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Infectious Diseases Module > EXAM THREE COVERAGE > Flashcards

EXAM THREE COVERAGE Flashcards

1
Q

What is the leading cause of global morbidity and mortality?

A

Dehydration

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2
Q

Infectious Diarrhea Types

A
  1. Enterotoxigenic Diarrhea
  2. Invasive Diarrhea
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3
Q

Enterotoxigenic Diarrhea

A
  1. Watery, non-inflammatory diarrhea
  2. Lower severity diarrhea
  3. Self-Limiting
  4. Increased colonic secretion caused by altered movement of ions and water
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4
Q

Invasive Diarrhea

A
  1. Dysentery/Inflammation
  2. Fever, blood/mucus in stool
  3. Requires close monitoring/follow up
  4. Disrupt GI mucosa via invasion and/or toxin production
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5
Q

Goal of Therapy for Infectious Diarrhea

A
  1. Prevent Dehydration
  2. All patients should receive supportive care via fluid and electrolyte replacement
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6
Q

Diagnosis of Infectious Diarrhea

A
  1. Stool Culture
  2. Not routinely recommended in patients with mild-moderate watery diarrhea
  3. Reserved for:
    * Dysenteric Diarrhea
    * High Risk (>65 w/comorbidites, neutropenia, HIV)
    * Suspected Outbreak
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7
Q

Treatment for Mild-to-Moderate Self Limiting Watery Diarrhea

A
  1. Oral Replacement Therapy
  2. Easily Digestible Foods
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8
Q

Treatment for Severe-Watery or Dysentric Diarrhea

A
  1. IV Rehydration Therapy
  2. Antibiotics
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9
Q

Antimotility Agents

A
  1. Diphenoxylate/Atropine
  2. Loperamide
  3. Bismuth Subsalicylate

AVOID in toxin-mediated dysenteric diarrhea

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10
Q

Adjunctive Agents to consider in Infectious Diarrhea Treatment

A
  1. Antimotility
  2. Probiotics
  3. Zinc: supplement with signs of malnutrition
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11
Q

Enterotoxigenic Diarrhea Causative Organisms

A
  1. E.Coli
  2. Cholera
  3. Viruses
  4. ETEC is most common form of E.Coli diarrhea
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12
Q

Enterotoxigenic Diarrhea Treatment

A
  1. Fluid and Electrolyte Replacement –> every patient should get
  2. Bismuth Subsalicylate and Loperamide
  3. Antibiotics for SEVERE cases:
    * Children: AZITHROMYCIN and CEFTRIAXONE
    * Adults: CIPROFLOXACIN
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13
Q

Cholera Treatment

Enterotoxigenic
1. Vibrio Cholerae: gram neg bacillus
2. Secretory Toxin

A
  1. Fluid and Electrolyte Replacement
  2. Antibiotics for SEVERE cases:
    * Children: AZITROMYCIN or ERYTHROMYCIN
    * Adults: DOXYCYCLINE
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14
Q

Viral Pathogen Treatment

Enterotoxigenic

A

Noroviruses: >90% of outbreaks, onset 12-48 hr
Rotavirsues: common in children, prevent with vaccination
Treatment: SUPPORTIVE CARE

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15
Q

Shigellosis Treatment

Invasive Diarrhea
1. Gram Negative Bacilli
2. Cytoxin Production = blood

A
  1. Typically Self Limiting 4-7 days
  2. Fluid and Electrolyte Replacement
  3. AVOID antimotility agents
  4. Antimicrobials (elderly, immune compromised, day care centers)
  5. Children: AZITROMYCIN or CEFTRIAXONE
  6. Adults: CIPROFLOXACIN or LEVOFLOXACIN
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16
Q

Salmonellosis Treatment

Invasive
1. Enterocolitis, bacteremia, localized infectious, and enteric

A
  1. Fluid and Electrolyte Replacement
  2. AVOID antimotility agent
  3. Antibiotics for those with bactermia or high risk
  4. Children: AZITHROMYCIN or CEFTRIAXONE
  5. Adults: CIPROFLOAXCIN
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17
Q

Campylobacteriosis Treatment

Invasive
1. Gram neg rods
2. Entertoxin/Cytotxin production

A
  1. Fluid and Electrolyte Replacement
  2. Antibiotics are not useful unless started within 4 days –> necessary for high fever, severe bloody diarrhea, prolonged illness (>7 days), pregnancy, and immunocomprised
  3. Children and Adults: AZITHROMYCIN or ERYTHROMYCIN
  4. NO Antimotility Agents
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18
Q

Anterohemorrhage E.Coli Treatment

Invasive
Watery diarrhea that is bloody in 1-5 days

A
  1. AVOID ABX as they increase the risk of HUS (hemolytic uremic syndrome)
  2. Fluid and Electrolyte Replacement
  3. Hemodialysis and/or blood transfusion in severe cases
  4. AVOID antimotility agents
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19
Q

Yersiniosis Treatment

Invasive
Gram neg bacilli, contaminated food/water

A
  1. Fluid and Electrolyte replacement
  2. Antibiotics in high risk patients who develop bacteremia
  3. Children: AZITHROMYCIN or CEFTRIAXONE
  4. Adults: CIPROFLOXACIN or LEVOFLOXACIN
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20
Q

Traveler’s Diarrhea

Malaise, anorexia, abdominal cramps with diarrhea

A
  1. Symptoms usually resolved in 1-2 days
  2. Fluid and Electrolyte Replacement
  3. Loperamide or Bismuth Subsalicylate for symptom relief
  4. Antibiotics
    * Single Dose of Fluoroquinolone
    * If diarrhea improves in 12-24 hrs, STOP therapy
    * If no improvement, continue for 3 DAYS
    * Pregnant and Children: AZITHROMYCIN
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21
Q

C. diff Epidemiology

A
  1. Gram Positive Spore Forming ANAEROBE
  2. Most common cause of infectious diarrhea
  3. CDI often occurs during/shortly after completion of antimicrobial therapy
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22
Q

What are the Risk Factors for C. diff?

A
  1. Elderly >70
  2. Altered gastric pH (PPIs)
  3. Immunosuppression, including active cancer
  4. Use of Antimicrobials:
    * Clindamycin
    * 3rd and 4th Generation Cephalosporins
    * Carbapenems
    * Fluoroquinolones
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23
Q

C. diff Clinical Presentation

A
  1. Colitis
  2. Pseudomembranous Colitis
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24
Q

Colitis

A
  1. Watery Diarrhea
  2. Malaise, abdominal pain, nausea
  3. Low-grade fever, leukocytosis
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25
Q

Pseudomembranous Colitis

A
  1. Severe abdmonial pain
  2. Perfuse diarrhea, high fever
  3. Marked Leukocytosis
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26
Q

Diagnosis of C. diff

A
  1. Stool testing recommended in patients with at least 3 UNEXPLAINED, New-Onset, UNFORMED Stools in 24 hours
  2. Two-Stepp Process
    * Nucleic Acid Amplification Test (PCR)
    * Toxin A&B Enzyme Immunoassay (Ab to Detect Toxins)
    * Both Positive = Treatment Indicated
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27
Q

C. diff Treatment Non-Severe

WBC <15,000
SCr <1.5

A

Preferred: Fidaxomicin 200 mg PO BID x 10 days
Alternative: Vancomycin 125 mg PO QID x 10 days
Metronidazole 500 mg PO QID x 10-14 days only if the two others are NOT available

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28
Q

C. diff Treatment Severe

WBC >15,000
SCr >1.5

A

Preferred: Fidaxomicin 200 mg PO BID x 10 days
Alternative: Vancomycin 125 mg PO QID x 10 days

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29
Q

C. diff Treatment Fulminant

Hypotension or Shock Toxic Megacolon or Ileus

A

Vancomycin 500 mg QID by mouth of NG tube + Metronidazole 500 mg IV Q8H
**If complete ileus, consider adding concomitant rectal instillation of vancomycin

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30
Q

Treatment of CDI First Recurrence

A

Preferred: Fidaxomicin 200 mg PO BID x 10 days or BID x 5 days followed by once every other day for 20 days
Alternative: Vancomycin PO in a tapered and pulsed regimen
Alternative: Vancomycin 125 mg PO QID x 10 days
Adjunct: Bezlotoxumab 10 mg/kg IV once

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31
Q

Treatment of CDI Second Recurrence

A
  1. Fidaxomicin 200 mg PO BID x 10 days or BID x 5 days followed by once every othery day for 20 days
  2. Vancomycin PO in a tapered and pulsed regimen
  3. Vancomycin 125 mg PO QID x 10 days, then Rifaximin 400 mg TID x 20 days
  4. Fecal Microbiota Transplantion
  5. Adjunctive Treatment: **Bezlotoxumab 10 mg/kg given IV once

NEVER give Bezlotoxumab MONOTHERAPY

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32
Q

If Fidaxomicin is not an option for recurrent CDI what can be a potential alternative?

A

Vancomycin TAPERED and PULSED regimen

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33
Q

Bezlotoxumab/Zinplava

Adjunct Therapy

A

Higher risk of HF exacerbation, infection, respiratory failure compared to placebo
**Concerns in patients with heart failure

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34
Q

Intra-Abdominal Infection IAI is what?

A
  1. Involves the peritoneal cavity or retroperitoneal space
  2. Localized or Diffuse
  3. May involve visceral organs: liver, spleen, pancreas, female pelvic organs
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35
Q

Normal Flora of the Stomach

A
  1. Streptococcus
  2. Lactobacillus
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36
Q

Normal Flora of the Colon

A
  1. Bacteroides
  2. Peptostreptococci
  3. Clostridium
  4. E.Coli
  5. Klebsiella
  6. Enterobacter
  7. Enterococci
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37
Q

Normal Flora of Small Intestine

A
  1. E. Coli
  2. Klebsiella
  3. Enterobacter
  4. Bacteroides
  5. Fragilis
  6. Clostridium
  7. Peptostreptococci
  8. Enterococci
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38
Q

Risk Factors of IAI

A
  1. Impaired host defenses/immunocompromised
  2. Decreased peristalsis
  3. Reduced stomach acid due to H2 blockers or PPIs
  4. Mucosal damage
  5. Disruption of normal flora due to antibiotic use
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39
Q

Classifications of IAIs

A
  1. Uncomplicated: Localized
    * Confined to visceral structures
  2. Complicated: Spreads
    * Anatomincal disruption
    * Extends beyond single organ
    * Leads to peritonitis and/or abscess
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40
Q

Peritonitis

IAI

A
  1. Inflammation of the peritoneal lining
  2. Primary –> not tested
  3. Secondary
  4. Tertiary
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41
Q

Secondary Peritonitis

Gram - and Polymicrobial

A
  1. Aerobes: E. coli and Klebsiella
  2. Anaerobes: Clostridium and Bacteroides
  3. Common Causes:
    * Appendicitis
    * Blunt or Penetrating Trauma
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42
Q

Tertiary Peritonitis

A
  1. Persistence or recurrence of peritoneal infection
  2. Occurs >48 hrs after adequate management of primary or secondary peritonitis
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43
Q

Abscess

IAI

A
  1. Purulent fluid collection separated from surrounding tissue by a wall consisting of inflammatory cells and adjacent organs
  2. Contains necrotic debris, large inoculum of bacteria, and inflammatory cells
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44
Q

Diagnosis of IAI

A

Subjective: rapid onset of abdominal pain, loss of appetitie, nausea and/or vomiting, bloating, constipation, pain/tenderness, abdominal guarding
Objective: vitals, WBC, radiologic (CT scan/ultrasound), microbiologic (blood/abscess cultures)

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45
Q

Treatment Goals of IAI

A
  1. Correction of intra-abdominal disease process
  2. Acheive resolution of infection without major organ injury or adverse drug effects
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46
Q

IAI Coordination of 3 MAJOR Modalities

A
  1. Hemodynamic and Organ Support
  2. Source Control
  3. Administratoin of appropriate antimicrobial therapy
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47
Q

Hemodynamic/Organ Support IAI

A
  1. Patients often require large volume IV fluids
  2. Maintenance of nutrition
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48
Q

Secondary/Tertiary Peritonitis Source Control

Managed Surgically

A

Patching perforated ulcers or removal of damaged/necrotic bowel segment

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49
Q

Intra-Abdominal Abscess Souce Control

A

DRAINAGE is CRITICAL to management
Without adequate drainage, antimicrobical therapy and fluid resuscitation likely to fail

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50
Q

Community Acquired IAI (CA-IAI)

Classified as Mild-Moderate of High

A

Risk Factors: sepsis, surgical intervention, advanced age, low albumin level, healthcare exposure

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51
Q

CA-IAI Mild-Moderate Treatment

Antimicrobials w/Narrow Spectrum

A
  1. Empiric Therapy: to cover aerobic gram-negative bacilli and anerobic baceria
  2. Single Agent Regimen: MOXIFLOXACIN, ERTRAPENEM, Cefoxitin, Ervacycline
  3. Double Agent Regimen: CEFTRIAXONE, CEFOTAXIME, CIPROFLOXACIN, Cefazolin, Cefuroxime, and Levofloxacin –> PLUS METRONIDAZOLE FOR ANAERBOIC COVERAGE
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52
Q

ANAEROBIC COVERAGE

A

Gram Pos = Clindamycin
Gram Neg = Metronidazole

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53
Q

CA-IAI High Treatment

Antimicrobials w/Broad Spectrum - concerned with Pseudomonas

A

Single Agent: ZOSYN, IMIPENEM/CILASTATIN, MEROPENEM, Meropenem/Vaborbactam, and Imipenem/Cilastatin/Relebactam
Double Agent: CEFEPIME, CEFTAZIDIME (+/- AVIBACTAM), CIPROFLOXACIN, Ceftoloxane/Tazobactam, Cefiderocol, Levofloxacin –> PLUS METRONIDAZOLE FOR ANAEROBIC COVERAGE

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54
Q

Hospital Associated IAI (HA-IAI)

A

Higher Risk of Resistant or Opportunitisc Organism

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55
Q

HA-IAI Treatment

A
  1. Use non FQ-containing regimen as in high severity CA-IAI
  2. BL-Allergy = Aztreonam + Metronidazole + Vancomycin
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56
Q

HA-IAI Enterococcus

A

Sensitive: Ampicillin +/- Sulbactam, Zosyn, and Imipenem
Resistant: Vancomycin, Linezolid, and Dapto

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57
Q

HA-IAI S. aureus

A

MSSA: Nafcillin, Oxacillin, and Cefazolin
MRSA: Vancomycin and Daptomycin

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58
Q

HA-IAI Candida

A

Sensitive: Fluconazole
Resistant/Severe: Echinocandin

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59
Q

Empiric Agents to AVOID in IAI

A
  1. Augmentin and Unasyn due to E. coli resistance
  2. FQs
  3. Cefotetan and Clindamycin due to B. fragilis resistance
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60
Q

What is the Duration of Therapy for IAI

A

FOUR DAYS for most infectious with adequate source control
-Longer 5-7 days fo severe/recurrent infections

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61
Q

Skin and Skin Structure Infectious SSTIs
Acute Bacterial Skin and Skin Structure Infections ABSSSIs

A
  1. Epidermis: thin layer, superficial
  2. Dermis: sebaceous glands
  3. Subcutaneous: fatty/muscle tissue
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62
Q

SSTIs Risk Factors

A
  1. High concentrations of bacteria >10^5
  2. Excessive skin moisture
  3. Inadequate blood supply
  4. Availability of bacterial nutrients
  5. Damage to the corneal layer
  6. Immunosuppression
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63
Q

Pathophysiology of SSTIs

A

Organisms Invade Skin
Damage Occurs to Surrounding Tissues
Inflammatory Response Ensues

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64
Q

Bacterial Etiology of SSTIs

A
  1. Majority caused by gram positive organisms present on skin
  2. Staph, Aureus
  3. Streptococcus Pyogenes
  4. Gram Neg/Anaerobic Bacteria in secondary or nosocomial infectious
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65
Q

Risk Factors for HA-MRSA SSTIs

A
  1. Recent exposure to antibiotis
  2. Health system exposure

Acquire genetic material to build resistance similar to MLS resistance

Sustain susceptibility to clindamycin

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66
Q

Risk Factors for CA-MRSA SSTIs

A
  1. Playing sports, attendance at day care or school
  2. Living in close quarters
  3. Producers of PANTON-VALENTINE LEUKOCIDIN TOXIN

PVL Factor = increased infection and invasiveness

Susceptible to: Bactrim/Clinda/and Tetracyclines

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67
Q

Primary SSTIs

A

Invasion of Healthy Skin

Usually due to single pathogen

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68
Q

Secondary SSTIs

A

Occurs in areas of previously damaged skin

Frequently polymicrobial

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69
Q

What is complicated SSTIs?

A

Involving deeps skin structures requiring significant surgical intervention, occuring in immunocompromised patients

DM OR HIV

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70
Q

Purulent vs Nonpurulent SSTI

A
  1. Purulent: Staphylococcus – MSSA or MRSA
  2. Non-Purulent: Streptococci
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71
Q

Purulent SSTI Folliculitis

Inflammation of the hair follicle

A
  • Papules that evolve into Pustules
  • Appear within 48 hrs
  • Found: butt, hips, areas in contact with bathing suits
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72
Q

Purulent SSTIs Furuncles and Carbuncles

Furuncle: boil
Carbuncle: coalescence of multiple furuncles

A

Infections of the hair follicle (deeper than folliculitis)

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73
Q

Purulent SSTIs Cutaneous Abscesses

A

Collection of pus within dermis and deeper skin tissues

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74
Q

Purulent SSTI MILD Treatment

A
  1. Incision and Drainage ALONE effective in most cases
  2. Antibiotic Therapy when ANY are present:
    * Abscess that cannot be drained
    * Associated comorbidites or immunosuppression
    * Associated septic phelbitis
    * Extremes of age
    * Lack of response to I&D alone

Warm moist compressess

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75
Q

Purulent SSTI MODERATE Treatment

Systemic Signs of Infection

A
  1. I&D with empiric oral antibiotics directed CA-MRSA
    * DOXYCYCLINE OR BACTRIM
  2. If MSSA is isolated
    * Cephalexin
    * Dicloxacillin

Warm moist compresses

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76
Q

Purulent SSTI SEVERE Treatment

Failed I&D+oral antibiotics or systemic sign of infection/immunocomprise

A
  1. I&D and IV antibiotics directed against MRSA
    * VANCOMYCIN
  2. If MSSA is isolated
    * Cefazolin, Oxacillin, and Nafcillin

Warm moist compresses

77
Q

Daptomycin

Secondary MRSA Bacteremia

A

BACTERICIDAL
Dapto >7 mg/kg/day is associated with lower mortality

78
Q

Linezolid

Secondary MRSA Bacteremia

A

BACTERIOSTATIC
Use PO for de-escalation after daptomycin

79
Q

Non-Purulent SSTIs Organisms

A
  1. Group A Streptococci S. Pyogenes especially ERYSIPELAS
  2. S. Aureus more common with cellulitis than erysipelas
80
Q

What are the Risk Factors specific to MRSA Non-Purulent SSTI?

A
  1. Penetrating Trauma
  2. Injection Drug Use
  3. Nasal Colonization w/MRSA
  4. Evidence of another MRSA infection
  5. Systemic inflammatory response syndrome
81
Q

Non-Purulent SSTI Erysipelas

Common in areas of pre-existing lymphatic obstruct/edema

A
  1. Brigh red erythematous lesion of superficial skin layers
  2. Raised border and well-demarcated margins
  3. Flu-like symptoms and burning pain
  4. Lower extremitiy most common site
82
Q

Non-Purulent SSTIs Cellulitis

A
  1. Acute inflammation of epidermis, dermis, and possible superfifical fascia
  2. Erythema and edema
  3. Non-elevated and poorly defined margins
  4. Organism can invade lymphatic tissue and blood
83
Q

Non-Purulent SSTI MILD Treatment

outpatient

A
  1. Oral antibiotics targeting streptococci
    * PENICLIIN VK
  2. immbolinzation and elevation of the affected extremity
84
Q

Non-Purulent SSTI MODERATE Treatment

Hospitalization

A
  1. IV Antibiotics
    * PENICILLIN G
  2. Switch to oral therapy once there is clinical response
  3. Immobilization and elevation of the affected extremity
  4. Concern for MRSA = VANCOMYCIN
85
Q

Non-Purulent SSTI SEVERE Treatment

Failed, immunocomprise, deep infection, or systemic

A
  1. Polymicrobial
  2. Rule out Necrotizing
  3. Surgical Debridement and IV Antibiotics
    * VANCOMYCIN + ZOSYN
  4. Immobilization and Elevation of the extremity
86
Q

Duration of Therapy for Non-Purulent SSTIs

A
  1. Outpatient: 5 days (may extend if slow to respond to therapy)
  2. Inpatient: 7-10 days
87
Q

What are the New Agents for SSTIs

All lack place in therapy

A
  1. Tedizolid
  2. Telavancin
  3. Dalbanacin/Oritavancin
  4. Delafloxacin
  5. Omadacycline
88
Q

Management for Recurrent Purulent SSTIs

A
  1. I&D
  2. Systemic Antibiotics
  3. Decolonization
    * Intranasal Mupirocin 2-3x times daily for 5 days
    * Daily chlorhexidine washes
    * Daily decontamination of personal items
89
Q

Necrotizing Infections

30-70% mortality rate

Caused by S.pyogenes fleshing eating bacteria

A
  1. Tracking along the superficial fascia
  2. Severe pain
  3. Skin crepitus
  4. Necrosis
90
Q

Necrotizing Fasciitis Treatment

A
  1. Immediate surgical debridement
  2. Repeat surgical debridement
  3. Antibiotic therapy active aganist anaerobes MRSA and anaerobes
91
Q

How long do you continue Necrotizing Fasciitis Treatment?

A
  1. Debridement is no longer needed
  2. Clinical improvement has occurred
  3. Afebrile for 48-72 hrs
  4. Duration of therapy is usually 2-3 weeks
92
Q

What is Fournier Gangrene?

A

Necrotizing Dasciits of the scotum, penis, or vulva

93
Q

Impetigo Characteristics

A
  1. Usually ocurs in children
  2. Highly communicable
94
Q

Impetigo Causative Organisms

A
  1. S. Aureus
  2. Beta-Hemolutic Streptococci
95
Q

Impetigo Treatment

TOPICAL

A
  1. Primary: Mupirocin 2-3x daily for 5 days
  2. Alternative: Ozenoxacin BID x5 days
  3. Empiric Treatment: Dicloxacillin, Cephalexin, Augmentin x7 days
  4. MRSA (suspected/confirmed) = Bactrim, Doxycycline, or Clindamycin
96
Q

Organisms in Human/Animal Bites

A

Mouth Flora = anerobes
Victim Skin = staph and strep
Purulent Wound = polymicrobial, aerobe, anaerobe
Non-Purulent Wound = staph and strep

97
Q

Pasteurella spp

A

ANIMAL bites

98
Q

Eikenella Corrodens

A

HUMAN bites

99
Q

Oral drugs for Bite Wounds

A

Augmentin
5-10 days

100
Q

IV drugs for Bite Wounds

A

Unasyn
7-14 days

Serious injuries, clenched fist, failed outpatient

101
Q

Tetanus Considerations

A

Tdap for those who have not had a vaccination in 10 years of a booster for dirsty wounds and 5 years have passed since last vaccination

102
Q

Diabetic Foot Infection Etiology

A

Mild Infections: monomicrobial
Severe Infections: polymicrobial
MRSA/MSSA/Strep/Gram Neg Bacilli/Anaerobes

103
Q

Definition of Diabetic Foot Infection

A

Presence of at lest 2 of the following:
1. Local swelling or induration
2. Erythema
3. Local tenderness or pain
4. Local warmth
5. Purulent discharge

104
Q

What classifies as MILD DFI?

A
  1. Local infection involving only skin/subcutaneous tissue
  2. Erythema <2cm
  3. Exclude other caues of inflammatory skin response
105
Q

What classifis as MODERATE DFI?

A
  1. Local infection
  2. Erythema >2 cm
  3. Involving structures deeper than skin/subcutaneous tissues
  4. No systemic inflammatory response signs
106
Q

What classifies as SEVERE DFI?

A
  1. Local infection with signs of SIRS manifested by >2 of the following:
    * Temperatures >38 C or <36 C
    * Heart Rate >90 bpm
    * Respiratory Rate >20 or PaCO2 <32
    * WBC >12,000 or <4,000 or >10% immature bands
107
Q

MILD DFI Treatment

Staph MSSA, Strep, and Staph MRSA

A

PO, 1-2 weeks
1. Dicloxacillin
2. Clindamycin
3. Cephalexin
4. Levofloxacin
5. Augmentin
6. Doxycycline
7. Bactrim

108
Q

MODERATE DFI Treatment

MSSA, Strep, Enterobacteriaceae, Obligate anaerobe, MRSA, pseudomonas

A

PO or IV, 1-3 weeks
1. FQ: levofloxacin/moxifloxacin
2. Cephalosporin: cefoxitin, ceftriaxone, ceftazidime, cefepime
3. Penicllin: unasyn and zosyn
4. Carbapenems
5. Levoflox + Clinda
6. Cipro + Clinda
7. Glycopeptide: vanc or dapto
8. Linezolid
9. Aztreonam
10. Tigecycline

109
Q

SEVERE DFI Treatment

MRSA, enteroacteriaceae, pseudomonas, and obligate anaerobes

A
  1. Vancomycin (dapto or linzeolid) + one of the following:
    * ZOSYN
    * CARBAPENEM
    * Ceftazidime
    * Cefepime
    * Aztreonam
110
Q

Predisposing Factors for Septic Arthritis

A
  1. Age >80 yrs or <2 yrs
  2. DM
  3. Rheumatoid Arhritis
  4. Prosthetic Joint
  5. Recent Joint Surgery
  6. Skin Infection
  7. Social IV drug use/Alcoholism
  8. Previous IA Steroid Injection
111
Q

Septic Arthritis Clinical Presentation

Painful, swollen joint

A
  1. Monoarticular: knee most common
  2. Polyarticular: gonococcal infection –> associated with DERMATITIS, TENOSYNOVITIS, & MIGRATORY POLYARTHRALGIA
112
Q

Septic Arthritis Etiology

A
  1. Gram Pos = staph, strep, and enterococci
  2. Gram Neg = pseudomonas common in IV drug users, other gram neg common in cchildren and elderly
  3. Gonococcal = exposure to STD, more common in women
113
Q

Treatment of Septic Arthritis Gram Pos

Gram stain, culture, WBC, crystals, based on synovial fluid aspirate

A

VANCOMYCIN, DAPTOMYCIN, & LINEZOLID

114
Q

Treatment of Septic Arthritis Gram Neg/Gonococcal

A

CEFTRIAXONE

115
Q

Treatment of Septic Arthritis if gram stain is negative

A

VANCOMYCIN AND CEFTRIAXONE

116
Q

Duration of therapy for Septic Arthritis

A

14-28 days

2-4 weeks

117
Q

Epidemiology of Osteomyelitis

A

Hematogenous: secondary to bacteria- monomicrobial
Contiguous: related to adjacent soft tissue infection- polymicrobial
Direct Inoculation: trauma or surgical procedure- polymicrobial

118
Q

Classification of Osteomyelitis

A
  1. Acute Infection: diagnosed <2 weeks from onset of signs/symptoms
  2. Chronic Infection: onset >2 weeks
119
Q

Etiology of Osteomyelitis

A
  1. STAPH AUREUS
  2. Coagulase Negative Staphylococcus: can cause infection via direct inoculation
120
Q

Treatment of Osteomyelitis

A
  1. If patient is stable, defer antibiotics until cultures are obtained
  2. Duration of Therapy: minimum 4-6 weeks (8 weeks for MRSA) up to 3 months
  3. Vertebral Osteomyelitis should be treated for 6-12 weeks
121
Q

Prosthetic Joint Infections Defintion

A

Patients with persistent wound drainage over joint prosthesis

122
Q

Surgical Strategies for PJI

A
  1. One Stage Exchange: remove infected prosthesis and replace during one surgical procedure, if suscepible to oral antimicrobials
  2. Two Stage Exchange: remove prosthesis, second surgery weeks/months later after antibiotic therapy
123
Q

PJI Staphylococci Treatment

A
  1. Debridement and Retention of Prosthesis
  2. IV antibiotics AND RIFAMPIN followed by:
  3. ORAL antibioitics AND RIFAMPIN for 3 months (hip/elbow/shoulder) or 6 months (knee)
  4. Treatment after resection arthroplasty = 4-6 weeks of IV or highly bioavailable oral therapy
124
Q

MSSA PJI Regimen

A
  1. Nafcillin
  2. Oxacillin
  3. Cefazolin
    May use Ceftriaxone after intiital therapy with primary agents
125
Q

MRSA PJI Regimen

A
  1. Vancomycin
    Alternative: Linzeolid, dapto, tigecycline, telavancin, ceftaroline
126
Q

Streptococci PJI Regimen

A
  1. Ampicillin
  2. Ceftriaxone
    Ceftriaxone may be preferable because of QD admin
127
Q

Enterococcus Faecalis PJI Regimen

A
  1. Ampicillin
    Vanc for penicillin allergic patients
128
Q

Sepsis-3 Definition

A
  1. Life threatening organ dysfunction caused by a dysregulated host response to infection
  2. Acute change in SOFA score >2 points
129
Q

What is Septic Shock?

SEPSIS-3

A

Sepsis + Persistent Hypotension

130
Q

Infections can lead to what causing sepsis?

A
  1. Coagulation
  2. Endothelial Cells
  3. Macrophages – PRO-inflammatory abundance
    = Organ Dysfunction = Loss of Homeostasis
131
Q

Sepsis-2 Defintion

SIRS + Infection = SEPSIS
Severe Sepsis = Sepsis + Organ Dysfunction

A

SIRS:
1. Temp >38/<36
2. HR>90
3. RR>20
4. WBC<12k

132
Q

Distributive Shock

Pathophysiology

A
  1. Lactate and intracellular acidosis = activate adenosine triphosphate-sensitive potassium channels
  2. Potassium efflux and cellular hyperpolarization
  3. Impaired calcium influx through voltage-gated calcium channels
  4. Impaired cellular depolarization and vasoconstriction
133
Q

Distributive Shock

Pathophysiology-Cytokines

A
  1. Proinflammatory cyttokines
  2. Increased expression of inducible nitric oxide synthase (iNOS)
  3. Nitric oxide NO production
  4. Vasodilation through cyclic guanosine monophosphate pathway
134
Q

Signs and Symptoms in Sepsis that Manifest Organ Damage

A
  1. Hyperventilation
  2. Arterial Hypotension
  3. Hyperglycemia or Hypoglycemia
  4. Decrerased Urine Output
135
Q

Sepsis-3 Performance Improvement Check

ONE HOUR BUNDLE

A
  1. Measure initial lactate
  2. Repeat in 2 hrs if initial lactate >2
  3. Obtain cultures prior to admin of antibiotics
  4. Admin broad IV antibiotics within 1 hr
  5. Initial fluid resuscitation of 30 mL/kg crystalloid for hypotension or lactate >4
  6. Vasopressors if MAP <65 or after completeion of fluid resuscitation
136
Q

Resuscitation

FLUIDS

A

30 mL/kg within 3 hours of sepsis recognition

Lactated Ringers or Plasmalyte

137
Q

Antibiotic Timing in Sepsis

A
  1. Antibiotics within 1 hr if possible **cultures first
  2. Broad Spectrum (MRSA and Pseudo)
138
Q

Gram Neg Pathogens in Sepsis

A
  • E. coli
  • Klebsiella
  • Proteus
  • Enterobacter
  • Pseudomonas
139
Q

Gram Pos Pathogens in Sepsis

A
  • S. aureus
  • Coagulase negative staph
  • Enterococcus
  • Strep pneumo
140
Q

When should you consider antifungals in spesis and what is the drug of choice for suspected/confirmed candidemia?

A
  1. Immunocomprised
  2. TPN
  3. Drug = Echinocandins (micafungin)
141
Q

Duration of Therapy of antibiotics in sepsis and pearls of antibiotic considerations?

A
  1. 10-14 days
  2. Possible spesis without shock = admin antimicrobials within 3hrs
  3. High risk for multidrug resistance = 2 antimicrobials with gram neg coverage

AVOID Procalcitonin

142
Q

MAP Formula and Goal

A

[(SBP) + (DBP x 2)]/3
Goal = 65

143
Q

Septic Shock Treatment Evidence

A
  1. Norepinephrine = 1st line
  2. Dopamine = high quality evidence
  3. Vasopressin = moderate quality
  4. Epinephrine = low quality
  5. Angiotensin II = very low quality
144
Q

Norepinephrine

A
  1. First line vasopressor in septic shock
  2. Potent alpha and less beta
  3. Increases MAP and SVR
145
Q

Vasopressin

A
  1. Second Line
  2. Vasoconstriction and Increased BP
  3. Decrease catecholamine NE + Epi requirements
146
Q

Epinephrine

A
  1. Third Line
  2. Non Specific Alpha and Beta Agonist
147
Q

Angiotensin II

A
  1. Increased BP
148
Q

Phenylephrine

A
  1. Selective Alpha-1 Agonist
  2. Salvage therapy
  3. DO NOT use in heart failure
149
Q

Dopamine

A
  1. Increased MAP and cardiac output by increasing HR and contractility
  2. Arrhytmogenic = tachycardia
150
Q

Stress Dose Steroids and Doses

A

Hydrocortisone 50 mg Q6h IV + Fludrocortisone 0.05 mg PO QD
**Start IV corticosteroids when NE or Epi is 0.25 mcg/kg/min at least 4 hours after initiation

151
Q

Endocardium

A

Endothelial membrane lining the chambers of the heart and covering the cusps of the heart valves (innermost layer of the heart wall)

endocarditis = inflammation of the endocardium

152
Q

Infective Endocarditis IE

A

Infection of heart valves by microorganisms
Mitral > Aortic > Tricuspid > Pulmonary

153
Q

Is blood a sterile environment?

154
Q

Bacteremia

A

Presence of bacteria in the bloodstream

155
Q

What are primary (focal) sources of infection into the bloodstream?

A
  1. Urinary tract
  2. respiratory
  3. Skin and soft tissue
  4. Bone and joint
156
Q

Pathogenesis of Infective Endocarditis

A
  1. Bacteremia
  2. Bacteria sticks to the clot via adhesion molecules
  3. Bacteria sticks and begins colonizing – vegetation of fibrin, platelets, and bacteria
  4. Protective layer of fibrin and platelets form over the bacterial colonization preventing host immune response
157
Q

What are the complications associated with Infective Endocarditis?

A
  1. Septic Emboli
  2. Formation of antibody complexes
  3. Vasculitis
  4. Glomerulonephritis = acute renal failure
158
Q

What are the 12 Risk Factors for Infective Endocarditis?

A
  1. PROSETHIC VALVE
  2. PRIOR ENDOCARDITIS INFECTION
  3. HEALTHCARE RELATED EXPOSURE
  4. Men > Women
  5. Age >60
  6. IV Drug Use
  7. Chronic IV Access
  8. Structural Heart Disease
  9. Cardiac Implantable Device
  10. DM
  11. CHF
  12. Poor Dentition
159
Q

Valvular Risk Factors

A

Stenosis: stiff valves = turbulent blood flow = damaged endothelium
Regurgitation: opposite direction blood flow = turbulent blood flow = damaged endothelium

160
Q

Staphylococci seen in Infective Endocarditis when?

A
  1. Skin Flora
  2. Due to healthcare exposure and IV drug use
  3. MOST COMMON cause of PVE within 1st year after valve surgery
  4. HIGHEST risk within 3 months after surgery
  5. MSSA/MRSA most often cause acute aggressive infections
161
Q

Streptococci seen in Infective Endocarditis when?

A
  1. Oral and Gingival Flora
  2. GI Flora
  3. Common in community acquired disease and underlying cardiac abnormalities
  4. COMMON in NATIVE valve endocarditis
162
Q

Enterococci seen in Infective Endocarditis when?

A
  1. GU Flora
  2. MOST COMMON with healthcare associated disease
  3. MUST HAVE DOUBLE THERAPY!!
163
Q

S/S of Infective Endocarditis

A

Symptoms: FEVER, chills, weakness
Signs: NEW OR CHANGING HEART MURMUR, embolic phenomea

164
Q

BIG KEY Endocarditis Signs

A
  1. Janeway Lesions
  2. Osler Nodes
  3. Roth Spots
  4. Splinter Hemorrhage
  5. Petechiae
  6. Clubbing Fingers
165
Q

Diagnosis of Infective Endocarditis

A
  1. Obtain at least 3 sets of blood cultures
  2. Cardiac Imaging (TTE vs TEE)
  3. Modified Duke’s Criteria
166
Q

What are the 2 MAJOR Criteria is Modified Duke’s Criteria?

A
  1. Positive blood culture x2 with typical microorganisms consistent with IE
  2. Evidence of endocardial involvement via echocardiography
167
Q

What are treatment considerations for IE?

A
  1. Prolonged
  2. IV
  3. BACTERICIDAL (beta lactam?)
168
Q

Empiric Therapy Considerations for IE

A
  1. Beta Lactams
  2. Vancomycin or Daptomycin (if allergic to first line)
  3. Gentamicin and Beta Lactam Synergy
169
Q

Gentamicin and Beta Lactase Synergy IE Dosing

A

LOW dose 3 mg/kg
Dosing Weight: IBW or AdjBW if actual greater than 1.25x
Trough <1 mcg/mL

170
Q

S. aureus Native Valve MSSA and MRSA Treatment

A

MSSA= Nafcillin or Oxacillin or Cefazolin
MRSA = Vancomycin or Daptomycin
Duration = 6 weeks

171
Q

S. aureus Prosthetic Valve MSSA Treatment

A
  1. Nafcillin or Oxacillin or Cefazolin
    PLUS
  2. Rifampin + Gentamicin Synergy*
    Duration = >6 weeks
    Duration Synergy* = first 2 weeks only
172
Q

S. aureus Prosthetic Valve MRSA Treatment

A
  1. Vancomycin
    PLUS
  2. Rifampin + Gentamicin Synergy*
    Duration = >6 weeks
    Duration Synergy* = first 2 weeks only
173
Q

Streptococci Highly Susceptible Native Valve MIC <0.12 Treatment

A
  1. Penicillin G
    OR
  2. Ceftriaxone +/- Gentamicin Synergy*
    Duration = 4 weeks
    Duration Synergy* = 2 weeks total for both
174
Q

Streptococci Highly Susceptible Prosthetic Valve MIC <0.12 Treatment

A
  1. Penicillin G
    OR
  2. Ceftriaxone +/- Gentamicin Synergy*
    Duration = 6 weeks
    Duration Synergy* = first 2 weeks only
175
Q

Streptococci Relatively Resistant MIC >0.12 <0.5 Native Valve Treatment

A
  1. Penicillin G
    OR
  2. Ceftriaxone + Gentamicin Synergy*
    Duration = 4 weeks
    Duration Synergy* = first 2 weeks only
176
Q

Streptococci Highly Resistant MIC >0.5 Native Valve Treatment

A
  1. Penicillin G
    OR
  2. Ceftriaxone + Gentamicin Synergy*
    Duration = 6 weeks
    Duration Synergy* = total duration
177
Q

Streptococci Relatively and Highly Resistant Prosthetic Valve Treatment

A
  1. Penicillin G
    OR
  2. Ceftriaxone + Gentamicin Synergy*
    Duration = 6 weeks
    Duration Synergy* = total duration
178
Q

Enterococci Susceptible Native or Prosthetic Valve

A
  1. Ampicillin or Penicillin G + Gentamicin Synergy* = 4-6 weeks, *total duration
  2. Ampicillin + Ceftriaxone = 6 weeks
179
Q

Enterococci PCN Resistant Native or Prosthetic Valve

A
  1. Ampicillin-Sulbactam
    OR
  2. Vancomycin + Gentamicin Synergy
    Duration = >6 weeks
180
Q

Enterococci PCN/VANC/AG Resistant Native or Prosthetic Valve

A

Linezolid or Daptomycin >6 weeks

181
Q

Why do you need double beta lactam therapy for Enterococci infective endocarditis treatment?

A
  1. Loss of penicillin-binding proteins
  2. 2 beta-lactams saturate various PBPs on the cell membrane = allows increased ampicillin activity against enterococci
  3. Lower risk of nephrotoxicity
182
Q

Beta Lactam Drug Monitoring

A
  1. Renal Function
  2. Hypersensitivity Reactions
183
Q

Vancomycin Drug Monitoring

A
  1. AUC vs Trough
  2. Nephrotoxicity
  3. Red Man Syndrome
184
Q

Gentamicin Drug Monitoring

A
  1. Peak and Trough
  2. Nephrotoxicity
  3. Ototoxicity
185
Q

Daptomycin Drug Monitoring

A
  1. CPK
  2. Myalgia/Myopathy
  3. Rhabdomyolysis
186
Q

What HIGH Risk groups need IE Prophylaxis?

A
  1. Prosthetic Cardiac Valve
  2. Prior IE
  3. CHD
  4. Cardiac Transplant with Valvulopathy
187
Q

What procedures need IE Prophylaxis?

A
  1. Dental Procedures
  2. Invasive Procedure of Respiratory Tract
  3. Surgical Procedures involving Infected Skin
188
Q

What are the ORAL Antibiotics for IE Prophylaxis?

A
  1. Amoxicillin
  2. Cephalexin
  3. Azithromycin or Clarithromycin
  4. Doxycycline
189
Q

What are the IM or IV Antibiotics for IE Prophylaxis?

A
  1. Amipicillin
  2. Cefazolin
  3. Ceftriaxone

Infectious Diseases Module (5 decks)

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