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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
Pseudomembranous Colitis
1. Severe abdmonial pain 2. Perfuse diarrhea, high fever 3. Marked Leukocytosis
26
Diagnosis of C. diff
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
27
C. diff Treatment Non-Severe | WBC <15,000 SCr <1.5
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
28
C. diff Treatment Severe | WBC >15,000 SCr >1.5
Preferred: Fidaxomicin 200 mg PO BID x 10 days Alternative: Vancomycin 125 mg PO QID x 10 days
29
C. diff Treatment Fulminant | Hypotension or Shock Toxic Megacolon or Ileus
Vancomycin 500 mg QID by mouth of NG tube + Metronidazole 500 mg IV Q8H **If complete ileus, consider adding concomitant rectal instillation of vancomycin
30
Treatment of CDI First Recurrence
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
31
Treatment of CDI Second Recurrence
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
32
If Fidaxomicin is not an option for recurrent CDI what can be a potential alternative?
Vancomycin TAPERED and PULSED regimen
33
Bezlotoxumab/Zinplava | Adjunct Therapy
Higher risk of HF exacerbation, infection, respiratory failure compared to placebo **Concerns in patients with heart failure
34
Intra-Abdominal Infection IAI is what?
1. Involves the peritoneal cavity or retroperitoneal space 2. Localized or Diffuse 3. May involve visceral organs: liver, spleen, pancreas, female pelvic organs
35
Normal Flora of the Stomach
1. Streptococcus 2. Lactobacillus
36
Normal Flora of the Colon
1. Bacteroides 2. Peptostreptococci 3. Clostridium 4. E.Coli 5. Klebsiella 6. Enterobacter 7. Enterococci
37
Normal Flora of Small Intestine
1. E. Coli 2. Klebsiella 3. Enterobacter 4. Bacteroides 5. Fragilis 6. Clostridium 7. Peptostreptococci 8. Enterococci
38
Risk Factors of IAI
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
39
Classifications of IAIs
1. Uncomplicated: Localized * Confined to visceral structures 2. Complicated: Spreads * Anatomincal disruption * Extends beyond single organ * Leads to peritonitis and/or abscess
40
Peritonitis | IAI
1. Inflammation of the peritoneal lining 2. Primary --> not tested 3. Secondary 4. Tertiary
41
Secondary Peritonitis | Gram - and Polymicrobial
1. Aerobes: E. coli and Klebsiella 2. Anaerobes: Clostridium and Bacteroides 3. Common Causes: * Appendicitis * Blunt or Penetrating Trauma
42
Tertiary Peritonitis
1. Persistence or recurrence of peritoneal infection 2. Occurs >48 hrs after adequate management of primary or secondary peritonitis
43
Abscess | IAI
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
44
Diagnosis of IAI
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)
45
Treatment Goals of IAI
1. Correction of intra-abdominal disease process 2. Acheive resolution of infection without major organ injury or adverse drug effects
46
IAI Coordination of 3 MAJOR Modalities
1. Hemodynamic and Organ Support 2. Source Control 3. Administratoin of appropriate antimicrobial therapy
47
Hemodynamic/Organ Support IAI
1. Patients often require large volume IV fluids 2. Maintenance of nutrition
48
Secondary/Tertiary Peritonitis Source Control | Managed Surgically
Patching perforated ulcers or removal of damaged/necrotic bowel segment
49
Intra-Abdominal Abscess Souce Control
DRAINAGE is CRITICAL to management Without adequate drainage, antimicrobical therapy and fluid resuscitation likely to fail
50
Community Acquired IAI (CA-IAI) | Classified as Mild-Moderate of High
Risk Factors: sepsis, surgical intervention, advanced age, low albumin level, healthcare exposure
51
CA-IAI Mild-Moderate Treatment | Antimicrobials w/Narrow Spectrum
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
52
ANAEROBIC COVERAGE
Gram Pos = Clindamycin Gram Neg = Metronidazole
53
CA-IAI High Treatment | Antimicrobials w/Broad Spectrum - concerned with Pseudomonas
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
54
Hospital Associated IAI (HA-IAI)
Higher Risk of Resistant or Opportunitisc Organism
55
HA-IAI Treatment
1. Use non FQ-containing regimen as in high severity CA-IAI 2. BL-Allergy = Aztreonam + Metronidazole + Vancomycin
56
HA-IAI Enterococcus
Sensitive: Ampicillin +/- Sulbactam, Zosyn, and Imipenem Resistant: Vancomycin, Linezolid, and Dapto
57
HA-IAI S. aureus
MSSA: Nafcillin, Oxacillin, and Cefazolin MRSA: Vancomycin and Daptomycin
58
HA-IAI Candida
Sensitive: Fluconazole Resistant/Severe: Echinocandin
59
Empiric Agents to AVOID in IAI
1. Augmentin and Unasyn due to E. coli resistance 2. FQs 3. Cefotetan and Clindamycin due to B. fragilis resistance
60
What is the Duration of Therapy for IAI
FOUR DAYS for most infectious with adequate source control -Longer 5-7 days fo severe/recurrent infections
61
Skin and Skin Structure Infectious SSTIs Acute Bacterial Skin and Skin Structure Infections ABSSSIs
1. Epidermis: thin layer, superficial 2. Dermis: sebaceous glands 3. Subcutaneous: fatty/muscle tissue
62
SSTIs Risk Factors
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
63
Pathophysiology of SSTIs
Organisms Invade Skin Damage Occurs to Surrounding Tissues Inflammatory Response Ensues
64
Bacterial Etiology of SSTIs
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
65
Risk Factors for HA-MRSA SSTIs
1. Recent exposure to antibiotis 2. Health system exposure | Acquire genetic material to build resistance similar to MLS resistance ## Footnote Sustain susceptibility to clindamycin
66
Risk Factors for CA-MRSA SSTIs
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 ## Footnote Susceptible to: Bactrim/Clinda/and Tetracyclines
67
Primary SSTIs
Invasion of Healthy Skin | Usually due to single pathogen
68
Secondary SSTIs
Occurs in areas of previously damaged skin | Frequently polymicrobial
69
What is complicated SSTIs?
Involving deeps skin structures requiring significant surgical intervention, occuring in immunocompromised patients | DM OR HIV
70
Purulent vs Nonpurulent SSTI
1. Purulent: Staphylococcus -- MSSA or MRSA 2. Non-Purulent: Streptococci
71
Purulent SSTI Folliculitis | Inflammation of the hair follicle
* Papules that evolve into Pustules * Appear within 48 hrs * Found: butt, hips, areas in contact with bathing suits
72
Purulent SSTIs Furuncles and Carbuncles | Furuncle: boil Carbuncle: coalescence of multiple furuncles
Infections of the hair follicle (deeper than folliculitis)
73
Purulent SSTIs Cutaneous Abscesses
Collection of pus within dermis and deeper skin tissues
74
Purulent SSTI MILD Treatment
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
75
Purulent SSTI MODERATE Treatment | Systemic Signs of Infection
1. I&D with empiric oral antibiotics directed CA-MRSA * DOXYCYCLINE OR BACTRIM 2. If MSSA is isolated * Cephalexin * Dicloxacillin | Warm moist compresses
76
Purulent SSTI SEVERE Treatment | Failed I&D+oral antibiotics or systemic sign of infection/immunocomprise
1. I&D and IV antibiotics directed against MRSA * VANCOMYCIN 2. If MSSA is isolated * Cefazolin, Oxacillin, and Nafcillin | Warm moist compresses
77
Daptomycin | Secondary MRSA Bacteremia
BACTERICIDAL Dapto >7 mg/kg/day is associated with lower mortality
78
Linezolid | Secondary MRSA Bacteremia
BACTERIOSTATIC Use PO for de-escalation after daptomycin
79
Non-Purulent SSTIs Organisms
1. Group A Streptococci S. Pyogenes especially ERYSIPELAS 2. S. Aureus more common with cellulitis than erysipelas
80
What are the Risk Factors specific to MRSA Non-Purulent SSTI?
1. Penetrating Trauma 2. Injection Drug Use 3. Nasal Colonization w/MRSA 4. Evidence of another MRSA infection 5. Systemic inflammatory response syndrome
81
Non-Purulent SSTI Erysipelas | Common in areas of pre-existing lymphatic obstruct/edema
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
Non-Purulent SSTIs Cellulitis
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
Non-Purulent SSTI MILD Treatment | outpatient
1. Oral antibiotics targeting streptococci * PENICLIIN VK 2. immbolinzation and elevation of the affected extremity
84
Non-Purulent SSTI MODERATE Treatment | Hospitalization
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
Non-Purulent SSTI SEVERE Treatment | Failed, immunocomprise, deep infection, or systemic
1. Polymicrobial 2. Rule out Necrotizing 3. Surgical Debridement and IV Antibiotics * VANCOMYCIN + ZOSYN 4. Immobilization and Elevation of the extremity
86
Duration of Therapy for Non-Purulent SSTIs
1. Outpatient: 5 days (may extend if slow to respond to therapy) 2. Inpatient: 7-10 days
87
What are the New Agents for SSTIs | All lack place in therapy
1. Tedizolid 2. Telavancin 3. Dalbanacin/Oritavancin 4. Delafloxacin 5. Omadacycline
88
Management for Recurrent Purulent SSTIs
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
Necrotizing Infections | 30-70% mortality rate ## Footnote Caused by S.pyogenes fleshing eating bacteria
1. Tracking along the superficial fascia 2. Severe pain 3. Skin crepitus 4. Necrosis
90
Necrotizing Fasciitis Treatment
1. Immediate surgical debridement 2. Repeat surgical debridement 3. Antibiotic therapy active aganist anaerobes MRSA and anaerobes
91
How long do you continue Necrotizing Fasciitis Treatment?
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
What is Fournier Gangrene?
Necrotizing Dasciits of the scotum, penis, or vulva
93
Impetigo Characteristics
1. Usually ocurs in children 2. Highly communicable
94
Impetigo Causative Organisms
1. S. Aureus 2. Beta-Hemolutic Streptococci
95
Impetigo Treatment | TOPICAL
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
Organisms in Human/Animal Bites
Mouth Flora = anerobes Victim Skin = staph and strep Purulent Wound = polymicrobial, aerobe, anaerobe Non-Purulent Wound = staph and strep
97
Pasteurella spp
ANIMAL bites
98
Eikenella Corrodens
HUMAN bites
99
Oral drugs for Bite Wounds
Augmentin 5-10 days
100
IV drugs for Bite Wounds
Unasyn 7-14 days | Serious injuries, clenched fist, failed outpatient
101
Tetanus Considerations
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
Diabetic Foot Infection Etiology
Mild Infections: monomicrobial Severe Infections: polymicrobial MRSA/MSSA/Strep/Gram Neg Bacilli/Anaerobes
103
Definition of Diabetic Foot Infection
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
What classifies as MILD DFI?
1. Local infection involving only skin/subcutaneous tissue 2. Erythema <2cm 3. Exclude other caues of inflammatory skin response
105
What classifis as MODERATE DFI?
1. Local infection 2. Erythema >2 cm 3. Involving structures deeper than skin/subcutaneous tissues 4. No systemic inflammatory response signs
106
What classifies as SEVERE DFI?
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
MILD DFI Treatment | Staph MSSA, Strep, and Staph MRSA
PO, 1-2 weeks 1. Dicloxacillin 2. Clindamycin 3. Cephalexin 4. Levofloxacin 5. Augmentin 6. Doxycycline 7. Bactrim
108
MODERATE DFI Treatment | MSSA, Strep, Enterobacteriaceae, Obligate anaerobe, MRSA, pseudomonas
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
SEVERE DFI Treatment | MRSA, enteroacteriaceae, pseudomonas, and obligate anaerobes
1. Vancomycin (dapto or linzeolid) + one of the following: * ZOSYN * CARBAPENEM * Ceftazidime * Cefepime * Aztreonam
110
Predisposing Factors for Septic Arthritis
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
Septic Arthritis Clinical Presentation | Painful, swollen joint
1. Monoarticular: knee most common 2. Polyarticular: gonococcal infection --> associated with DERMATITIS, TENOSYNOVITIS, & MIGRATORY POLYARTHRALGIA
112
Septic Arthritis Etiology
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
Treatment of Septic Arthritis Gram Pos | Gram stain, culture, WBC, crystals, based on synovial fluid aspirate
VANCOMYCIN, DAPTOMYCIN, & LINEZOLID
114
Treatment of Septic Arthritis Gram Neg/Gonococcal
CEFTRIAXONE
115
Treatment of Septic Arthritis if gram stain is negative
VANCOMYCIN AND CEFTRIAXONE
116
Duration of therapy for Septic Arthritis
14-28 days | 2-4 weeks
117
Epidemiology of Osteomyelitis
Hematogenous: secondary to bacteria- monomicrobial Contiguous: related to adjacent soft tissue infection- polymicrobial Direct Inoculation: trauma or surgical procedure- polymicrobial
118
Classification of Osteomyelitis
1. Acute Infection: diagnosed <2 weeks from onset of signs/symptoms 2. Chronic Infection: onset >2 weeks
119
Etiology of Osteomyelitis
1. STAPH AUREUS 2. Coagulase Negative Staphylococcus: can cause infection via direct inoculation
120
Treatment of Osteomyelitis
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
Prosthetic Joint Infections Defintion
Patients with persistent wound drainage over joint prosthesis
122
Surgical Strategies for PJI
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
PJI Staphylococci Treatment
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
MSSA PJI Regimen
1. Nafcillin 2. Oxacillin 3. Cefazolin May use Ceftriaxone after intiital therapy with primary agents
125
MRSA PJI Regimen
1. Vancomycin Alternative: Linzeolid, dapto, tigecycline, telavancin, ceftaroline
126
Streptococci PJI Regimen
1. Ampicillin 2. Ceftriaxone Ceftriaxone may be preferable because of QD admin
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Enterococcus Faecalis PJI Regimen
1. Ampicillin Vanc for penicillin allergic patients
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Sepsis-3 Definition
1. Life threatening organ dysfunction caused by a dysregulated host response to infection 2. Acute change in SOFA score >2 points
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What is Septic Shock? | SEPSIS-3
Sepsis + Persistent Hypotension
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Infections can lead to what causing sepsis?
1. Coagulation 2. Endothelial Cells 3. Macrophages -- PRO-inflammatory abundance = Organ Dysfunction = Loss of Homeostasis
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Sepsis-2 Defintion | SIRS + Infection = SEPSIS Severe Sepsis = Sepsis + Organ Dysfunction
SIRS: 1. Temp >38/<36 2. HR>90 3. RR>20 4. WBC<12k
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Distributive Shock | Pathophysiology
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
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Distributive Shock | Pathophysiology-Cytokines
1. Proinflammatory cyttokines 2. Increased expression of inducible nitric oxide synthase (iNOS) 3. Nitric oxide NO production 4. Vasodilation through cyclic guanosine monophosphate pathway
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Signs and Symptoms in Sepsis that Manifest Organ Damage
1. Hyperventilation 2. Arterial Hypotension 3. Hyperglycemia or Hypoglycemia 4. Decrerased Urine Output
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Sepsis-3 Performance Improvement Check | ONE HOUR BUNDLE
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
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Resuscitation | FLUIDS
30 mL/kg within 3 hours of sepsis recognition | Lactated Ringers or Plasmalyte
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Antibiotic Timing in Sepsis
1. Antibiotics within 1 hr if possible **cultures first 2. Broad Spectrum (MRSA and Pseudo)
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Gram Neg Pathogens in Sepsis
* E. coli * Klebsiella * Proteus * Enterobacter * Pseudomonas
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Gram Pos Pathogens in Sepsis
* S. aureus * Coagulase negative staph * Enterococcus * Strep pneumo
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When should you consider antifungals in spesis and what is the drug of choice for suspected/confirmed candidemia?
1. Immunocomprised 2. TPN 3. Drug = Echinocandins (micafungin)
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Duration of Therapy of antibiotics in sepsis and pearls of antibiotic considerations?
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
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MAP Formula and Goal
[(SBP) + (DBP x 2)]/3 Goal = 65
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Septic Shock Treatment Evidence
1. Norepinephrine = 1st line 2. Dopamine = high quality evidence 3. Vasopressin = moderate quality 4. Epinephrine = low quality 5. Angiotensin II = very low quality
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Norepinephrine
1. First line vasopressor in septic shock 2. Potent alpha and less beta 3. Increases MAP and SVR
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Vasopressin
1. Second Line 2. Vasoconstriction and Increased BP 3. Decrease catecholamine NE + Epi requirements
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Epinephrine
1. Third Line 2. Non Specific Alpha and Beta Agonist
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Angiotensin II
1. Increased BP
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Phenylephrine
1. Selective Alpha-1 Agonist 2. Salvage therapy 3. DO NOT use in heart failure
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Dopamine
1. Increased MAP and cardiac output by increasing HR and contractility 2. Arrhytmogenic = tachycardia
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Stress Dose Steroids and Doses
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
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Endocardium
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
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Infective Endocarditis IE
Infection of heart valves by microorganisms Mitral > Aortic > Tricuspid > Pulmonary
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Is blood a sterile environment?
YES
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Bacteremia
Presence of bacteria in the bloodstream
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What are primary (focal) sources of infection into the bloodstream?
1. Urinary tract 2. respiratory 3. Skin and soft tissue 4. Bone and joint
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Pathogenesis of Infective Endocarditis
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
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What are the complications associated with Infective Endocarditis?
1. Septic Emboli 2. Formation of antibody complexes 3. Vasculitis 4. Glomerulonephritis = acute renal failure
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What are the 12 Risk Factors for Infective Endocarditis?
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
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Valvular Risk Factors
Stenosis: stiff valves = turbulent blood flow = damaged endothelium Regurgitation: opposite direction blood flow = turbulent blood flow = damaged endothelium
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Staphylococci seen in Infective Endocarditis when?
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
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Streptococci seen in Infective Endocarditis when?
1. Oral and Gingival Flora 2. GI Flora 3. Common in community acquired disease and underlying cardiac abnormalities 4. COMMON in NATIVE valve endocarditis
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Enterococci seen in Infective Endocarditis when?
1. GU Flora 2. MOST COMMON with healthcare associated disease 3. MUST HAVE DOUBLE THERAPY!!
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S/S of Infective Endocarditis
Symptoms: FEVER, chills, weakness Signs: NEW OR CHANGING HEART MURMUR, embolic phenomea
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BIG KEY Endocarditis Signs
1. Janeway Lesions 2. Osler Nodes 3. Roth Spots 4. Splinter Hemorrhage 5. Petechiae 6. Clubbing Fingers
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Diagnosis of Infective Endocarditis
1. Obtain at least 3 sets of blood cultures 2. Cardiac Imaging (TTE vs TEE) 3. Modified Duke's Criteria
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What are the 2 MAJOR Criteria is Modified Duke's Criteria?
1. Positive blood culture x2 with typical microorganisms consistent with IE 2. Evidence of endocardial involvement via echocardiography
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What are treatment considerations for IE?
1. Prolonged 2. IV 3. BACTERICIDAL (beta lactam?)
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Empiric Therapy Considerations for IE
1. Beta Lactams 2. Vancomycin or Daptomycin (if allergic to first line) 3. Gentamicin and Beta Lactam Synergy
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Gentamicin and Beta Lactase Synergy IE Dosing
LOW dose 3 mg/kg Dosing Weight: IBW or AdjBW if actual greater than 1.25x Trough <1 mcg/mL
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S. aureus Native Valve MSSA and MRSA Treatment
MSSA= Nafcillin or Oxacillin or Cefazolin MRSA = Vancomycin or Daptomycin Duration = 6 weeks
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S. aureus Prosthetic Valve MSSA Treatment
1. Nafcillin or Oxacillin or Cefazolin PLUS 2. Rifampin + Gentamicin Synergy* Duration = >6 weeks Duration Synergy* = first 2 weeks only
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S. aureus Prosthetic Valve MRSA Treatment
1. Vancomycin PLUS 2. Rifampin + Gentamicin Synergy* Duration = >6 weeks Duration Synergy* = first 2 weeks only
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Streptococci Highly Susceptible Native Valve MIC <0.12 Treatment
1. Penicillin G OR 2. Ceftriaxone +/- Gentamicin Synergy* Duration = 4 weeks Duration Synergy* = 2 weeks total for both
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Streptococci Highly Susceptible Prosthetic Valve MIC <0.12 Treatment
1. Penicillin G OR 2. Ceftriaxone +/- Gentamicin Synergy* Duration = 6 weeks Duration Synergy* = first 2 weeks only
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Streptococci Relatively Resistant MIC >0.12 <0.5 Native Valve Treatment
1. Penicillin G OR 2. Ceftriaxone + Gentamicin Synergy* Duration = 4 weeks Duration Synergy* = first 2 weeks only
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Streptococci Highly Resistant MIC >0.5 Native Valve Treatment
1. Penicillin G OR 2. Ceftriaxone + Gentamicin Synergy* Duration = 6 weeks Duration Synergy* = total duration
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Streptococci Relatively and Highly Resistant Prosthetic Valve Treatment
1. Penicillin G OR 2. Ceftriaxone + Gentamicin Synergy* Duration = 6 weeks Duration Synergy* = total duration
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Enterococci Susceptible Native or Prosthetic Valve
1. Ampicillin or Penicillin G + Gentamicin Synergy* = 4-6 weeks, *total duration 2. Ampicillin + Ceftriaxone = 6 weeks
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Enterococci PCN Resistant Native or Prosthetic Valve
1. Ampicillin-Sulbactam OR 2. Vancomycin + Gentamicin Synergy Duration = >6 weeks
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Enterococci PCN/VANC/AG Resistant Native or Prosthetic Valve
Linezolid or Daptomycin >6 weeks
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Why do you need double beta lactam therapy for Enterococci infective endocarditis treatment?
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
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Beta Lactam Drug Monitoring
1. Renal Function 2. Hypersensitivity Reactions
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Vancomycin Drug Monitoring
1. AUC vs Trough 2. Nephrotoxicity 3. Red Man Syndrome
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Gentamicin Drug Monitoring
1. Peak and Trough 2. Nephrotoxicity 3. Ototoxicity
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Daptomycin Drug Monitoring
1. CPK 2. Myalgia/Myopathy 3. Rhabdomyolysis
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What HIGH Risk groups need IE Prophylaxis?
1. Prosthetic Cardiac Valve 2. Prior IE 3. CHD 4. Cardiac Transplant with Valvulopathy
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What procedures need IE Prophylaxis?
1. Dental Procedures 2. Invasive Procedure of Respiratory Tract 3. Surgical Procedures involving Infected Skin
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What are the ORAL Antibiotics for IE Prophylaxis?
1. Amoxicillin 2. Cephalexin 3. Azithromycin or Clarithromycin 4. Doxycycline
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What are the IM or IV Antibiotics for IE Prophylaxis?
1. Amipicillin 2. Cefazolin 3. Ceftriaxone

Infectious Diseases Module (5 decks)

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