in AIDS; often resistant to multiple drugs
  • prophylactic tx c azithromycin
  • all mycobacteria are acid fast organisms
  • TB symtoms: fever, night sweats, wt loss, hemoptysis
  • cord factor in virulent strains inhibits macrophage maturation and induces release TNF alpha
  • sulfatides- surface glycolipids; inhibit phagolysosmal fusion
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103
Q

leprosy (Hansen’s dz)

  1. caused by
  2. 2 forms
  3. drug therapy
A
  • caused by Mycobacterium leprae, an acid-fast bacillus that likes cool temperature (infects skin & superficial nerves–“glove & stocking” loss of sensation) and cannot be grown in vitro
  • reservoir in US: armadillos
  1. Lepromatous- presents diffusely over skin and is communicable; characterized by low cell-mediated immunity with a humoral Th2 response
  2. Tuberculoid-limited to a few hypoesthetic, hairless skin plagues; characterized by high cell-mediated immunity with a largerly Th1-type immune response
    - multidrug therapy consisting of dapsone nad rifampin for 6 months for tuberculoid form and dapsone, rifampin, clofazimine for 2-5 yrs for lepromatous form
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104
Q

lactose-fermenting enteric bact

A
  • grow pink colonies on MacConkey’s agar
  • eg: Citrobacter, Klebsiella, E. coli, Enterobacter, and Serratia
  • **-lactose is KEE
  • Test with MacConKee’s agar
  • E. coli produces beta-galactosidase, which breaks down lactose into glucose & galactose
  • EMB agar-lactose fermenters grow as purple/black colonies
  • E.coli grows purple colonies c a green sheen
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105
Q

penicillin & gram negative bugs

A
  • gram- bacilli are resistant to penicillin G but may be usceptible to penicillin derivatives such as ampicillin and amoxicillin
  • gram neg outer membrane layer inhibits entry of penicillin G and vancomycin
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106
Q

Neisseria

2 types

A
  • gram neg diplococci
  • both ferment glucose and produce IgA proteases
  • N. gonorrhoeae within polymorphonuclear leukocytes
  • *MeninGococci ferment Maltose and Glucose.
  • *Gonococci ferment Glucose
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107
Q

gonococci vs. meningococci

A

gonococci

  1. no polysaccharide capsule
  2. no maltose fermentation
  3. no vaccine-due to rapid antigenic variation of pilus proteins
    - sexually transmitted
    - causes gonorrhea, septic arthritis, neonatal conjunctivitis, PID, Fitz-Hugh-Curtis syndrome
    - tx: ceftriaxone + (azithromycin, doxycycline) for possible chlamydia coinfection

meningococci

  1. polysaccharide capsule
  2. maltose fermentation
  3. vaccine–none for type B
  4. respiratory & oral secretions
  5. causes meningococcemia & meningitis, Waterhouse-Friderichsen syndrome
  6. rifampin, ciprofloxacin, ceftriaxone prophylaxis in close contacts
  7. tx: ceftriaxone or penicillin G
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108
Q

Haemophilus influenzae

A
  • HaEMOPhilus causes Epiglottis (cherry red in children), menigitis, otitis media, pneumonia
  • small gram- (coccobacillary) rod
  • aerosol transmission
  • most invasive dz caused by capsular type B
  • nontypeable strains cause mucosal infections (otitis media, conjunctivitis, bronchitis)
  • produces IgA protease
  • culture on chocolate agar requires factors V (NAD+) and X (hematin) for growth; can also be grown with S. aureus, which provides factor V.
  • treat meningitis with ceftriaxone
  • rifampin prophylaxis in close contacts
  • when a child has flu, mom goes to five (V) and dime (X) store to buy some chocolate
  • vaccine contains type B capsular polysaccharide (polyribosylribitol phosphate) conjugated to diptheria toxoid or other protein
  • given btw 2-18 mos of age
  • does not cause the flu (influenza virus does)
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109
Q

Legionella pneumophilia

A

Legionnaire’ dz=severe pneumonia, fever, GI, CNS symptoms

  • pontiac fever-mild flu-like syndrome
  • gram neg rod
  • gram stains poorly- use silver stain
  • grow on charcoal yeast extract culture with iron & cysteine
  • detected clinically by presence of antigen in urine
  • aerosol transmission from environmental water source habitat
  • no person-to-person transmission
  • tx: macrolide or quinolone
  • think of a French legionnaire (soldier) with his silver helmet, sitting around a campfire (charcoal) with his iron dagger–he is no sissy (cystein)
  • labs show hyponatremia
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110
Q

pseudomonas aeruginosa

A

PSEUDOmonas is associated with wound and burn infections, Pneumonia (especially in cycstic fibrosis), Sepsis (black lesions on skin), external otitis (swimmer’s ear), UTI, Drug use and Diabetes Osteomyelitis, and hot tub folliculitis

  • malignant otitis externa in diabetics
  • aerobic gram- rod
  • nonlactose fermenting, oxidase positive
  • produces pyocyanin (blue-green) pigment; has a grape-like odor
  • water source
  • produces endotocin (fever, shock), and exotoxin A (inactivates EF-2)
  • tx: aminoglycoside plus extended spectrum penicillin (eg. piperacillin, ticarcillin)
  • Aeruginosa-aerobic
  • think water connection and blue-green pigment
  • think Pseudomonas in burn victims
  • chronic pneumonia in CF patients is associated with biofilm
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111
Q
  1. E. coli

2. 4 strains

A
  1. E. coli virulence factors: fimbriae—cystitis & pyelonephritis; K capsule–pneumonia, neonatal meningitis; LPS endotoxin—septic shock
  2. EIEC, ETEC, EPEC, EHEC (P.I.T.H)
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112
Q

E. coli strain:toxin & mechaism, presentation

EIEC

A
  • microbe invades intestinal mucosa and causes necrosis & inflammation. No toxins produced. Clinical manifestatios similar to Shigella
  • Invasive; dysentery
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113
Q

E. coli strain:toxin & mechaism, presentation

ETEC

A
  • labile toxin/stable toxin. No inflammation or invasion

- Traveler’s diarrhea (watery)

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114
Q

E. coli strain:toxin & mechaism, presentation

EPEC

A
  • no toxin produced. adheres to apical surface, flattens villi, prevents absorption
  • diarrhea usually in children (Pediatrics)
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115
Q

E. coli strain:toxin & mechaism, presentation

EHEC

A
  • O157:H7 is the most common serotype. Produces Shiga-like toxin and Hemolytic-uremic syndrome (triad of anemia, thrombocytopenia, and acute renal failure)
  • endothelium swells and narrows lumen, leading to mechanical hemolysis and reduced renal blood flow; damaged endothelium consumes platelets
  • dysentery (toxin alone causes necrosis and inflammation)
  • does not ferment sorbitol (distinguishes it from other E. coli)
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116
Q

Klebsiella

A
  • an intestinal flora that causes lobar pneumoni in alcoholics and diabetics when aspirated
  • very mucoid colonies caused by abundant polysaccharide capsule
  • red currant jelly sputum
  • also cause of nosocomial UTIs
  • **4 As
    1. Aspiration pneumonia
    2. Abscess in lungs & liver
    3. Alcoholics
    4. diAbetics
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117
Q

Salmonella vs. Shigella

A

Salmonella

  1. have flagella (salmon swim)
  2. can disseminate hematogenously
  3. have many animal reservoirs
  4. produce hydrogen sulfide
  5. antibiotics may prolong symptoms
  6. invades intestinal mucosa and causes a monocytic response
  7. can cause bloody diarrhea
  8. does not ferment lactose

Shigella

  1. no flagella
  2. cell to cell transmission; no hematogenous spread
  3. only reservoirs are human & primates
  4. does not produce hydrogen sulfide
  5. antibiotics prolong excretion of organism in feces
  6. invades intestinal mucosa and causes PMN infiltration
  7. often causes bloody diarrhea
  8. does not ferment lactose
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118
Q

salmonella typhi

A
  • causes typhoid fever
  • found only in humans
  • characterized by rose spots on the abdomen, fever, HA, diarrhea
  • can remain in gallbladder and cause a carrier state
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119
Q

campylobacter jejuni

A
  • major cause of bloody diarrhea, especially in children
  • fecal-oral transmission through foods such as poultry, meat, unpasteurized milk
  • comma or S-shaped, oxidase positive, grows at 42C
  • **Campylobacter likes the hot campfire
  • common antecedent to Guillain-Barre syndrome and reactive arthritis
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120
Q

vibrio cholerae

A
  • produces profuse rice-water diarrhea via toxin that permanently activates Gs, inc cAMP
  • comma shaped, oxidase positive, grows in alkaline media
  • endemic to developing countries
  • prompt oral rehydration is necessary
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121
Q

Yersinia enterocolitica

A
  • usually transmitted from pet feces (eg. puppies), contaminated milk, pork
  • causes mesenteric adenitis that can mimic Crohn’s or appendicitis
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122
Q

Helicobacter pylori

A
  • causes gastritis and up to 90% of duodenal ulcers
  • risk factor for peptic ulcer, gastric adenocarcinoma, lymphoma
  • curved gram neg rod
  • urease positive (can use urea breath test for dx)
  • creates alkaline environment
  • most common initial tx is triple therapy: proton pump inhibitor; clarithromycin; amoxicillin or metronidazole
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123
Q

spirochetes

A
  • the spirochetes are spiral-shaped bact c axial filaments and include Borrelia (big size), Leptospira, Treponema
  • *BLT; B is big
  • only Borrelia can be visualized using aniline dyes (Wright’s or Giemsa stain) in light microscopy.
  • Treponema is visualized by dark-field microscopy
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124
Q

Leptospira interrogans

A
  • found in water contaminated with animal urine, causes leptospirosis: flu-like symptoms, jaundice, photophobia with conjunctivitis
  • prevalent among surfers and in tropics
  • Weil’s dz (icterohemorrhagic leptospirosis) severe form with jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, anemia
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125
Q

Lyme dz

  1. caused by
  2. stages
A

caused by Borrelia burgdorferi, which is transmitted by the tick Ixodes (also vector for Babesia)

  • natural reservoir is mouse, important for tick life cycle
  • common in northeastern US
  • tx: doxycycline, ceftriaxone

Stage
1.erythema chronicum migrans (expanding bull eye red rash with central clearing), flu like symptoms
2.neurologic (facial nerve palsy) and cardiac (AV block) manifestations
3.musculoskeletal (chronic monoarthritis and migatory polyarthritis), neurologic (encephalopathy and polyneuropathy) and cutaneous manifestations
***FAKE a key Lyme pie
Facial nerve palsy (typically bilateral)
Arthritis
Kardiac block
Erythema migrans

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126
Q

1’ syphilis

A

-caused by spirochete Treponema pallidum
-tx penicillin G
1’
-localized disease presenting c painless chancre. screen c VDRL and confirm diagnose c FTA-ABS

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127
Q

2’ syphilis

A

-caused by spirochete Treponema pallidum
-tx penicillin G
2’
-disseminated dz c constitutional symptoms, maculopapular rash (palms & soles), condylomata lata
-treponemes are present in chancres of 1’ and condylomata lata of 2’ syphilis and may be directly visualized through dark-field microscopy
-screen with VDRL and confirm diagnosis with FTA-ABS
-secondary syphilis=Systemic

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128
Q

3’ syphilis

A

-caused by spirochete Treponema pallidum
-tx penicillin G
3’
-Gummas (chronic granulomas), aortitis (vasa vasorum destruction), neurosyphilis (tabes dorsalis), Argyll Robertson pupil
-signs: broad-based ataxia, positive Romberg, Charcot joint, stroke w/o HTN
-test spinal fluid c VDRL

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129
Q

congenital syphilis

A

-caused by spirochete Treponema pallidum
-tx penicillin G
congenital
-Saber shins, saddle nose, CN VIII deafness, Hutchinson’s teeth, mulberry molars
-early prevention is key, as placental transmission typically occurs after first trimester

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130
Q

Argyll Robertson pupil

A
  • Argyll Robertson pupil constricts c accomondation but is not reactive to light
  • associated c 3’ syphilis
  • prostitute’s pupil–accommodates but does not react
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131
Q

VDRL false positives

A

VDRL detects nonspecific antibody that reacts with beef cardiolipin
-used for dx of syphilis, but many false positives, including viral infection (mononucleosis, hepatitis), some drugs, rheumatic fever, SLE, and leprosy
**VDRL
Viruses (mono, hepatitis)
Drugs
Rheumatic fever
Lupus and leprosy

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132
Q

Jarisch-Herxheimer reaction

A

-flu-like syndrome immediately after abx are started due to killed bact releasing pyrogens

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133
Q

Zoonotic bact

A

zoonosis: infectious dz transmitted btw animals & humans

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134
Q

Zoonotic bact species: dz, transmission & source

Bartonella spp.

A
  • Cat scratch dz

- cat scratch

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135
Q

Zoonotic bact species: dz, transmission & source

Borrelia burgdorferi

A
  • lyme dz

- Ixodes ticks (live on deer & mice)

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136
Q

Zoonotic bact species: dz, transmission & source

Borrelia recurrentis

A
  • recurrent fever

- louse (recurrent bcuz of variable surface antigens)

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137
Q

Zoonotic bact species: dz, transmission & source

Brucella spp.

A
  • Brucellosis/undulant fever

- unpasteurized diary

138
Q

Zoonotic bact species: dz, transmission & source

Campylobacter

A
  • bloody diarrhea

- puppies, livestock (fecal-oral, ingestion of undercooked meat)

139
Q

Zoonotic bact species: dz, transmission & source

Chlamydophila psittaci

A
  • psittacosis

- parrots, other birds

140
Q

Zoonotic bact species: dz, transmission & source

Coxiella burnetii

A
  • Q fever

- aerosols of cattle/sheep amniotic fluid

141
Q

Zoonotic bact species: dz, transmission & source

Ehrlichia chaffeensis

A
  • Ehrlichiosis

- lone star tick

142
Q

Zoonotic bact species: dz, transmission & source

Francisella tularensis

A
  • Tularemia

- Ticks, rabbits, deer fly

143
Q

Zoonotic bact species: dz, transmission & source

Leptospira spp.

A

Leptospirosis

-animal urine

144
Q

Zoonotic bact species: dz, transmission & source

Mycobacterium leprae

A

leprosy

-armadillos and humans with lepromatous leprosy

145
Q

Zoonotic bact species: dz, transmission & source

Pasteurella multocida

A
  • cellulitis, osteomyelitis

- animal bite, cats, dogs

146
Q

Zoonotic bact species: dz, transmission & source

Rickettsia prowazekii

A

epidemic typhus

-Louse

147
Q

Zoonotic bact species: dz, transmission & source

Rickettsia ricketsii

A

rocky mountain spotted fever

-Dermacentor tick bite

148
Q

Zoonotic bact species: dz, transmission & source

Rickettsia typhi

A

endemic typhus

-fleas

149
Q

Zoonotic bact species: dz, transmission & source

Yersinia pestis

A

plague

-fleas (rats & prairie dogs are reservoirs)

150
Q

Gardnerella vaginalis

A
  • A pleomorphic, gram-varibale rod that causes vaginosis presenting as a gray vaginal discharge with a fishy smell; nonpainful.
  • Associated with sexual activity but not STD.
  • bact vaginosis is characterized by overgrowth of certain bacteria in vagina.
  • Clue cells or vaginal epithelial cells covered with bact are visible under microscope.
  • Tx: metronidazole.
  • *I don’t have a clue why I smell fish in the vagina garden
151
Q

Rickettsial dz and vector-borne illness.

A
  • Rash vs. No Rash

- treatment for all: doxycycline

152
Q

Rickettsial dz and vector-borne illness

Rash

A

-Rocky Mountain spotted fever (tick)–Rickettsia rickettsii
-Broadly distributed in US
-rash typically starts at wrists and ankles and then spreads to trunk, palms, and soles
-Rickettsiae are obligate intracelluar organisms that need CoA and NAD+
Typhus:
-endemic (fleas)–R. typhi
-epidemic (human body louse)–R.. prowazekii. Rash starts centrally and spreads out, sparing palms & soles
-classic triad–HA, fever, rash (vasculitis)
**Rickettsii on the wRist, Typhus on the Trunk
**Palm & sole rash is seen in:
-Coxsackievirus A infection (hand, foot, mouth disease)
-Rocky Mountain spotted fever, secondary Syphilis ***you drive CARS using your palms & soles

153
Q

Rickettsial dz and vector-borne illness

No Rash

A

Ehrlichiosis (tick)–Ehrlichia
-monocytes c morula (berry-like inclusion) in cytoplasma
-anaplasmosis (tick)–Anaplasma. Granulocytes c morula in cytoplasma
-Q fever (tick feces & cattle placenta release spores that are inhaled as aerosols)–Coxiella burnetii.
No arthropod vector. Presents as pneumonia
**Q fever is Queer bcuz it has no rash or vector and its caustive organism can survive outside in its endospore form. not int he Rickettsia genus, but closely related

154
Q

Chlamydiae

A

-Chlamydiae cannot make their own ATP
-they are obligate intracelluar organisms that cause mucosal infections
2 forms:
1.elementary body-small dense is Enfectious and Enters cell via Endocytosis
2.Reticulate body Replicates inc ell by fission; form seen on tissue culture
-Chlamydia trachomatis causes reactive arthritis, conjunctivitis, nongonococcal urethritis and PID
-C. pneumoniae & C. psittaci cause atypical pneumonia; transmitted by aerosol
-treatment: azithromycin–favored bcuz one-time tx or doxycycline
***Chlamys=cloack (intracelluar)
**Chamydophila psittaci-notable for an avian reservoir
-lab dx: cytoplasmic inclusions seen on Giemsa or fluorescent antibody–stained smear. The chlamydial cell wall is unusual in that it lacks muramic acid

155
Q

Chlamydia trachomatis serotypes:

  1. Types A, B, C
  2. Types D-K
  3. Types L1, L2, L3
A
  1. Types A, B, C
    - chronic infection, cause blindness due to follicular conjunctivitis in Africa
    - ABC=Afric/Blindness/Chronic infection
  2. Types D-K
    - Urethritis/PID, ectopic pregnancy, neonatal pneumonia (staccato cough), neonatal conjunctivitis
    - D-K=everything else
    - neonatal dz can be cquired during passage through infected birth canal
  3. Types L1, L2, L3
    - lymphogranuloma venereum
156
Q

Mycoplasma pneumoniae

A
  • classic cause of atypical “walking”pneumonia (insidious onset, HA, nonproductive cough, diffuse interstitial infiltrate)
  • X-ray looks worse than patient
  • high titer of cold agglutinins (IgM) which can agglutinate or lyse RBCs
  • grown on Eaton’s agar
  • treatment: macrolide or fluoroquinolone (penicillin ineffective since Mycoplasma have no cell wall)
  • no cell wall. not seen on gram stain
  • bact membrane contains sterols for stability
  • mycoplasmal pneumonia is more common in patients <30 yo
  • frequent outbreaks in military recruits and prisons
157
Q

systemic mycoses

  1. characteristics
  2. types (4)
A
  • all of following can cause pneumonia and can disseminate
  • all caused by dimorphic fungi: cold (20C); heat (37C)
  • only exception is coccidioidomycosis, which is a spherule (not yeast) in tissue
  • treatment: fluconazole or itraconazole for local infection; amphotericin B for systemic infection
  • systemic mycoses can mimic TB (granuloma formation), except unlike TB, have no person-person transmission
    1. Histoplasmosis
    2. Blastomycosis
    3. Coccidioidomycosis
    4. Paracoccidiodomycosis
158
Q

systemic mycoses: endemic location & pathologic features

Histoplasmosis

A
  • Mississippi nad ohio river valleys
  • causes pneumonia
  • macrophage filled with Histoplasma (smaller than RBC)
  • Histo hides (within macrophages)
  • bord or bat droppings
159
Q

systemic mycoses: endemic location & pathologic features

Blastomycosis

A
  • States east of Mississippi River and central America
  • causes inflammatory lung dz and can disseminate to skin and bone
  • forms granulomatous nodules
  • broad-base budding (same size as RBC)
  • **Blasto buds (broadly)
160
Q

systemic mycoses: endemic location & pathologic features

Coccidioidomycosis

A
  • Southwestern US, Califeronia.
  • causes penumonia and menigitis; can disseminate to bone and skin
  • case rate increase after earthquakes (spores in dust are thrown up in the air and become spherule filled with endospores (much larger than RBC)
  • *Coccidio crowds
  • San Joaquin Valley or desrt (desert bumps) valley fever
161
Q

systemic mycoses: endemic location & pathologic features

Paracoccidiodomycosis

A

-latin american
-budding yeast with captain’s wheel formation (much larger than RBC)
Captain wheel appearance
-Paracoccidio parasails with the captain’s wheel all the way to Latin America

162
Q

Cutaneous mycoses: Tinea versicolor & other

A

Tinea versicolor

  • caused by Malassezia furfur
  • degradation of lipids produces acids that damage melanocytes and cause hypopigmented and/or hyperpigmented patches
  • occurs in hot, humid weather
  • treament: topical miconazole, selenium sulfide (selsun)
  • spaghetti and meatball appearance on KOH prep

Other Tinea

  • includes tinea pedis (foot), tinea cruris (groin), tinea corporis (ringworm, on body), tinea capitis (head, scalp), tinea unguium (onychomycosis, on fingernails)
  • pruritic lesions with central clearing resembling a ring, caused by dermatophytes (Microsporum, Trichophyton, Epidermophyton
  • see mold hyphae in KOH prep, not dimorphic
163
Q

Opportunistic fungal infections:

Candida albicans

A

alba=white

  • systemic or superficial fungal infection
  • oral and esophageal thrush in immunicompromised (neonates, steroids, DM, AIDS), vulvovaginitis (DM, use of abx), diaper rash, endocardidiasis (to any organ), chronic mucocutaneous candidiasis
  • treatment: topical azole for vaginal; fluconazole or caspofungi for oral/esophageal; fluconazole, amphotericin B, or caspofungin for systemic
164
Q

Opportunistic fungal infections:

Aspergillus fumigatus

A
  • invasive aspergillos, especially in immunocompromised and those with chronic granulomatous dz
  • allergic bronchopulmonary aspergillosis (ABPA): with asthma or CF
  • aspergillomas in lungc cavities, especially after TB infection
  • some species of Aspergillus produce aflatoxins, which are associated with HCC
  • **Think A for Acute Angles in Aspergillus. Not dimorphic
165
Q

Opportunistic fungal infections:

Cryptococcus neoformans

A
  • cryptococcal meningitis, cryptococcosis
  • heavily encapsulated yeast
  • not dimorphic
  • found in soil, pigeon droppings
  • acquired through inhalation with hematogenous dissemination to meninges
  • culture on Sabouraud’s agar
  • stains with India ink
  • latex agglutination test detects polysaccharide capsular antigen and is more specific
  • soap bubble lesions in brain
166
Q

Opportunistic fungal infections:

Mucor & Rhizopus

A
  • Mucomycosis. Dz mostly in ketoacidotic diabetic & leukemia pts
  • fungi proliferate in blood vessel walls when there is excess ketone and glucose, penetrate cribriform plate and enter brain
  • rhinocerebral, frontal lobe abscesses
  • HA, facial pain, black necrotic eschar on face, may have cranial nerve involvement
167
Q

pneumocystis jirovecii

A
  • causes Pneumocystis pneumonia (PCP), a diffuse interstitial pneumonia
  • yeast (originally classified as protozoan)
  • inhaled
  • most infections are asymptomatic
  • immunosuppression (eg AIDS) predispose to dz
  • diffuse, bilateral CXR appearnace
  • diagnosed by lung biopsy or lavage
  • disc-shaped yeast forms on methenamine silver stain of lung tissue
  • treatment: TMP-SMX, pentamidine, dapsone
  • start prophylaxis when CD4 drops<200 cells/mm3 in HIV pts
167
Q

pneumocystis jirovecii

A
  • causes Pneumocystis pneumonia (PCP), a diffuse interstitial pneumonia
  • yeast (originally classified as protozoan)
  • inhaled
  • most infections are asymptomatic
  • immunosuppression (eg AIDS) predispose to dz
  • diffuse, bilateral CXR appearnace
  • diagnosed by lung biopsy or lavage
  • disc-shaped yeast forms on methenamine silver stain of lung tissue
  • treatment: TMP-SMX, pentamidine, dapsone
  • start prophylaxis when CD4 drops<200 cells/mm3 in HIV pts
168
Q 
Protozoa-GI infections
1. three types
Protozoa-CNS infections
1.three types
Protozoa- Hematologic infections
1.Two types
Protozoa-Others
1. three types
A

Protozoa-GI infections

  • Giardia lamblia
  • Entamoeba histolytica
  • Cryptosporidium

Protozoa-CNS infections

  • Toxoplasma gondii
  • Naegleria fowleri
  • Trypanosoma brucei: T. gambiense, T. Rhodesiense

Protozoa- Hematologic infections

  • Plasmodium: P. vivax/ovale, P. falciparum, P. malariae
  • Babesia
Protozoa-Others
visceral infections
-Trypanosoma cruzi
-Leishmania donovani
STDs
-Trichomonas vaginalis
168
Q

sporothrix schenckii

A
  • sporotrichosis
  • dimorphic, cigar-shaped budding yeast that lives on vegetation
  • when spores are traumatically introduced into the skin, typically by a thorn (rose gardeners’s dz), causes local pustules or ulcer with nodules along draining lymphatics (ascending lymphangitis)
  • little systemic illness
  • treatment: itraconazole or potassium iodide
  • plant a rose in the pot
169
Q 
Protozoa-GI infections
1. three types
Protozoa-CNS infections
1.three types
Protozoa- Hematologic infections
1.Two types
Protozoa-Others
1. three types
A 
Protozoa-GI infections
1. three types
-Giardia lamblia
-Entamoeba histolytica
-Cryptosporidium
Protozoa-CNS infections
1.three types
-Toxoplasma gondii
-Naegleria fowleri
-Trypanosoma brucei: T. gambiense, T. Rhodesiense
Protozoa- Hematologic infections
1.Two types
-Plasmodium: P. vivax/ovale, P. falciparum, P. malariae
-Babesia
Protozoa-Others
1. three types
visceral infections
-Trypanosoma cruzi
-Leishmania donovani
STDs
-Trichomonas vaginalis
170
Q

Protozoa-GI infections: dz, transmission, dx, tx

Giardia lamblia

A

Giardia lamblia

  • Giardiasis: bloating, flatulence, foul-smelling, fatty diarrhea (often seen in campers/hikers). Think fat-rich Ghirardelli chocolates for fatty stools of Giardia
  • cysts in water
  • Trophozoites or cysts in stool
  • metronidazole
171
Q

Protozoa-GI infections: dz, transmission, dx, tx

Entamoeba histolytica

A
  • amebiasis: bloody diarrhea (dysentery), liver abscess (anchovy paste exudate), RUQ pain (histology shows flask-shaoed ulcer if submucosal abscess of colon ruptures)
  • cysts in water
  • serology and/or trophozoites (c RBCs in the cytoplasm) or cyst (c multiple nuclei in stool
  • metronidazole; iodoquinol for asymptomatic cyst passers
172
Q

Protozoa-GI infections: dz, transmission, dx, tx

-Cryptosporidium

A
  • severe diarrhea in AIDS Mild dz (watery diarrhea) in non-immunocompromised
  • cyst in water
  • cysts on acid-fast stain
  • prevention(by filtering city water supplies); nitazoxanide in immunocompetent hosts
173
Q

Protozoa-CNS infections: dz, transmission, dx, tx

-Trypanosoma brucei: T. gambiense, T. Rhodesiense

A
  • African sleeping sickness: enlarged lymph nodes, recurring fever (due to antigenic variation), somnolence, coma
  • Tsetse fly, a painful bite
  • blood smear
  • Suramin for bloodborn dz or melarsoprol for CNS penetration (it sure is nice to go to sleep; melatonin helps with sleep_
174
Q

Protozoa-CNS infections: dz, transmission, dx, tx

-Naegleria fowleri

A
  • rapidly fatal meningoencephalitis
  • swimming in freshwater lakes (think Nalgene bottle filled with freshwater containing Naegleria); enters via cribriform palte
  • amoebas in spinal fluid
  • amphotericin has been effective for a few survivors
175
Q

Protozoa-CNS infections: dz, transmission, dx, tx

-Trypanosoma brucei: T. gambiense, T. Rhodesiense

A
  • African sleeping sickness: enlarged lymph nodes, recurring fever (due to antigenic variation), somnolence, coma
  • Tsetse fly, a painful bite
  • blood smear
  • Suramin for bloodborn dz or melarsoprol for CNS penetration (it sure is nice to go to sleep; melatonin helps with sleep_
176
Q

Protozoa- Hematologic infections: dz, transmission, dx, tx

-Plasmodium: P. vivax/ovale, P. falciparum, P. malariae

A
  • Malaria: fever, HA, anemia, splenomegaly
  • P. vivax/ovale-48 hr cycle (tertian; includes fever on first day and third day thus fevers are actually 48 hr apart); dormant form (hypozoite) in liver
  • P. falciparum–severe; irregular fever patterns; parasitized RBCs occlude capillaries in brain (cerebral malaria), kidneys, lungs
  • P. malariae–72 hr cycle (quartan)
  • mosquito (anopheles)
  • blood smear, trophozoite ring form, RBC schizont with meroites
  • begin with chloroquine, which blocks Plasmodium heme polymerase; if resistant, use mefloquine
  • if life threatening, use intravenous quinidine (test for G6PD deficiency)
  • Vivax/ovale add primaquine for hypnozoite (test for G6PD deficiency)
179
Q

Protozoa- Hematologic infections: dz, transmission, dx, tx

-Babesia

A
  • babesiosis: fever & hemolytic anemia; predominantly in northeastern US; asplenia inc risk of severe dz
  • Ixodes tick (same as Borrelia burgdorferi of Lyme disease; may often coinfect humans)
  • blood smear, ring form, Maltese cross; PCR
  • Atovaquone + azithromycin
180
Q

Protozoa-Others: dz, transmission, dx, tx

Trypanosoma cruzi

A
  • Chagas’ dz: dilated cardiomyopahty, megacolon, megaesophagus; predominantly in South AMerica
  • Reduviid bug (kissing bug), a painless bite (much like a kiss)
  • blood smear
  • Nifurtimox
181
Q

Protozoa-Others: dz, transmission, dx, tx

Leishmania donovani

A
  • visceral leishmaniasis (kala-azar): spiking fevers, hepatosplenomegaly, pancytopenia
  • sandfly
  • macrophages containing amastigotes
  • sodium stibogluconate
182
Q

Protozoa-Others: dz, transmission, dx, tx

STD: Trichomonas vaginalis

A
  • vaginitis: foul smelling, greenish discharge; ithcing and burning; do not confuse with Gardnerella vaginalis, a gram-variable bacterium that causes vaginosis
  • sexual (cannot exist outside human because it cannot form cysts)
  • trophozoites (motile) on wet mount
  • metronidazole for patient and partner (prophylaxis)
183
Q 
Nematodes (roundworms): intestinal
organism, transmission, dz, trx
1.Enterobius vermicularis (pinworm)
2.Ascaris lumbricoides (giant roundworm)
3.Strongyloides stercoralis
4.Ancylostomas duodenale, Necator americanus
(hookworms)
A
  1. Enterobius vermicularis (pinworm)
    - food contaminated c eggs
    - intestinall infection causing anal pruritus (dx via the Scotch Tape test)
    - Bendazoles or pyrantel pamoate (worms are bendy; tx c mebendazole)
  2. Ascaris lumbricoides (giant roundworm)
    - fecal-oral; eggs visible in feces under microscope
    - intestinal infection
    - bendazoles or pyrantel pamoate
  3. Strongyloides stercoralis
    - larvae in soil penetrate the skin
    - intestinal infection causing vomiting, diarrhea, anemia
    - Ivermectin or albendazole

4.Ancylostomas duodenale, Necator americanus
(hookworms)
-larvae penetrate skin
-intestinal infection causing anemia by sucking blood from intestinal walls
-Bendazoles or pyrantel pamoate

184
Q 
Nematodes (roundworms): tissue
organism, transmission, dz, trx
1.Dracunculus medinensis
2.Onchocerca volvulus
3.Loa Loa
4.Wuchereria bancrofti
5.Toxocara canis
A
  1. Dracunculus medinensis
    - in drinking water
    - skin inflammation and ulceration
    - slow extraction of worm
  2. Onchocerca volvulus
    - female blackfly bite
    - hyperpigmented skin and river blindness (black flies, black skin nodules, black sight; allergic reaction to microfilaria possible
    - ivermectin (ivermectin for river blindness)
  3. Loa Loa
    - deer fly, horse fly, mango fly
    - swelling in skin, worm in conjunctiva
    - Diethylcarbamazine
  4. Wuchereria bancrofti
    - female mosquito
    - blocks lymphatic vessels: elephantiasis; takes 9 mo-1 yr after bite to become symptomatic
    - Diethylcarbamazine
  5. Toxocara canis
    - food contaminated with eggs
    - visceral larva migrans
    - albendazole or mebendazole
185
Q

nematode routes of infection

A
  • ingested: Enterobius, Ascaris, Trichinella
  • *you’ll get sick if you EAT these
  • cutaneous: Strongyloides, Ancyclostoma, Necator
  • *These get into your feet from the SANd
186
Q

Cestodes (tapeworm): transmission, dz, tx

  1. Taenia solium
  2. Diphyllobothrium lactum
  3. Echinococcus granulosus
A
  1. Taenia solium
    - ingestion of larvae encysted in undercooked pork–>intestinal infection–>Praziquantel
    - Ingestion of eggs–>cysticercosis, neurocycticercosis–>Praziquantel; bendazoles for neurocysticercosis
  2. Diphyllobothrium lactum
    - ingestion of larvae from raw freshwater fish–>Vit B12 deficiency (tapeworm competes for B12 in intestine)–>anemia–>praziquantel
  3. Echinococcus granulosus
    - ingestion of eggs from dog feces–>cysts in liver, causing anaphylaxis if antigens released (surgeons preinject c ehtanol to kill cysts b4 removal)–>bendazoles
187
Q

Trematodes (flukes): transmission, dz, tx

  1. schistosoma
  2. clonorchis sinensis
  3. paragonimus westermani
A
  1. schistosoma
    - snails are host; cercariae penetrate skin of humans–>liver & spleen granulomas, fibrosis, inflammation. Chronic infection c S. haematobium can lead to squamous cell carcinoma of the bladder–>Praziquantel
  2. clonorchis sinensis
    - undercooked fish–>biliary tract inflammation–>pigmented gallstones associated c cholangiocarcinoma–>Praziquantel
  3. paragonimus westermani
    - undercooked crab meat–>lung inflammation and 2’ bact infection c hemoptysis–>Praziquantel
188
Q

Parasite hints: findings & organism

  1. brain cysts, seizures
  2. liver cysts
  3. vit B12 deficiency
  4. biliary tract dz, cholangiocarcinoma
  5. hemoptysis
  6. portal HTN
  7. hematuria, bladder cancer
  8. microcytic anemia
  9. perianal pruritus
A
  1. Taenia solium (cysticercosis)
  2. Echinococcus granulosus
  3. diphyllobothrium latum
  4. clonorchis sinensis
  5. paragonimus westermani
  6. schistosoma mansoni
  7. schistosoma haematobium
  8. ancylostoma, Necator
  9. enterobius
189
Q

viral genetics:

  1. recombination
  2. reassortment
  3. complementation
  4. phenotypic mixing
A
  1. xchange genes btw 2 chromosomes by crossing over within regions of significant base sequence homology
  2. when viruses c segmented genomes (eg.influenza virus) xchange segments. High frequency recombination. cause of worldwide influenza pandemics
  3. 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 making a functional protein that serves both viruses
  4. occurs c simultaneous infection of a cell c 2 viruses. Genome of virus A can be partially or completely coated (forming pseudovirion) c the surface proteins of virus B. Type B protein coat determines the tropism (infectivity) of the hybrid virus. However, progeny from this infection have a type A coat that is encoded by its type A genetic material
190
Q

Viral vaccines:

  1. live attenuated vaccines
  2. killed
  3. recombinant
A
  1. live attenuated vaccines
    - induce humoral & cell-mediated immunity but have reverted to virulence on rare occasion
    - killed/inactivated vaccines induce only humoral immunity but are stable
    - live attentuated–smallpox, yellow fever, chickenpox (VZV), Sabin’s polio virus, MMR, influenza (intranasal)
    * **Live! One night only. See small yellow chickens get vaccinated with Sabin’s and MMR. It’s incredible.
    - NO booster needed for live attentuated vaccines
    - dangerous to give live vaccines to immunocompromised pts or their close contacts
    - MMR=measles, mumps, rubella (live attenuated vaccine that can be given to HIV-pos pts who do not show signs of immunnodeficiency
  2. killed
    - Rabies, Influenza (injected), Salk Polio, and HAV vaccines
    - SalK=Killed
  3. recombinant
    - HBV (antigen=recombinant HBsAg), HPV (types 6, 11, 16, 18)
191
Q

DNA viral genome

A
  • all DNA viruses except Parvoviridae are dsDNA
  • all are linear except papilloma-, polyoma-, and hepadnaviruses (circular)
  • All are dsDNA (like our cells) except “part-of-a-virus (parvovirus) is ssDNA
  • Parvus=small
192
Q

RNA viral genomes

A
  • all RNA virses except Reoviridae are ssRNA
  • positive-stranded RNA viruses: I went to a retro (retrovirus) toga (togavirus) party, where I drank flavored (flavivirus) Corona (coronavirus) and are hippy (hepevirus) California (calicivirus) pickles (picornavirus)
  • all are ssRNA (like our mRNA) except repeato-virus (reovirus) is dsRNA
193
Q

Naked viral genome infectivity

A
  • purified nucleic acid of most dsDNA (except poxviruses and HBV) and (+) strand ssRNA (=mRNA) viruses are infectioous.
  • naked nucleic acids of (-) strand ssRNA and dsRNA viruses are not infectious
  • they require polymerases contained in the complete virion
194
Q

virus ploidy

A

all viruses are haploid (c 1 copy of DNA or RNA) except retroviruses, which have 2 identical ssRNA molecules (=diploid)

195
Q

Viral replication

  1. DNA viruses
  2. RNA viruses
A
  1. all replicate in the nucleus (except poxvirus)

2. all replicate in the cytoplasm (except influenza virus & retroviruses)

196
Q

viral envelope

A
  • NAKED (nonenveloped) viruses include Papillomavirus, Adenovirus, Picornavirus, Polyomavirus, Calcivirus, Parvovirus, Reovirus, Hepevirus
  • generally enveloped viruses acquire their envelopes from plasma membrane when they exit from cell. Exceptions include herpesviruses, which acquire envelopes from nuclear membrane
  • give PAPP smears and CPR to a naked Heppy (hippy)
  • DNA=PAPP; RNA=CPR and hepevirus
197
Q

DNA virus characteristics/general rules

A
  • some general rules-all DNA viruses
    1. Are HHAPPPy viruses
  • *Hepadna, Herpes, Adeno, Pox, Parvo, Papilloma, Polyoma
    2. are double stranded
  • *except parvo (single stranded)
    3. are linear
  • *except papilloma and ployoma (circular, supercoiled) and hepadna (circular, incomplete)
    4. are icosahedral
  • *except pox (complex)
    5. replicate in the nucleus
  • *except pox (carries own DNA-dependent RNA polymerase)
198
Q

DNA viruses:

  1. enveloped?
  2. DNA structure
  3. medical importance

Herpesvirus

A
  1. Yes
  2. DS and linear
  3. HSV-1- oral (some genital) lesions, spontaneous temporal lobe encephalitis, keratoconjunctivitis
    - HSV-2– genital (some oral) lesions
    - VZV (HHV-3)–chickenpox, zoster (shingles); vaccine available
    - EBV (HHV_4)–mononucleosis, Burkit’s lumphoma, Hodgkin’s lymphonma
    - CMV (HHV-5)–infection in immunosuppressed pts (AIDS retinitis), especially transplant recipients; congenital defects (sightomegalovirus)
    - HHV-6–roseola (exanthem subitum)
    - HHV-7–less common cause of roseola
    - HHV-8–Kaposi’s sarcoma-associated herpesvirus (KSHV)
199
Q

DNA viruses:

  1. enveloped?
  2. DNA structure
  3. medical importance

Hepadnavirus

A
  1. yes
  2. DS & partial circular
  3. HBV:
    - acute or chronic hepatitis
    - vaccine available –contains HBV surface antigen
    - not a retrovirus but has reverse transcriptase
200
Q

DNA viruses:

  1. enveloped?
  2. DNA structure
  3. medical importance

Adenovirus

A
  1. No
  2. DS, Linear
  3. Febrile pharyngitis–sore throat; acute hemorrhagic cystitis, pneumonia, conjunctivitis-pink eye
201
Q

DNA viruses:

  1. enveloped?
  2. DNA structure
  3. medical importance

Parvovirus

A
  1. No
  2. SS & linear (-); smallest DNA virus
  3. B19 virus–aplastic crises in sickle cell dz, slapped cheeks rash in children–erythema infectiosum (5th dz), RBC destruction in fetus leads to hydrops detalis and death, pure RBC aplasia and rheumatoid arthritis–like symptoms in adults
202
Q

DNA viruses:

  1. enveloped?
  2. DNA structure
  3. medical importance

Papillomavirus

A
  1. No
  2. DS & circular
  3. HPV–warts (1,2,6,11), CIN, cervical cancer (16,18) vaccine available
203
Q

DNA viruses:

  1. enveloped?
  2. DNA structure
  3. medical importance

Polyomavirus

A
  1. no
  2. DS & circular
  3. JC virus–progressive multifocal leukoencephalopathy (PML) in HIV; BK virus–transplant pts, commonly targets kidney
    - JC:Junky cerebrum; BK-Bad kidney
204
Q

DNA viruses:

  1. enveloped?
  2. DNA structure
  3. medical importance

Poxvirus

A
  1. Yes
  2. DS & linear (largest DNA virus)
  3. Smallpox, although eradicated, could be used in germ warfare. Vaccinia–cowpox (milkmaids’ blisters); Molluscum contagiosum–flesh-colored dome lesions c central dimple
205
Q

Herpesviruses:

7 types

A
  1. HSV1
  2. HSV2
  3. VZV (HHV3)
  4. EBV (HHV4)
  5. CMV (HHV5)
  6. HHV6
  7. HHV8

HHV7 is rare

206
Q

Herpesviruses: dz & route of transmission

HSV1

A
  • gingivostomatitis, keratoconjunctivitis, temporal lobe encephalitis (most common cause of sporadic encephalitis in the US), herpes labialis. Latent in trigeminal ganglia
  • respiratory secretions, saliva
207
Q

Herpesviruses: dz & route of transmission

HSV2

A
  • Herpes genitalis, neonatal herpes. Latent in sacral ganglia
  • sexual contact, perinatal
208
Q

Herpesviruses: dz & route of transmission

VZV (HHV3)

A
  • varicella-zoster (chickenpox, shingles), encephalitis, pneumonia, Latent in dorsal root or trigeminal ganglia
  • respiratory secretions
209
Q

Herpesviruses: dz & route of transmission

EBV (HHV4)

A
  • infectious mononucleosis, Burkitt’s/Hodgkin’s lymphoma, nasopharyngeal carcinoma. latent in B cells
  • respiratory secretion, saliva
210
Q

Herpesviruses: dz & route of transmission

CMV (HHV5)

A
  • congenital infection, mononucleosis (negative Monospot), pneumonia, retinitis. INfected cells have characteristic “owl eye” inclusions. latent in mononuclear cells
  • congenital, transfusion, sexual contact, saliva, urine, transplant
211
Q

Herpesviruses: dz & route of transmission

HHV6

A
  • roseola: high fevers for several days that can cause seizures, followed by a diffuse macular rash
  • route of transmission not determined
212
Q

Herpesviruses: dz & route of transmission

HHV8

A
  • Kaposi’s sarcoma (HIV pts)

- sexual contact

213
Q

HSV identification

A
  • PCR is test of choice
  • Tzanck test–a smear of an opened skin vesicle to detect multinucleated giant cells commonly seen in HSV1, HSV2, VZV
  • infected cells also have intranuclear Cowdry A inclusions
  • Tzanck heavens I do not have herpes
214
Q

EBV (HHV4)

A
  • A perpesvirus
  • can cause mononucleosis
  • infects B cells
  • characterized by fever, hepatosplenomegaly, pharyngitis, lymphadenopathy (especially posterior cervical nodes)
  • peak incidence 15-20 yo
  • atypical lymphocytes seen on peripheral blood smear
  • are not infected B cells but rather reactive cytotoxic T cells
  • positive Monospot test–heterophile antibodies detected by agglutination of sheep or horse RBCs
  • also associated with development of Hodgkins’ and endemic Burkitt’s lymphomas as well as nasopharyngeal carcinoma
  • most common during peak kissing years
215
Q

15 RNA viruses

A
  1. Reovirus
  2. Picornaviruses
  3. Hepevirus
  4. Calicviruses
  5. flaviviruses
  6. togaviruses
  7. retroviruses
  8. coronaviruses
  9. orthomyxoviruses
  10. paramyxoviruses
  11. rhabdoviruses
  12. filoviruses
  13. arenaviruses
  14. bunyaviruses
  15. delta virus
216
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Reoviruses

A
  1. envelope,
    - NO
  2. RNA structure,
    - DS linear
    - 10-12 segments
  3. Capsid symmetry
    - icosahedral (double)
  4. Medical importance
    - Coltivirus; negative sense=arbovirus, transmitted by arthropods (mosquitoes or tick)
    - Colorado tick fever
    - Rotavirus- #1 cause of fatal diarrhea in children
217
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Picornaviruses

A
  1. envelope
    - NO
  2. RNA structure,
    - SS (+) linear
  3. Capsid symmetry,
    - Icosahedral
  4. Medical importance
    - Poliovirus–polio-Salk/Sabin vaccine–IPV/OPV
    - Echovirus–aseptic meningitis
    - Rhinovirus–common cold
    - Coxsackievirus–aseptic meningitis; herpangina (mouth blisters, fever); hand, foot, and mouth dz; myocarditis
    - HAV–acute viral hepatitis
    * **PERCH
218
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Hepevirus

A
  1. envelope,
    - No
  2. RNA structure,
    - SS (+) linear
  3. Capsid symmetry,
    - Icosahedral
  4. Medical importance
    - HEV
219
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Caliciviruses

A
  1. envelope
    - No
  2. RNA structure,
    - SS (+) linear
  3. Capsid symmetry,
    - icosahedral
  4. Medical importance
    - Norovirus–viral gastroenteritis
220
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Flaviviruses

A
  1. envelope
    - yes
  2. RNA structure,
    - SS (+) linear
  3. Capsid symmetry,
    - icosahedral
  4. Medical importance
    - HCV
    - yellow fever
    - dengue
    - St.Louis encephalitis
    - west nile virus
    - all above transmitted through mosquitoes/ticks
221
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Togaviruses

A
  1. envelope,
    - Yes
  2. RNA structure,
    - SS (+) linear
  3. Capsid symmetry,
    - Icosahedral
  4. Medical importance
    - Rubella
    - Eastern equine encephalitis (mosquitoes/ticks)
    - Western equine encephalitis (mosq/ticks)
222
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Retroviruses

A
  1. envelope
    - Yes
  2. RNA structure,
    - SS (+) linear
  3. Capsid symmetry,
    - Icosahedral (HTLV), complex and conical (HIV)
  4. Medical importance
    - have reverse transcriptase
    - HTLV–T-cell leukemia
    - HIV–AIDS
223
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Coronaviruses

A
  1. envelope,
    - Yes
  2. RNA structure,
    - SS (+) linear
  3. Capsid symmetry,
    - Helical
  4. Medical importance
    - coronavirus–common cold and SARS
224
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Orthomyxoviruses

A
  1. envelope
    - Yes
  2. RNA structure,
    - SS (-) linear
    - 8 segments
  3. Capsid symmetry,
    - helical
  4. Medical importance
    - influenza virus
225
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Paramyxoviruses

A
  1. envelope,
    - YES
  2. RNA structure,
    - SS (-) linear
    - nonsegmented
  3. Capsid symmetry,
    - helical

4.Medical importance
-Paramyxovirus:
parainfluenza–croup
RSV–bronchiolitis in babies; Rx–ribavirin
Measles, Mumps

226
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Rhabdoviruses

A
  1. envelope,
    - yes
  2. RNA structure,
    - SS (-) linear
  3. Capsid symmetry,
    - Helical
  4. Medical importance
    - Rabies
227
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Filoviruses

A
  1. envelope
    - Yes
  2. RNA structure,
    - SS (-) linear
  3. Capsid symmetry,
    - Helical
  4. Medical importance
    - Ebola/marburg hemorrhagic fever–often fatal
228
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Arenaviruses

A
  1. envelope
    - Yes
  2. RNA structure,
    - SS (-) linear
    - 2 segments
  3. Capsid symmetry,
    - helical
  4. Medical importance
    - LCMV–lymphocytic choriomeningitis virus
    - lassa fever encephalitis–spread by mice
229
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Bunyaviruses

A
  1. envelope,
    - Yes
  2. RNA structure,
    - SS (-) circular
    - 3 segments
  3. Capsid symmetry,
    - helical
  4. Medical importance
    - California encephalitis (mosq/ticks)
    - Sandfly/Rift Valley fever (mosq/ticks)
    - Crimean-Congo hemorrhagic fever (mosq/ticks)
    - Hantavirus–hemorrhagic fever, pneumonia
230
Q

RNA viruses:

  1. envelope,
  2. RNA structure,
  3. Capsid symmetry,
  4. Medical importance

Delta virus

A
  1. envelope,
    - Yes
  2. RNA structure,
    - SS (-) circular
  3. Capsid symmetry,
    - uncertain
  4. Medical importance
    - HDV is a defective virus that requires HBV co-infection
231
Q

Negative-stranded viruses

A
  • must transcribe negative strand to positive
  • Virion brings its own RNA-dependent RNA polymerase
  • they include Arenaviruses, Bunyaviruses, Paramyxoviruses, Orthomyxoviruses, Filoviruses, Rhabdoviruses

**Always Bring Polymerase Or Fail Replication

232
Q

Segmented viruses

A
  • all are RNA viruses
  • they include Bunyaviruses, Orthomyxoviruses (influenza viruses), Arenaviruses, Reoviruses

**BOAR

233
Q

Picornavirus

A
  • includes Poliovirus, Echovirus, Rhinovirus, Coxsackievirus, HAV
  • RNA is translated into 1 large polypeptide that is cleaved by proteases into functional viral proteins
  • can cause aseptic (viral) meningitis (except rhinovirus and HAV)
  • all are enteroviruses (fecal oral spread) except rhinovirus

**PicoRNAvirus=small RNA virus
PERCH on a peak (pico)

234
Q

Rhinovirus

A

-a picovirus
-nonenveloped RNA virus
-cause of common cold
>100 serologic types
-acid labile–destroyed by stomach acid
-therefore does not infect the GI tract (unlike the other piconaviruses)

235
Q

Yellow fever virus

A
  • a flavivirus (also a arbovirus=negative sense; transmitted through mosquitoes/ticks)
  • transmitted by Aedes mosquitoes
  • virus has a monkey or human reservoir
  • symptoms: high fever, black vomitus, jaundice
  • *Flavi=yellow, juandice
236
Q

Rotavirus

A
  • Rotavirus, most important global cause of infantile gastroenteritis, is a segmented dsRNA virus (a reovirus)
  • major cause if acute diarrhea in US during winter espeically in day care, kindergartens
  • villous destruction c atrophy leads to dec absroption of Na+ and loss of K+

**ROTAvirus=Right Out The Anus
CDC recommends routine vaccination of all infants

237
Q

influenza viruses

A
  • Orthomyxoviruses
  • enveloped, neative single stranded RNA viruses c 8 segment genome
  • contain hemagglutinatin (promotes viral entry) and neuraminidase (promotes progeny virion release) antigens
  • patients at risk for fatal bacterial superinfection
  • rapid genetic changes
  • killed viral vaccine is major mode of protection; reformulated vaccine offered each fall
  • vaccine containing live, temperature-sensitive mutant that replicates in the nose but not in the lung is also available. Used in children
238
Q

Genetic shift/antigenic shifts

Genetic drift

A
  • causes pandemics
  • reassortment of viral genome
  • segments undergo high frequency recombination, such as when human flu A virus recombines c swine flu A virus
  • Sudden shift is more deadly than gradual drift
  • genetic drift causes epidemics
  • minor (antigentic drift) changes based on random mutation
239
Q

rubella virus

A
  • a togavirus
  • causes rubella, once known as German (3 days) measles
  • fever, postauricular adenopathy, lymphadenopathy, arthralgias, fine truncal rash that starts at head and moves down
  • causes mild disease in children but serious oncgenital disease (a ToRCHeS infection)
240
Q

Paramyxovirus

A
  • paramyxovirus cause dz in children
  • they include those that cause parainfluenza (croup:seal-like barking cough), mumps, measles as well as RSV, which cause respiratory tract infection (bronchiolitis, pneumonia) in infants.
  • all contain surface F (fusion) protein, which causes resp epithelial cells to fuse and form multinucleated cells
  • palivizumab (monoclonal antibody against F protein) prevents pneumonia caused by RSV infection in premature infants
241
Q

measles virus

A
  • a paramyxovirus that causes measles
  • Koplik spots (red spots c blue white center on buccal mucosa) and descending maculopapular rash are characteristic
  • SSPE (subacute sclerosing panencephalitis, occuring yrs later), encephalitis (1:2000), and giant cell pneumonia (rarely, in immunosuppresed) are possible sequalae
  • rash presents last & spreads from head to toe
  • includes hands feet (vs. truncal rash in rubella)
  • do not confuse c roseola (caused by HHV-6)

**3 C’s of measles:
Cough
Coryza
Conjunctivitis

242
Q

Mumps virus

A
  • a paramyxovirus
  • symptoms: Parotitis, Orchitis (inflammation of testes), aseptic Meningitis
  • can cause sterility (especially after puberty)
  • mumps makes your parotid glands & testes as big as POM-poms
243
Q

Rabies virus

A
  • bullet-shaped virus
  • Negri bodies are characteristic cytoplasmic inclusions in neurons infected by rabies virus
  • commonly found in purkinje cells of cerebellum
  • rabies has long incubation period (wks to months) before symptoms onset
  • postexposure tx is wound cleansing & vaccination +/- rabies immune globulin
  • travels to CNS by migrating in a retrograde fashion up nerve axons
  • progression of dz: fever, malaise–>agitation, photophobia, hydrophobia–>paralysis, coma–>death
  • more commonly from bat, raccoon, skunk bites than dog bites in US
244
Q

Hepatitis viruses: HAV

  1. virus,
  2. transmission,
  3. carrier,
  4. incubation
  5. HCC risk
  6. Notes
A

Hepatitis viruses: HAV

  1. virus
    - RNA picornavirus
  2. transmission,
    - fecal-oral
  3. carrier,
    - no
  4. incubation
    - short (wks)
  5. HCC risk
    - no
  6. Notes
    - asymptomatic (usually) acute, alone (no carriers)
    - naked viruses do not rely on an envelope so they are not destroyed by the gut
245
Q

Hepatitis viruses: HBV

  1. virus,
  2. transmission,
  3. carrier,
  4. incubation
  5. HCC risk
  6. Notes
A 
Hepatitis viruses: HBV
1. virus,
DNA hepadnavirus
2.transmission,
-parenteral, sexual, maternal-fetal
3.carrier, 
-Yes
4.incubation
-long (months)
5.HCC risk
Yes: integrates into host genome, acts as oncogene
6.Notes
-virus uses its own DNA-dependent DNA polymerase to make full dsDNA. The host RNA polymerase transcribes mRNA from viral DNA and then makes viral proteins from the mRNAs
246
Q

Hepatitis viruses: HCV

  1. virus,
  2. transmission,
  3. carrier,
  4. incubation
  5. HCC risk
  6. Notes
A

Hepatitis viruses: HCV

  1. virus,
    - RNA flavivirus
  2. transmission
    - primarily blood, IVDU, post transfusion
  3. carrier,
    - yes
  4. incubation
    - long
  5. HCC risk
    - yes: chronic inflammation
  6. Notes
    - chronic, cirrhosis, carcinoma, carrier
247
Q

Hepatitis viruses: HDV

  1. virus,
  2. transmission,
  3. carrier,
  4. incubation
  5. HCC risk
  6. Notes
A

Hepatitis viruses: HDV

  1. virus
    - RNA delta virus
  2. transmission,
    - parenteral, sexual, maternal-fetal
  3. carrier,
    - yes
  4. incubation
    - superinfection-short
    - co-infecton-long
  5. HCC risk
    - yes
  6. Notes
    - defective virus
    - dependent on HBV; superinfection–>dec prognosis
248
Q

Hepatitis viruses: HEV

  1. virus,
  2. transmission,
  3. carrier,
  4. incubation
  5. HCC risk
  6. Notes
A

Hepatitis viruses: HEV

  1. virus
    - RNA hepevirus
  2. transmission,
    - fecal-oral, especially c waterborne epidemics
  3. carrier,
    - no
  4. incubation
    - short
  5. HCC risk
    - no
  6. Notes
    - high mortality in pregnant women; enteric, expectant mothers, epidemic
    - naked viruses do not rely on an envelope so they are not destroyed by the gut
249
Q

Hepatitis serologic markers

  1. anti-HAV (IgM)
  2. anti-HAV (IgG)
  3. HBsAg
  4. Anti-HBs
  5. HBcAg
  6. Anti-HBc
  7. HBeAg
  8. Anti-HBe
A
  1. anti-HAV (IgM)—IgM antibody to HAV; best test to detect active hepatitis A
  2. anti-HAV (IgG)–IgG antibody indicates prior HAV infection and/or prior vaccination; protects against reinfection
  3. HBsAg–Antigen found on surface of HBV; indicates hepatitis B infection
  4. Anti-HBs–antibody to HBsAg; indicates immunity to hep B
  5. HBcAg—antigen associated c core of HBV
  6. Anti-HBc–antibody to HBcAg; IgM=acute/recent infection; IgG=prior exposure or chronic infection. Positive during window period
  7. HBeAg–second, different antigenic determinant in the HBV core. HBeAg indicates active viral replication and therefore high transmissibility
  8. Anti-HBe–antibody to e antigen; indicates low transmissibility
250
Q

HIV

A
  • diploid genome (2 molecules of RNA)
  • 3 structural genes (protein coded for):
    1. env (gp120 & gp41)–formed from cleavage of gp160 to form envelope proteins
    1a) .gp120–attachment to host CD4+ T cell
    1b) .gp41–fusion & entry
    2. gag (p24)–capsid protein
    3. pol–reverse transcriptase, aspartate protease, integrase
  • reverse transcriptase synthesizes dsDNA from RNA; dsDNA integrates into host genome
  • virus binds CCR5 (early or CXCR4 (late) co-receptor and CD4 on T-cells; binds CCR5 & CD4 on macrophages
  • homozygous CCR5 mutation=immunity
  • heterozygous CCR5 mutation=slower course
251
Q

HIV diagnosis

A
  • presumptive dx made c ELISA (sensitive, high false-positive rate, low threshold, rule out test)
  • positive results are then confirmed c Western blot assay (specific, high false-negative rate and high threshold, rule in test)
  • ELISA/Western blot test look for antibodies to viral protein
  • these tests often are falsely negative in 1st 1-2 mos of HIV infection and falsely positive initially in babies born to infected mothers (anti-gp120 crosses placenta)
  • HIV PCR/viral load tests determine the amount of viral RNA in plasma
  • high viral load associated c poor prognosis
  • also use viral load to monitor effect of drug therapy
  • AIDS dx <1.5
252
Q

common dz of HIV positive adults

A

-as CD4 count dec, risk of reactivation of past infections (TB, HSV, shingles), dissemination of bacterial infections and fungal infections (eg. coccidiodomycosis), and non-Hodgkin’s lymphoma increase

253
Q

common dz of HIV positive adults: systemic

  1. clinical presentation
  2. findings/labs
  3. pathogen
A
  1. clinical presentation
    - low grade fevers, cough, hepatosplenomegaly, tongue ulcer
  2. findings/labs
    - oval yeast cells withinin macrophages, CD4 <100 cells/mm3
  3. pathogen
    - Histoplasma capsulatum (causes only pulmonary symptoms in immunocompetent hosts)
254
Q

common dz of HIV positive adults: Dermatologic

  1. clinical presentation
  2. findings/labs
  3. pathogen
A
  • fluffy white cottage-cheese lesions–>pseudohyphae, commonly oral if CD4C. albicans (causes thrush)
  • superficial vascular proliferation–>biopsy reveals neutrophilic inflammation–>Bartonella henselae (causes bacillary angiomatosis)
255
Q

common dz of HIV positive adults: Gastrointestinal

  1. clinical presentation
  2. findings/labs
  3. pathogen
A

common dz of HIV positive adults:

  1. clinical presentation
    - chronic watery diarrhea
  2. findings/labs
    - acid-fast cysts seen in stool especially when CD4 <200
  3. pathogen
    - Cryptosporidium spp.
256
Q

common dz of HIV positive adults: Neurologic

  1. clinical presentation
  2. findings/labs
  3. pathogen
A
  • encephalopathy–>due to reactivation of a latent virus; results in demyelination, CD4 JC virus reactivation (cause of PML)
  • abscesses–>many ring-enhancing lesions on imaging, CD4 Toxoplasma gondii
  • meningitis–>India ink stain reveals yeast with narrow-based budding and large capsule, CD4 Cryptococcus neoformans
  • retinitis–>cotton-wool spots on funduscopic exam and may also occur with esophagitis, CD4 CMV
  • dementia–>must differentiate from other causes–>directly associated with HIV
257
Q

common dz of HIV positive adults: Oncologic

  1. clinical presentation
  2. findings/labs
  3. pathogen
A
  • superficial neoplastic proliferation of vasculature–>biopsy reveals lymphocytic inflammation–>HHV8 (causes Kaposi’s sarcoma), do not confuse with bacillary angiomatosis caused by B. henselae
  • hairy leukoplakia–>often on lateral tongue–>EBV
  • Non-Hodgkin’s lymphoma (large cell type)–>often on oropharynx (Waldeyer’s ring)–>may be associated with EBV
  • Squamous cell carcinoma–>often in anus (men who have sex with men) or cervix (female)–>HPV
  • primary CNS lymphoma–>focal or multiple, differentiate from toxoplasmosis–>often associated with EBV
258
Q

common dz of HIV positive adults: respiratory

  1. clinical presentation
  2. findings/labs
  3. pathogen
A
  • interstitial pneumonia–>biopsy reveals cells with intranuclear (owl’s eye) inclusion bodies–>CMV
  • invasive aspergillosis–>pleuritic pain, hemoptysis, infiltrates on imaging–>Aspergillus fumigatus
  • Pneumonia–>especially with CD4 Pneumocystis jirovecii
  • Tuberculosis-like disease–>especialy with CD4 Mycobacterium avium-intracellulare
259
Q

Prions

A
  • prion dzs are caused by the conversion of normal cellular protein termed prion protein (PrPc) to a beta-pleated form (PrPsc), which is transmissible
  • PrPsc resists degradation and facilitates conversion of still more PrPc
  • accumulation of PrPsc results in spongiform encephalopathy and dementia, ataxia, death
  • it can be sporadic (Creutzfeldt-Jakob dz–rapidly progressive dementia), inherited (Gerstmann-Straussler-Scheinker syndrome), or acquired (kuru)
260
Q

normal flora: dominant (6)

  1. location
  2. microorganism
A
  1. skin–>Staphylococcus epidermidis
  2. Nose–>S. epidermidis; colonized by S. aureus
  3. Oropharynx–>viridans group streptococci
  4. Dental plaque–>streptococcus mutans
  5. colon–>bacteroides fragilis > E.coli
  6. vagina–>Lactobacillus, colonized by E.coli and group B strep

neonates delivered by cesarean section have no flora but are rapidly colonized after birth

261
Q

Bugs causing food poisoning (7)

  1. microorganism
  2. source of infection
A
  • S. aureus and B. cereus food poisoning starts quickly and end quickly
    1. Vibrio parahaemolyticus and V. vulnificus–>contaominated seafood; V. vulnificus can also cause wound infections from contact with contaminated water or shellfish
    2. bacillus cereus–>reheated rice. Food poisoning from reheated rice? Be serious! (B. cereus)
    3. Clostridium perfringens–>reheated meat dishes
    4. C. botulinum–>improper canned foods (sign is bulging cans)
    5. E. coli O157:H7–>undercooked meat
    6. Salmonella–>poultry, meat, eggs
262
Q

Bugs that can mimic appendicitis

A
  • Yersinia enterocolitica is most common cause of mesenteric adenitis, a disease that mimics appendicitis
  • nontyphoidal Salmonella can also be a cause
  • Camplyobacter jejuni may also mimic appendicitis
263
Q

Bugs causing diarrhea: bloody (7)

A
  1. campylobacter–comma or S-shaped organisms; growth at 42C
  2. Salmonella–lactose negative; flagellar motility; has animal reservoir, especially poultry & eggs
  3. Shigella–lactose negative; very low ID50; produces Shiga toxin (human reservoir only)
  4. Enterohemorrhagic E. coli–O157:H7; can cause HUS; makes Shiga-like toxin
  5. Enteroinvasive E. coli–invades colonic mucosa
  6. Yersinia entercolitica–Day-care outbreaks, pseudoappendicitis
  7. Entamoeba histolytica–protozoan
264
Q

Bugs causing diarrhea: watery (6)

A
  1. Enterotoxigenic–Traveler’s diarrhea; produces ST & LT toxins
  2. Vibrio cholerae–common-shaped organisms; rice water diarrhea
  3. C. difficile–can also cause bloody diarrhea. Pseudomembranous colitis
  4. C. perfringens–also causes gas gangrene
  5. Protozoa–Giardia, Cryptospordium (in immunocompromised)
  6. Viruses–rotavirus, norovirus
265
Q 
common causes of pneumonia in:
1.neonates
2 children (4wks-18yo)
3. adults (18-40 yo)
4. adults (40-65 yo)
5. elderly
A

1.neonates
-Group B streptococci
-E. coli
2 children (4wks-18yo)
-viruses (RSV)
-Mycoplasma
-Chlamydia trachomatis (infants-3 yo)
-C. pneumoniae (school-age)
-Streptococcus pneumoniae
-Ransv May Cough Chunky Sputum
3. adults (18-40 yo)
-Mycoplasma
-C. pneumonoiae
-S. pneumoniae
4. adults (40-65 yo)
-S. pneumonia
-H. influenzae
-Anaerobes
-viruses
-mycoplasma
5. elderly
-S. pneumoniae
-influenza virus
-anaerobes
-H. influenzae
-Gram negative rods

266
Q

Special groups

  1. nosocomial (hospital acquired)
  2. immunocompromised
  3. aspiration
  4. alcoholic/IV drug user
  5. cystic fibrosis
  6. postviral
  7. atypical
A
  1. nosocomial (hospital acquired)
    - Staphylococcus, enteric gram negative rods
  2. immunocompromised
    - Staphylococcus, enteric gram neg rods, fungi, viruses, pneumocystic jirovecii–with HIV
  3. aspiration
    - anaerobes
  4. alcoholic/IV drug user
    - S. pneumoniae, Klebsiella, Staphylpcoccus
  5. cystic fibrosis
    - Pseudomonas, S. aureus, S. pneumoniae
  6. postviral
    - Staphylococcus, H. influenze, S. pneumoniae
  7. atypical
    - Mycoplasma, Legionella, Chlamydia
267
Q

Common causes of meningitis:

  1. Newborn (0-6mos)
  2. Children (6mos-6yo)
  3. 6-60 yo
  4. 6O+
A

1.Newborn (0-6mos)
-Group B streptococci
-E. coli
-Listeria
2.Children (6mos-6yo)
-Streptococcus pneumoniae
-Neisseria meningitidis
-Haemophilus influenzae type B
-Enteroviruses
3. 6-60 yo
-S. pneumoniae
-N. meningitidis (#1 in teens)
-Enteroviruses
-HSV
4. 6O+
-S. pneumoniae
-gram neg rods
-Listeria
-

268
Q

Osteomyelitis: condition & cause

  1. assume if no other info is available
  2. sexually active
  3. diabetics and IV drugs users
  4. sickle cell
  5. prosthetic replacement
  6. vertebral disease
  7. cat & dog bites or scratches
A

-most osteomylitis occurs in children. Elevated CRP & ESR classic but nonspecific

  1. S. aureus
  2. Neisseria gonorrhoeae (rare), septic arthritis more common
  3. Pseudomonas aeruginosa, Serratia
  4. Salmonella
  5. S. aureus & S. epidermidis
  6. Mycobacterium tuberculosis (Pott’s diasese)
  7. Pasteurella multocida
269
Q

urinary tract infections

A
  • Cystitis presents with dysuria, frequency, urgency, suprapubic pain, WBCs (but not WBC casts) in urine
  • primiarly caused by ascension of microbes from urethra to bladder
  • males–infants with congenital defects, vesicouretal reflux
  • elderly–enlarged prostate in male
  • ascension to kidney results in pyelonephritis, which presents with fever, chills, flank pain, CVA tenderness, hematuria, WBC casts
  • tentimes more common in women (shorter urethras colonized by fecal flora)
  • other predisposing factors include obstruction, kidney surgery, catherization, GU malformation, diabetes, and pregnancy
  • diagnostic markers: positive leukocyte esterase test=bact UTI; positive nitrite test=gramneg bacterial UTI
270
Q

UTI bugs (7)

A
  1. escherichia coli
    - leading cause of UTI
    - colonies show green mettalic sheen on EMB agar
  2. Staphylococcus saprophyticus
    - 2nd leading cause of community-acquired UTI in sexually active women
  3. Klebsiella pneumoniae
    - 3rd leading cause of UTI. large mucoid capsule and viscous colonies
  4. Serratia marcescens
    - some strains produce a red pigment; often nosocomial and drug resistant
  5. Enterobacter cloacae
    - often nosocomial and drug resistant
  6. Proteus mirabillis
    - motility causes swarming on agar; produces urease; associated with struvite stones
  7. Pseudomonas aeruginosa
    - blue-green pigment and fruity odor; usually nosocomial and drug resistant

-diagnostic markers: +leukocytes esterase=bacterial; +nitrite test=gram negative; +urease test=urease-producing bugs (eg Proteus, Klebsiella); -urease test=E coli, enterococcus

271
Q

ToRCHes infections

  1. toxoplasma gondii
  2. rubella
  3. CMV
  4. HIV
  5. Herpes simplex virus-2
  6. syphilis
A
  • microbes that may pass from mother to fetus
  • transmission is transplacental in most cases or via delivery (especially HSV-2)
  • nonspecific signs common to many ToRCHeS infections include hepatosplenomegaly, jaundice, thrombocytopenia, growth retardation
  • other important infectious agents include Streptococcus agalactiae (group B streptococci), E coli, Listeria monocytogenes–all causes of meningitis in neonates
  • parvovirus B19 causes hydrops fetalis
272
Q

Toxoplasma gondii

  1. mode of transmission
  2. maternal manifestation
  3. neonatal manifestation
A
  1. mode of transmission
    - cat feces or ingestion of undercooked meat
  2. maternal manifestation
    - usually asymptomatic; lymphadenopathy (rarely)
  3. neonatal manifestation
    - classic triad: chorioretinitis, hydrocephalus, and intracranial calcifications
273
Q

rubella

  1. mode of transmission
  2. maternal manifestation
  3. neonatal manifestation
A
  1. mode of transmission
    - respiratory droplets
  2. maternal manifestation
    - rash, lymphadenopathy, arthritis
  3. neonatal manifestation
    - classic triad: PDA (or pulmonary artery hypoplasia), cataracts, deafness +/- blueberry muffin rash
274
Q

CMV

  1. mode of transmission
  2. maternal manifestation
  3. neonatal manifestation
A
  1. mode of transmission
    - sexual contact, organ transplants
  2. maternal manifestation
    - usually asymptomatic; mononucleosis-like illness
  3. neonatal manifestation
    - hearing loss, seizures, petechial rash, blueberry muffin rash
275
Q

HIV

  1. mode of transmission
  2. maternal manifestation
  3. neonatal manifestation
A

1.mode of transmission
-sexual contact, needlestick
2.maternal manifestation
-variable presentation depending on CD4+ count
3.neonatal recurrent infections, chronic diarrhea
-

276
Q

Herpes simplex virus-2

  1. mode of transmission
  2. maternal manifestation
  3. neonatal manifestation
A
  1. mode of transmission
    - skin or mucous membrane contact
  2. maternal manifestation
    - usually asymptomatic; herpetic (vesicualr) lesions
  3. neonatal manifestation
    - encephalitis, herpetic (vesicular) lesions
277
Q

Sphyllis

  1. mode of transmission
  2. maternal manifestation
  3. neonatal manifestation
A
  1. mode of transmission
    - sexual contact
  2. maternal manifestation
    - chancre 1’ and disseminated rash 2’ are the two stages likely to result in fetal infection
  3. neonatal manifestation
    - often results in stillbirth, hyfrops fetalis; if child survives, presents with facial abnormalities (notched teeth, saddle nose, short maxilla), saber shins, CN VIII deafness
278
Q

red rashes of childhood

7 types and its associated syndrome and clinical presentation

A
  1. rubella virus–>rubella–>rash begins at head, moves down–>fine truncal rash; postauricular lymphadenopathy
  2. measles virus–>measles–>paramyxovirus; beginning by cough, coryza, conjunctivitis, blue-white (Koplik) spots on buccal mucosa
  3. VZV (HHV3)–>chickenpox–>vesicular rash begins on trunk; spreads to face and extremities with lesions of different age
  4. HHV6–>roseola–>macular rash over body appears after several days of high fever; can present with febrile seizures; usually affects infants
  5. Parvovirus B19–>erythema infectiosum–>slapped cheek rash on face (can cause hydrops fetalis in pregnant women)
  6. Streptococcus pyogenes–>scarlet fever–>erythematous, sandpaper-like rash with fever and sore throat
  7. Coxsackievirus type A–>hand-foot mouth disease–>vesicular rash on palms and soles; ulcers in oral mucosa
279
Q

13 sexually transmitted diseases:

clinical features and organism

A
  1. gonorrhea–>urethritis, cervicitis, PID, prostatitis epididymis, arthritis, creamy purulent discharge–>Neisseria gonorrhoeae
  2. 1’ syphilis–>painless chancre–>Treponema pallidum
  3. 2’ syphilis–>fever, lymphadenopahty, skin rashes, condylomata lata
  4. 3’ syphilis–>Gummas, tabes dorsalis, general paresis, aortitis, Argyll Robertson pupil
  5. Chancroid–>painful genital ulcer, inguinal adenopathy–>Haemophilus ducreyi (it’s so painful you do cry)
  6. genital herpes–>painful penile, vulvar, or cervical vesicles and ulcers; can cause systemic symptoms such as fever, HA, myalgia–>HSV2, less commonly HSV1
  7. chlamydia–>urethritis, cervicitis, conjunctiviti, Reiter’s syndrome, PID–>Chlamydia trachomatis (D-K)
  8. Lymphogranuloma venereum–>infecton of lymphatics; genital ulcers, lymphadenopathy, rectal strictures–>C. trachomatis (L1-L3)
  9. trichomoniasis–>vaginitis, strawberry-colored mucosa, motile in wet prep–>Trichomonas vaginalis
  10. AIDS–>opportunistic infection, Kaposi’s sarcoma, lymphoma–>HIV
  11. Condylomata acuminata–>genital warts, koilocytes–>HPV6 and HPV 11
  12. Hepatitis B–>jaundice—>HBV
  13. Bacterial vaginosis–>noninflammatory, malodorous discharge (fishy smell); positive whiff test, clue cells, not exclusively an STD—>Gardnerella vaginalis
280
Q

pelvic inflammatory disease

A
  • top bugs: chlamydia trachomatis (subacute, often undiagnosed), Neisseria gonorrhoeae (acute).
  • C. trachomatis–the most common bacterial STD in US
  • cervical motion tenderness (chandelier sign), purulent cervical discharge
  • PID may include salpingitis, endometritis, hydrosalpinx, tubo-overian abscess
  • can lead to Fitz-Hugh-Curtis syndrome—infection of the liver capsule and violin string adhesions of parietal peritoneum to liver
  • Salpingitis is a risk factor for ectopic pregnancy, infertility, chronic pelvic pain, adhesions
281
Q

nosocomial infections: risk factors

  1. CMV, RSV
  2. E. coli, Proteus mirabilis
  3. Pseudomonas aeruginosa
  4. HBV
  5. Candida albicans
  6. Legionella
A
  1. CMV, RSV–>newborn nursery
  2. E. coli, Proteus mirabilis–>urinary catherization–>2 most common causes of nosocomial infections are E. coli (UTI) and S. aureus (wound infection)
  3. Pseudomonas aeruginosa–>respiratory therapy equipment–>presume Pseudomonas “airuginosa” when air or burns are involved
  4. HBV–>work in renal dialysis unit
  5. Candida albicans–>hyperalimentation
  6. Legionella–>water aerosols–>Legionella when water source is involved
282
Q

Bugs affecting unimmunized children: findings/labs & pathogen

  1. dermatologic
  2. neurologic
  3. respiratory (2)
A
  1. dermatologic
    - Rash—>beginning at head and moving down c postauricular lymphadenopathy—>rubella virus
    - Rash–>beginning at head and move down; rash preceded by cough, coryza, conjunctivitis, blue-white (Koplik) spots on buccal mucosa–>measles virus
  2. neurologic
    - Meningitis–>microbe colonizes nasopharynx–>H. influenzae type B
    - meningitis–> can lead to myalgia and paralysis–>Poliovirus
  3. respiratory (2)
    - Pharyngitis–>grayish oropharyngeal exudate (“pseudomembranes may obstruct airway); painful throat—>Corynebacterium diphtheriae (elaborates toxin that causes necrosis in pharynx, cardiac, and CNS tissue)
    - Epiglottitis–>fever c dysphagia, drooling, difficulty breathing due to edematous “cherry red” epiglottis–>H. influenzae type B (also capable of causing epiglottis in fully immunized children)
283
Q

Bug hints (if all else fails): chacteristics & organism

  1. pus, empyema, abscess
  2. pediatric infection
  3. pneumonia in cystic fibrosis, burn infection
  4. branching rods in oral infection, sulfur granules
  5. traumatic open wound
  6. surgical wound
  7. dog or cat bite
  8. currant jelly sputum
  9. positive PAS stain
  10. sepsis/meningitis in newborn
  11. healthcare provider
  12. fungal infection in diabetic or immunocompromised patient
  13. asplenic patient
  14. chronic granulomatous disease
  15. neutropenic patients
  16. facial nerve palsy
A
  1. S. aureus
  2. Haemophilus influenzae (including epiglottitis)
  3. Pseudomonas aeruginosa
  4. Actinomyces israelii
  5. Clostridium perfringens
  6. S. aureus
  7. Pasteurella multocida
  8. Klebsiella
  9. Tropheryma whipplei (whipple’s disease)
  10. Group B strep
  11. HBV (from needle stick)
  12. Mucor or Rhizopus spp
  13. Encapsulated microbes, especially SHiN (S. pneumoniae, H. influenzae type B, N. meningitidis)
  14. Catalase-positive microbes, especially S. aureus
  15. Candida albicans (systemic), Aspergillus
  16. Borrelia burgdorferi (lyme disease)
284
Q

antimicrobial therapy: mechanism of action & drugs

  1. block cell wall synthesis by inhibition of peptidoglycan cross-linking
  2. block peptidoglycan synthesis
  3. block nucleotide synthesis by inhibiting folic acid synthesis (involved in methylation)
  4. block DNA topoisomerases
  5. block mRNA synthesis
  6. damage DNA
  7. block protein synthesis at 50S ribosomal subunit
  8. block protein synthesis at 30S ribosomal subunit
A
  1. penicillin, methicillin, ampicillin, piperacillin, cephalosporins, aztreonam, imipenem
  2. bactracin, vancomycin
  3. sulfonamides, trimethroprim
  4. fluoroquinolones
  5. rifampin
  6. metronidazole
  7. chloramphenicol, macrolides, clindamycin, streptogramins (quinupristin, dalfopristin), linezolid
  8. aminoglycosides, tetracyclines
285
Q

Penicillin:

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A

Penicillin G (IV & IM form), penicillin V (oral). Prototype beta-lactam antibiotics

  1. mechanism
    - bind penicillin-binding proteins (transpeptidases)
    - block transpeptidase cross-linking of peptidoglycan
    - activate autolytic enzymes
  2. clinical use
    - mostly used for gram-postive organisms (S. pneumoniae, S. pyogenes, Actinomyces)
    - also used for Neisseria meningitidis, Treponema pallidum, syphilis
    - bactericidal for gram-positive cocci, gram-positive rods, gram-neg cocci, spirochetes
    - not penicillinase resistant
  3. toxicity
    - hypersensitivity reactions, hemolytic anemia
  4. resistance
    - beta-lactamases cleave beta-lactam ring
286
Q

Oxacillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of beta-lactamase to beta-lactam ring
    - use naf (nafcillin) for staph
  2. clinical use
    - S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site)
  3. toxicity
    - hypersensitivity reactions, interstitial nephritis
287
Q

ampicillin, amoxicillin (aminopenicillins)

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A
  1. mechanism
    - same as penicillin
    - wider spectrum; penicillinase sensitive
    - also combine with clavulanic acid to protect against beta-lactamase
    - amoxicillin has greater oral bioavailability than ampicillin
    - ***AMinoPenicillins are AMPed-up penicillin
  2. clinical use
    - extended-spectrum penicillin-Haemophilus influenzae, E.coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci
    - Coverage: ampicillin/amoxicillin HELPSS kill enterococci
  3. toxicity
    - hypersensitivity reactions; ampicillin rash; pseudomembranous colitis
  4. resistance
    - beta-lactamases cleave beta-lactam ring
288
Q

Ticarcillin, piperacillin (antipseudomonals)

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - same as penicillin. Extended spectrum
  2. clinical use
    - Pseudomonas spp. and gram negative rods; susceptible to penicillinase; use with clavulanic acid
  3. toxicity
    - hypersensitivity reactions
289
Q

Beta-lactamase inhibitors:

A
  • include Clavulanic Acid, Sulbactam, Tazobactam
  • often added to penicillin antibiotics to protect the antibiotics to protect the antibiotic from destruction by beta-lactamase (penicillinase)
  • ***CAST
290
Q

Cephalosporins:

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - Beta-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases
    - bactericidal
    - organisms typically not covered by cephalosporins are LAME: Listeria, Atypicals (Chlamydia, Mycoplasma), MRSA, and Enterococci.
    - Exception: ceftaroline covers MRSA
  2. clinical use
    - 1st generation (cefazolin, cephalexin)–gram-pos cocci, Proteus mirabilis, E.coli, Klebsiella pneumoniae
    - cefazolin used prior to surgery to prevent S. aureus wound infections
    * *1 st generation—>PEcK
    - 2nd generation (cefoxitin, cefaclor, cefuroxime)–gram-pos cocci,
    - Haemophilus, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens
    * **2nd generation—>HEN PEcKS
    - 3rd generation (ceftriaxone, cefotaxime, ceftazidime)–serious gram-neg infections resistant to other beta-lactams
    - **ceftriaxone–meningitis and gonorrhea
    * **ceftazidine–pseudomonas
    - 4th generation (cefepime)–inc activity against Pseudomonas and gram pos organisms
  3. toxicity
    - hypersensitivity reactions, vitamin K deficiency
    - low cross-reactivity with penicillins
    - inc nephrotoxicity of aminoglycosides
291
Q

Aztreonam:

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - a monobactam resistant to beta-lactamases
    - prevents peptidoglycan cross-linking by binding to PBP3
    - syngergistic with aminoglycosides
    - no cross-allergenicity with penicillins
  2. clinical use
    - gram negative rods only–
    - no activity against gram-positive or anaerobes
    - for penicillin-allergic patients and those with renal insufficiencyn who cannot tolerate aminoglycosides
  3. toxicity
    - usually nontoxic; occasional GI upset
292
Q

Imipenem/cilastatin, meropenem

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - imipenem is a broad-spectrum, beta-lactamase-resistant carbapenem
    - always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules
    - with imipenem, :the kill is lastin’s with cilastatin.”
    - newer carbapenems include ertapenem and doripenem
  2. clinical use
    - gram-positive cocci, gram-negative rods, and anaerobes
    - wide spectrum, but the significant side effects limit use to life-threatening infections, or after other drugs have failed
    - Meropenem, however, has a reduced risk of seizures and is stable to dehydropeptidase I.
  3. toxicity
    - GI distress, skin rash, CNS toxicity (seizures) at high plasma levels
293
Q

vancomycin

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A

1.mechanism
-inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors.
-bactericidal
2.clinical use
-gram-positive only–serious, amultidrug-resistant organisms, including MRSA, enterococci, and Clostridium difficile (oral dose for pseudomembranous colitis)
3.toxicity
Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing–red man syndrome (can largerly prevent by pretreatment with antihistamines and slow infusion rate)
-well tolerated in general–does NOT have many problems
4.resistance
-occurs with amino acid change of D-ala D-ala to D-ala D-lac
-pay back 2 D-alas (dollars) for vandalizing (vancomycin)

294
Q

protein synthesis inhibitors:

  • 30S inhibitors:
  • 50S inhibitors
A
  • specifically target smaller bacterial ribosome (70S, made 30S and 50S subunits), leaving human ribosome (80S) unaffected
  • buy AT 30, CCEL (sell) at50
  • 30S inhibitors: A=aminoglycosides (bactericidal), T=tetracyclines (bacteriostatic)
  • 50S inhibitors: C=chloramphenicol, Clindamycin (bacteriostatic), E=erythromycin (macrolides) (bacteriostatic), L=linezolid (variable)
295
Q

aminoglycosides:

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A

Aminoglycosides: Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

  • Mean (aminoglycoside) GNATS cannot kill anaerobes
    1. mechanism
  • bactericidal; inhibit formation of initiation complex and cause misreading of mRNA
  • also block translocation
  • require O2 for uptake; therefore ineffective against anaerobes
  • A initiates the Alphabet
    2. clinical use
  • severe gram-negative rod infections
  • synergistic with beta-lactam antibiotics
  • neomycin for bowel surgery
    3. toxicity
  • Nephrotoxicity (especially when used with cephalosporins), Neuromuscular blockade, Ototoxicity (especially when used with loop diuretics). Teratagen
    4. resistance
  • transferase enzymes that inactivate the drug by acetylation, phosphorylation, adenylation
296
Q

Tetracyclines:

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A

Tetracyclines: tetracycline, doxycycline, demeclocycline, minocycline

  • Demeclocycline–ADH antagonist; acts as a diuretic in SIADH. Rarely used as antibiotic
    1. mechanism
  • bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA
  • limited CNS penetration
  • doxycycline is decally eliminated and can be used in patients with renal failure
  • do not take with milk, antacids, or iron-containing preparations because divalent cations inhibit its absorption in the gut
    2. clinical use
  • Borrelia burgdorferi, M. pneumoniae
  • drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and chlamydia
    3. toxicity
  • GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity
  • contraindicated in pregnancy
    4. resistance
  • decrease uptake into cells or increase influx out of cell by plasmid-encoded transport pumps
297
Q

Metronidazole:

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - forms free radical toxic metabolites in the bacterial cell that damage DNA
    - bactericidal, antiprotozoal
  2. clinical use
    - treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. difficile)
    - used with a proton pump inhibitor and clarithromycin for triple therapy against H. pylori
    - GET GAP on the Metro with metronidazole.
    - treats anaerobic infection below the diaphragm vs. clindamycin (anaerobic infections above diaphragm)
  3. toxicity
    - disulfiram-like reaction with alcohol; HA, metallic taste
298
Q

Chloramphenicol

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A

1.mechanism
blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic
2.clinical use
-meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae)
-conservative use owing to toxicities but often still used in developing countries because of low cost
3.toxicity
-anemia (dose dependent), aplstic anemia (dose independent), gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase)
4.resistance
-plasmid-encoded acetyltransferase that inactivates drug

299
Q

Clindamycin

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A
  1. mechanism
    - blocks peptide transfer (transpeptidotion) at 50S ribosomal subunit. Bacteriostatic
  2. clinical use
    - anaerobic infections (eg. Bacteroides fragilis, Clostridium perfringens) in aspiration pneumonia or lung abscesses
    - also oral infections with mouth anaerobes
    - treats anaerobes above the diaphragm vs. metronidazole (anaerobic infections below diaphragm)
  3. toxicity
    - pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea
300
Q

Sulfonamides:

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

  1. mechanism
    - PABA antimetabolites inhibit dihydropteroate synthase. Bacteriostatic
  2. clinical use
    - gram positive, gram negative, Nocardia, Chlamydia.
    - triple sulfas or SMX for simple UTI
  3. toxicity
    - hypersensitivity rxn, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (eg. warfarin)
  4. resistance
    - altered enzyme (bacterial dihydropteroate synthase), dec uptake,or inc PABA synthesis
301
Q

Trimethoprim:

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A
  1. mechanism
    - inhibits bacterial dihydrofolate reductase. Bacteriostatic
  2. clinical use
    - used in combination with sulfonamides (trimethoprin-sulfamethoxazole (TMP-SMX)), causing sequential block of folate synthesis
    - combination used for UTIs, Shigella, Salmonella, Pneumocystic jirovecii pneumonia (tx & prophylaxis)
  3. toxicity
    - megaloblastic anemia, leukopenia, granulocytopenia
    - may alleviate c supplemental folinic acid (leucovorin rescue)
    - Abbreviated TMP: treat Marrow Poorly
302
Q

Fluoroquinolones:

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A

-Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfloxacin, moxifloxacin, gat
ifloxacin, enoxacin (fluoroquinolones), nalidic acid (a quinolone)
1.mechanism
-inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.
-bactericidal
-must not be taken with antacids
2.clinical use
-gram negative rods of urinary and GI tracts (including Pseudomonas), Neisseria, some gram positive organisms
3.toxicity
-GI upset, superinfections, skin rashes, HA, dizziness
-less common: tendonitis, tendon rupture, leg cramps, myalgia
-contraindicated in pregnant women and in children because animal studies show damage to cartilage
-some may cause prolonged QT interval
-may cause tendon rupture in people >60 yo and in pt taking prednisone
-Fluoroquinolones hurt attachment to your bones
4.resistance
-chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps

303
Q

Macrolides

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A

Azithromycin, clarithromycin, erythromycin

  1. mechanism
    - inhibit protein synthesis by blocking translation (macroslides); bind to 23S rRNA of the 50S ribosomal subunit
    - bacteriostatic
  2. clinical use
    - atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STDs (for chlamydia), and gram positive cocci (streptococcal infections in patients allergic to penicillin)
  3. toxicity
    - MACRO: Motility issues, Arrhythmia caused by prolonged QT, acute Cholestatic hepatitis, Rash, eOsinophilia
    - increases serum concentration of theophyllines, oral anticoagulants
  4. resistance
    - methylation of 23S rRNA binding site
304
Q

Isoniazid (INH)

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A

1.

  • dec synthesis of mycolic acods
  • bacterial catalase-peroxidase (KatG) needed to convert INH to active metabolite
  • INH injures Neurons and Hepatocytes
    2. clinical use
  • Mycobacterium tuberculosis
  • the only agent used as solo prophylaxis against TB
  • different INH half-lives in fast vs. slow acetylators
    3. toxicity
  • neurotoxicity, hepatotoxicity,
  • pyridoxine (vit B6) can prevent neurotoxicity, lupus
    4. resistance
305
Q

Rifampin

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A
  1. mechanism
    - inhibits DNA dependent RNA polymerase
    - Rifampin’s 4 R: RNA polymerase inhibitor, Revs up microsomal P-450, Red/orange body fluids, Rapid resistance if used alone
  2. clinical use
    - Mycobacterium tuberculosis; delays resistance to dapsone when used for leprosy
    - used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus influenzae type B
  3. toxicity
    - minor hepatotoxicity and drug interactions (inc P-450); orange body fluids (nonohazardous side effect)
306
Q

Pyrazinamide:

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A
  1. mechanism
    - uncertain. Thought to acidify intracellular environment via conversion to pyrazinoic acid.
    - effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found
  2. clinical use
    - Mycobacterium tuberculosis
  3. toxicity
    - Hyperuricemia, hepatotoxicity
307
Q

Ethambutol:

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A
  1. mechanism
    - dc carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase
  2. clinical use
    - mycobacterium tuberculosis
  3. toxicity
    - optic neuropathy (red-green color blindness)
308
Q

Antimycobacterial prophylaxis and treat drugs for bacterium:

  1. M. tuberculosis
  2. M. avium-intracelluare
  3. M leprae
A
  1. M. tuberculosis–>isoniazid–>Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE for tx)
  2. M. avium-intracelluare–>Azithromycin–>azithromycin, rifampin, ethambutol, streptomycin
  3. M leprae–>N/A–> long term tx with dapson and rifampin for tuberculoid form. Add clofazimine for lepromatous form
309
Q

Antimicrobial prophylaxis: condition & medication

  1. Meningococcal infection
  2. Gonorrhea
  3. Syphylis
  4. History of recurrent UTIs
  5. Endocarditis with surgical or dental procedures
  6. Pregnant woman carrying group B strep
  7. Prophylaxis of strep pharyngitis in child with prior rheumatic fever
  8. Prevention of postsurgical infection due to S. aureus
  9. Prevention of gonococcal or chlamydial conjunctivitis in newborn
A
  1. Ciprofloxacin (drug of choice), rifampin for children
  2. Ceftriaxone
  3. Benzathine penicillin G
  4. TMP-SMX
  5. Penicillins
  6. Ampicillin
  7. Oral penicillin
  8. Cefazolin
  9. Erythromycin ointment
310
Q

HIV prophylaxis & infection with cell count

1.CD4<50

A
  1. TMP-SMX—>Pneumoncystis pneumonia
  2. TMP-SMX–>Pneumoncystis pneumonia and toxoplasmosis
    * *TMP-SMX: aerosilzed pentamidine may be used if patients is unable to tolerate TMP-SMX, but this may not prevent toxoplasmosis infection concurrently
  3. Azithromycin—>Mycobacterium avium complex
311
Q

Treatment of highly resistant bacteria

A
  • MRSA–vancomycin

- VRE—linezolid and streptogramins (quinupristin/dalfopristin)

312
Q

Amphotericin B

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes
    - Amphotericin “tears” holes in the fungal membrane by forming pores
  2. clinical use
    - serious, systemic mycoses
    - Cryptococcus (amphotericin B w/wout flucytosine for cryptococcal meningitis), Blastomyces, Coccidioides, Histoplasma, Candida, Mucor
    - intrathecally for fungal meningitis
    - supplement K & Mg because of altered renal tubule permeability
  3. toxicity
    - fever/chills (shake & bake), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (amphoterrible)
    - hydration reduces nephrotoxicity
    - liposomal amphotericin reduced toxicity
313
Q

Nystatin

  1. mechanism
  2. clinical use
A
  1. mechanism
    - same as amphotericin B
    - topical form because too toxic for systemic use
  2. clinical use
    - Swish and swallow for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis
314
Q

Azoles

  1. mechanism
  2. clinical use
  3. toxicity
A

Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole

  1. mechanism
    - inhibit fungal sterol (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to ergosterol
  2. clinical use
    - local and less serious systemic mycoses
    - fluconazole for chronic suppression of cryptococcal meningitis in AIDS pts and candidal infections of all types
    - Itraconazole for Blastomyces, Coccidiodes, Histoplasma,
    - Clotrimazole, miconazole for topical fungal infections
  3. toxicity
    - testesterone synthesis inhibition (gynecomastia, esp. with ketoconazole), liver dysfunction (inhibits cytochrome P-450)
315
Q

Flucytosine

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - inhibits DNA & RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase
  2. clinical use
    - used in systemic fungal infections (esp. meningitis caused by Cryptococcus) in combination with amphotericin B
  3. toxicity
    - bone marrow suppression
316
Q

Caspofungin, micafungin

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - inhibits cell wall synthesis by inhibiting synthesis of beta-glucan
  2. clinical use
    - invasive aspergillosis, Candida
  3. toxicity
    - GI upset, flushing (by histamine release)
317
Q

Terbinafine

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - Inhibits the fungal enzyme squalene epoxidase
  2. clinical use
    - used to treat dermatophytoses (especially onychomycosis–fungal infection of finger or toe nails
  3. toxicity
    - abnormal LFTs, visual disturbances
318
Q

Griseofulvin

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - interferes with microtubule function; disrupts mitosis
    - deposits in keratin-containing tissues (eg. nails)
  2. clinical use
    - oral tx of superficial infections; inhibit growth of dermatophytes (tinea, ringworm)
  3. toxicity
    - teratogenic, carcinogenic, confusion, HA, inc P-450 and warfarin metabolism
319
Q

Chloroquine

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - block detoxification of heme into hemozoin
    - heme accumulates and is toxic to plasmodia
  2. clinical use
    - tx of plasmodial species other than P. falciparum (frquency of resistance in P.faciparum is too high)
    - resistance due to membrane pump that dec intracelullar concentration of drug
    - treat P. falciparum with artemether/lumifantrine or atovaquone/proguanil
    - for life-threatnening malaria, use quinidine in US (quinine elsewhere) or artisunate
  3. toxicity
    - retinopathy
320
Q

Antiprotozoan therapy

A

-pyrimethamine (toxoplasmosis), suramin and melarsoprol (Trypanosoma brucei), nifurtimox (T.cruzi), sodium stibogluconate (leishmaniasis)

321
Q

Antihelminthic therapy

A

Mebendazole, pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel’ immobilize helminths
-use praziquantel against flukes (trematodes) such as Schistosoma

322
Q

Zanamivir, oseltamivir

Mechanism
Clinical use

A
  1. mechanism
    - inhibit influenza neuraminidase, decreasing the release of progeny virus
  2. clinical use
    - tx and prevention of both influenza A & B
323
Q

Ribavirin

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - inhibit synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase
  2. clinical use
    - RSV, chronic hepatitis C
  3. toxicity
    - hemolytic anemia, severe teratogen
324
Q

Acyclovir

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A
  1. mechanism
    - monophorphorylated by HSV/VZV thymidine kinase
    - guanosine analog
    - triphosphate formed by cellular enzymes
    - preferentially inhibits viral DNA polymerase by chain termination
  2. clinical use
    - HSV & VZV
    - weak activity against EBV
    - no activity against CMV
    - used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis.
    - prophylaxis in immunocompromised patients
    - no effect on latent forms of HSV and VZV
    - valacyclovir, a prodrug of acyclovir, has better oral bioavailability
    - for herpes zoster, use a related agent, famciclovir
  3. toxicity
    - few serious adverse effects
  4. resistance
    - mutated viral thymidine kinase
325
Q

Ganciclovir

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A
  1. mechanism
    - 5’-monophosphate formed by a CMV viral kinase
    - guanosine analog
    - triphosphate formed by cellular kinases
    - preferentially inhibits viral DNA polymerase
  2. clinical use
    - CMV, especially in immunocompromised patients
    - valganciclovir, a prodrug of ganciclovir, has better oral bioavailability
  3. toxicity
    - leukopenia, neutropenia, thrombocytopenia, renal toxicity
    - more toxic to host enzymes than acyclovir
  4. resistance
    - mutated CMV DNA polymerase or lack of viral kinase
326
Q

Foscarnet

  1. mechanism
  2. clinical use
  3. toxicity
  4. resistance
A
  1. mechanism
    - viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme
    - does not require activiation by viral kinase
    - foscarnet=pyrofosphate analog
  2. clinical use
    - CMV retinitis in immunocompromised pts when gangciclovir fails; acyclovir-resistant HSV
  3. toxicity
    - nephrotoxicity
  4. resistance
    - mutated DNA polymerase
327
Q

Cidofovir

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - preferentially inhbits viral DNA polymerase
    - does not require phosphorylation by viral kinase
  2. clinical use
    - CMV retinitis in immunocompromised pts, acyclovir-resistant HSV, long half0life
  3. toxicity
    - nephrotoxicity (co-administer with probenecid and IV saline to reduce toxicity)
328
Q

Interferons

  1. mechanism
  2. clinical use
  3. toxicity
A
  1. mechanism
    - glycoproteins synthesized by virus-infected cells; block replication of both RNA and DNA viruses
  2. clinical use
    - IFN alpha-chronic hepatitis B & C, Kaposi’s sarcoma. IFN beta-MS, IFN-gamma-NADPH oxidase deficiency
  3. toxicity
    - neutropenia, myopathy
329
Q

HIV therapy

A

HIghly active antiretroviral therapy (HAART): initiated when patients present with AIDS-defining illness, low CD4 cell counts (<500 cell/mm3), or high viral load

  • regimen consists of 3 drugs to prevent resistance
  • 2 nucleoside reverse transcriptase inhibitors (NRTIs) + 1 non-nucleoside reverse transcriptase inhibitor (NNRTI) or 1 protease inhibiot or 1 integrase inhibitor
330
Q

Protease inhibitors:

  1. drugs (7)
  2. mechanism
  3. toxicity
A
  1. lopinavir
    - atazanavir
    - darunavir
    - fosamprenavir
    - saquinavir
    - ritonavir
    - indinavir
  2. assembly of virions depends on HIV-1 protease (pol gene) which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.
    - Ritonavir can boost other drug concentrations by inhibiting cytochrome P-450
    - all protease inhibitors end in –navir
    - Navir (never) tease a protease
  3. Hyperglycemia, GI intolerance (nasea, diarrhea), lipodystrophy.
    - nephropathy, hematuria (indinavir)
331
Q

NRTIs

  1. drugs 7
  2. mechanism
  3. toxicity
A
  1. Tenofovir (TDF)
    - Emtricitabine (FTC)
    - Abacavir (ABC)
    - Lamivudine (3TC)
    - Zidovudine (ZDV, formerly AZT)
    - Didanosine (ddl)
    - Stavudine (d4T)
  2. Competitvely inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group)
    - Tenofovir is a nucleotide analog and does not have to be activated; the others are nucleoside analogs and do need to be phosphorylated to be active
    - ZDV is used for general prophylaxis and during pregnancy to reduce risk of fetal transmission
    - **have you dined (vudine) with my nuclear (nucleosides) family?

3.bone marrow suppression (can be reversed with G-CSF and erythropoicitin), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), anemia (ZDV)

332
Q

NNRTIs:

  1. drugs 3
  2. mechanism
  3. toxicity
A
  1. Nevirapine, Efavirenz, Delavirdine
  2. bind to reverse transcriptase at site different from NRTIs. do not require phosphorylation to be active or compete with nucleotides
  3. same as NRTIs:bone marrow suppression (can be reversed with G-CSF and erythropoicitin), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), anemia (ZDV)
333
Q

integrase inhibitors:

Raltegravir

A
  • inhibits HIV genome integration into host cell chromosome by reversibily inhibiting HIV integrase
  • toxicity: hypercholesterolemia
334
Q

antibiotics to avoid in pregnancy and its side effect

A
  1. Sulfonamides–>Kernicterus
  2. Aminoglycosides–>Ototoxicity
  3. Fluoroquinolones–>Cartilage damage
  4. Clarithromycin–>Embryotoxic
  5. Tetracyclines–>discolored teeth, inhibition of bone growth
  6. Ribavirin (antiviral)–>teratogenic
  7. Griseofulvin (antifungal)—>teratogenic
  8. Chloramphenicol–>gray baby
    * *SAFe Children Take Really Good Care
335
Q

Staphylococcus aurcus:

  1. incubation
  2. symptoms
  3. mechanism of action
  4. typical food contamination
A
  1. incubation- 2-4 hrs
  2. symptoms–sudden vomiting, cramps, diarrhea, no fever
  3. mechanism of action- enterotoxin
  4. typical food contamination- ham, meats, custards, cream filling
336
Q

Clostridium perfringens

  1. incubation
  2. symptoms
  3. mechanism of action
  4. typical food contamination
A
  1. incubation- 6-24 hrs, usually 10-12 hrs
  2. symptoms- abd pain, diarrhea, N/V, usually no fever
  3. mechanism of action- enterotoxin
  4. typical food contamination- meat, poultry
337
Q

Salmonella (non-typhoid)

  1. incubation
  2. symptoms
  3. mechanism of action
  4. typical food contamination
A
  1. incubation- 6-48 hrs
  2. symptoms- diarrhea, fever, cramps
  3. mechanism of action- intestinal invasion of bact
  4. typical food contamination- poultry, eggs, meat
338
Q

Shigella species

  1. incubation
  2. symptoms
  3. mechanism of action
  4. typical food contamination
A
  1. incubation-2-4 days
  2. symptoms-diarrhea, often bloody, cramps, little-no fever
  3. mechanism of action- intestinal invasion of bact
  4. typical food contamination- food handlers usually contaminates the food, not food-borne
339
Q

E.coli

  1. incubation
  2. symptoms
  3. mechanism of action
  4. typical food contamination
A
  1. incubation- 3-4 days
  2. symptoms- diarhhea, abd cramps, little-no fever, bloody urine in children
  3. mechanism of action- cytotoxin
  4. typical food contamination- beef, raw milk, water
340
Q

Norwalk-like viruses

  1. incubation
  2. symptoms
  3. mechanism of action
  4. typical food contamination
A
  1. incubation– 24-48 hrs
  2. symptoms— vomiting, cramps, HA, fever, diarrhea
  3. mechanism of action- unknown
  4. typical food contamination– raw or undercooked shellfish, sandwiches, salads, water

USMLE First AID (9 decks)

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