In patients with liver disease, vibrio vinificulis is a risk if eating or working with shellfish or sea water. Similiar syndrome caused by aeromonas hydrophilia is caused by freshwater
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HIV |
IVDA |
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Splenomegaly |
ETOH |
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heart murmur or any prosthetics |
Steroids |
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Chemotherapy |
Diabetes |
(from EM Reports)
Staph and strep pyogenes
Periorbital/orbital usually secondary to sinus infection
Mild is <2cm in adults
Mod/Severe systemic signs or symptoms, labs abnormal, >2cm
Need blood cultures only if signs of systemic toxicity. Blood cultures are usually useless as isolates rarely correlate with actual bug.
Wound cultures if patient is failing to improve on the current antibiotic regimen. If you do sample, take deep tissue from ulcer base.
Treatment
augment c probenicid (inhibits tubular pcn secretion)?
Fake nails give pseudomonal infections, Also the pads in any shoes. Rx with Diclox/Bactrim?
Infection in bursa vs. joint, have patient pronate/supinate arm to differentiate
Always admit cellulitis overlying a weight bearing joint.
PCN resistant bugs skyrocket if you have a child in daycare
Outbreaks of persistent furunculosis on the lower extremities have been reported in patrons of nail salons. The causative organism has been identified as Mycobacterium fortuitum
think wooden foreign bodies
bullous=staph, otherwise strep. Thick amber/honey crust
raised lesions, painful and demarcated
group A strep
Lower ext 70%, Face 20%
I/D
If surrounding cellulitis, needs broad antibiotics
Chronic
Non-Healing Ulcers: if traveler,
consider leishmaniasis. From Sandfly
bite. Cutaneous leishmania is also
endemic to
intensely pruritic
seen in diabetic males
genitocrural distribution
Looks like candida, but there are no satellite lesions
Under Wood's lamp, it turns bright red
Treat with Erythromycin
Clostridium perfringens is the classic organism responsible for "gas gangrene" or clostridial myonecrosis, although any Clostridial species can produce such infections. Clostridium perfringens is especially likely in wounds contaminated with soil. Clinically, Clostridium infections begin within hours of an inciting trauma, or surgery, with the sudden onset of pain that rapidly extends beyond the wound. A thin, watery discharge may develop, and large hemorrhagic bullae appear. A Gram’s stain of the discharge often reveals gram-positive bacilli with a paucity of white blood cells.
Clostridium septicum can cause spontaneous, nontraumatic necrotizing infections. A colonic lesion, such as carcinoma, will predispose to this highly lethal disease.
Presents with high fever, rash and hypotension. Prodrome of malaise, low grade fever, myalgias and vomiting. Sx may occur 2-3 days after tampon use, soft tissue infection, or within a week of other inciting factors.
Rash is a diffuse, non-pruritic, blanching, macular erythroderma leading to desquamation.
Clinical Criteria
Hypotension
Fever >102
Rash
· Erythroderma followed by desquamation
· Mucous membrane involvement
BP < 90 mmHg
Three or more of the following clinical signs:
1. CNS-altered mental status without focal deficit
2. Cardiovascular
a. Distributive shock
b. Arrhythmia
c. Heart failure
d. AV block
3. Pulmonary
a. ARDS
b. Pulmonary Edema
4. Gastrointestinal
a. Vomiting
b. Diarrhea
5. Liver involvement
a. SGPT > 2 ´ normal
b. Total billirubin > 2 ´ normal
c. Liver enzymes twice normal for age
d. Twofold elevation of liver enzymes
6. Renal impairment
a. Creatinine greater than > 2 mg/dL
b. Creatinine greater than twice upper limit of normal for age
c. Twofold elevation over the baseline level
7. Hematologic
a. Anemia
b. Coagulopathy-Platelets less than 100,000/mm3
c. Disseminated intravascular coagulopathy
8. Metabolic
a. Hypocalcemia
b. hypophosphatemia
Pts will have pain out of proportion to physical findings (85%)
Often coexistent with necrotizing fasciitis
Staph Aureus that produces TSST-1 a pyogenic exotoxin
Rx remove source of infection, toxin mediated (Staph).
Isolation
of group A Streptococcus taht produces extoxin SPE (Strep pyogenic exotoxins):
higher mortality than staph
Aggressive
fluid resuscitation
ABX
may help in Staph TSS, use
Even more important in Strep TSS, use Pen G or Ampicillin plus clindamycin and possibly aminoglycoside. Culture and debride all infected tissue.
Scalded skin syndrome often starts in a child with a bullous impetigo. The lesion begins as a vesicle, and then gradually enlarges into flaccid bullae that rupture. New bullae typically appear over the next 2-3 days, during which time hair and nails may also shed. Fever, skin tenderness, and a scarlatiniform rash are common. The exfoliation toxin can be also secreted by localized infection in the nasopharynx, umbilicus, or urinary tract. In some children, exposed dermal surfaces will weep, while fluid and electrolyte losses may lead to hypovolemia. Exposed surfaces may also serve as a portal for other infections. Most children recover in about 10 days if appropriately treated.
Scalded skin syndrome should be treated with parenteral antibiotics. In a community-acquired infection, beta-lactamase-resistant antibiotics are appropriate. When the infection appears to have been acquired in a hospital or extended care facility, methicillin-resistant Staphylococcus aureus should be considered and vancomycin is the drug of choice. Intranasal mupirocin may provide benefits by eliminating intranasal colonization.
Staph Scalded Skin-Nikolsky’s Sign-easy separation of outer skin
Group A streptococcus, known as the "flesh-eating bacteria" in the lay press, causes a wide spectrum of soft-tissue infections. They range from the mild and superficial, such as impetigo, to a rapidly progressive and deadly necrotizing contagion.
Many of these patients develop hypotension, renal dysfunction, and coagulopathies resembling staphylococcal toxic shock syndrome. The mortality rate remains higher than 30% but with appropriate antibiotics and supportive care, can be reduced to 12%.
Recognition-suspect if pain is out of proportion to clinical findings, then progression to anesthesia.
All present with hypotension, initially or soon afterwards. Progressing to multiorgan dysfunction.
Will at first look just like a cellulitis with/without abcess. One clue is that area will become anesthetic as infection progresses. May not see bubbles of air on radiography b/c only some organisms will produce. Not necessarily clostridium if you do see bubbles, e. coli and others can produce as well. Broad spectrum abx and surgical consult. Unasyn/Genta or Amp/Genta/Flagyl or Imipenem/Flagyl Unasyn plus clindamycin
Stat surgical consult
Type I, or polymicrobial NF, usually occurs after trauma
or surgery.
This form may initially be mistaken for a simple wound cellulitis. However,
severe pain and systemic toxicity reflect widespread tissue necrosis
underlying apparently viable skin.
This disease process may also be observed in association with urogenital or
anogenital infections (see Physical).
Type II, or group A streptococcal NF, is the so-called flesh-eating bacterial infection.
Type III NF, or clostridial myonecrosis, is gas gangrene. This skeletal muscle infection may be associated with recent surgery or trauma.
Type II — Type II necrotizing fasciitis is caused by GAS and
was previously called "streptococcal gangrene" [ 7]. There was a dramatic
increase in the number of invasive infections such as necrotizing fasciitis
caused by GAS during the 1990s. In Ontario, Canada, for example, the incidence
of GAS necrotizing fasciitis increased from 0.085 per 100,000 in 1991 to 0.40
per 100,000 in 1995 [10] . Most cases were community-acquired but 20 percent
were nosocomial or acquired in a nursing home. Almost one-half had streptococcal
toxic shock syndrome. ( See "Streptococcal toxic shock syndrome"). That most
cases are community-acquired is further supported by a recent epidemic in a
small town in Minnesota where the incidence approached 24 cases/100,000
population.
In contrast to type I necrotizing fasciitis, which primarily occurs in patients
who are immunocompromised or have certain chronic diseases such as diabetes,
type II can occur in any age group and among patients who do not have
complicated medical illnesses [9]. Predisposing factors include a history of
blunt trauma, varicella (chickenpox), injection drug use, a penetrating injury
such as laceration, surgical procedures, childbirth, exposure to a "case," and
perhaps nonsteroidal antiinflammatory drugs.
The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool
for distinguishing necrotizing fasciitis from other soft tissue
OBJECTIVE: Early operative debridement is a major determinant of outcome in
necrotizing fasciitis. However, early recognition is difficult clinically. We
aimed to develop a novel diagnostic scoring system for distinguishing
necrotizing fasciitis from other soft tissue infections based on laboratory
tests routinely performed for the evaluation of severe soft tissue infections:
the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score. DESIGN:
Retrospective observational study of patients divided into a developmental
cohort (n = 314) and validation cohort (n = 140) SETTING: Two teaching tertiary
care hospitals. PATIENTS: One hundred forty-five patients with necrotizing
fasciitis and 309 patients with severe cellulitis or abscesses admitted to the
participating hospitals. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The
developmental cohort consisted of 89 consecutive patients admitted for
necrotizing fasciitis. Control patients (n = 225) were randomly selected from
patients admitted with severe cellulitis or abscesses during the same period.
Hematologic and biochemical results done on admission were converted into
categorical variables for analysis. Univariate and multivariate logistic
regression was used to select significant predictors. Total white cell count,
hemoglobin, sodium, glucose, serum creatinine, and C-reactive protein were
selected. The LRINEC score was constructed by converting into integer the
regression coefficients of independently predictive factors in the multiple
logistic regression model for diagnosing necrotizing fasciitis. The cutoff value
for the LRINEC score was 6 points with a positive predictive value of 92.0% and
negative predictive value of 96.0%. Model performance was very good (Hosmer-Lemeshow
statistic, p =.910); area under the receiver operating characteristic curve was
0.980 and 0.976 in the developmental and validation cohorts, respectively.
CONCLUSIONS: The LRINEC score is a robust score capable of detecting even
clinically early cases of necrotizing fasciitis. The variables used are
routinely measured to assess severe soft tissue infections. Patients with a
LRINEC score of > or = 6 should be carefully evaluated for the presence of
necrotizing fasciitis. (Crit Care Med. 2004 Jul;32(7):1535-41)
J Am Acad Derm (2004;51:308)
Deep space infection of skeletal muscle, without overlying cellulitis. Causative agents are usual skin bacteria
pelvis, hip, or leg
usually, but not always, have some increased risk of infection
MRI or CT scan
2/3 of pts will need surg drainage
Cipro/clinda is very good combination
think wooden foreign bodies
a free-living, gram-negative, curved bacillus found in warm marine waters. It is capable of causing terrifying life- and limb-threatening infections, especially in those with underlying liver disease (usually due to alcoholism or viral hepatitis). Skin infection may follow exposure of open wounds to contaminated seawater or shellfish or may spread hematogenously following ingestion of contaminated seafood, usually raw oysters. Skin involvement may range from mild cellulitis to rapidly progressing necrotizing fasciitis and myositis. Patients may develop hemorrhagic bullae. Treatment requires prompt recognition, surgical debridement, and early institution of antimicrobial therapy. Clinical trials are lacking, but some authors recommend third-generation cephalosporins (e.g., ceftazidime) with an aminoglycoside. Others suggest adding doxycycline to the empiric antibiotic regimen based on animal studies and in vitro susceptibility testing
3rd generation cephalosporin + tetracycline may be best choice. retrospective article Arch Intern Med 2006;166:2117-2123.
gram-negative bacillus found in freshwater lakes and streams. Serious soft-tissue infection may follow wound exposure to such water. These suppurative infections progress rapidly, often requiring surgical drainage. Cephalosporins (second-, third-, or fourth-generation), trimethoprim/sulfamethoxazole, and fluoroquinolones are active against Aeromonas
develops following exposure to contaminated water and is generally seen in swimmers and fishermen. A small papule, or nodule, develops after 2-6 weeks of incubation. This "fish tank" or "swimming pool" granuloma will then ulcerate and drain serosanguinous fluid. In approximately 20%-40% of patients, nodular lesions develop along the lymphatics (known as the "sporotrichoid" distribution). Bacterial culture may require 2-4 weeks of incubation.
M. marinum is resistant to isoniazid and pyrazinamide. Treatment options include clarithromycin, minocycline, or trimethoprim/sulfamethoxazole as single agents, or a combination of ethambutol and rifampin. The duration of antimicrobial therapy is approximately 12-24 weeks, and surgical debridement is often required
Fire Coral: local reactions
Sponges: abrasions with mild toxin
Marine
Hematoma
If infected, I/D
Mondor's Disease
phlebitis of thoracoepigastric vein (runs from axilla to epigastrum)
Rx only needed for pain control
Subcutaneous Rupture
usually from seatbelt trauma
if in non-lactating woman, consider malignancy
Milk Stasis
Mastitis
Epidemic-nosocomial ~1st week of life. Usually progresses to abcess. Spread from infant to infant and then to mother. Staph. Use diclox. If abcess, aspiration and possible surgical drainage along with parenteral antibiotics. Do not breast feed from that side.
Endemic-usually more benign. 1-2 weeks. Staph/strep. Must continue to feed from that breast. Moist heat pads. Oral abx (keflex or diclox) unless systemic symptoms
cyclical breast pain
Drugs and Breast Feeding
avoid flagyl, sulfonamides, nitrofurantoin, ergotamine, lithium, Hold breast feeding for 4 days after radioactive compounds.
Emerging MRSA
MRSA susceptibilities were as follows: 100 percent were susceptible to trimethoprim–sulfamethoxazole (217 of 217) and to rifampin (186 of 186); 95 percent were susceptible to clindamycin (215 of 226), 92 percent to tetracycline (207 of 226), 60 percent to fluoroquinolones (106 of 176), and 6 percent to erythromycin (13 of 226). Although the proportion of all S. aureus isolates (MRSA and MSSA) that were resistant to clindamycin was less than 15 percent at 10 of the study sites, 6 of 10 S. aureus isolates from New York City (60 percent) were resistant to clindamycin. Among the isolates that were sent to the CDC, 11 of 218 MRSA isolates (5 percent) and 7 of 55 MSSA isolates (13 percent) were not susceptible to clindamycin, including 4 (2 percent) MRSA isolates and 5 (9 percent) MSSA isolates with inducible clindamycin resistance detected by an antimicrobial-susceptibility D-zone disk-diffusion test. Sixty-six patients with MRSA infections (27 percent) had one or more established risk factors for health care–associated MRSA; these included 43 patients who had been hospitalized within the past year, 28 with a history of MRSA infection, 2 who resided in a long-term care facility, and 1 who was undergoing dialysis. Isolates from 55 of these patients were evaluated at the CDC, and 54 (98 percent) had pulsed-field types characteristic of community-associated MRSA.
Features associated with the isolation of MRSA as compared with the isolation of any other bacteria (Table 2) included antibiotic use in the month before enrollment, the presence of an abscess or a lesion attributed to a spider bite at enrollment, history of MRSA infection, and a recent history of close contact with someone with a similar skin infection. The presence of an underlying illness and characterization as belonging to the "other" category of race or ethnic background were negatively associated with the isolation of MRSA. In multivariate logistic-regression analyses, all these factors were associated with MRSA infection, with the exception of the presence of an abscess (Table 3). Black race was independently associated with MRSA infection. Controlling for study site did not affect the association between any of these factors and MRSA infection. Among 64 patients with none of these factors, 31 (48 percent) were infected with MRSA. The only factor that was significantly associated with isolation of MRSA, as compared with MSSA, was the presence of abscess at enrollment (odds ratio, 2.3; 95 percent confidence interval, 1.2 to 4.4).
(NEJM 2006;355(7):666)
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