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Edward Island)

Canada (N/A)

GPCs utilisés pour le GUO sur la

rhinosinusite Données contextuelles

Populations cibles Otherwise healthy

hosts and compromised hosts of all age groups.

Methicillin- Resistant Staphylococcus aureus Infections in Adults and Children.

Suspected skin/soft tissue infection in children > 44 weeks CGA.

Management of common infectious diseases presenting to the ED.

Non-spécifié Chow 2012:

Children and Adults Desrosiers 2011:

Limited to the adult population

Rosenfeld 2015:

Adults Skye 2013:

Non-immune compromised adults Wald 2013:

Children Aged 1 to 18 Years

Généralités Pathogènes Combined data from

specimen cultures, serologic studies [41, 48–51], and other methods (eg,

immunohistochemical staining to detect antigens in skin

In the pre–CA MRSA era, microbiologic investigations using needle aspiration or punch biopsy cultures of

nonpurulent cellulitis

Nonpurulent cellulitis is usually due to group A streptococci (although studies are limited due to the difficulty culturing from these infections)

∅ Pathogens in typical cellulitis can include β-hemolytic

Streptococcus (Group A, B, C, and G) with Group B more common with diabetics, PVD, recurrent infections,

Rhinosinusites bactériennes (pouvant se compliquer en cellulite

périorbitaire/orbitaire:

Chow 2012, Desrosiers

Dumaresq 2016, CISSS Chaudière-Appalaches : Les streptocoques bêta-hémolytiques (groupes A, B, C et G) sont les

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(score 57)

Nassisi 2012 États-Unis Qualité modérée

(score 51)

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biopsies [51, 52]), suggests that the vast majority of these infections arise from streptococci, often group A, but also from other groups, such as B, C, F, or G.

Staphylococcus aureus less frequently causes cellulitis, but cases due to this organism are typically associated with an open wound or previous penetrating trauma, including sites of illicit drug injection.

MRSA is an unusual cause of typical cellulitis. A prospective study of patients with cellulitis in a medical center with a high incidence of other MRSA-related SSTIs demonstrated that treatment with β-lactams, such as cefazolin or oxacillin, was successful in 96%

of patients, suggesting that cellulitis due to MRSA is uncommon

identified b-hemolytic

streptococci and S.

aureus as the main pathogens.

In the majority of cases, a bacterial etiology was not identified, but MSSA was the most common pathogen among those who were culture positive [128–133]. A retrospective case-control study in children with nonpurulent cellulitis found that,

compared with b-lactams, clindamycin provided no

additional benefit, whereas TMP-SMX was associated with a slightly higher failure rate [134].

The only prospective study of

nonculturable cellulitis among hospitalized inpatients found that b-hemolytic

streptococci (diagnosed by acute- and

Purulent cellulitis may be caused by MSSA, MRSA, or group A streptococci (GAS).

• Approximately 27%

of S. aureus isolates from wounds are MRSA at Seattle Children’s (2012-13 data)

trauma/excoriation, and lymphedema.

Staphylococcus aureus in

non-immunocompromised patients typically presents with folliculitis or trauma leading to an abscess. Community acquired MRSA can occasionally present as streptococcal disease above.

Outside of water exposure, bites, burns, or trauma (including through footwear), Gram-negatives do not have a significant role in an immunocompetent host.

2011, Rosenfeld 2015, Skye 2013, Wald 2013:

Streptococcus pneumoniae,

Haemophilus influenza, Moraxella catarrhalis, Staphylococcus aureus,

Autres pathogènes Chow 2012, Desrosiers 2011, Skye 2013 : Streptococcus pyogenes (or other streptococcus), oral anaerobes Autres pathogènes Chow 2012, Desrosiers 2011 :

gram-negative bacilli

principaux agents étiologiques des cellulites /érysipèles.

Tétrault 2016, INSPQ/LSPQ : La proportion de souches de SARM parmi le nombre total de

Staphylococcus aureus isolés de pus superficiels et pus profonds de la peau et des tissus mous de patients provenant de la communauté est de 10 %. Ce taux varie de 4 à 15 % selon les régions, en excluant les régions

«Nunavik, Baie James»

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Hospital) États-Unis Qualité modérée

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and treatment for that organism is usually unnecessary [50]

In nonpurulent cellulitis, the clinical isolation rate of a pathogen is <20%.

This leaves the modern clinician with an unconfirmed diagnosis 80% of the time.

Several other organisms can cause cellulitis, but usually only in special circumstances, such as animal bites, freshwater or saltwater immersion injuries, neutropenia, or severe cell-mediated

immunodeficiency.

(Animal bites) Purulent bite wounds and abscess are more likely to be polymicrobial (mixed aerobes and anaerobes), whereas nonpurulent wounds commonly yield staphylococci and streptococci [156, 157].

Pasteurella species are commonly isolated from both nonpurulent

convalescent-phase serological testing for anti-streptolysin-O and anti-DNase-B antibodies or positive blood culture results) accounted for 73%

of the cases; despite the lack of an identifiable etiology in 27% of cases, the overall clinical response rate to b-lactam therapy was 96% [135]. Although additional research is needed to characterize the microbiology of nonpurulent cellulitis, currently available data suggests that b-hemolytic

streptococci may be the primary

pathogen.

Among patients presenting with purulent SSTI to 11 emergency departments throughout the United States, CA-MRSA was the

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wounds with or without lymphangitis and from abscesses.

Additionally, nonpurulent wound infections may also be polymicrobial [156].

Human bites may occur from accidental injuries, purposeful biting, or closed-fist injuries. The bacteriologic

characteristics of these wounds are complex, but include aerobic bacteria, such as Streptococci, S. aureus, and Eikenella

corrodens, as well as with multiple anaerobic organisms, including Fusobacterium, Peptostreptococcus, Prevotella, and Porphyromonas species.

Compléments d’information tirés du GPC IDSA 2005:

Many other infectious agents can produce cellulitis, but usually only in special

circumstances. With cat or dog bites, for

dominant organism, isolated from 59% of patients, followed by MSSA (17%); b- hemolytic streptococci accounted for a much small

proportion (2.6%) of these infections [11].

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example, the organism responsible is typically Pasteurella species, especially P. multocida, or Capnocytophaga canimorsus. A.

hydrophila may cause cellulitis following immersion in fresh water, whereas infection after saltwater exposure can arise from Vibrio species, particularly V. vulnificus in warm climates.

Periorbital cellulitis due to Haemophilus influenza can occur in children. Diagnostic and therapeutic considerations of this infection have been reported by the Committee on Infectious Diseases, American Academy of Pediatrics [6]. In neutropenic hosts, infection may be due to Pseudomonas

aeruginosa or other gram-negative bacilli, and in patients infected with HIV, the

responsible organism may be Helicobacter cinaedi [71].

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of America) États-Unis Qualité modérée

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Occasionally, Cryptococcus neoformans causes cellulitis in patients with deficient cell-mediated immunity.

The predominant pathogens in bite wounds are the normal oral flora of the biting animal, along with human skin organisms and occasional secondary invaders (e.g., S. aureus and S.

pyogenes).

The average wound yields 5 types of bacterial isolates (range, 0–16 types of bacterial isolates), with

∼60% yielding mixed aerobic and anaerobic bacteria. Pasteurella species are isolated from 50% of dog bite wounds and 75% of cat bite wounds.

Staphylococci and streptococci are found in ∼40% of bites from both types of animals.

Facultative gram-negative rods are uncommon.

Bacteroides species,

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fusobacteria, Porphyromonas species, Prevotella heparinolytica, proprionibacteria, and peptostreptococci are common anaerobes isolated from both dog bite wounds and cat bite wounds [113].

The bacteriologic characteristics of these [human bite] wounds reflect the normal oral flora of the biter, with streptococci (especially viridans streptococci) in 80% of wounds, as well as staphylococci, Haemophilus species, and Eikenella

corrodens as prominent aerobic pathogens [112, 115].

Définition

“Cellulitis” and

“erysipelas” refer to diffuse, superficial, spreading skin infections. The term

“cellulitis” is not appropriate for

cutaneous inflammation associated with collections of pus, such as in septic bursitis,

∅ Cellulitis is an infection of the skin and underlying soft tissue. It is

characterized by pain, erythema, edema and warmth.

- Purulent cellulitis is cellulitis associated with drainage or

∅ ∅ ∅ ∅

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furuncles, or skin abscesses. For example, when cutaneous redness, warmth, tenderness, and edema encircle a suppurative focus such as an infected bursa, the appropriate terminology is “septic bursitis with

surrounding

inflammation,” rather than “septic bursitis with surrounding cellulitis.” This distinction is clinically crucial, for the primary treatment of cellulitis is antimicrobial therapy, whereas for purulent collections the major component of management is drainage of the pus, with antimicrobial therapy either being unnecessary or having a subsidiary role (Figure 1 and Table 2).

exudate, currently or by history. A drainable abscess may or may not be present.

- Nonpurulent cellulitis has no drainage, exudate or abscess present.

Autres These infections arise

when microbes breach the cutaneous surface, especially in patients with fragile skin or diminished

∅ ∅ ∅ ∅ Desrosiers 2011:

Periorbital or orbital cellulitis is the most common complication of Acute Bacterial RhinoSinusitis and

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local host defenses from such conditions as obesity, previous cutaneous trauma (including surgery), prior episodes of cellulitis, and edema from venous insufficiency or lymphedema

[36, 37]. The origin of the disrupted skin surface may be obvious, such as trauma, ulceration, and preexisting cutaneous inflammation, but often the breaks in the skin are small and clinically unapparent.

These infections are most common on the lower legs.

Compléments d’information tirés du GPC IDSA 2005:

The origin of the disrupted cutaneous barrier may be trauma, preexisting skin infections such as impetigo or ecthyma, ulceration, fissured toe webs from maceration

most often caused by acute ethmoid and/or frontal disease [36,37].

Infection spreads from the sinuses to the orbit with relative ease [38,39].

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or fungal infection, and inflammatory

dermatoses, such as eczema.

Prévention

Facteurs de risque et mesures préventives Patients with a previous

attack of cellulitis, especially involving the legs, have annual recurrences rates of about 8%–20% [65–

67].

Edema, especially lymphedema and other local risk factors such as venous insufficiency, prior trauma (including surgery) to the area, and tinea pedis or other toe web abnormalities [65–71], increase the frequency of

recurrences. Other predisposing conditions include obesity, tobacco use, a history of cancer, and homelessness [66, 67, 71].

Addressing these factors might decrease the frequency of recurrences, but evidence for any such a

Recurrent SSTIs Preventive educational messages on personal hygiene and appropriate wound care are recommended for all patients with SSTI.

Instructions should be provided to:

i. Keep draining wounds covered with clean, dry bandages (A-III).

ii. Maintain good personal hygiene with regular bathing and cleaning of hands with soap and water or an alcohol-based hand gel, particularly after touching infected skin or an item that has directly

contacted a draining wound (A-III).

∅ ∅ Foot Care.

Treatment of tinea pedis.

Control of eczema.

MRSA decolonization (selective)

∅ ∅

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benefit is sparse.

Elevation of the affected area and treatment of

predisposing factors, such as edema or underlying cutaneous disorders, are

recommended (strong, moderate) In lower-extremity cellulitis, clinicians should carefully examine the interdigital toe spaces because treating fissuring, scaling, or maceration may eradicate colonization with pathogens and reduce the incidence of recurrent infection (strong, moderate).

The source of these pathogens is frequently unclear, but in many cases of leg cellulitis, the responsible streptococci reside in macerated, scaly, or fissured interdigital toe spaces [53, 54]. This observation

underscores the importance of detecting

iii. Avoid reusing or sharing personal items (eg,

disposable razors, linens, and towels) that have contacted infected skin (A-III).

Environmental hygiene measures should be

considered in patients with recurrent SSTI in the household or community setting:

Decolonization may be considered in selected cases if:

i. A patient develops a recurrent SSTI despite optimizing wound care and hygiene measures (C-III).

ii. Ongoing transmission is occurring among household members or other close contacts despite optimizing wound care and hygiene measures (C-III).

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and treating tinea pedis, erythrasma, and other causes of toe web abnormalities.

Identify and treat predisposing conditions such as edema, obesity, eczema, venous insufficiency, and toe web

abnormalities (strong, moderate).

These practices should be performed as part of routine patient care and certainly during the acute stage of cellulitis (strong, moderate).

Compléments d’information tirés du GPC IDSA 2005:

Surgical procedures that increase the risk for cellulitis,

presumably due to disruption of lymphatic drainage, include saphenous venectomy [49, 50], axillary node dissection for breast cancer [51, 52], and operations for gynecologic malignancies that

Decolonization strategies should be offered in

conjunction with ongoing reinforcement of hygiene measures.

Oral antimicrobial therapy is recommended for the treatment of active infection only and is not routinely recommended for decolonization (A-III). An oral agent in combination with rifampin, if the strain is susceptible, may be considered for decolonization if infections recur despite above measures (CIII).

In cases where household or interpersonal transmission is suspected:

i. Personal and environmental hygiene measures in the patient and contacts are recommended

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involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical

hysterectomy [53, 54].

III).

ii. Contacts should be evaluated for evidence of S.

aureus infection:

a. Symptomatic contacts should be evaluated and treated (A-III); nasal and topical body decolonization strategies may be considered following treatment of active infection

(C-III).

b. Nasal and topical body decolonization of asymptomatic household contacts may be considered (C-III).

Antibiotiques en prophylaxie Administration of

prophylactic antibiotics, such as oral penicillin or erythromycin bid for 4–52 weeks, or intramuscular benzathine penicillin every 2–4 weeks, should be considered in patients who have 3–4 episodes of cellulitis per year despite attempts to treat or control predisposing factors

∅ ∅ ∅ ∅ ∅ ∅

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(weak, moderate).

This program should be continued so long as the predisposing factors persist (strong,

moderate).

Two randomized trials using twice-daily oral penicillin or

erythromycin demonstrated a substantial reduction in recurrences among the antibiotic recipients compared to controls [72, 73]. An

observational trial of monthly intramuscular injections of 1.2 million units of benzathine penicillin found that this regimen was beneficial only in the subgroup of patients who had no identifiable

predisposing factors for recurrence [74]. In a study of patients with recurrent cellulitis involving arm

lymphedema caused by breast cancer

treatment, 2.4 million units of biweekly intramuscular

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benzathine penicillin seemed to reduce the frequency of episodes, but there was no control group [75]. The duration of therapy is indefinite, and infections may recur once prophylaxis is discontinued.

For example, a recent double-blind

comparative trial demonstrated that phenoxymethyl-penicillin given as 250 mg twice daily for 12 months increased the time to recurrence to 626 days compared with 532 days in the control group and decreased the

frequency of recurrence from 37% to 22% [76].

Symptômes These infections cause

rapidly spreading areas of erythema, swelling, tenderness, and warmth, sometimes accompanied by lymphangitis and inflammation of the regional lymph nodes.

∅ • Erythema, warmth,

edema universally present

• Induration or fluctuance (the latter diagnostic of fluid collection) may be present

∅ ∅ Rosenfeld 2015:

Patients with a reconfirmed diagnosis of ABRS who fail treatment, especially those with a worsening pattern of illness, should be examined for complications that include orbital or intracranial spread of

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The skin surface may resemble an orange peel (peau d’orange) due to superficial cutaneous edema surrounding hair follicles and causing skin dimpling because the follicles remain tethered to the underlying dermis.

Vesicles, bullae, and cutaneous

haemorrhage in the form of petechiae or ecchymoses may develop.

Systemic

manifestations are usually mild, but fever, tachycardia, confusion, hypotension, and leukocytosis are sometimes present and may occur hours before the skin abnormalities appear.

Surgical Site Infections (SSIs) rarely occur during the first 48 hours after surgery, and fever during that period usually arises from noninfectious or

• When first

• When first

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