Cat bites - epidemiology (how many get infected) - etiology - management

- 80% of cat bites get infected - Pastuerella multocida most common but POLYMICROBIAL - Treat empirically with amoxil-clav

Dog bites - epidemiology (how many get infected) - etiology - management

- 5% of dog bites get infected - Pastuerella canis most common but POLYMICROBIAL - Treat only if severe or immune-compromised host with amoxil-clav

Clenched fist injury - epidemiology (how many get infected) - etiology

- high risk of infection - patients present late - POLYMICROBIAL

Cat scratch disease - epidemiology (who gets it) - etiology - clinical presentation - diagnosis - Treatment

- children and young adults - Bartonella henselae - local LAD +/- cutaneous lesion but can be atypical - serology, blood culture - Azithromycin

SSTIs Flashcards by Bethany Woodrow

Cat bites

epidemiology (how many get infected)
etiology
management

80% of cat bites get infected
Pastuerella multocida most common but POLYMICROBIAL
Treat empirically with amoxil-clav

How well did you know this?

Not at all

Perfectly

Dog bites

epidemiology (how many get infected)
etiology
management

5% of dog bites get infected
Pastuerella canis most common but POLYMICROBIAL
Treat only if severe or immune-compromised host with amoxil-clav

How well did you know this?

Not at all

Perfectly

Human bites

-etiology

POLYMICROBIAL
Viridens strep
Staph epidermidis
Corynebacterium
S. aureus
Bacteroides
Peptostreptococcus

How well did you know this?

Not at all

Perfectly

Clenched fist injury

epidemiology (how many get infected)
etiology

high risk of infection
patients present late
POLYMICROBIAL

How well did you know this?

Not at all

Perfectly

Other animal bites

-general considerations

Tetanus vaccine booster or IgG if never vaccinated

- Rabies vaccine and IgG

How well did you know this?

Not at all

Perfectly

Cat scratch disease

epidemiology (who gets it)
etiology
clinical presentation
diagnosis
Treatment

children and young adults
Bartonella henselae
local LAD +/- cutaneous lesion but can be atypical
serology, blood culture
Azithromycin

How well did you know this?

Not at all

Perfectly

Disseminated gonococcal infection

-2 classic clinical presentations

-Triad of tenosynovitis, polyarthritis, dermatitis
OR
-purulent arthritis

How well did you know this?

Not at all

Perfectly

Infectious lymphadenopathy

-etiology

Viral: HIV, CMV, EBV
Bacterial: GAS, S. aureus, Bartonella henselae and many others
Mycobacteria: TB and atypical
Parasite: toxoplasma, histoplasma
Fungal: Sporotrichosis

How well did you know this?

Not at all

Perfectly

Septic arthritis

-etiology

disseminated gonoccocal infection
staph aureus
strep
G(-)
TB
Fungal

How well did you know this?

Not at all

Perfectly

Septic arthritis

-risk factors

Age > 80
diabetes
pre-existing joint disease
recent surgery/injection
prosthetic joint
IVDU

How well did you know this?

Not at all

Perfectly

Septic arthritis

-clinical presentation

Triad: fever, pain (cannot bear weight), decreased range of motion

How well did you know this?

Not at all

Perfectly

Septic arthritis

-diagnosis

aspirate synovial fluid and Gram stain and C&S
blood cultures
Xray to rule out osteomyelitis

How well did you know this?

Not at all

Perfectly

Septic arthritis

-management

antibiotics based on C&S

- aspire fluid/ surgical drainage

How well did you know this?

Not at all

Perfectly

Septic arthritis

-how does the infective agent get there

hematogenous> trauma >post-surgery > from osteomyelitis

How well did you know this?

Not at all

Perfectly

Disseminated gonococcal infection

-diagnosis

cervical/urethral swab usually +

- blood, skin, synovial culture can be -

How well did you know this?

Not at all

Perfectly

Disseminated gonococcal infection

-management

Cefotaxime+ Doxyxline
aspirate fluid
treat partners

How well did you know this?

Not at all

Perfectly

Ludwig’s angina

-definition

-cellulitis of bilateral sublingual/submandibular spaces

Ludwig’s angina

-risk factors

recent dental work
tooth pain
immune compromise
tongue piercing
mandibular fracture

almost always the result of an oral infection

Ludwig’s angina

-etiology in immunecompetent and immunocompromised

POLYMICROBIAL

Immunecompetent: strep, G+ anaerobes, bacteroides

Immunocompromised: pseudomonas, clostridium, candida

Ludwig’s angina

-management

monitor airway (1/3 require intubation)

- Antibiotics IV (e.g penicillin+clindamycin+metronidazole)

Non-bullous impetigo

-clinical presentation

bilateral skin lesions that are painless and pruritic

- bumps–>blisters–>golden crust

Non-bullous impetigo

-etiology

-Staph aureus, often preceded by URTI

Non-bullous impetigo

-epidemiology (who gets it)

-school-aged children

Non-bullous impetigo

-treatment

Topical antibiotic (Mupirocin)

Bullous impetigo - epidemiology (who gets it) - etiology

- Neonates>> children> adults | - Toxin producing S. aureus

Bullous impetigo | -diagnosis in neonate

-blood cultures and septic evaluation

Bullous impetigo | -management (treatment and complications)

- cloxacillin or vancomycin (if MRSA) Complications: dehydration +/- sepsis

Diabetic foot infection | -2 factors that contribute to diabetic foot infection

1) peripheral neuropathy | 2) decreased blood flow (macro and microvascular)--> decreased immune system

Diabetic foot infection | - patient assessment

1) The whole patient: systemic illiness? social support? comorbidities? 2) The affected limb: problems that will impair healing (e.g. charcot joint, vascular disease)? 3) The infection: is it there? how severe?

Diabetic foot infection | -how to quantify peripheral vascular disease

- use (ankle/brachial) blood pressure

Diabetic foot infection | -risk factors

- previous amputation - wound extending to the bone - peripheral vascular disease Are the top three.

Diabetic foot infection | -how to determine presence and severity of infection

- Presence: inflammation +/- purulent discharge | - Severity: IDSA criteria (grade 1-4)

Diabetic foot infection | -management

1) imaging if required 2) wound culture if pt has recently received ab 3) Ab for infected wounds: usually can just cover staph and strep (e.g. cloxacillin). This changes if risk of MRSA, or pt has received ab recently or pseudomonas risk factors 4) good wound care: cleaning, elevation

Cellulitis - how it happens - etiology

- break in skin allows normal flora to invade dermis and subcutaneous tissue - almost always staph and strep

Cellulitis | -clinical presentation

Localized: erythema, LAD, lymphangitis Systemic: bullae, sever swelling, hemorrhage, systemic symptoms

Cellulitis | -management

- empiric Ab based on presentation - elevate - analgesic - draw a line around cellulitis

Erisypelas - what is it? - what causes it?

- Infection limited to upper dermis and superficial lymphatics (cellulitis is deeper) - almost always B-hemolytic strep

Erisypelas - clinical presentation - management

Clinical presentation: well-demarcated, raised erythema, rapid onset, fever Management: Penicillin V or Amoxil

Necrotizing fasciitis - what is it? - what types? - etiology of each type - which type is more common?

- Deep infection of subcutaneous tissue, sever destruction of fat and fascia - Type 1: immunocompromised/post-operative (Polymicrobial) - Type 2: healthy individuals (GAS) **Type 1 is far more common**

Necrotizing fasciitis | -clinical presentation

- bullae - disproportionate pain - swelling - erythema - systemic signs (fever, tachycardia, hypotension) - rapidly progressing

Necrotizing fasciitis | -management

- IMMEDIATE surgical consult - Cultures of deep tissue (surgical) and blood - IMMEDIATE antibiotics: piperacillin-tazo +metronidazole or clindamycin+ carbapenem+cefepime (cover everything)

Osteomyelitis - what is it? - possible etiology - management (in Vancouver)

Definition: infection of the bone or bone marrow Etiology: extrapulmonary TB, staph aureus Management: - Imaging - Blood cultures - Surgical debridement and bone cultures - Ab based on bone culture - Check for endocarditis