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295 Cards in this Set
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Introduction to SSTI
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Commonly encountered infections in community and hospital settings.
Over the last decade, there has been a 71% increase in hospitalization rates for SSTI. Exact incidence unknown, but majority are believed to be mild, therefore are treated outpatient. Community pharmacists often frontline in helping to prevent, or spotting an existing infection Group A Strep infections causing necrotizing fasciitis are on the rise. Community-acquired MRSA also increasing. Patterns of resistance among geographical areas must be taken into account when treating patients empirically. Complications of skin infections include abscesses and osteomyelitis |
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Integumentary System
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The Skin is the largest organ in the body
Accessory structures including hair, nails, glands, and nerve receptors are in the dermis Functions as major defense mechanism against infections: Covers internal structures to protect from external environment Reduced pH (4-6.5) Sebaceous secretions hydrolyzed to free fatty acids Epithelial shedding Sensory receptors (pressure, pain, temperature monitoring) Bacterial skin/soft tissue infections may be: Primary or secondary in nature; Complicated or uncomplicated. |
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edidermis
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Avascular proliferative layer, constantly regenerating protein and lipid
About as thick as a sheet of paper |
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dermis
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Contains blood vessels, nerve receptors, lymphatics, and fibroblasts
The eccrine sweat glands, sebaceous glands, and hair follicles originate here |
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suncutaneous tissue
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An effective cushion and energy storage reserve of variable thickness
cellullitis and necortizing occur at this level |
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Uncomplicated (Primary)
SSTI |
Superficial:
Impetigo Deeper: Erysipelas Cellulitis Hair follicle associated: Folliculitis Furunculosis Abscess: Carbuncle Other cutaneous abscesses |
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Complicated (Secondary)
SSTI |
Acute wound infections (cellulitis):
Traumatic Bite-related Post-operative Necrotizing fasciitis Chronic wound infections: Diabetic foot infections Venous stasis ulcers Decubitus ulcers Perianal cellulitis ± abscess (difficult to treat because of fecal contamination) Periorbital (secondary to eye infection such as conjunctuvitsis, if left untreated can lead to blindness) |
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Normal Flora of the Skin
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Resident nonpathogenic flora reside on the skin
Predominant inhabitants of most of the body’s skin include Staphylococcus epidermidis and propionobacterium (including P. acnes). S. Aureus, corynebacterium (diphtheroids), and some gram negative organisms in moist environments of the body. Nares typically colonized by S. Aureus. Nares can be colonized with CA-MRSA. If the skin looses its integrity, this is an opportunity for flora to become pathogenic. more gram negative in moister areas |
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Self Care of Minor Wounds
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Wound healing starts immediately after injury and consists of three phases:
Inflammatory Proliferative Maturation Wound healing is impaired if locally infected A primary goal of wound treatment is to protect the wound from infection |
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cleansing of minor wounds
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Cleanse
Saline or bottled water irrigation to remove debris should always be step in preventing an infection. |
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Apply Antiseptic (+/-) to minor wounds
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May consider for reduction of microbial activity around the area of the wound to reduce infection risk.
Only apply to intact skin (or will cause tissue damage) |
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Wound dressings to minor wounds
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protect the injured skin from further insult and bacterial contamination.
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ointments and minor wounds
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(vaseline) can be applied under dressing of minor wounds to maintain moisture and reduce scarring. (Except for puncture wounds.)
apply after inflammatroy phase to prevent eschar formation and ultimately scarring |
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Self Care of Minor Wounds
topical AB |
Topical Antibiotics:
Minor cuts, scrapes, and burns do not usually require antibiotics. Wounds that are a little deeper, bigger or the patient is unable to get entirely clean may benefit. OTC Products: Bacitracin: Inhibits bacterial cell wall synthesis in some gram positives Polymyxin B: Affects bacterial cell membrane function in gram-negatives Neomycin: Aminoglycoside; active against gram negatives Triple ABX therapy no better than double in studies Hypersensitivity to neomycin is high (up to 11% in adults)1 dont need as much gram - coverage as the triple AB provides |
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OTC Topical Antibiotics for Minor Wounds
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Routine use of topical antibiotics should not be encouraged, but probably little harm in most patients
Apply 1-3 times/day for first few days as desired Combine with good initial wound cleaning, use of antiseptics, keeping wound covered & clean |
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wound Conditions that usually require referral include:
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Wounds with large or impacted foreign materials
Unusually deep or wide wounds Chronic or slow-healing (>5 days after injury) wounds Extensive wounds involving face, mucous membranes, or genitals Bite or puncture wounds Wounds already obviously infected w/ more extensive tissue involvement or systemic symptoms fever |
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Patient presents with niece shortly after a bike accident and asks what you would recommend to care for the wound. You observe the nieces knee and shin wounds, which are dirty with gravel and bloody. She is crying and doesn’t want her aunt to touch the wounds. What do you recommend as the first step to reduce the risk of infection in this patient?
Recommend irrigation with povidone iodine. Recommend irrigation with saline solution. Recommend referral Apply hydrogen peroxide, then bandages to cover the wounds |
Recommend irrigation with saline solution.
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what is the site of infection of folluculitis
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hair follicle
just inflammation of the hair follice\ doesn't always turn into furuncles |
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Folliculitis
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Inflammation of the hair follicles
Associated with small (2-5 cm) erythematous, pruritic, papular lesions S. Aureus overgrowth in and around the follicle |
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self care of follicuitis
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Self Care options
Warm compresses benzoyl peroxide (non-specific antimicrobial) More extensive infections of the hair follicle include furuncles and carbuncles. Rx topicals include clindamycin, erythromycin, mupirocin |
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A 27 yo male presents to the pharmacy with a sore that has developed on his chin. He tells you he sometimes gets ingrown hairs in his beard area but that they usually heal quickly. He’s concerned because the sore seems to be larger and he wants to know what he should do about it. You tell him:
That’s gross! You should see your dermatologist To pop it and get the healing process going. To put moist heat on it to promote drainage. To go to the doctor to get a prescription because it’s infected. |
To put moist heat on it to promote drainage.
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what part of the skin does a furuncel effect
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hair follicle and surrunding dermis
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Furuncles and Carbuncles
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Furuncle are S. Aureus infections around the hair follicle involving deeper areas of the skin.
Firm, tender, red nodules Carbuncle is two or more confluent furuncles with separate heads This is distinctly different from Acne. Furuncles/Carbuncles are the most common type of SSTI caused by CA-MRSA Appearance resembles a spider bite |
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most common site of a furuncle
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Most frequent sites include hairy skinned areas (neck, axillae, buttocks, face).
Larger, deeper lesions Swelling of surrounding tissue Undrained pus common Symptoms include fever, chills , malaise, leukocytosis (+/-) |
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Small furuncles self treated with
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with moist heat
Promotes localization (congestion reduced) =drainage of pus |
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Large furuncles and carbuncles tx
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incision and drainage
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if fever or cellulitis is present with a furuncle how is it treated
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treat with oral antibiotics*
Dicloxacillin Cephalexin Clindamycin (PCN allergic) TMP/SMX for suspect CA-MRSA |
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how are repeated facial furuncles treated
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Repetitive facial involvement may be secondary to nasal colonization
Mupirocin ointment applied to nares BID for 5 consecutive days per month may decrease recurrent furunclulosis (~50% overall reduction in recurrence.) Once daily clindamycin 150 mg x 3 months recurrent infections by 80% |
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Impetigo
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Superficial cellulitis
Staphylcoccus aureus (Bullous Impetigo) Group A streptococci Most common among children ages 2-5 years old Most common during hot, humid weather Initially pruritic, with fluid filled vesicles Develops into pustular blisters that easily rupture. Lesions dry, to form golden-yellow crusts Highly communicable |
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a kid should with impetigo not return to regular daily activities for ______ hours after Ab treatment
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24 hours
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Impetigo tx for uncomplicated
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Topical treatment may be considered in:
Uncomplicated course Relatively small surface area affected Agents: Mupericin 2% ointment TID Retapamulin 1% (Altabax®) ointment BID x 7-10 days |
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impetigo tx for complicated (bigger SA, sick child)
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Oral antistaphylococcal empiric treatment of choice
dicloxacillin cephalexin amoxacillin/clavulanate clindamycin for PCN-allergic |
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what type of organims are being covered in the tx of impetigo
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gram +
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Patients with uncomplicated course of Impetigo may be
treated topically with: bacitracin ointment TID mupericin 2% ointment TID Coal tar shampoo BID salicylic acid gel 1% |
mupericin 2% ointment TID
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treatment duration of impetigo
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7-10 days
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Erysipelas treatment duration
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7-10 days
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Erysipelas
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Superficial cellulitis with extensive lymphatic involvement
Group A streptococci (30% of patients have had strep throat) (but infection arose from a break in the skin not the infection itself) Infection most common in infants, young children, the elderly, and patients with nephrotic syndrome Lower extremities are most common site S/Sx include painful or burning pain, fever, malaise, leukocytosis |
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Erysipelas tx
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Mild-Moderate
Procaine Penicillin G or Penicillin VK Dicloxacillin Cephalexin Clindamycin (or erythromycin) for PCN-allergic +/- Prednisolone1 (increases patient comfort) |
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why is PCN benzathine not used for erysipelas
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because it has a prolonged duration of action and erysipelas does not reaquire that long of tx
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is PCN procaine or benzathine ever administered IV
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no will kill the patient
JUST IM (only) |
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how do you distinguis eryispelas from cellulitis
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the skin is raised in eryispelas and a very distinct boarder
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cellulitis
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Acute, serious infection that involves the deeper layers of the dermis / subQ tissue
Spreads to superficial fascia, through the lymphatic tissue to the bloodstream if left untreated. Resultant complication: thrombophlebitis, abscesses, osteomyelitis, necrotizing fasciitis, septic arthritis, sepsis Patients of all ages are affected. Half with underlying drug or alcohol abuse, obesity, diabetes, or PVD |
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JD is a 69 yo male with a history of diabetes who presents to the clinic with a painful, bright red area with distinct raised borders on his face. There appears to be some edema, but no blisters or vesicles. Which of the penicillin regimens below is appropriate for treatment?
Benzathine 1,200,000 units SQ BID x 7 days Benzathine 2,400,000 units IM once Procaine 600,000 units IV BID x 7 days Procaine 600,000 units IM BID x 10 days |
Procaine 600,000 units IM BID x 10 days
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etiology of cellulitis
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History of wound or trauma often identified, but not always
Poor circulation or altered immune function Legs and feet are most common sites in non-IV drug abusers (in port of entry) |
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Periorbital Cellulitis
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Most common in kids < 6
Complication of primary infection (URI, conjunctivitis, facial surgeries) Watch for patients who progress to cellulitis from conjunctivitis. infection in SQ tissue around eye eyes can be clear can cause blindness REFER |
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common S/S of cellitits
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Erythema and edema of affected area
Lesions are non-elevated Margins are poorly defined Inflammation Vesicles Chills, malaise, anorexia, N/V Fever Leukocytosis |
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what is cellulitis usually caused by in healthy patients
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Infections in “healthy” are generally caused by skin flora and are monomicrobic.
S. Pyogenes (group A strep) S. Aureus CA-MRSA ? |
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in more complicated patients what is cellulitis typically caused by (DM, IVDA< Surgical incisions)
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Diabetics, IVDA, traumatic injuries, surgical incision sites, immunocompromised
Mixed aerobic/anaerobic polymicrobial infections including gram negatives and positives These are considered complicated SSTI |
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diagnostic work up for cellulitis
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Culture collection from advancing edges
Needle aspiration or punch biopsy culture +ive only 5-40% of the time1 Any wound drainage or fluid should be cultured CBC leukocytosis is common Blood cultures bacteremia may be present (< 5% of the time) (concerned for endocarditis) If +, pathogen-directed therapy can be instituted |
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local care for cellulitis
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Elevate affected area
Rest affected area ( so do not further irritate) Apply cool, sterile saline dressings (to decrease edema) After inflammation controlled, apply moist heat Pain management may be indicated Incision, drainage, debridement if severe skin abscesses < 5 cm in diameter can often be cured without antibiotics by incision and drainage Antibiotic therapy |
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cellulitis treatment duration
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7-14 days
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cellulitis Considerations in Antibiotic Selection
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Tissue penetration
Targeted microbiology Empiric therapy must cover S. Aureus and streptococci CA-MRSA should be considered when choosing Gram negative anaerobes (immunocompromised) Anaerobes (abscesses, post-op wounds) (DM, IVDA...) |
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empiric tx of cellulitis for outpatient
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Empiric treatment of mild infections with antistaphylcoccal PCN
dicloxicillin |
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cellulitis tx for more severe cases (when to hospitalize??)
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Head, neck, face involvement
Rapidly progressing Severe systemic symptoms Suspected fascia or bone involvement Unstable underlying diseases DM IVDA these patients need IV therapy |
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Oral Agents for Mild-Moderate Cellulitis
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Dicloxacillin
Cephalexin Cefadroxil Amoxicillin/clavulanate (not typically 1st line) Moxifloxacin used for CA-MRSA Clindamycin* TMP/SMX* Doxycycline* |
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what agents are used when CA-MRSA are suspected
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Clindamycin*
TMP/SMX* Doxycycline* used when MRSA suspected, must add agent to Bactrim for empiric coverage vs. Group A Strep |
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Empiric Antibiotics for Hospitalized Community-Acquired SSTI
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General (IV therapy)
Cefazolin 1 gm IV q8h Nafcillin/oxacillin 2 gm IV q4h +/- SMX/TMP (if CA-MRSA suspect) Penicillin allergic Clindamycin 600 mg IV q8h Levofloxacin 750 mg IV q24h + Metronidazole 500 mg IV q8h Injection drug users Cefazolin 1 gm IV q8h + Metronidazole 500 mg IV q8h |
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is bactrim useful against strep A
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not really
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MB is a 36 yo male who presents to the clinic with a painful, red, swollen ankle. The patient has been taking cephalexin for 5 days as prescribed by his PCP for a presumed cellulitis. He’s at the urgent care because the infection has continued to spread. It’s really painful. What pathogen is the likely cause of MB’s infection?
CA-MRSA MSSA Clostridium S. Epidermidis |
CA-MRSA
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CA-MRSA Cellulitis epidemic proportions
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CA-MRSA predominantly presents as SSTIs
Currently, the most common single pathogen isolated from SSTI (Microbiology data from U.S. Emergency Depts.) Most common for infection to occur on unbroken skin, but linked to focal lesion such as an ulcer, abscess, or folliculitis Localized necrosis is typical Dark center where abscess formed often exists Patients present to the ED, majority successfully treated as outpatients |
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MB is a 36 yo male who presents to the clinic with a painful, red, swollen ankle. The patient has been taking cephalexin for 5 days as prescribed by his PCP for a presumed cellulitis. He’s at the urgent care because the infection has continued to spread. It’s really painful. What is your recommendation to treat MB’s infection?
daptomycin IV Cefazolin IV SMX/TMP PO dicloxacillin PO |
SMX/TMP PO
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CA MRSA Cellulitis
Adjunctive antibiotics after I&D recommended if |
Complicated abscesses (defined as presence of one of the following
Fever Cellulitis surrounding it Lymphangitis > 5 cm diameter abscess Rapidly progressive or severe local disease Comorbid conditions or immune suppression Inability to completed drain abscess cavity Extremes of age Failed prior I&D |
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drug of choice for outpatient CA-MRSA cellulitis
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TMP/SMX currently the drug of choice for outpatient management. Susceptibility range of CA-MRSA is 83-100%.
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MB presents to the ED after starting the outpatient therapy you chose in the last slide. The infection has continued to spread. His temperature is 39.5 C and he is confused and in pain (rated as 8 on scale of 10). What is the most appropriate recommendation for therapy at this time, given his previous antibiotic failures and current clinical condition?
doxycycline 500 mg PO BID + MSO4 5 mg IVP nafcillin 2 g IV every 4 hrs + MSO4 5 mg IVP SMX-TMP 2.5 mg/kg IV BID + MSO4 5 mg IVP vancomycin 1 g IV Q12H + MSO4 5 mg IVP |
vancomycin 1 g IV Q12H + MSO4 5 mg IVP
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Treatment of Hospitalized MRSA Patients
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In geographic areas with high prevalence of CA-MRSA (>15% of community isolates), treat empirically:
First line: vancomycin (CA-MRSA is 99-100% susceptible.) Second-line: TMP-SMX 2.5 mg/kg IV Q12 hrs + oxacillin, nafcillin, cefazolin for streptococci Note: Addition of Gram-negative coverage may be recommended in higher-risk patients |
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alternative therapies for MRSA cellulitis
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very expensive
linezolid daptomycin tigecycline telavancin |
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Inappropriate Empiric Therapy for Hospitalized MRSA cellulitis Patients
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Fluoroquinolones
Risk factor for MRSA infection (Most common ABX) Macrolides erythromycin (existing resistance) clindamycin (existing resistance and/or inducible resistance) Rifampin monotherapy Rapid resistance develops vancomycin + rifampin is used by some in clinical practice, but data is lacking for this combination. |
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What makes SSTI “complicated”?
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Fascia or muscle layer involvement
Significant surgical intervention required Co-morbidities: Diabetics, HIV infected, others that are likely to compromise response to treatment. Superficial infections on/at regions of the body that are at risk for Gram negative or anaerobic pathogens. |
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Examples of cSSTI
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Infected surgical wounds
Cellulitis with purulent drainage post-traumatic wound infections Diabetic foot infections Decubitus ulcers Necrotizing fasciitis Deep soft-tissue abscesses |
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Microbiology of cSSTI
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Although monomicrobial infections do occur, polymicrobic (“mixed”) bacterial infections are far more common
Gram-positive aerobes S. aureus (may be MRSA), other staphylococci, streptococci (Groups A, C, D, G), enterococci Gram-negative aerobes Enterobacteriaceae, Pseudomonas aeruginosa Anaerobes Bacteroides fragilis, B. fragilis group, Fusobacterium, anaerobic streptococci |
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Treatment of cSSTI Determinants of antimicrobial selection depends on....
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Community versus hospital acquired
Patient specific factors Site of infection Diabetic IVDA Immunosuppression Presence of prosthesis Previous surgeries Organ dysfunction that could affect ADME Recent antimicrobial therapy or failed agents for less severe SSTI (i.e. fluoroquinolone) |
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Post-operative wounds
cSSTI bugs |
Gram + aerobes: S. aureus, Enterococcus spp.
Gram – aerobes: P. aeruginosa, Enterobacter spp., E. coli Anaerobes: B. fragilis, other Bacteroides group |
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Abscesses in injection drug users cSSTI bugs
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Gram + aerobes: S. aureus, coagulase-negative staphylococci, S. pyogenes, S. milleri, S. viridans
Gram – aerobes: Eikenella corrodens, H. parainfluenzae Anaerobes: Bacteroides spp., Peptostreptococcus spp., Clostridium spp., Fusobacterium spp., Prevotella spp. |
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Cellulitis in immunocompromised patients bugs
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Gram + aerobes: S. aureus, S. pyogenes
Gram – aerobes: Pseudomonas spp., E. coli, Enterobacter spp. |
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Antibiotic Options for Treatment of Complicated Skin/Skin Structure Infections
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Penicillins: Nafcillin, oxacillin
Cephalosporins: Cefazolin, cefoxitin, cefotetan, ceftriaxone, ceftazidime, cefepime -Lactam/ -Lactamase Inhibitor Combinations:Amoxicillin/clavulanate,ampicillin/sulbactam, ticarcillin/clavulanate, piperacillin/tazobactam Carbapenems:Imipenem/cilastatin, meropenem, ertapenem Fluoroquinolones:Ciprofloxacin, levofloxacin Aminoglycosides:Gentamicin, tobramycin, amikacin Anaerobic agents:Metronidazole, clindamycin Miscellaneous (Gram +):Vancomycin, linezolid, daptomycin, telavancin, quinupristin/dalfopristin |
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Empiric Antibiotic Selection: Nosocomial cSSTI in general
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Piperacillin/tazobactam 3.375 gm IV q6h
± Vancomycin 1 gm IV q12h Imipenem/cilastatin 500 mg IV q8h ± Vancomycin 1 gm IV q12h Meropenem 1 gm IV q8h ± Vancomycin 1 gm IV q12h Cefepime 1 gm IV q8h or Ceftazidime 1 gm IV q6h ± Vancomycin 1 gm IV q12h ± Metronidazole 500 mg IV q8h |
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Empiric Antibiotic Selection: Nosocomial cSSTI PCN allergic
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Clindamycin 600 mg IV q8h + aminoglycoside or aztreonam ± Vancomycin
Vancomycin 1 gm IV q12h + aminoglycoside or aztreonam ± Metronidazole |
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Necrotizing Fasciitis type I
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(Trauma or Sx): mixed anaerobes, Streptococci and enterobacteriaceae
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Necrotizing Fasciitis type 2
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(virulent gram positive organisms)
S. Pyogenes S. Aureus |
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Toxic Shock Syndrome may result from ....
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infections that involve streptococcal or staphylococcal organisms.
Symptoms include shock, coagulopathy, organ failure and necrotizing infection. exotoxin mediated |
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Necrotizing Fasciitis Empiric Treatment
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Immediate, aggressive debridment of necrotic tissue
Administer broad spectrum antibiotics to cover streptococci, enterobacteriacae, anaerobes until pathogen is identified Culture will allow for targeted therapy Known Type II cause antistaphylococcal PCN (oxacillin, dicloxacillin) + toxin directed therapy (clindamycin or linezolid) +/- Vanco if MRSA suspected |
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Toxin-directed Antimicrobial Therapy for necortizing fas
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Some S. Aureus strains produce protein cytotoxins that are able to lyse neutrophils, eliminating cellular defenses against MRSA infections.
Clindamycin 600-900 mg IV Q8H (also linezolid) have ability to inhibit toxin by suppressing protein and should be added as “antitoxin antimicrobial” in severe systemic infections. (don't want to use alone will induce R) BUT use of clindamycin empirically must be deliberate, due to potential for inducible resistance in up to 50% of CA-MRSA strains. |
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Clostridial Myonecrosis
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Skeletal muscle infection known as Gas Gangrene
World War II: 30% of battlefield wounds were associated Occurs most often from traumatic injury that becomes contaminated with clostridial spores C. Perfringens typically isolated Gram + anaerobic rod Most common clostridial species isolated from mammalian intestinal tracts Ubiquitous in soil, GI tract Produces protein toxins |
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contributing factors of Clostridial Myonecrosis
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Crushing injuries, burn victims, GI surgical pts, septic abortions, PVD, diabetic fool ulcers, recently - IVDA injecting contaminated coal-tar heroin.
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what bacteria is typically isolated from Clostridial Myonecrosis
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Perfringens typically isolated
Gram + anaerobic rod Most common clostridial species isolated from mammalian intestinal tracts Ubiquitous in soil, GI tract Produces protein toxins |
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Clostridial Myonecrosis begins...
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Begins 24-72 hrs after trauma or surgery
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Clostridial Myonecrosis S/S
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Signs and symptoms
Severe pain despite absence of obvious physical signs Within hours of symptom onset, edema and gas in the infected tissue are detectable by physical evaluation +/- hemorrhagic Bullae Foul odor Absence of fever Tachycardia Black tissue appearance |
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Clostridial Myonecrosis leads to .....
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profound ischemia, tissue hypoxia
obstructed microvascular circulation caused by platelet aggregation within vessels and fibrin deposition |
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Clostridial Myonecrosis tx
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Promptly debride, possibly amputate, hysterectomy (uterine involvement)
Early, aggressive antibiotic treatment High dose Penicillin G Hyperbaric Oxygen (+/-) |
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dog bite wound epidemiology
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~ 80% of animal bites that require medical attention are from Dogs.
~ 1000 dog bite wounds present to ED per day in the U.S. ~ 50% of bites occur in individuals < 20 Infection risk greatest: If bite involves a puncture If presentation is > 12 hrs after injury If pts are > 50 y/o results in punctures planting the microbes deep in the fascia |
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Cat Wound Epidemiology:
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~5-15% of animal bites
Scratches or bites may cause infection Infection rates are estimated at 30-50%, which is more than double that seen with dog bites. |
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dog bites
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Normal oral flora (aerobic and anaerobic) and pressure of the bite wound result in increased infection risk.
Bite wounds can result in crushing injury, causing devitalized tissue. |
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microbiology of dog bits
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Common aerobes: Pasteurella multocida (most common), Streptococci, staphylcocci, Moraxella, Neisseria
Common anaerobes: Fusobacterium, Bacteroides, Porphyromonas, Provotella |
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clinical presentation of dog bites
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Local cellulitis: Pain, purulent discharge (malordorous), swelling
P. multocida more likely if rapid progression (24-48 hrs of bite). (stink, purulenc) Fever uncommon |
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Cat Bites
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Normal oral flora (aerobic and anaerobic) and puncture depth of the bite increase infection risk.
Sharp, long teeth that penetrate to bone may lead to septic arthritis or osteomyelitis. |
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cat bites microbiology
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Same as dogs, but P. Multocida responsible for 75% of bites/scratches
~ 25-30% of cultures grow only anaerobes. |
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clinical presentation of cat bites
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Local cellulitis: Pain, purulent discharge (malordorous), swelling
P. multocida more likely if rapid progression (24-48 hrs of bite). Fever uncommon more pasteurella becausequick bite and not as much tissue trauma |
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Evaluation of Bite Wounds
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Patients seen within 8-12 hours after bite have not yet acquired infection, usually require only general wound care & repair (irrigation)
Patients seen >8-12 hours after injury are usually seeking care for infection-related complaints Detailed history, including timing of injury Careful inspection of the wound with attention to deepness, whether tendons or ligaments are affected, presence of foul odor |
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Evaluation of Bite Wounds if coming in infected
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Cultures (aerobic and anaerobic) and CBC when possible
Surgical consults should be obtained for wounds which are: Deep Obviously infected Extensive injury to tissues, ligaments, or tendons, particularly if hand is affected |
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Bite Wound Treatment
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Promptly irrigate the wound with soap or iodine
Immunization Status of Animal: Rabies Dog bites account for ~ 3% of rabies Reminder: Promptly irrigate the wound with soap or iodine If known dog infection with rabies, then initial rabies treatment protocol Immunoglobulin into and around the wound and IM vaccination Immunization status of Patient: Tetanus Boost if unknown or > 5 yrs since last dose (it’s a presumed dirty wound) DTaP versus Tdap versus Td |
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DTap is used in
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kids
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Tdap is used in
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in adults that did not receive tdap
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Td used in
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adults if had tdap in last 10 years
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bite wound treatment duration
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7-10 days
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prophylaxis for dog bits
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Prophylaxis (x 3-5 days) is controversial, should probably be reserved for high-risk patients
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tx for dog bites
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Amoxacillin-Clavulanate
1st or 2nd generation cephalosporin + clindamycin TMP/SMX + clindamycin or metronidazole |
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prophylaxis for cat bites
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Prophylaxis (x 3-5 days) considered for all due to higher wound infection rates
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tx for cat bites
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Amoxacillin-Clavulanate
PCN ceftriaxone doxycycline |
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Human Bites
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Often sustained during fights
Clenched-fist or “fight bite” Generally more serious than animal bites with higher risk of infection Risk for infection: 10-50% of human bites become infected Hands carry higher risk for infection Patients often present late for treatment after infection has already been established Typically polymicrobial, involve normal flora of both mouth & skin Streptococci, S. aureus, Haemophilus spp., Eikenella corrodens Anaerobes in ~40% of infections |
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micorobes involved in humna bites
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Streptococci, S. aureus, Haemophilus spp., Eikenella corrodens
Anaerobes in ~40% of infections |
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Human Bites: Treatment wound management
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Surgical & radiographic evaluation if deep wounds or accumulations of pus evident
Wound Management: Aggressive irrigation of wound Fist infections move proximally once fingers open, harder to irrigate Debridement of dead/infected tissue Immobilization of limb to minimize inflammation/spread of infection Assess HIV status of biter, if possible |
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Human Bites: Treatment AB
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Treat both non-infected (x 3-5 days) and infected (x 7-10 days)
Amoxicillin/clavulanate Doxycycline Dicloxacillin + Penicillin VK Clindamycin + Fluoroquinolone or TMP/SMX |
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Bioterrorism def.
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Deliberate release of viruses, bacteria, or other germs (agents) used to cause illness or death in people, animals, or plants.
directly on humans or secondary |
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agents used for bioterrorism def.
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Typically found in nature
Altered to increase their ability to cause disease, resistant to current medicines, or ability to be spread into an environment modified strain that is more virulent and R, spread more easily than the normal enviromental one |
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Category A bioter (know)
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High-priority agents that pose the greatest risk to the public and national security
Easily spread High death rates or major public health impact Public panic or social disruption Require special action for public health preparedness person to person spread forcus on these agents for public perparedness |
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Category B bioter (know)
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Second highest priority
Moderately easy to spread Moderate illness and low death rates Require specific enhancements of CDC’s laboratory and disease monitoring |
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Category C bioter (know)
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Third highest priority – Emerging threats for disease (future implications)
Easily available Easily produced and spread Potential for high morbidity and mortality rates and major health impact could cause serious harm CDC is worried about but trying to figure out if a risk or not |
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bioter agents cat A
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Bacillus anthracis (Anthrax)
Variola virus (Smallpox) Yersinia pestis (Plague) Botulinum toxins Francisella tularensis (Tularemia) Hemorrhagic Fever Viruses (when get cause a major systemic response and crazy bleeding--> 1/3 of people die and there is nothing to use against ift but provide supportive care) Crimean Congo Ebola Marburg Rift Valley Fever |
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bioter agents cat B
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Brucella spp.
Coxiella burnetti (Q fever) Food safety threats Salmonella E.coli O157:H7 Shigella Clostridium perfringens toxin Ricin toxin Bulkholderia mallei (Glanders) Bulkholderia pseudomallei (Melioidosis) Chlamydia psittaci (psittacosis) Staphylococcal enterotoxin B Rickettsia prowazekii (Typhus fever) Water Safety threats Vibrio cholerae, cryptosporidium parvum Viral encephalitis bateria related such as toxins and infections |
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bioter agents cat C
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Nipah virus
Hantavirus Influenza |
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Why would Terrorists Choose Biological Weapons?
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Ability to inflict large numbers of casualties over a large area
Cheap Relatively easy to produce Difficult to detect Vulnerability of the population and the system |
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Biological Warfare & Terrorism in History
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Pre-Modern warfare - use of carcasses
Early American colonial period WWI - Glanders WWII Japanese Unit 731 UK - US fear of Nazis Cold War - USSR; UK; US; France; PRC (China) “Third World” - Iran; Iraq; North Korea; Libya; Syria; … The Dalles, Oregon - 1984 Iran-Iraq War - 1980s Aum Shin Rykio - 1990s Anthrax - 2001 In the 13th and 14th centuries, enemies used infectious diseases such as plague as a weapon by laying siege to castles and throwing dead bodies over the walls. Around Pittsburgh area, Lord Amherst spread smallpox to the native Americans. In WW I, the Germans are suspected of infecting American cattle with Glanders. The first real incident of bioterrorism in the U.S. occurred in The Dalles, Oregon in 1984. The followers of Bhagwan Sri Rashneesh wanted to influence a local election so they spread Salmonella on salad bars. Public health quickly identified the disease agent but it took longer to find an informant who could explain who had done it and why. Iraq did produce about 8500 L of anthrax Aum Shim Rykio – 1990s. Most people associate the subway sarin attacks in Tokyo with Aum Shim Rykio, but this group was also developing biological agents. Anthrax – Fall of 2001. |
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BioWar
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Stereotypical attack scenarios
Cold War Big attacks 100,000s |
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BioTerror
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Unconventional attack scenarios
Creative terrorism “New” “War” Small attacks 10 – 100 hard to detect Change: move away from big bio war to small bioterrorism, creative terrorism Implications for detection, response and containment |
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Anthrax meaning of word
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Greek word that means coal – derived from its black escar with cutaneous infection)
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Anthrax as a Biologic Weapon
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Spores are durable
Could be delivered by cutaneous contact, contaminated food, or aerosolized Intentional release of 1 kg of spores could lead to over 100,000 deaths in a city of 10 million Virulence depends on bacterial capsule and toxin complex Incubation: range 1 day – 8 weeks Depends on exposure route and dose |
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aerosol delivery of anthrax
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Aim is to generate invisible clouds of particles of 0.5-1.0 microns in diameter
Can stay suspended for long periods of time Perfect size to reach the alveoli get into lungs to increase morbidity and mortality |
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The 2001 anthrax attacks in
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in the United States, also known as Amerithrax from its Federal Bureau of Investigation (FBI) case name, occurred over the course of several weeks beginning on September 18, 2001. Letters containing anthrax spores were mailed to several news media offices and two Democratic U.S. Senators, killing five people and infecting 17 others. The primary suspect was not publicly identified until 2008.
In mid-2008, the FBI narrowed its focus to Bruce Edwards Ivins, a scientist who worked at the government's biodefense labs at Fort Detrick in Frederick, Maryland. Ivins had been told about the impending prosecution and died from an overdose of "Tylenol with Codeine," which was reported as a suicide on August 1, 2008.[1][2] On August 6, 2008, federal prosecutors declared Ivins to be the sole culprit of the crime.[3] Two days later, Sen. Charles Grassley and Rep. Rush Holt called for hearings into the DOJ and FBI's handling of the investigation.[4] |
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outcomes of 2001 anthrax attacks
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Washington DC, Florida, New Jersey, New York City, Maryland, Pennsylvania, Virginia
15 cases, 3 deaths 7 inhalational, 8 cutaneous Postal workers and workers who sorted mail at the end receiving company Florida media company targeted 1100 persons started on antimicrobial prophylaxis 555 worked full-time or part time in the building Majority of others reported spending > 1 hour in building |
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Bacillus anthracis (Anthrax)
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Aerobic, gram-positive rod, encapsulated, spore-forming
Defense mechanisms: anti-phagocytic capsule and toxin release Lethal toxin and Edema Toxin Soil reservoir; acute infection in animals & humans |
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toxins of anthrax
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Toxin causes cellular edema, release of TNF, and IL-1. Effects lungs and brain.
Lethal toxin is responsible for the tissue damage, shock, and high probability of death Edema toxin causes extensive systemic edemas due to disruptions of electrolyte and water transport across cellular membranes |
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Anthrax in animals (zoonotic disease of herbivores)
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Ingest spores while grazing on contaminated land
Global: Middle East, Asia, Africa, S&E Europe, S&C America U.S.: TX, LA, MS, OK, SD |
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Anthrax in humans
naturally |
Exposure to infected animals or animal products
Agricultural and industrial exposure NO person to person transmission |
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Inhalation Anthrax
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5% of global cases: 18 cases in U.S. (1900-1978)
inhaled spores from contaminated hides, wool, hair BW aerosol (8,000-10,000 spores, 1 ng - lethal dose) |
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Cutaneous Anthrax
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95% of global cases pre-Oct 2001
U.S.: 1 case/year (1990-2000) entry of spores thru skin abrasion or cut |
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Gastrointestinal and Oropharyngeal Anthrax
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rare form: ingestion of contaminated meat
incubation period 1-7 days; oropharyngeal or abdominal disease |
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Mortality from inhalation anthrax
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95% in untreated patients
Soviet biological weapons facility Sverdlovsk, 1979 Affected 94 persons and killed at least 64 Wind direction saved > 100,000 United States, 1900-200016/18 (89%) United States, 2001 5/22 (23%) |
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Early Symptoms of Inhalation Anthrax
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1-7 days (up to 60 day incubation period)
Low-grade fever, chills, weakness, myalgia, dyspnea, cough, headache, malaise, fatigue Abdominal pain, vomiting, chest pain Widened mediastinum (seen on CXR or CT scan) Pleural effusion on CXR earlier if a bioter attack because such a large number of spiores |
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Late Symptoms of Inhalation Anthrax
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1-5 days after early symptoms
High fever, dyspnea, extreme diaphoresis, cyanosis, and stridor secondary to massive lymphadenopathy 50% develop meningitis - may present w/ seizures 90-95% mortality after late onset w/ or w/o antibiotic Rx Shock and death within 24-36 hours |
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Diagnosis of Anthrax Infection (tests)
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Chest x-ray: widened mediastinum, infiltrates, pleural effusion
Chest CT: Hyperdense hilar and mediastinal nodes, mediastinal edema, infiltrates, pleural effusion Thoracentesis: hemorrhagic pleural effusions |
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microbiology of antrax
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Peripheral blood smear: gram-positive on blood smear
Blood culture growth of large gram-positive bacilli with preliminary identification of Bacillus species Cutaneous: culture of vesicle fluid |
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what does anthrax look like under a microscope
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gram + rod
narrows it down to 5-6 types of bacteria |
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Inhalational Anthrax Treatment inital therapy
|
Ciprofloxacin 400 mg iv Q12h or Doxycycline 100 mg IV Q12h
Plus 1-2 additional antibiotics until the patient is clinically stable or sensitivities obtained (clindamycin, vancomycin, imipenem, meropenem, chloramphenicol, penicillin, ampicillin, rifampin, and clarithromycin) bioter anthrax is going to be very R so start broad spectur because if the treatment is unsuccessful can die in 1-2 days |
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Inhalational Anthrax Treatment prolonged therapy
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Ciprofloxacin 500 mg po Q12h or doxycycline 100 mg po Q12h
(Children should be switched to PCN or amoxicillin if susceptible) |
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duration of treatment of anthrax
|
(1) 60 days of treatment (most common recommendation),
(2) 100 days of treatment, or (3) 100 days of treatment plus AVA (3 doses) |
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Anthrax Treatment inital therapy
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Initial therapy
Ciprofloxacin 400 mg iv Q12h or Doxycycline 100 mg IV Q12h Plus 1-2 additional antibiotics until the patient is clinically stable or sensitivities obtained (clindamycin, vancomycin, imipenem, meropenem, chloramphenicol, penicillin, ampicillin, rifampin, and clarithromycin) Prolonged therapy Ciprofloxacin 500 mg po Q12h or doxycycline 100 mg po Q12h (Children should be switched to PCN or amoxicillin if susceptible) Total Duration options (1) 60 days of treatment (most common recommendation), (2) 100 days of treatment, or (3) 100 days of treatment plus AVA (3 doses) |
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AVA
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anthrax vaccine
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is anthrax spore forming
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yep so hard to erradicate
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Anthrax Treatment in addition to AB
|
Corticosteroids
Consider for meningitis or significant mediastinal edema Drainage For pleural effusions – chest tube Supportive care Mechanical ventilation Volume repletion Vasopressors |
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Early Symptoms of Cutaneous Anthrax after Direct contact with spores or bacilli
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Usually an immediate response (within first day)
Incubation period 1-12 days Small papule or pruritic macule for 1-2 days Vesicle (1-2 cm) containing serosanguinous fluid Vesicles ruptures leaving necrotic ulcer, satellite vesicles Prominent inflammation and edema surround lesion mortality is a lot less thatn the inhaltion form |
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Late Symptoms of Cutaneous Anthrax after Direct contact with spores or bacilli
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1 week after early symptoms
painless, depressed, black eschar lymphangitis, painful lymphadenopathy and systemic symptoms may occur 20% mortality w/o and <1% w/ antibiotic Rx |
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Cutaneous Anthrax Treatment
|
Systemic involvement, Extensive edema, Lesions on the head and neck
See inhalational anthrax treatment (IV therapy) Therapy Ciprofloxacin 500 mg po Q12h or doxycycline 100 mg po Q12h Alternative therapy – amoxicillin 500 mg po TID Total Duration 60 days of treatment |
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adults Postexposure Prophylaxis
|
Ciprofloxacin 500 mg PO Q12h
Doxycycline 100 mg PO Q12h |
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children Postexposure Prophylaxis
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Ciprofloxacin 10-15 mg/kg/day divided Q12h
Doxycycline > 8 years/>45 kg: 100 mg Q12h 8 years/ 45 kg: 2.2 mg/kg/dose Q12h < 8 years: 2.2 mg/kg/dose Q12h Amoxicillin 80 mg/kg/day divided Q8h |
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pregnant or breastfeeding women Postexposure Prophylaxis
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Ciprofloxacin or Doxycycline
Amoxicillin 500 mg Q8h |
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prophylaxis duraition in all groups of peopels
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30 days (vaccine + abx)
60 days (abx only) |
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anthrax vacination schedule
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if available
0, 2, 4 weeks may shorten duration of tx |
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Active immunization against B. anthracis
|
Vaccine: AVA Anthrax Vaccine Absorbed (BioPort, Lansing, MI)
vaccine: culture filtrate of attenuated strain strain: unencapsulated, non-proteolytic composed predominantly of protective antigen (PA) Vaccination Schedule: 0.5 mL subcutaneous injection: at 0, 2, 4 weeks boosters at 6, 12, and 18 months then annual boosters if potential exposure Seroconversion: 95% after initial 3 doses (measured by EIA) |
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Anthrax vaccine - Safety
|
Anecdotal reports of autoimmune responses (vertigo, muscle and joint pain, or mental impairment)
Gulf War syndrome Vaccine Adverse Event Reporting System Reviewed 1841 reports describing 3991 adverse events Concluded that there is no evidence for an unusual rate of any serious adverse events attributable to AVA AVA may cause significant local inflammation has not been linked |
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effects of reduced dose schedule and IM admin of anthrax vaccine adsorbed on immunogenicity and safety at 7 months
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1005 participants
3 IM doses provided adequate antibody titers Adverse effects Injection site reactions and pain most common Possible serious ADR – 7 patients Allergic reactions, seizures, breast cancer, arthralgias |
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Future of anthrax vaccine
|
Recombinant protective antigen (rPA) – in clinical trials
Delivery systems – in animal testing stage Skin patch Inhalation |
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small pox is part of what family
|
Part of the orthopoxvirus family: variola, vaccinia, cowpox, and monkeypox)
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Smallpox as a Biologic Weapon
|
Aerosolized delivery
Large susceptible population Few health-care professionals have seen cases Long incubation period, contagious Likelihood of secondary and tertiary cases |
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does small pox spread person to person
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very easily
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small pox epidemiology
|
Person to person continuing chain of transmission
Droplet Aerosol Incubation 12 days (7-17 days) Virus transmitted from the onset of rash until all scabs separated |
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Smallpox: clinical course
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day 1: oral entry -> regional lymph nodes (multiplication)
day 3-4: asymp viremia -> multiplication of virus in spleen, bone marrow, lymph nodes day 8: secondary viremia -> localized in small blood vessels day 12-14: high fever, malaise, headache and backache, +/- severe abdominal pain & delirium progresses to: maculopapular rash, initially on oral mucosa, face, and forearms day 15-16: rash -> vesicular -> pustular 30% fatality rate: circulating immune complexes and toxemia day 20: crust forms -> scabs -> pitted scarring |
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small pox vs chicken px symptoms
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when was the small pox vaccine introduced
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1798 by edward jenner from cow pox
he realized that milk mades did not get small px |
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Smallpox: Treatment
|
Up to 4 days post-exposure: vaccine (live vaccinia)
Within 2-3 days of exposure: Protect against disease Within 4-5 days of exposure: Protect against death After 5 days post-exposure: no treatment U.S. vaccine program: terminated in 1972 Adequate stockpile to vaccinate everyone in the US give vaccine as early as possible |
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vaccine preparation
|
Dryvax by Wyeth Lab.
Prepared from calf lymph containing live vaccinia virus Contains trace amounts of polymyxin B, streptomycin, tetracycline and neomycin |
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how to administer small pox vaccine
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Use bifurcated needle to puncture skin in deltoid area
2-3 punctures for primary 15 punctures for secondary vaccination |
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Clinical Response to Vaccination
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Symptom/sign
Papule 2-5 days Pustule 7-10 days Maximum erythema 8-10 days Scab 14 days Scab separation 21 days keep bandage on until it scabs over because is infective |
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Smallpox Vaccine Local Reactions Among Susceptible Adults
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Pain, swelling, erythema at vaccination site
Regional lymphadenopathy Begins 3-10 days after vaccination Can persist for 2-4 weeks after vaccination site heals Elevated temperature 17% >100o F 1.4% >102o F Systemic symptoms (malaise, myalgias) 36% sufficiently ill to miss work, school, or recreational activities or had trouble sleeping |
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Smallpox: vaccine complications
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Fever: 70% of children develop fever
Postvaccine encephalitis: 1 in 300,000 vaccinees Progressive vaccinia: immunodeficient vaccinees Eczema vaccinatum: vaccinia lesions extend over previous area of eczema - treat with vaccinia IG Generalized vaccinia: blood-borne dissemination, lesions 6-9 days post-vaccination |
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dealths related to the samll pox vaccine
|
9 deaths in 1968 in 14 million vaccinees
Approximately 173 deaths per 270 million vaccinees Assumes all vaccinees are receiving primary vaccination Does not take into account the larger immunocompromised population |
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Contraindication to Vaccination (small pox)
|
In the event of bioterrorist attack, there are no contraindications to vaccination in exposed
Immunodeficiency / immunosuppressive tx HIV infection and AIDS Skin disorders – “eczema”, atopic dermatitis Ocular or periorbital disease Pregnancy |
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if someone is exposed to bioter small pox are there any CI for the vaccine
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nope
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New Smallpox Vaccines
|
Live vaccinia virus produced using cell culture technology
Modified vaccinia Ankara (MVA) VaxGen, Inc. California Developing new stronger vaccine |
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Cidofovir
|
Nucleotide analogue of cytosine
Broad spectrum of activity against herpesviruses Currently approved for treatment of CMV retinintis in persons with AIDS Activity against orthopoxviruses in cell-based and animal models Available for treatment of vaccinia under IND Second line treatment of complications of smallpox vaccination Use if patient fails to respond to VIG treatment 5 mg/kg IV during a 60 minute period; probenecid given to reduce risk of renal failure Second dose one week later may be considered |
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Cidofovir is a...
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anit-viral agent
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Cidofovir Adverse Events
|
Renal toxicity
Neutropenia Proteinuria Anterior uveitis/iritis Metabolic acidosis Possible carcinogenicity and teratogenicity Probenecid adverse events |
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Ribavirin
|
Still investigational
Data limited to case reports Adverse effects Severe anemia anti-viral |
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Yersinia pestis (Plague)
|
Enterobacteriaceae – gram (-) bacillus
Transmission Flea bites (infected from feeding on rats/rodents), handling infected animals, or exposure to persons or animals with plague pneumonia or cough Signs/symptoms Fever, chills, HA, fatigue Swollen gland in groin, armpit, or neck – “bubo” (bubonic plague) Pneumonia, sepsis Mortality 50-60% without treatment 14% in US with (early treatment is key) |
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S/S of the plague
|
Fever, chills, HA, fatigue
Swollen gland in groin, armpit, or neck – “bubo” (bubonic plague) Pneumonia, sepsis |
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treatment for the plague
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Treatment
First line Streptomycin or gentamicin (because the best data we have) Alternative Chloramphenicol or tetracyclines Fluoroquinolones |
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Botulinum toxins Clostridium botulinum
|
Anaerobic gram (+) spore forming rod
Biological weapon Aerosolized toxin Symptoms Symmetrical cranial neuropathies Difficulty swallowing or speaking, diplopia, dilated pupils Respiratory dysfunction (requiring mech vent) Flaccid paralysis Intact mental state |
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Botulism toxin treatment
|
Botulism Anti-Toxin
Neutralizing antibody Supportive care (respiratory support) very acute process will die quickly become paralyzed very quickly complete paralysis, cant even breath mentally all there |
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Francisella tularensis (Tularemia)
|
Aerobic gram-negative coccobacillus
Water, moist soil, hay, straw, animal carcasses No person to person transmission Infected arthopods can transmit through bites South-central and western states Symptoms High fever, headache, chills, rigors, myalgias Hemorrhagic airway inflammation, lymphadenopathy bleed into lungs |
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Tularemia vaccination
|
Live attenuated vaccine used to protect lab workers who work with the bacteria
Available as IND. Under review by the FDA |
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Tularemia treatment
|
Streptomycin or gentamicin x 10 days (1st line)
Chloramphenicol, tetracyclines x 14 days Ciprofloxacin |
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Health Care Providers in Emergency Preparedness
|
Preparedness and prevention
Detection and surveillance Diagnosis and characterization of agents Response Communication |
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Metropolitan Medical Response system (MMRS)
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CDC: National Pharmaceutical Stockpile (NPS)
|
NPS has 2 components: Push Package and VMI
Push Package: emergency response, Category A agents 50 ton packages held in 8 locations in U.S. delivery < 12h contents: pharmaceuticals, med supplies, equipment Vaccines antibiotics for: anthrax, plague, and tularemia prophylaxis for 250,000 people x 7 days treatment for 6,000 people x 60 days Vendor-managed inventory (VMI): CDC contract delivery within 24-36h plan: treat 12 million people (60d for anthrax) |
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VMI
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vender managed enventory, which is the second step in the stock pile porcess
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what is the 1st step in the stock pile process
|
NPS has 2 components: Push Package and VMI
Push Package: emergency response, Category A agents 50 ton packages held in 8 locations in U.S. delivery < 12h contents: pharmaceuticals, med supplies, equipment Vaccines antibiotics for: anthrax, plague, and tularemia prophylaxis for 250,000 people x 7 days treatment for 6,000 people x 60 days Vendor-managed inventory (VMI): CDC contract delivery within 24-36h plan: treat 12 million people (60d for anthrax) |
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How is the NPS deployed ?
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Event reported to local health and law enforcement officials via 911
State Dept of Health notifies Director of CDC Final decision to deploy NPS is made by: Director of CDC in conjunction with U.S. Surgeon General and Secretary of Health and Human Services Who should receive post-exposure prophylaxis? Decision made by local and federal public health officials investigating bioterrorism cases |
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Role of a Pharmacist in bioter attack
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The selection, handling, and deployment of medications and related supplies
Planning for providing interim treatment of patients before nationally stockpiled drugs arrive on scene Advise public health officials on appropriate public messages related to the use of medications Collaborate with physicians and other prescribers in the drug therapy management |
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bone structure
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Hematogenous osteomyletis
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Infection originates elsewhere, travels through blood to bone (bone often already injured)
Affected population Pediatrics IVDU, hemodialysis, sickle cell Slower onset of infection, symptoms occur gradually Considered acute despite slow development |
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what is the periosteum
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the hard outer layer of the bone
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classifications of osteomyelitis
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hematogenous
contiguous |
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osteomyelitis Contiguous - No vascular insufficiency
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Direct contact of organisms to bone tissue
Often secondary to trauma or surgery More localized area of infection Faster onset of symptoms and infection, classified as acute shortly after trauma or surgery |
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osteomyelitis Contiguous - Vascular insufficiency
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Usually originates from cellulitis or wound
Affects high-risk populations Patients with diabetes, PVD, neuropathies, decubitis ulcers Considered chronic in nature spread is very slow necorsis of the outside of the bone occurs result of DM, neuopathies, PVD |
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hematogenous osteomyelitis in <1 yr
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site involved:: invovled in long bones and joints
risk factors: prematurity, catheters |
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hematogenous osteomyelitis 1-20 yrs
|
site involved: long bones (femur, tibia, humerus)
risk factors: infection, sickle cell, trauma, puncture wound |
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hematogenous osteomyelitis >50 yrs
|
site involved: vertebrea
risk factors: DM, trauma, UTI, IVDA |
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Contiguous-
No Vascular Insufficiency in those 20-50 yrs |
site involved: Femur, Tibia, Mandible
risk factors: Hip/open fracture, surgeries, trauma |
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Contiguous-
Vascular Insufficiency in those >50 |
sites involved: Feet, Toes
risk factors: DM, PVD, neuropathies, trauma, pressure sores usually polymicrobial |
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how bone growth in children affects bone infections
|
Growth occurs at the metaphesis and it is highly vascularized (lots of caps) so it is easy for bacteria to get lodged in the bone
the madullary cavity becomes infected the periosteum is flexible in kids an dit keeps growing because it is still getting blood suply, but the bacteria cannot get out so the destory the inner bone |
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bone infections in adults
|
periosteum is hard and bone is thicker so the inside of the bone necorsis
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Osteomyelitis: Clinical Signs
|
Clinical Signs
Pain, swelling, fever, chills, malaise, erythema Often difficult to identify when secondary to trauma differ based on mode of transmission |
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Osteomyelitis: Diagnosis
|
Precipitating factors
Trauma Surgery Imaging CT, MRI, Ultrasound, X-Ray, Bone scan Laboratory evaluation ESR, WBC, CRP Bone biopsy and culture If abscess found, gram stain aspirate MRI is the most sensitive to see how much bone is involved may need to debride the bone so new bone can grow |
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Osteomyelitis: Etiology in Hematogenous Infections in Children
|
S. aureus (60-90%), Enterobacter, Haemophilus spp.
Neonates: S. aureus, Group B streptococci, E. Coli |
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Osteomyelitis: Etiology in Hematogenous Infections in adults
|
Vertebral: S. aureus (60%), E. coli
IVDA: S. aureus most common, Pseudomonas second Other Gram-negatives: Klebsiella, Serratia, Enterobacter > 50% of infections in the vertebral column Sickle cell: ~70% due to Salmonella secondary to bowel infarctions |
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Osteomyelitis: Etiology in Contiguous Infections with good blood flow
|
S. aureus most common
Enterobacter, Pseudomonas also seen Can really be just about anything! |
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Osteomyelitis: Etiology in Contiguous Infections with vascular insufficiency
|
Diabetic foot, PVD, decubitis ulcers most common
Consider source of infection Usually polymicrobial S. aureus, S. epidermidis Pseudomonas, E. coli, Proteus Anaerobes (previous fracture and diabetes = predisposing factors) POLYMICROBIAL |
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Management of Osteomyelitis
|
Surgical intervention often required
Debridement and removal of hardware Radiographic studies; MRI is most sensitive Radiographic-guided histological sampling Obtain culture & sensitivities to guide drugs Biopsy sample or swab sampling of drainage (important for infectious control purposes; S. aureus growth is highly correlated with deep seeded infection.) Acute osteomyelitis: Begin antibiotics ASAP (may avoid surgery) High-dose, IV antibiotics are standard Long durations are required Infection “walled off” with sequestra (dead bone) and involuca (new bone) Penetration of drugs becomes major consideration 4-6 weeks of therapy typical (up to 3 months) Takes 6 weeks for debrided bone to be covered with vascularized tissue Chronic osteomyelitis: High-dose IV initially, then PO x 6-12 months |
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what bug for bone infections are you coving in newborns
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S. aureus, streptococci, E. Coli
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what bug for bone infections are you covering in children <5 (don't need to know doses just wanted to remined you what drugs are used)
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S. aureus, streptococci
IV nafcillin 150mg/kg/day or IV cefazolin 100mg/kg/day |
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what bug for bone infections are you covering in children >5 and adults (don't need to know doses justwanted to remined you what drugs are used)
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S. aureus
IV nafcillin 150mg/kg/day or IV cefazolin 100mg/kg/day |
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what bug for bone infections are you covering in IVDA
(don't need to know doses just wanted to remined you what drugs are used) |
Pseudomonas, other Gram-negatives
IV ceftazidime 2g q8h plus IV tobramycin 5mg/kg/day |
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what bug for bone infections are you covering in Post-op, trauma patients
(don't need to know doses just wanted to remined you what drugs are used) |
Gram-positive and Gram-negative organisms
IV piperacillin/tazobactam 3.325 g IV q6h |
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what bug for bone infections are you covering in Pts with vascular insufficiency
(don't need to know doses just wanted to remined you what drugs are used) |
Gram-positives and Gram-negatives, anaerobes
IV Cefotetan 1-2g q12h IV piperacillin/tazobactam |
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IV Antibiotics for Osteomyelitis
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Clindamycin
Ceftazidime Ceftriaxone Cefazolin Nafcillin Ampicillin/sulbactam Piperacillin/tazobactam Vancomycin Ciprofloxacin |
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Eligibility for conversion to oral therapy for bone infections
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Confirmed infection with susceptible organism(s)
Improvement in signs/symptoms with IV therapy Compliant patient Agent with good absorption No DM/PVD No significant drug interactions Note that not all clinicians believe in oral therapy as an effective treatment option Home infusion therapy is another option when long-term therapy is needed but PO antibiotics are not an option |
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What AB are used for gram + bone infections
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Dicloxacillin
Cephalexin Clindamycin Fluoroquinolones Addition of Rifampin (+/- for sensitive staphylococci) |
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What AB are used for gram - bone infections
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Pseudomonas: ciprofloxacin
Other pathogens per susceptibilities |
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What AB are used for polymicrobial bone infections
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FQ + clindamycin or metronidazole
Amoxicillin/clavulanate |
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GK is a 13 yo female presenting to the ED after being thrown from her horse. There is clear evidence of a large, open wound. She reports that her arm hit the ground with traumatic force and in a pile of manure. Her forearm was crooked, with blood at the site of compound fracture. She pushed it back in. An ambulance arrives on the scene. Which type of osteomyelitis is she most at risk of developing?
Contiguous, with vascular insufficiency Contiguous, without vascular insufficiency Hematogenous She is at risk for both contiguous and hematogenous |
Contiguous, without vascular insufficiency
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HD, a 45 yo man, is admitted to the hospital with a suspected osteomyelitis in his right lower limb. His past medical history is significant for DM II x 13 years, hernia repair at age 41, and open fracture repair of right tibia 5 months ago. He drinks 3-4 alcoholic beverages per week. He was recently treated for 14 days with amoxacillin/clavulanate for an ulcer on his right foot. Which of the following is true?
Anaerobes should be covered empirically Bone aspirate should be cultured before therapy initiation Recent fracture and SSTI increases the risk of osteomyelitis All of the above are true |
All of the above are true
this is a very complicated patient the infection is not in direct contact with the bone |
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HD, a 45 yo man, is admitted to the hospital with a suspected osteomyelitis in his right lower limb. His past medical history is significant for DM II x 13 years, hernia repair at age 41, and open fracture repair of right tibia 5 months ago. He drinks 3-4 alcoholic beverages per week. He was recently treated for 14 days with amoxacillin/clavulanate for an ulcer on his right foot.
Tobramycin + cefazolin Clindamycin + ciprofloxacin Nafcillin + TMP/SMX Ampicillin/sulbactam The most appropriate choice for empiric treatment for HD’s osteomyelitis is: |
Clindamycin + ciprofloxacin
already had PCN so may have some R doesn't need pseudo coverage he is not an IVDA |
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Infectious Arthritis
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Septic arthritis due to bacterial pathogens is the most potentially dangerous and destructive form of acute arthritis.
can result in perminant joint damage damaged joints are at higher risk |
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Infectious Arthritis: Direct contamination of bone space
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Deep-penetrating wounds (bite wounds, IVDA, trauma to small joints of hands and feet most common)
Intraarticular steroid injection Arthroscopy, prosthetic joint surgery joints are very vascular |
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Infectious Arthritis: Hematogenous dissemination
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(most common)
Synovial tissue is highly vascular and susceptible to infection during bacteremia Neisseria gonorrhoeae infections travel this way, and joint is commonly involved in these infections. |
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Predisposing factors for septic arthritis (non-gonococcal) in adults with acutely painful joints (2 or more significantly increases the risk):
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Age greater than 80 years
Diabetes mellitus Rheumatoid arthritis Prosthetic joint Recent joint surgery Skin infection, cutaneous ulcers IV drug abuse, alcoholism Previous intra-articular corticosteroid injection |
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Poor joint outcomes occur in over 30% of patients recovering from septic arthritis.
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Elderly patients, presence of preexisting joint disease, or patients with joint containing infected material are likely to experience reduced joint mobility upon recovery.
Cartilage degradation is accelerated in the presence of purulent exudate accumulation and alteration in synovial blood flow. |
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Disseminated Gonococcal Infectious Arthritis
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Result from bacteremia following untreated genitourinary gonococcal infection.
Recent exposure to sexual encounters should raise suspicion of gonococcal infectious arthritis when symptomatic patients present. Young women with h/o untreated genitourinary tract infections due to asymtomatic infxn prior to bacteremia. Population most affected are women 15-50, otherwise healthy. Co-infection with Chlamydia trachomatis reported in 20-40% patients with gonococcal infection |
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Disseminated Gonococcal Infectious Arthritis clinical presentation
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Fever (especially children, but often absent in elderly)
Painful swollen joints, unless patient taking DMARDS or corticosteroids Note: Infectious Arthritis can be difficult to differentiate from RA flair Effusion, restriction of motion, tenderness, joint warmth “Classic Triad” of Neisseria gonorrhoeae infectious arthritis includes migratory polyarthritis, dermatologic lesions, tenosynovitis in addition to systemic inflammatory symptoms. |
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is a joint effusion painful
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yep
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is bursitis painful
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nope
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Disseminated Gonococcal Infectious Arthritis Laboratory Finds
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↑ ESR (erythrocyte sedimentaion rate)
Leukocytosis with left shift (50% of patients) Blood cultures (may or may not be positive) (gonococcal is hard to grow so have to look at the patient factors) Elevated lactic acid in sinovial fluid (nongonoccal infections only) Positive culture of synovial fluid Elevated synovial fluid leukocyte count (50,000 – 100,000 cells/mm3) unless on immunosuppressive agents for RA. Gonococcal: Simultaneous culture of synovial fluid and cervix, urethra, and/or rectum should be obtained. Culture of synovial fluid are positive in < 50% of cases |
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Clinical differentiation between gonococcal (G) and nongonococcal (NG) arthritis patient characteristics
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G: Sexually active young adults, female>male
NG: Newborns or adults with chronic disease (RA, OA, DM) |
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Clinical differentiation between gonococcal (G) and nongonococcal (NG) arthritis presentation
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G: Migratory polyarthritis, dermatitis, tenosynovitis
NG: Single joint involvement |
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Clinical differentiation between gonococcal (G) and nongonococcal (NG) arthritis pattern of joint involvement
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G: Polyarticular ~ 50%
NG: Mono or oligoarticular ~ 90% |
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Clinical differentiation between gonococcal (G) and nongonococcal (NG) arthritis culture positivity
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G: Less than 50%
NG: nearly 90% |
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Clinical differentiation between gonococcal (G) and nongonococcal (NG) arthritis prognosis
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G: Good with adequate antibiotic therapy
NG: Usually bad prognosis (predisposing factors make more complicated) |
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Infectious Arthritis Microbiology (non-gonococcal)
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S. Aureus most common
Group A Streptococcus and Pneumococcus Gram negative (10-20% of infections, and secondary to bacteremia associated with GI or UTI) E. coli and P. aeruginosa most common Anaerobes: 5-7% of cases Wound infections, joint arthroplasty, or immunocompromised hosts. |
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Treatment (non-gonococcal)
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Antibiotics (empiric, then pathogen directed)
Joint drainage every 5-7 days as needed Joint rest |
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Infectious Arthritis AB therapy general principles
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General Principles
Treatment must begin immediately after clinical evaluation and appropriate cultures have been taken. Initially managed with intravenous antibiotics, most have good penetration into joint space. Intra-articular antibiotics are not appropriate for septic arthritis Length of therapy varies but a total of 3-4 weeks is typical, with 15-21 days of IV antibiotic initially and course completion with oral antibiotics |
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Infectious Arthritis AB empiris therapy
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Neonates: broad-spectrum with [nafcillin or oxacillin or vanco] + [gentamicin or cefotaxime]
Children age < 5: nafcillin or oxacillin or cefazolin Age > 5 and adults: empirically treat with vanco + cefotaxime or ceftazdime or (celphlasorin allergy FQ or AG), then tailor to gram stain and culture results. Bite wounds infecting joints: Cefuroxime or pip/tazo or ampicillin/sulbactam Gonococcal: Ceftriaxone rest the joint to prevent further damage |
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Pathogen-Directed Treatment for infectious arthritis
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gram +: Cefazolin 2 g or cefotaxime 1 IV g q 8 hr
MRSA: Vancomycin 1 g IV Q 12 h Non-psuedo, gram - rods: Ceftriaxone 1 g IV Q 24 h P. Aeruginosa: [Cefepime or piperacillin-tazobactam or ceftazidime or ciprofloxacin] + aminoglycoside Gonococcal Initial: ceftriaxone 1 g IV q 24 hrs As long as confirmed culture and sensitivity, switch to oral amoxicillin or doxycycline or tetracycline on the 4th day of therapy Duration is 7-10 days, since organism responds will to antibiotics. |
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Infective Endocarditis
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Turbulent blood flow from congentital or acquired heart disease results in endothelial damage
Infection of valves is most common 75-95% of IE cases involve native valves, 5-25% prosthetic valves Affects 10,000 - 20,000 persons annually in U.S. 4th leading cause of life-threatening infectious syndromes Nearly 2/3 of cases are male Most commonly occurs in persons >50 years of age Mortality rates range from 5% to 50% depending on pathogens and risk factors |
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Endocarditis =
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infection of endocardium (membrane lining the chambers of heart and cusps of heart valves)
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Pathophysiology of Endocarditis
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Endothelial surface of heart damaged through blood-flow turbulence and/or high pressures associated with valvular lesions or other pathology
Immune-mediated processes can also lead to tissue injury (e.g. rheumatic fever) Bacteria may directly adhere to prosthetic valves Platelet and fibrin deposition occurs at site of injury Bacteremia (either transient or sustained) results in colonization of damaged epithelial surface Continued deposition of platelets and fibrin forms infected “vegetations” Bacterial loads may reach 1010 organisms/gram of veg. Infected vegetations are resistant to penetration of both host immune defenses (e.g. leukocytes) and antibiotics |
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high risk for endocarditis
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Prosthetic valves (400x risk)
Cyanotic congenital heart disease (e.g. single ventricle) Non-valvular intracardiac prostheses Surgical reconstruction of cardiac anatomy h/o previous endocarditis (400x increases risk) |
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moderate risk for endocarditis
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Rheumatic heart disease
Hypertrophic cardiomyopathy Mitral valve prolapse Aortic or mitral regurgitation Congenital bicuspid aortic valve Central IV lines - right atrium Intravenous drug use |
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non-ivda valvular involvement
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Mitral: 28 - 45%
Aortic: 5 - 36% Mitral + Aortic: 0 - 35% Tricuspid: 0 - 6% Pulmonic: rare |
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ivda valvular involvement
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(IVDA and IVDU)
involves the trisupid (right sided) not only IVDA get Tricuspid: 50% Aortic: 18% Mitral: 11% Mitral + Aortic: 12% |
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Complications of IE
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Inflamed valves become thickened, may adhere to surrounding tissue valvular insufficiency, regurgitation
Leads to acute or chronic heart failure Continued inflammation & destruction of valvular tissue may also lead to: Perforation of valve leaflets Rupture of chordae tendineae, papillary muscles Valvular stenosis 2o scarring Valvular or myocardial abscesses Myocardial conduction defects, arrhythmias |
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Complications of IE (cont.)
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Embolic complications may result from fragments of vegetations breaking off into bloodstream
“Septic emboli” may result in abscesses or infarction in multiple organs downstream from infection Right-sided vegetations pulmonary emboli Left-sided vegetations emboli to brain, spleen, kidneys, liver, eyes, heart, skin, bone Most common presenting feature in developed countries Circulating immune complexes may deposit in organs & tissues, producing local inflammation and damage Glomerulonephritis, skin lesions (bodies response to Iand gs being depositied in tissues) Bacteremic complications such as sepsis and abscess |
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Microbial Etiology of IE
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Gram-positive bacteria
Streptococci 55-65% Viridans streptococci 30-40% Other streptococci 15-25% Staphylococci 25-35% S. aureus 10-27% Coag.-negative staph. <5% Enterococcus 5-18% Gram-negative aerobic bacilli 2-13% Fungi 2-4% |
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Viridans Streptococci in IE
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Commonly found as part of normal flora in oropharynx
Among most common pathogens in native-valve endocarditis (30-40% of cases) Almost always in presence of risk factors (e.g. cardiac abnormalities) due to overall low virulence of pathogen Most common cause of IE in persons > 50 y.o. (because have under lying heart problem) Streptococcus bovis causes 15-25% of IE cases. Treated pharmacologically the same as S. viridans not a very virulent organism |
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Staphylococci in IE
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Staphylococcus aureus
Very virulent organism, capable of causing infection even in normal valves (patients with no risk facotrs) Causes 50% of endocarditis in IVDU Staphylococcus epidermidis Less virulent, rarely effects normal valves Common cause of prosthetic-valve endocarditis Greatest risk within 2 months of valve replacement |
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Enterococci in IE
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Gram positive organisms which reside in GI tract
Causes 15% of endocarditis in IVDU GU & GI procedures most commonly associated with enterococcal endocarditis GU manipulation because present in the urethra E. faecalis & E. faecium most common pathogens |
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Why Staph, Strep, and Enterococcus in IE??
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Adhesins
Attach readily to fibrin-protein matrix of not yet infected Also attach to matrix proteins that coat implantable medical devices before they endothelialize. This is basis for Early Prosthetic Valve Endocarditis (PVE). If < 2 months since valve replacement: S. aureus and epidermidis (nosocomial usually the cause – direct inoculation of through post-op hematogenous spread) likely. By > 12 months since replacement surgery, etiology is same as native valve endocarditis. This is termed Late PVE. For both Early and Late PVE, duration of treatment is longer and includes rifampin in addition to longer course of gentamicin for treatment of S. aureus. |
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Weird causes of IE: Gram Negatives
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Gram-negative aerobic rods
Unusual cause of endocarditis (no adhesins) Still a possibility in patients with PVE IVDUs at greater risk Pseudomonas aeruginosa and Serratia spp. have commonly been reported, often linked to shared use of contaminated paraphernalia “HACEK” organisms Haemophilus spp. H. parainfluenzae, H. aphrophilus, H. paraphrophilus Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingella kingae Gram-negative bacilli or coccobacilli Slow growing, fastidius organisms not easily isolated on common agars/media |
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HACEK” organisms
(IE) |
organisms that colonize the GIT, respiratory tract
Haemophilus spp. H. parainfluenzae, H. aphrophilus, H. paraphrophilus Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingella kingae |
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More Weird Cause of IE: Fungal
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Candida spp. most common cause of fungal IE
Aspergillus spp. (rare) At-risk patient populations: Immunocompromised hosts IVDUs Patients with chronic indwelling IV lines Prosthetic heart valves Surgery usually required for effective management most likely polymicrobial |
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Culture negative Endocarditis
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#1 cause is prior antibiotic use
Get cultures and TEE before starting antibiotic therapy Others associated with organism: HACEK Legionella, Chlamydia Bartonella, Brucella, Burnetti (Q Fever) Fungal Alternative method if identification: Collect serologies Hold cultures for 21-days PCR of emboli or valvular vegetation Does not provide susceptibility data, persists despite clinical cure Use growth media recommended for suspected organism |
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when fo you try to get cultrues for IE
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hour 1 and then 12 later therefore making sure it is not transient bacteremia
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Clinical Signs & Symptoms of IE acute
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Marked toxicity
Sepsis frequent Progresses over days to weeks Metastatic infections frequent (abseses in other parts of he body) Usually caused by S. aureus |
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Clinical Signs & Symptoms of IE subacute
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Modest toxicity (fever, chills, night sweats, weight loss, malaise)
Progresses over weeks to months Metastatic infections unusual Most common with streptococci, other staphylococci, enterococci, Gram-negatives |
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Diagnosis of IE is often difficult
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Incorporates clinical, laboratory, & echocardiographic findings
“Duke Criteria” based on presence of major and minor criteria |
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Examples of Modified Duke major Criteria for IE
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> 2 positive blood cultures drawn > 12 hrs apart, or
3 of 4 separate blood cultures positive Single positive blood culture positive for Coxiella burnetii, or Antiphase I immunoglobulin G antibody titer > 1:800. Evidence of endocardial involvement TEE or TTE, abscess identification, new or worsening murmur |
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Examples of Modified Duke minor Criteria for IE
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High risk for IE, IVDA, blood cultures (2 out of 4), physical findings
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Friable vegetation (IE) -->
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septic emboli-->organ abscess or infarction (hematogenous seeding)
above may be responsible for skin manifestations observed in patients with IE. |
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Formation of immune complexes (IE)-->
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organ deposition --> local inflammation/organ damage
above may be responsible for skin manifestations observed in patients with IE. |
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Non-specific constitutional symptoms commonly seen in subacute infections in IE
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Low grade fever (< 39oC) 80 - 85%
Chills 42 - 75% Malaise, generalized fatigue 25 - 40% Anorexia 25 - 55% Weight loss 25 - 35% Night sweats |
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cliical signs of IE
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Fever 80 - 90%
Heart murmur (sometimes new or changing) 80 - 85% Peripheral “stigmata” of IE Petechiae 10 - 40% Splinter hemorrhages 5 - 15% Osler’s nodes 7 -10% Janeway lesions 6 - 10% Roth spots 4 - 10% Embolism-related organ dysfunction Splenomegaly |
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Embolic Signs of IE: Splinter Hemorrhages
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not specific to IE
linear heorrhages on finger nails or toe nails emboli that damages tissue |
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Peripheral Signs of IE: Osler’s Nodes
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indicative of a hemmorhage somewhere
nodule, purple hurts |
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Embolic Signs of IE: Janeway Lesions
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indicative of a hemmorhage somewhere
shows up on hands and feet |
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Embolic Signs of IE: Roth Spots
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signs of hemmorhage in the retina
circular w/ white center |
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Clinical Signs & Symptoms of IE
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Laboratory findings (lack specificity):
WBC may be normal or only slightly elevated anemia ESR, CRP Abnormal UA (proteinuria, microscopic hematuria) Blood cultures are cornerstone of diagnosis due to continuous bacteremia with IE. Cultures provide live bacterial for susceptibility testing. Collect blood cultures over 24 hr period before starting therapy unless patient is acutely ill. If acutely ill, 3 sets drawn 30 min apart is appropriate. Echocardiogram Transthoracic (TTE) = 40-63% sensitive Transesophageal (TEE) = 90-100% sensitive (more invasive) |
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In IE why may WBC levels be normal
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because the bacteria is protected from the immune system
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General Considerations in Treatment of Infective Endocarditis
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Empiric Therapy
Antibiotic selection dependent on certain factors: IVDU vs. non-IVDU Native vs. prosthetic valve If prosthetic, when was surgery performed (early versus late PVE) History of valvular disease Suspected pathogens Antibiotics should be high-dose, parenteral, and bactericidal Penetration into vegetations, lack of effective immune response are major considerations Determination of MICs important |
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usual empiric theay for IE
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= vancomycin + gentamicin
Modification of therapy based on subsequent cultures & susceptibilities is crucial. -lactams preferred over vancomycin if organism is susceptible. Addition of gentamicin to many regimens is based on good penetration into vegetations, rapid clearance of bacteremia resulting in patient feeling better. Aminoglycosides have not been shown to reduce mortality in most types of IE Aminoglycosides usually used for ≤2 weeks due to toxicity concerns, lack of proven benefits with longer duration At this time, extended interval dosing is appropriate for Streptococcal infections only. |
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AHA Guidelines for Treatment of IE viridans
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Viridans Streptococci and S. Bovis (PCN MIC < 0.12 mcg/ml)
PCN G IV 12-18 MU/ 24 hrs x 4 weeks Ceftriaxone 2 g IV q 24 hrs x 4 weeks Short course: PCN G IV or ceftriaxone IV + gentamicin x 2 weeks (short course = low risk patients only) PCN allergy: Vancomycin IV x 4 weeks (NO gentamicin) (PCN MIC > 0.12mcg/ml, < 0.5mcg/ml) PCN G IV x 4 weeks + gentamicin IV x 2 weeks PCN allergy: Vancomycin IV x 4 weeks (NO Gentamicin) |
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AHA Guidelines for Treatment of IE staphylococcus aureus
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Staphylococcus aureus
Nafcillin IV x 4-6 weeks +/- gentamicin IV* x 3-5 days or Cefazolin IV x 4-6 weeks +/- gentamicin IV x 3-5 days PCN allergy or MRSA: Vancomycin IV 6 weeks May consider 2 week course in IVDA with uncomplicated right-sided MSSA. If prosthetic valve: add rifampin to therapy for MSSA and MRSA (if susceptible) Provided CrCl > 30 mL/min, then gentamicin is added for 2 weeks to either beta lactam or vancomycin.(adding vanco because want good penetration) treat for > 6 weeks |
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AHA Guidelines for Treatment of IE enterococcus
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Enterococcus
Must be treated with 2 drugs including a cell wall active agent an aminoglycoside (target peaks 3-4 mcg/mL) Culture and sensitivity should tailor therapy Treat for 6 weeks, unless resistant organism. Then, treat for > 8 weeks with susceptible combination antibiotic therapy Empiric Options: Base on risk factors and local susceptibility patterns [ampicillin or high dose Penicillin G] + [gentamicin or streptomycin] or Vancomycin + [gentamicin or streptomycin] |
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General Considerations for IE
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Durations of intravenous therapy will be long, i.e. 4-6 weeks
Surgery may be required: Certain pathogens (e.g. coagulase-negative staphylococci, Candida) Prosthetic heart valves (placement or replacement) Severe cases with myocardial complications (e.g., valvular dysfunction, abscess, failure to resolve vegetations) |
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Because of the long treatment durations for IE required and the frequent occurrence of significant complications, appropriate monitoring of patients is crucial
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Prompt recognition of complications
Proper drug dosing Favorable response to therapy Minimizing adverse effects of drugs Renal failure: interstitial nephritis (PCN, gentamicin, vancomycin) Ototoxicity Drug related fever Newly developed allergy |
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Prognosis of IE
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Rapid and correct diagnosis improves outcomes
Increased mortality associated with: Heart failure Culture-negative endocarditis Resistant organisms Left sided endocarditis caused by S. aureus Prosthetic-valve (PV) endocarditis Relapses usually occur within 2 months of treatment completion enterococcal and PVE most frequently associated. If valve is replaced, morbidity remains elevated due to need for anticoagulation, risk of valve thrombosis, or additional surgeries. (long term complications ass. with anti-coag) |
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DG is a 56 yo male who presents to the ED with chest pain, fatigue, muscle pain and low-grade fever that he states has progressed over the last week. His past medical history includes hypertension and mitral valve replacement 6 weeks ago. Laboratory values reveal elevated ESR and CRP, and thrombocytopenia. Medications include warfarin, metoprolol, and lisinopril. The medical team suspects infective endocarditis. What is the most likely pathogen?
H. influenza S. viridans Staphylcoccus spp. Enterococcus spp. |
Staphylcoccus spp.
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DG is a 56 yo male who presents to the ED with chest pain, fatigue, muscle pain and low-grade fever that he states has progressed over the last week. His past medical history includes hypertension and mitral valve replacement 6 weeks ago. Laboratory values reveal elevated ESR and CRP, and thrombocytopenia. Medications include warfarin, metoprolol, and lisinopril. The medical team suspects infective endocarditis. The most appropriate choice for empiric treatment for DG’s endocarditis is:
PCN G Procaine + gentamicin nafcillin + gentamicin ampicillin / sulbactam Vancomycin + gentamicin |
Vancomycin + gentamicin
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