Antibacs I, Anaerobes, Oppor.infections

Front 1

Lowest concentration of drug required to inhibit growth of bacterium in vitro

Back 1

MIC- min inhibitory concentration

Front 2

the MIC that defines whether a bacterium is resistant or susceptible to a drug. Determined by usual drug serum levels

Back 2

break point

Front 3

All penicillin-family antibiotics have ____________

Back 3

beta-lactam ring (called beta-lactam antibiotics)

Front 4

What happens when transpeptidase enzyme is bound by beta-lactam ring?

Back 4

Competitively inhibited -> cell wall synthesis is arrested --> DEATH of bacteria

Front 5

Lowest antibiotic concentration (in μg/ml) that kills 99.99%

Back 5

Minimal bactericidal concentration (MBC)

Front 6

b-lactams, aminoglycosides, quinolones, vancomycin have what in common?

Back 6

they are bacteriacidal

Front 7

In gram negative bugs, what must penicillin pass through?

Back 7

Porins

Front 8

What is one way that only gram negative bacteria can defend against penicillin?

Back 8

Altering the porins

Front 9

How do both gram neg and pos bacteria defend against penicillin?

Back 9

They can have beta-lactamase enzymes that cleave the C-N bond in beta lactam ring.

They can have an efflux pump to actively pump out the penicillin

Front 10

Gram _____ secrete beta-lactamase (penicillinase) and thus try to intercept antibiotic outside peptidoglycan wall

Back 10

Positive (like staph)

Front 11

Gram _____ try to destroy beta-lactam penicillins in the periplasmic space, locally

Back 11

neg

Front 12

How is MRSA resistant to all penicillin family drugs?

Back 12

It alters the sturcture of the transpeptidase so beta-lactam can't bind

Front 13

polymixin, daptomycin: mech of action

Back 13

membrane perturbation

Front 14

beta-lactams, vancomycin: mech of action

Back 14

interference with cell wall synthesis

Front 15

sulfonamides and trimethoprim: mech of action

Back 15

Interference with folic acid metabolism/aka antimetabolite

Front 16

Most important adverse effect of penicllins

Back 16

allergic reaction (IgE mediated). Bronchospasm, urticaria, anaphylactic shock

Front 17

Original penicillin used in 1940s.

Back 17

Penicillin G

Front 18

Penicillins offering better coverage of gram-neg bacteria

Back 18

Aminopenicillins

Front 19

Penicillins useful against beta-lactamase-producing S. aureus

Back 19

penicillinase-resistant penicillins
(methicillin, nafcillin, oxacillin)
MET a NAsty OX

Front 20

Group offering even wider coverage against gram-neg bacteria, including pseudomonas aeruginosa. Includes carboxypenicillins, ureidopenicillins, and monobactams

Back 20

Anti-Pseudomonal penicillins

Front 21

Widely used group of antibiotics with a beta-lactam ring, resistant to beta-lactamase, cover broad spectrum of gram postive and neg bacteria

Back 21

cephalosporins

Front 22

What is penicillin G used for?

Back 22

pneumonia caused by Strep pneumoniae, group A Strep (Strep pyogenes)

Front 23

oral form of penicillin

Back 23

Penicillin V

Front 24

What is penicillin V used for?

Back 24

Group A beta hemolytics strep-caused pharyngitis

Front 25

Ampicillin and Amoxicillin part of what class?

Back 25

Aminopenicillins. broader spectrum (gram negative) than penicillin G

Front 26

6 bacteria most resistant to current antibiotics

Back 26

Enterococcus faecium
Staphylococcus aureus
Klebsiella pneumonia
Acinetobacter baumanii
Pseudomonas aeruginosa
Enterobacter species
(ESKAPE)

Front 27

One of few drugs effective against gram-positive enterococci

Back 27

aminopenicillins

Front 28

Drug of choice for Listeria infections

Back 28

amoxicillin (more effective orally)

Front 29

What is the amp-gent combo?

Back 29

Ampicillin-gentamicin (aminoglycosides); often started until cultures reveal exact organism. broad spectrum

Front 30

Penicillinase - resistant penicillins (3)

Back 30

methicillin, nafcillin, oxacilin
I MET a NAsty Ox.

Front 31

What are the oral beta-lactamase resistant penicillins?

Back 31

The CLOX were ticking.

CLOXacillin, diCLOXacillin

Front 32

Once MRSA has been excluded, what are DOC for penicillinase resistant S aureus?

Back 32

Penicillinase-resistant penicillins.

Front 33

Resistance that is innate to every membrane of a species or genus;characteristic of a species or genus

Back 33

Intrinsic resistance

Front 34

Resistance acquired by microbes due to genetic mutation or acquisition of new genes (due to conjugation, transduction, or transformation)

Back 34

Acquired resistance

Front 35

Anti-Pseudomonal Penicillins

Back 35

Remember James Bond weapons:
CAR, TICK, PIPE

carbenicillin, ticarcillin, piperacillin

Front 36

beta Lactamase inhibitors: what are they, when are they used?

Back 36

Inhibits beta lactamase, given in combination with penicillins.

Amoxicillin and clavulanic acid (augmentin).

Ticaricillin and clavulanic acid (Timentin)

Ampicillin and sulbactam

Piperacillin and tazobactam

Front 37

What are the beta-lactamase inhibitors (without combos)

Back 37

Clavulanic acid, sulbactam, tazobactam

Front 38

Advantages of cephalosporins over penicillins

Back 38

1) Addition of new basement makes more resistant to beta-lactamases

2) New R group side chain (new antenna cable) allows for double the manipulation in lab

Front 39

Why is MRSA resistant to all cephalosporins?

Back 39

because it's changed the structure of its penicilin binding protein (transpeptidase)

Front 40

First generation cephalosporins have what sound in their name?

Back 40

CEF (like all cephalosporins) but usually spelled with a PH. EXCEPT: cefazolin (don't let it FAZE you)

Front 41

T/F any disruption to beta lactam ring ruins the antibiotic

Back 41

T

Front 42

Second generation cephalosporins have what in their names?

Back 42

fam, fa, fur, fox, tea

Front 43

Third generation cephalosporins have what in their name?

Back 43

Cef followed by a TRI (T)

Front 44

Only 4th gen cephalosporin

Back 44

Cefepime

Front 45

Advantages of 2nd gen cephalosporins

Back 45

Covers more gram negs. Good when cmomunity acquired pneumonia sputum is neg and don't know what organism is

Front 46

What is charge of most beta-lactams?

Back 46

negative

Front 47

Which beta-lactams are highly albumin bound (>80%)

Back 47

nafcillin and ceftriaxone

Front 48

How are most beta lactams eliminated?

Back 48

by kidney (secretion mainly)

Front 49

How long is serum half-life for most beta lactam antibiotics?

Back 49

short (30-120 minutes) necessitating frequent dosing intervals (4-8 hours) for serious infection.

Front 50

What is the exception to the short half-life rule of beta-lactams?

Back 50

Ceftriaxone-6-8 hour half life can be dosed daily

Front 51

What are 3 2nd-gen cephalosporins covering anaerobic bacteria and therefore useful for intra-abdominal infections, aspiration pneumonias, and colorectal surfery prophylaxis?

Back 51

Cefotetan, cefoxitan, cefmetazole

Front 52

Gram positive and gram neg coccal bacterial infections generally treated by what class?

Back 52

penicillins

Front 53

T/F Cephalosporins generally more active against enteric gram-neg rods with activity increasing with later generations

Back 53

T

Front 54

How is broader spectrum of later generation cephalosporins obtained?

Back 54

1) Resistance to beta lactamase
2) Increase penetrance thru gram-negative outer membrane

Front 55

___________ has broadest spectrum of any beta lactam

Back 55

imipenem

Front 56

imipenem is administered with _______ to prevent enzymatic degradation

Back 56

cilastatin

Front 57

Identical spectrum to 3rd gen cephalosporins, but with fewer allergic reactions

Back 57

Aztreonam

Front 58

Major dose-related side fx of beta-lactams other than allergies

Back 58

seizures, bleeding due to platelet dysfunction (high doses)

Front 59

Drug of choice for syphilis

Back 59

penicillin

Front 60

Drug of choice for Group A and B strep

Back 60

penicillin

Front 61

Drug of choice for viridans strep endocarditis

Back 61

penicillin

Front 62

Drug of choice for tetanus

Back 62

penicillin

Front 63

Drug of choice for listeria monocytogenes meningitis

Back 63

Ampicillin/Amoxicillin (po)

Front 64

Drug of choice for all staph infections except those caused by MRSA

Back 64

methicillin, oxacillin, nafcillin

Front 65

One of drugs of choice for pseudomonas and acinetobacter; susceptible to all beta-lactamase

Back 65

piperacillin

Front 66

Drug of choice for broad spectrum hospital gram-neg coverage including pseudomonas aeruginosa

Back 66

amoxicillin + clavulanic acid; piperacillin + tazobactam

Front 67

Gram negatives producing class C β-lactamase

Back 67

Serratia, Providentia,indole-pos proetus, citrobacter, Enterobacter

SPICE

Front 68

Drug of choice for Gram negatives producing class C β-lactamase

Back 68

imipenem (a carbapenem)

Front 69

Drug of choice for patients with immediate hypersensitivity (Type I) reactions to other β lactam antibiotics

Back 69

aztreonam

Front 70

T/F pathogenic anaerobic bacteria are immediately killed by O2

Back 70

False. They're usually bacteriostatic - O2 will prevent growth but won't immediately kill

Front 71

Characteristics (4) of anaerobic infection

Back 71

1) Predisposing conditions (eg, tissue damage or impaired circulation)

2) Endogenous organisms (usually normal flora) cause the infection

3) Multiple types of organisms in infection site

4) Abscess formation and tissue necrosis present

5) Foul odor due to fermentative end products

Front 72

T/F Stomach and small intestine contain high numbers of bacteria

Back 72

F. There are increasing numbers of bacteria with distance from stomach

Front 73

Bacteroides fragilis
Prevotella melanogenicus
Fusobacterium nucleatum


All fall into what category?

Back 73

Anaerobic, gram-negative bacteria encountered clinically

Front 74

Clostridium perfringens
Clostridium difficile


All fall into what category?

Back 74

Anaerobic, Gram-positive spore forming bacilli encountered frequently clinically

Front 75

Most common colonic bacteria

Back 75

In decreasing order: Bacteroides, Bifidobacterium, coliforms, strep, clostridium

Front 76

What are functions of normal intestinal microflora?

Back 76

1) Metabolize dietary fiber resulting in increased caloric intake (increased in obese people)

2) Gas metabolism (Produces H2S, Co2, H2, CH4) depending on diet

3) Biosynthesis of Vitamin K and B12

4) Protects against colonization of pathogens

5) Stimulates non specific immunity and induces antibacterial peptides

Front 77

T/F Essentially every type of infection can be caused by anaerobic bacteria

Back 77

T

Front 78

Most common blood culture in patients with anaerobic bacteremia

Back 78

Bacteroides fragilis (gram neg, non spore forming obligately anaerobic rods)

Front 79

Most predominant species of Bacteroides isolated from clinical specimens

Back 79

bacteroides fragilis

Front 80

Major virulence factor of B fragilis

Back 80

Capsular polysaccharide, that inhibits phagocytosis and induces abscesses. The purified capsule alone can induce abscess formation in lab animals.

Front 81

Type of infections caused by B fragilis

Back 81

Disease:
Causes abscesses alone or in mixed infections
Usually in the peritoneal cavity

Front 82

Minor virulence factors

Back 82

Proteolytic enzymes
Same strains (10%) produce an “exotoxin” - metalloprotease, may disrupt colonic epithelial cells

Front 83

Gas Gangrene

Back 83

generally occurs at the site of trauma or a recent surgical wound in patients with vascular disease. The onset of gas gangrene is sudden and dramatic.

Front 84

Gas gangrene: common causative agent

Back 84

Clostridium perfringens

Front 85

characteristics of clostridium

Back 85

gram positive, spore forming bacteria, naturally in intestinal tracts of man and animals

Front 86

What do most species of clostridium ferment?

Back 86

carbs or AMINO ACIDS via stickland rxn producing large amounts of gas.

Front 87

What is lecithinase and what does it do?

Back 87

An α toxin produced by C perfringens causing membrane damage by destruction of lecithin --> increased vascular permeability

Front 88

Has box car shaped rod on gram stain and rapid generation time

Back 88

C perfringens

Front 89

Major virulence factor of C perfringens

Back 89

alpha toxin: lecithinase

Front 90

Types of wound infections caused by C perfringens

Back 90

Wound contamination; Anaerobic cellulitis; Myonecrosis (aka gas gangrene)

Front 91

What happens in clostridial myonecrosis?

Back 91

Clostridia infects necrotic tissue. Associated with toxemia, local edema, gas, and 15-30% death rate in untreated cases.

Front 92

CAUSATIVE AGENT OF PSEUDOMEMBRANOUS COLITIS (PMC)

Back 92

C difficile

Front 93

Major virulence factors of C difficile

Back 93

Ability to overgrow in the colon if predominant colonic anaerobes decimated by antibiotics
Toxins A and B

Front 94

Food poisoning by __________ is 2nd in incidence behind Staph Aureus

Back 94

C perfringens

Front 95

What is the course of illness for C perfringens food poisoning?

Back 95

After ingested, bacteria sporulates in small intestines producing enterotoxin causing diarrhea lasting 24-48hours. Usually no vomiting.

Front 96

Major risk factor for pseudomembranous colitis

Back 96

Recent antimicrobial use

Front 97

What antibiotics implicated in pseudomembranous colitis?

Back 97

Almost all except vancomycin and metronidazole, parentally administered aminoglycosides and erythromycin

Front 98

What do C difficile's A and B toxins do?

Back 98

Catalyze a monoglycosylation of GTP binding proteins (Rho, Rac, CDC 42) known to be involved in regulation structural proteins controlling cell shape

Front 99

What is used to treat C difficile?

Back 99

Vancomycin, metronidazole

Front 100

Gram-positive rod
Obligate anaerobe
Sporeformer
Normally found in less than 5% of people outside of hospitals


Characteristics of what?

Back 100

C difficile

Front 101

Structure of C diff toxin

Back 101

Binding domain – binds mammalian cell receptor
TcdA – receptor is disaccharide
TcdB – receptor unknown
Translocation domain – translocation of enzymatic domain into host cell
Enzymatic domain – catalyzes glucosylation of G protein

Front 102

Difference between frank and opportunistic infections

Back 102

frank infections cause disease in normal, unvaccinated humans. Opportunistic pathogens show low invasiveness but once established can cause life-threatening disease

Front 103

Pseudomonas aeruginosa
is an example of what?

Back 103

opportunistic infection

Front 104

Pseudomonas aeruginosa: characteristics

Back 104

The premier opportunistic pathogen
Gram-negative rod
Single Polar flagellum
Aerobe, Nonfermenter (no acid from glucose).
Grows from 20° to 42°C (i.e., body temp.)
Ubiquitous - free-living in all environmental habitats (especially soil/water)
Simple growth requirements
Versatile nutrition

Front 105

What is electron acceptor for Pseudomonas aeruginosa?

Back 105

Inorganic - eg., O2, NO3

Front 106

What color is characteristic of the species?

Back 106

Green (can be blue in pyocyanin)

Front 107

Common infections by P. aeruginosa

Back 107

1) Pulmonary infections (from respirator)
2) Bacteremia/fatal sepsis
3) Otitis externa (swimmer's ear)
4) UTI
5) Meningitis
6) Septic arthritis, endocarditis
7) Folliculitis/Dermatitis/Vasculitis
8) Eye infections

Front 108

Cause and characteristics of P. aeruginosa pulmonary infections

Back 108

Very severe. Happens to people on ventilators (because of the humidifiers). Common in cystic fibrosis - 90% have chronic pulmonary disease from P aeruginosa

Front 109

seen in leukemia patients on immunosuppressive drugs, burn patients, diabetes patients, patients with neutropenia

Back 109

Bacteria/fatal sepsis caused by P. aeruginosa

Front 110

After bacteremia, invasion/destruction of blood vessel walls --> cutaneous papules --> black necrotic ulcers

Back 110

Ecthyma gangrenosum

Front 111

Ulcerative keratitis following corneal trauma caused by infection with what?

Back 111

P aeruginosa

Front 112

Presumptive Lab Dx of P aeruginosa

Back 112

Gram stain shows Gm-neg. rods
Lactose non-fermenting(white colonies on Lac-MacConkey).
Oxidase Positive
Blue-green pigment
Fruity-aroma (grapes).

Front 113

P aerignosa: oxidase pos or neg

Back 113

pos

Front 114

P aerignosa:gram neg or pos

Back 114

neg

Front 115

P aerignosa:MacConkey results

Back 115

Lactose non-fertilizing (white colonies)

Front 116

What is treatment for P aerignosa?

Back 116

Difficult because high innate resistance. Must be tailored to sensitivity of each isolate (can change during tx!)

Use combo therapy:
Gentamycin+ppiperacillin

Cipro for UT infections


Aminoglycoside (gentamycin or tobramycin) + new b-lactam (azlocillin, ceftazidime, or imipenem) or a new Quinolone (Ciprofloxacin)

Front 117

Treatment of Cystic Fibrosis

Back 117

Antibiotics to minimize lung damage and treat lung infections. Nebulizer is sometimes used to deliver aerosolized antibiotics to the lungs to help open up the airways and prevent or treat respiratory infections.


Postural drainage using “chest physical therapy [CPT]” requires vigorous percussion (by using cupped hands) on the back and chest to dislodge the thick mucus from the lungs.

Front 118

Why are CF patients especially susceptible to P aeruginosa?

Back 118

The CFTR Cl- ion pump is normally a cell receptor for P aeruginosa to internalize the organisms for destruction, so they can't get internalized

Front 119

T/F • Desquamation of bacteria-laden epithelial cells is a host defense mechanism to reduce the bacterial load.

Back 119

T

Front 120

What is mucoid conversion by Pseudomonas aeruginosa?

Back 120

Change whereby alginate (capsule, slime layer, glycocalyx) is produced, conferring resistance to opsonic phagocytosis

Front 121

What causes mucoid conversion by Pseudomonas aeruginosa?

Back 121

pathoadaptive mutation” in a gene (mucA) encoding an anti-sigma factor in vivo causes mucoid conversion.

Front 122

What are the virulence factors of Pseudomonas aeruginosa?

Back 122

Many - numerous toxic exoproducts secreted into the environment or directly into cells by type III secretion apparatus.

Exotoxin A blocks protein synthesis; Exoenzyme S, Proteases, PLC, etc

Front 123

Characteristics of Exotoxin A (ETA)

Back 123

Secreted to environment, Extremely toxic
ADPR Transferase - modifies elongation factor-2
Blocks protein synthesis

Front 124

Why is P. aeruginosa highly tolerant to most antibiotics ?

Back 124

P. aeruginosa is highly tolerant to most antibiotics due in part to efflux pumps

Front 125

What is quorum sensing?

Back 125

system of stimulus and response correlated to population density. Many species of bacteria use quorum sensing to coordinate gene expression according to the density of their local population.

Bacteria that use quorum sensing constantly produce and secrete certain signaling molecules (called autoinducers or pheromones). These bacteria also have a receptor that can specifically detect the signaling molecule (inducer). When the inducer binds the receptor, it activates transcription of certain genes, including those for inducer synthesis.

There is a low likelihood of a bacterium detecting its own secreted inducer. Thus, in order for gene transcription to be activated, the cell must encounter signaling molecules secreted by other cells in its environment. When only a few other bacteria of the same kind are in the vicinity, diffusion reduces the concentration of the inducer in the surrounding medium to almost zero, so the bacteria produce little inducer. However, as the population grows, the concentration of the

Front 126

What are quorum sensing methods used by Pseudomonas aeruginosa?

Back 126

When cell density is high, virulence genes are turned on.

N-(3-oxododecanoyl) homoserine lactone (3O-C12-HSL) re-enters cell when cell density high, activates LasR and turns on numerous virulence genes.

Front 127

causes Melioidosis - acute/chronic pneumonia, usually in tropical areas (SE Asia)

Back 127

Burkholderia pseudomallei (gram neg)

Front 128

Pulmonary infection in CF patients
(other than P aeruginosa)

Back 128

Burkholderia cepacia

Front 129

Causes the following: Pneumonia - inhalation therapy infection
Urinary Infection - infected catheters
Bacteremia - iv puncture
Often antibiotic resistant, making treatment difficult

Back 129

Acinetobacter

Front 130

TX for acinetobacter infections

Back 130

Difficult due to high resistance.

Imipenem, meropenem

Front 131

Morphology and Characteristics of Legionella pneumophila

Back 131

Gram-negative rod, motile
Difficult to stain
Require a very rich medium to grow
Grow slowly (5 days to form colonies)

Front 132

Where is legionella pneumophila typcially found?

Back 132

Common parasite of protozoa and amoeba in fresh water and soil

Front 133

Legionella pneumophila is gram (neg, pos)

Back 133

neg

Front 134

Typical sources of Legionella pneumophila infection

Back 134

Inhalation of mist from warm stagnant water (whirlpools, showers, cooling towers, Hotel AC)


NO person to person spread

Front 135

Symptoms of Legionellosis

Back 135

Non-Specific Symptoms
Fever, chills, and a cough (dry or may produce sputum)
Other symptoms: muscle aches, headache, tiredness, loss of appetite, abdominal pain, diarrhea, and confusion.
Chest X-ray often shows pneumonia.
The symptoms do not readily distinguish Legionnaires' disease from other types of pneumonia.

Front 136

What is the range of Legionellosis?

Back 136

From Severe toxic pneumonia (Legionnaire's disease) to Pontiac Fever (100% recovery)

Front 137

Most severe form of legionellosis

Back 137

Legionnaire's disease. Severe toxic pneumonia. 15% die.

A severe, toxic, progressive pneumonia
2-10 day incubation after exposure
Fever, cough, chest pain, chills, shock
15% Mortality due to respiratory failure

Front 138

Pontiac Fever: characteristics

Back 138

A Non-pneumonic Febrile Illness
1-2 days incubation after exposure, acute onset
Flu-like: Fever, dry cough, spontaneous recovery

Front 139

Risk factors for Legionnaire's disease

Back 139

Age (middle age and older), smoking or chronic lung disease, immune system suppression

Front 140

What causes the lung damage seen in Legionnaire's disease?

Back 140

Inflammatory response due to ingestion by alveolar macrophages.

Cellular immune response dominant
Influx of monocytes and neutrophils leads to development of abscesses (seen as infiltrates on chest x-rays

Front 141

How is Legionnaire's disease diagnosed?

Back 141

Must order special tests when suspected.

Methods to detect bacteria in sputum:
Gram stain shows no bacteria
Direct fluorescent antibody stain
PCR with specific DNA probe
Detection of Legionella antigens in urine:
Enzyme immunoassay
Antibody levels in 2 blood samples taken 3-6 weeks apart (usually in a retrospective diagnosis).
Culture organisms (specimen from lower respiratory tract)
Takes 3-5 days, but most definitive for diagnosis

Front 142

What is Legionnaire's disease treatment?

Back 142

Antibiotics effective

Use a -mycin or fluoroquinolone + rifampin.

Front 143

T/F Legionnaire's is sensitive to penicillin derivatives

Back 143

F. Usually resistant.

Front 144

Category of Klebsiella pneumoniae

Back 144

Lac+ Enterobacteriacea, Normal flora
respiratory / intestinal tracts of 5% healthy individuals

Related to e. Coli

Front 145

What is the most common cause of nosocomial pneumonia?

Back 145

Klebsiella pneumoniae

Front 146

Most common cause of bacteremia

Back 146

E coli

Front 147

Second most common cause of bacteremia

Back 147

Klebsiella pneumoniae

Front 148

What kind of infections does klebsiella pneumoniae cause?

Back 148

Pneumonia - severe and destructive • most common cause of nosocomial pneumonia

Bacteremia - 2nd most common cause (1st is E. coli)

Urinary tract infections - especially hospital acquired

Burn wound infections

Front 149

Causes of virulence of Klebsiella pneumoniae

Back 149

Capsule - ~80 serotypes

High resistance to antimicrobial agents

Front 150

Tx of Klebsiella pneumoniae

Back 150

Cefotaxime, ceftriaxome, ceftazidime, cefepime

Front 151

What does Klebsiella pneumoniae look like when cultured on Endo agar?

Back 151

Slimy, mucoid, raised, forms long stringy threads when drawn with a loop

Front 152

Characteristics and risks of Serratia sp.

Back 152

Normal flora
Produces a bright red pigment
Opportunistic pathogen
Causes serious hospital acquired infections, particularly in the newborn and debilitated.

Front 153

Treatment of serratia

Back 153

imipenem, meropenem

Front 154

Which bacteria produces urease, raising urine pH which can facilitate formation of renal stones?

Back 154

Proteus vulgaris

Front 155

Classification of proteus vulgaris

Back 155

rod-shaped, Gram negative bacterium.

Enterobacteriaceae

Extremely motile - tend to "swarm" on an agar plate instead of forming distinct colonies

Front 156

Proteus vulgaris is implicated in what infection?

Back 156

Urinary tract infections

Front 157

Tx of proteus vulgaris

Back 157

Cefotaxime, ceftriaxome, ceftazidime, cefepime

ampicillin; TMX-SMP