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Block 6: Microbio, ID, Derm, Heme-Onc > Bacteria Cont, Cell-Wall Antimicrobials (Week 3) > Flashcards

Bacteria Cont, Cell-Wall Antimicrobials (Week 3) Flashcards

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Dermatology Board Prep flashcards
1
Q

Streptococcus pneumoniae

A

Pneumococcus

Gram +, encapsulated, lancet shaped, diplococci, facultative anaerobe, alpha-hemolytic, naturally competent

Most common cause of community-acquired pneumonia, bacterial meningitis and meningitis in adults

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2
Q

What allows us to defend against encapsulated bacteria?

A

ANTIBODIES!

Complement cannot opsonize/phagocytize/membrane attack complex encapsulated bacteria

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3
Q

Pneumococcal pneumonia

A

From Streptococcus pneumoniae

Purulent exudate-filled alveoli –> bronchopneumonia, lobar pneumonia, cough

Immunity by antibodies because it is encapsulated (infection or vaccine)

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4
Q

Neisseria meningitidis

A

Gram -, diplococci, encapsulated

Nasopharyngeal carriage and transmitted in respiratory droplets

Virulence factors: LOS endotoxin, secretes IgA1 protease, pili, capsule

Can do transcytosis (bind apical side of cell, transit through cell and exit basolateral side of cell)

Diseases: meningitis (CNS diesase), meningococcemia (septicemia), both together

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6
Q

Drug classes that inhibit cell wall synthesis

A

Beta-lactam antibiotics: penicillins, cephalosporins; contain 4-membered beta-lactam ring structure

Vancomycin

Bacitracin

Bactericidal; only work on actively proliferating microorganisms

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7
Q

Beta lactam antibiotics

A

Inhibit transpeptidase enzmes that cross-link peptidoglycan matrix

Ex: Penicillins, cephalosporins

Contain 4-membered beta-lactam ring structure

Bactericidal

Effective against mixture of gram + and gram - bacteria

If bacteria contains beta-lactamase (ie penicillinase or cephalosporinase) then will be resistant to beta-lactam drugs

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8
Q

Penicillins

A

Interfere with one of final steps in bacterial cell wall synthesis and cause cell lysis

Can cause hypersensitivity

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9
Q

Transpeptidase

A

Bacterial enzyme that cross-links peptidoglycan matrix to form cell wall

Located in cytoplasmic membrane

AKA penicillin binding proteins (PBPs)

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10
Q

Bordetella pertussis

A

Gram - coccobacillus (small)

Obligate aerobe

NOT part of normal flora, but live in healthy ciliated epithelial cells in infected people

Disease: Pertussis (whooping cough)

Transmission: respiratory droplets, highly communicable

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11
Q

Clinical features of pertussis (whooping cough)

A

Incubation period: 7-14 days

Catarrhal phase: 7 days; mild cold-like symptoms

Paroxysmal phase: 1-4 weeks or longer; severe forceful spasmodic coughing followed by inspiratory gasp (whoop), lymphocytosis

Convalescent phase: several weeks; paroxysms less frequent/severe, gradual recovery

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12
Q

In vaccinated populations, where is the reservoir of B. pertussis?

A

In adolescents and adults, who may be asymptomatic but can give B. pertussis to infants

Note: most cases occur in infants before the vaccine has given immunity

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13
Q

Toxins secreted by B pertussis

A

1) Adenylate cyclase toxin: binds receptors on neutrophils, CDs, monocytes, is internalized, is activated by calmodulin to turn ATP to cAMP which inhibit the phagocytic cell form phagocytizing (disrupt chemotaxis, phagocytosis, killing bacteria)
2) Pertussis toxin (Ptx): A/B toxin takes ADP portion of NAD and links it to G alpha protein to inhibit its activity, but this G protein is itself inhibitory to adenylate cyclase in the host cell so this causes increase in cAMP in the host cell
3) Tracheal cytotoxin: is a fragment of bacterial peptidoglycan cell wall that stops cilia from beating and kills ciliated cells (this same toxin used by gonococcus)

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14
Q

Haemophilus influenzae

A

Gram - coccobacillus (small)

Requires hemin (X factor) and NAD (V factor)

Grown on chocolate agar

Strains a-f are encapsulated and nontypeable are nonencapsulated

Diseases: otitis media in kids, pneumonia, epiglottitis, meningitis

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15
Q

Which pathogens have conjugate vaccines?

A

Streptococcus pneumoniae

Neiserria meningitis

H. influenza

Note: all encapsulated (duh)

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16
Q

Trimethoprim sulfonamide (TMP/SMX)

A

Widely active against Gram +/-

Used to be used for UTIs but no longer because E coli are more resistant

Tx CA-MRSA, Pneumocystis jiroveci pneumonia

NOT to tx Group A streap or enterococci (intrinsically resistant)

AKA Bactrim

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17
Q

Important properties of sulfonamides

A

Highly protein bound

Undergo hepatic metabolism

Metabolite excreted by urine (may form crystals or stones in urinary tract)

Many possible toxicities (SJS)

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18
Q

Drug interaction of sulfonamide and phenytoin

A

Sulfonamide produces phenytoin toxicity (too much phenytoin) because sulfa binds albumin and displaces phenytoin from albumin

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19
Q

How do bacteria become resistant to sulfonamides?

A

1) Overproduce PABA (increase concentration of substrate so even though sulfa there to inhibit, reaction still proceeds)
2) Mutations in DHFR so that trimethoprim can’t bind/inhibit it

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20
Q

Trimethoprim

A

Toxicities: nausea and vomiting, hematopoetic problems, interferes with Na/K exchange in kidney (hyperkalemia)

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21
Q

Combination sulfa drugs

A

Pyrimethamine-sulfadoxine (Fansidar) used to treat malaria

Pyrimethamine-sulfadiazine used to treat toxoplasmosis

Note: sulfa drugs almost never prescribed alone

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22
Q

Use of sulfonamides for other things

A

Use 1% silver sulfadiazine cream for prophylaxis against infection

Use sodium sulfacetamide drops for conjunctivitis

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23
Q

Where do beta-lactams act?

A

Act on cell wall

If acting on gram - then must get through porins in outer membrane to act in periplasmic space

Note: mycobacteria have complex cell wall (or NO cell wall??) and beta-lactams usually don’t work against them

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24
Q

Three groups of cell wall synthesis inhibitors

A

Beta-lactams

Glycopetides

Inhibitor of peptidoglycan precursor transport (Bacitracin, only used topically)

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25
Q

Resistance to beta-lactams and our response

A

Degradation by beta-lactamases (all S. aureus is resistant because of this), but we combat this by using beta-lactamase inhibitors

Decreased permeability through porins (outer membrane of Gram -), but we combat this by adding different “R” groups to make drugs better able to penetrate (add amino group)

Altered penicillin binding proteins/transpeptidases (MRSA), but all we can do to combat this is to use another type of drug :(

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26
Q

Beta-lactamase inhibitors

A

Since bacteria make beta-lactamase to avoid being killed by beta-lactams (penicillins), we created beta-lactamase inhibitors!

Ex: clavulanate, sulbactam, tazobactam

Note: amoxicillin + clavulanate = Augmentin

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27
Q

Beta-lactam toxicity

A

Hypersensitivity

Nausea, vomiting, diarrhea

Neutropenia

GI disease (C difficile)

Neurotoxicity (seizure risk)

Cation toxicity: Na and K disturbances when large doses of ticarcillin/carbenicillin given; Na load with piperacillin/tazobactam

Interstitial nephritis (methicillin, others)

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28
Q

Vibrio cholerae

A

Curved gram - rod (comma)

Single polar flagellum for motility

Secretory diarrhea (“rice water diarrhea”)

Transmission is fecal-oral

Cholera toxin is phage-encoded

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29
Q

Campylobacter jejuni

A

Curved, spiral, gram - rods

Reservoir in wild and domesticated animals

Transmission: contaminated food, water, milk

Common cause of diarrhea

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30
Q

Helicobacter pylori

A

Most common cause of gastritis and gastric ulcers after NSAIDs

Associated with cancer (gastric adenocarcinoma and gastric (MALT) lymphoma)

Motile

Urease +

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31
Q

Cholera toxin

A

Secreted by V. cholera when in the lumen of gut

A/B toxin

“A” subunit enters cytoplasm, takes ADP ribose part of NAD and links it to G-alpha protein to lock it in active/GTP-bound state (links at GTPase portion so can no longer do GTP –> GDP!)

Continually active adenylate cyclase –> huge amounts of cAMP –> alteration of ion flux (Cl- and HCO3 secreted; Na and K uptake is blocked) –> water follows salt to lumen of small intestine –> watery diarrhea

Note: genes for cholera toxin are on lysogenic bacteriophage

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32
Q

Is cholera caused only by cholera toxin?

A

No, even when gene for cholera toxin (ctxAB) is deleted, still some people get sick

Note: if gene for pilus (tcpA) is deleted, nobody gets sick because V cholerae can’t colonize!

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33
Q

Which cephalosporins can cause you to bleed more (increase PT time) and how?

A

Cefotetan and Cefoperazone

Both have MTT side chain (R2) which interacts with vitamin K synthesis (remember, vit K needed for clotting) by specifically affecting enzymes in the vitamin K synthesis pathway

Note: in general, any antimicrobial can decrease vitamin K metabolism by wiping out gut flora because that gut flora needed for vitamin K synthesis and this can lead to bleeding too; however Cefotetan and Cefoperazone cause MORE bleeding because they are specifically targeting vitamin K synthesis pathway

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34
Q

What two types of antibiotics can be used synergistically to treat enterococcal infections?

A

Beta-lactams and aminoglycosides (gentamycin)

(Because beta-lactams might not be fully bactericidal alone)

35
Q

Salmonella

A

Gram - bacillus, motile, enterobacteriaceae

Non-lactose fermenter, produces H2S

Enteric (typhoid) fever: S. typhi, S. paratyphi

Nontyphoidal enteritis: S. typhimurium, S. enteriditis, etc

Pathogenesis: typhoidal strains get into macrophages and prevent phagosome from killing them; Type III secretion system uses SopE and SptP to turn on/off Ras-Cdc42 to polymerize actin to open/close cell membrane to infect cell

36
Q

Carrier state of salmonella

A

Some people infected with salmonella become chronic carriers and have S typhi in their gallbladders

“Typhoid Mary” contaminated food to everyone she cooked for

37
Q

Shigella

A

Gram - bacilli, non-motile (shigella has no flagella)

S. dysenteriae, S. flexneri, S. boydii, S. sonnei

Pathogenesis: similar to EIEC because both invade intestinal epithelial cells and release Shiga toxin to cause cell destruction; cell-to-cell spread

Clinical manifestations: dysentery, bloody diarrhea, complications (bacteremia, HUS)

38
Q

Shiga toxin

A

Cleaves 28S rRNA, inhibits protein synthesis

Causes cell destruction (usually in GI tract/intestinal epithelial cells) to cause bloody diarrhea

39
Q

Listeria monocytogenes

A

Gram + rod, non-spore forming, tumbling motility (tail of actin filaments being polymerized/depolymerized)

Virulence factors: listeriolysin O allows escape from phagolysosomes of macrophages (avoid intracellular killing); invasins (InlAB), ActA polymerizes actin

Diseases: pregnant women during 3rd trimester, immunocompromised/elderly meningitis, neonatal meningitis

Note: need CD4 T cell response to activate macrophages to kill L monocytogenes before it escapes and doesn’t allow macrophage killing!

40
Q

Enterobacteriaceae

A

Gram -

Some are normal flora that become opportunistic (E. coli, Klebsiella, Proteus) or acquire virulence factor (toxigenic E. coli)

Some are always a pathogen (Salmonella, shigella, yersinia)

Virulence factors in general: flagella (H antigen), capsule (K or Vi antigen), LPS, sequestration of growth factors, antimicrobial resistance

41
Q

Escherichia coli

A

Gram - bacillus (rod)

Lactose fermenting, oxidase negative, reduces nitrates to nitrites

Virulence factors: adhesins (pili), exotoxins (LT and ST, shiga-like toxin), endotoxin (lipid A of LPS)

Diseases: diarrhea, UTI, neonatal meningitis, neonatal pneumonia, sepsis secondary to infection at other site

42
Q

Different types of E. coli infections

A

1) Enterotoxigenic E. coli (ETEC)
2) Enteropathogenic E. coli (EPEC)
3) Enteroinvasive E. coli (EIEC)
4) Enterohemorrhagic E. coli (EHEC)
5) Enteroaggregative E. coli (EAEC)

APITH

43
Q

Enterotoxigenic E. coli (ETEC)

A

Watery (secretory) diarrhea (but milder than cholera)

No histologic changes in bowel mucosa (no inflammatory response)

Traveler’s diarrhea (T for traveler’s)

Heat labile AB toxin increases cAMP to cause ion secretion (labile like the Air)

Heat stable monomer toxin increases cGMP (stable like the Ground)

44
Q

Enteropathogenic E. coli (EPEC)

A

Watery diarrhea, fever, nausea and vomiting

Infant diarrhea in developing countries; rare in adults

E coli destroy/flatten microvilli to cause malabsorption, so would see histological changes (inflammation)

Type III secretion injects intimin receptor to bind adhesin; get attachment/effacement lesions

45
Q

Enteroinvasive E. coli (EIEC)

A

Very similar to Shigella (main virulence factor encoded by plasmid shared by Shigella and E. coli = shiga-like toxin)

Watery diarrhea may become a little bloody; fever, WBCs in intestinal wall and stool; dysentery in developing countries

E. coli actually invades epithelial cells and host causes inflammation to get rid of bacteria

46
Q

Enterohemorrhagic E. coli (EHEC)

A

Bloody diarrhea, severe abdominal cramps (hemorrhagic colitis), usually no fever

Hemolytic uremic syndrome (HUS) with anemia, thrombocytopenia, renal failure when have E. coli 0157:H7 (most common in US)

Most common in developed countries (from contaminated meat, cheese, etc)

Secrete shiga-like toxin (verotoxin) which destroys intestinal cells; get attachment/effacement lesions

47
Q

Enteroaggregative E. coli (EAEC)

A

Chronic watery diarrhea (infants in developing countries; AIDS pts)

Bundle-forming fimbriae AAF-I and -II, no cytotoxin

Not as common

48
Q

Shiga toxin

A

Stx-1, Stx-2

Phage transduced

AB toxin

Gets into submucosa and capillaries to halt protein synthesis (inhibits 60S ribosome of host)

Causes destruction of intestinal villus cells, A/E lesions

Hemolytic uremic syndrome associated with Stx-2

Shiga toxin secreted by EHEC, EIEC

49
Q

Klebsiella

A

Encapsulated with thick capsule (with O antigen) but non-motile (so no H antigen)

Causes sepsis, UTIs and pneumonia (bloody sputum = currant jelly; lobar pneumonia) in hospitalized patients

Increasing drug resistance is emerging (KPC carbapenemase producing strain is spreading)

50
Q

Proteus mirabilis

A

Motile, urea-splitting (will find alkaline/high urine pH), doesn’t ferment lactose, oxidase negative

Increased pH precipitates ammonium magnesuim phosphate, leading to urinary stones

Swarms, forms confluence on agar plate

Common cause of UTIs and nosocomial infections

Note: also have Proteus vulgaris, similar?

51
Q

Nosocomial gram negative rods

A

Enterobacter

Citrobacter

Morganella

Serratia

These can cause nosocomial pneumonia, UTI, bloodstream infection, meningitis (after neurosurg procedure)

Have increased antimicrobial resistance (extended spectrum beta lactamase production; inducible chromosomal resistance (initially appears susceptible but resistant strains emerge quickly))

52
Q

Pseudomonas aeuginosa

A

Aerobic, Gram - rod

Lactose negative, oxidase positive, produces green-blue pigment, has grape-like odor

Virulence factors: pili, capsule (slime layer), lipid A endotoxin, pyocyanin, exotoxin A, exoenzymes S and T, elastases, alkaline protease, phospholipase C, rhamnolipid, antimicrobial resistance

Diseases: nosocomial pathogen; pneumonia, UTI, medical device infection; skin infection (hot tub folliculitis, nails); (malignant) otitis externa; corneal infection

Opportunistic pathogen,usually affects people already in hospital or sick

Treatment: double coverage (2 agents of diff classes: beta lactam plus aminoglycoside or quinolone)

53
Q

Stenotrophomonas maltophila

A

Non-fermenter

Nosocomial pneumonia, meningitis, sepsis

Opportunistic infections when impaired host defense

54
Q

Burkholderia cepacia

A

Non-fermenter

Pneumonia in cystic fibrosis, sepsis, nosocomial UTI

Relatively low virulence

55
Q

Burkholderia pseudomallei

A

Causes melioidosis, skin infection w/adenitis, necrotizing pneumonia w/cavitation

Endemic to Southeast Asia

56
Q

Acinetobacter

A

A. baumannii, A. lwoffii, A. haemolytics

May be a colonizer

Nosocomial pneumonia, sepsis, UTI, wound infection

Antimicrobial resistance

57
Q

Moraxella catharralis

A

Bronchopneumonia in elderly, sinusitis, otitis media in kids

Produce beta-lactamases

58
Q

Bacteroides fragilis

A

Gram - rod, aerobic

No activity of LPS!

59
Q

Anaerobic infection

A

Usually part of mixed infection with other gram - or gram +

Necrotizing infections, abscesses (lung, intra-abdominal, soft tissue, gynecologic)

60
Q

Anaerobic and mixed infection: necrotizing pneumonia, lung abscess,empyema

A

Rare, but commonly someone aspirating oral secretion

Prevotella, porphyromonas, fusobacterium, anaerobic gram + (peptostreptococcus)

Foul smelling breath, cavitation

61
Q

Anaerobic and mixed infection: brain abscess

A

Odontogenic source, chronic sinusitis, otitis media

Prevotella, porphyromonas, fusobacterium, peptostreptococcus

Presents with fever, headache, altered mental status

62
Q

Anaerobic and mixed infection: intra-abdominal infection

A

Comes from gut: perforation of bowel due to trauma, ischemia, diverticulitis, pancreatitis –> spill intestinal contents into peritoneum

B. fragilis, B. thetaiotaomicron

Abscess formation

63
Q

Anaerobic and mixed infection: gynecologic infection

A

Pelvic inflammatory disease (chlamydia, gonorrhea), tubo-ovarian abscess, salpingitis, endometritis

64
Q

Anaerobic and mixed infection: skin and soft tissue infection

A

Human bite wound, diabetic foot infection (devitalized tissue due to arterial insufficiency with superimposed infection (wet gangrene)

65
Q

How do you treat anaerobic infection?

A

Surgical treatment is critical: must debride and remove necrotic tissue, drain abscesses (poor penetration of antibiotics)

Broad therapy

66
Q

HACEK organisms

A

Slow-growing gram - rods

Mostly odontogenic source

Cause endocarditis, brain abscesses

Treat with ceftriaxone

Haemophilus aphrophilus

Actinobacillus actinomycetemcomitans

Cardiobacterium hominis

Eikenella corrodens

Kingella kingae

67
Q

Pasteurella multocida

A

Animal borne (get from cat/dog bites)

Often requires debridement or drainage

Treat with amoxicillin/clavulanate (enteral) or ampicillin/sulbactam (parenteral)

68
Q

Bartonella

A

Slow-growing aerobic gram -

Get from animals, particularly insects

B. bacilliformis, B. quintana, B. henselae

69
Q

Bartonella bacilliformis

A

Oroya fever

Chronic skin manifestations (verruga)

Sandfly vector

70
Q

Bartonella quintana

A

Trench fever (common in WWI)

Headache, fever for 5 days, weakness, bone pain

Person to person spread via body louse

71
Q

Bartonella henselae

A

Cat-scratch disease

Bacillary angiomatosis in AIDS patients

Peliosis hepatis

72
Q

Vibrio vulnificus

A

Salt-water bacteria (surfers!)

Skin infection with bullae, necrosis; sepsis

73
Q

Vibrio parahaemolyticus

A

Salt water bacteria (get from oysters)

Get this in Japan

Diarrhea, can cause fever

74
Q

Aeromonas

A

Water organism

Associated with wound infection and enteritis

75
Q

Plesiomonas shigelloides

A

Water organism

Not associated with wound infections

Polar flagella

76
Q

Legionellaceae

A

Gram - rod, slender

In water (lakes, streams, air conditioning, respiratory devices)

Intracellular pathogen

L. pneumophila, L. micdadei

Pathogenesis: binds complement but then prevents fusion with phagolysosome and kills by releasing proteolytic enzymes, phosphatase, lipase, nuclease

Diseases: Legionnaires’ Disease, Pontiac Fever

77
Q

Coxiella burnetii

A

Gram - coccobacillus

Intracellular pathogen

Associated with farm animals (cows, sheep)

Disease: Q fever (mild atypical pneumonia that can lead to hepatitis, chronic endocarditis)

78
Q

Typical vs. atypical pneumonia

A

Typical: focal lobar infiltrate (Strep pneumonia, H. influenzae, M. catarrhalis, Strep pyogenes)

Atypical: patchy infiltrates looks more like viral pneumonia (legionella, chlamydia, mycoplasma)

79
Q

Reasons to use genome sequencing of bacteria

A

1) Determine the origin of bacteria causing an outbreak
2) Determine what virulence factors bacteria may be using

80
Q

Why wouldn’t you want to use an antibiotic that damages DNA (fluoroquinolones) to kill bacteria?

A

If the bacteria contains a phage, it can sense host becoming damaged and will make more phage (so more toxin if is phage-encoded) and escape the cell

81
Q

Human gut microbes associated with obesity

A

More firmicutes in obese (fatty) people and bacteroidetes in skinny people

82
Q

What is the significance of germ free mice having no gut flora?

A

Germ free mice (no bacteria in gut) do not get as obese when over-fed –> gut microbes modulate energy production and storage

Block 6: Microbio, ID, Derm, Heme-Onc (10 decks)

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