Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Infectious Diarrhea Types

A
  1. Enterotoxigenic Diarrhea
  2. Invasive Diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Goal of Therapy for Infectious Diarrhea

A
  1. Prevent Dehydration
  2. All patients should receive supportive care via fluid and electrolyte replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment for Mild-to-Moderate Self Limiting Watery Diarrhea

A
  1. Oral Replacement Therapy
  2. Easily Digestible Foods
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Treatment for Severe-Watery or Dysentric Diarrhea

A
  1. IV Rehydration Therapy
  2. Antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Antimotility Agents

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

AVOID in toxin-mediated dysenteric diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Adjunctive Agents to consider in Infectious Diarrhea Treatment

A
  1. Antimotility
  2. Probiotics
  3. Zinc: supplement with signs of malnutrition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Enterotoxigenic Diarrhea Causative Organisms

A
  1. E.Coli
  2. Cholera
  3. Viruses
  4. ETEC is most common form of E.Coli diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

C. diff Clinical Presentation

A
  1. Colitis
  2. Pseudomembranous Colitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Colitis

A
  1. Watery Diarrhea
  2. Malaise, abdominal pain, nausea
  3. Low-grade fever, leukocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pseudomembranous Colitis

A
  1. Severe abdmonial pain
  2. Perfuse diarrhea, high fever
  3. Marked Leukocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

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

A

Vancomycin TAPERED and PULSED regimen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Bezlotoxumab/Zinplava

Adjunct Therapy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Normal Flora of the Stomach

A
  1. Streptococcus
  2. Lactobacillus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Normal Flora of the Colon

A
  1. Bacteroides
  2. Peptostreptococci
  3. Clostridium
  4. E.Coli
  5. Klebsiella
  6. Enterobacter
  7. Enterococci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Peritonitis

IAI

A
  1. Inflammation of the peritoneal lining
  2. Primary –> not tested
  3. Secondary
  4. Tertiary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Tertiary Peritonitis

A
  1. Persistence or recurrence of peritoneal infection
  2. Occurs >48 hrs after adequate management of primary or secondary peritonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

IAI Coordination of 3 MAJOR Modalities

A
  1. Hemodynamic and Organ Support
  2. Source Control
  3. Administratoin of appropriate antimicrobial therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Hemodynamic/Organ Support IAI

A
  1. Patients often require large volume IV fluids
  2. Maintenance of nutrition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Secondary/Tertiary Peritonitis Source Control

Managed Surgically

A

Patching perforated ulcers or removal of damaged/necrotic bowel segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Intra-Abdominal Abscess Souce Control

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

ANAEROBIC COVERAGE

A

Gram Pos = Clindamycin
Gram Neg = Metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Hospital Associated IAI (HA-IAI)

A

Higher Risk of Resistant or Opportunitisc Organism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

HA-IAI Treatment

A
  1. Use non FQ-containing regimen as in high severity CA-IAI
  2. BL-Allergy = Aztreonam + Metronidazole + Vancomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

HA-IAI Enterococcus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

HA-IAI S. aureus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

HA-IAI Candida

A

Sensitive: Fluconazole
Resistant/Severe: Echinocandin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Pathophysiology of SSTIs

A

Organisms Invade Skin
Damage Occurs to Surrounding Tissues
Inflammatory Response Ensues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Primary SSTIs

A

Invasion of Healthy Skin

Usually due to single pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Secondary SSTIs

A

Occurs in areas of previously damaged skin

Frequently polymicrobial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is complicated SSTIs?

A

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

DM OR HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Purulent vs Nonpurulent SSTI

A
  1. Purulent: Staphylococcus – MSSA or MRSA
  2. Non-Purulent: Streptococci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Purulent SSTIs Furuncles and Carbuncles

Furuncle: boil
Carbuncle: coalescence of multiple furuncles

A

Infections of the hair follicle (deeper than folliculitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Purulent SSTIs Cutaneous Abscesses

A

Collection of pus within dermis and deeper skin tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

YES

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions