Since antibodies to citrullinated peptides have been demonstrated to precede development of RA by several years (12–15), anticitrulline immunity has increasingly been hypothesized to be causatively involved in the development of RA

Antibodies to autoantigens modified by citrullination through deimination of arginine to citrulline are present in about two-thirds of all RA patients but are rare (<2%) in healthy individuals and relatively rare in other inflammatory conditions

smoking, that in the context of HLA–DR SE genes may trigger RA-specific immune reactions to citrullinated proteins

(i.e., antibodies to proteins modified by citrullination).

triggering immune reactions to citrulline-modified proteins.

xist on environmental surfaces for 3-8 weeks and still be infectiou

It spreads most often through the air as aerosolized droplets through sneezes or coughs, and also from inanimate surfaces on which those aerosolized droplets have been deposited, such as door handles, silverware, and handkerchiefs

throughout spring, and early summer,

VZV is transmitted through respiratory droplets, direct and indirect contact.

VZV is present globally and incidences of disease caused by VZV tend to increase from March to May (CDC Website).

The West Nile virus virion is an icosahedral particle with the capsid protein associating with the RNA genome to form the nucleocapsid, which is surrounded by a lipid bilayer. A high proportion of capsid protein localizes to the nucleus, while viral assembly takes place in the cytoplasm, with budding in the endoplasmic reticulum (ER) (17, 41, 183). Although the nuclear functions of capsid are not fully understood, recent evidence suggests a role in gene regulation through binding with histone proteins

The virus-containing endosome matures during internalization from the cell surface, with the pH dropping from neutral to slightly acidic in the early endosome and becoming more acidic during maturation to the late endosome. Within the late endosome, the envelope protein will undergo a conformational change resulting in fusion of the viral lipid membrane with the endocytic membrane and the release of the viral RNA genome into the cell cytoplasm (134)

In situ hybridization of DNA probes specific for viral RNA demonstrated the trafficking of uncoated viral RNA genomes to the endoplasmic reticulum.

The E protein of flaviviruses has been demonstrated to play crucial role in mediating virus-host cellular receptors interaction

Cleavage of prM by cellular furin or related proteases during virus maturation pathway would then release matured virus particles containing M proteins (37).

Flavivirus RNA genome encodes for three structural proteins (capsid [C], precursor of membrane [prM], and envelope [E]), and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5) that are essential for intracellular replication of the virus (12, 13, 49, 58). The RNA genome is packaged within a spherical nucleocapsid that composed of multiple copies of the capsid proteins (11, 59). The nucleocapsid is further enwrapped by a modified lipid bilayer derived from host cellular membranes through the insertion of virus structural proteins, envelope, and precursor membrane.

he family Flaviviridae are positive-sense, single-stranded RNA viruses that replicate in the cytoplasm of infected cells.

Heterodimers of prM and E protein become embedded in the lipid bilayer of the virus during assembly and are exposed on the virion surface [32]. The prM protein is thought to protect the immature virion from undergoing premature fusion prior to viral budding from the cell surface by blocking the fusion loop of E and is cleaved off during the viral maturation process [32–36]. During infection, mature, immature, and partially mature virus particles are produced, containing a varying number of immature prM protein molecules on the surface [37]. The E protein mediates both binding of the receptor on the cell surface for viral entry and fusion with the membrane of the host cell [38–40].

Urinary tract infections caused by P. mirabilis occur usually in patients under long-term catherization

ccording to our results, Escherichia coli was the most common etiological agent of UTI (74.6%), followed by Klebsiella spp (11.7%), Staphylococcus saprophyticus (6.4%), and Pseudomonas aeruginosa (2.2%). Analysis of the frequency of isolated bacteria according to the age of the patients revealed that Klebsiella infections are more prevalent in the older age groups (>10 years) and Pseudomonas infections are more prevalent in children and the elderly (<9 years and >60 years).

The risk factors associated with UTI include sex (distance between the anus and urethral meatus (short in women and long in men), moisture content surrounding urethra), genetic predisposition (e.g. blood group), the antibacterial activity of prostatic fluid (in men), behavioral factors (such as recent sexual intercourse, use of spermicidal agents and diaphragm, frequency of urination, aspects of personal hygiene or use of the birth control pill), low concentration of lactobacilli in elderly women, urologic structural abnormalities, diabetes, immune-suppression, pregnancy, hypertension, stone formation, nosocomial acquired infections and instrumentation like catheterization

E.coli causes 70-95% upper and lower UTIs

UTI caused by Escherichia coli and female gender (p<0.05).

The most common uropathogenic Gram negative bacteria are Escherichia coli and Klebsiella pneumoniae.

R-LPS without O-chains was described in S. putrefaciens (21, 28). The reduced lipopolysaccharide structure allows for better adhesion of bacteria to the iron-containing surface, and therefore more efficient use of this metal as an electron acceptor in respiration. The core of LPS has high concentrations of carboxyl and phosphoryl sites, which indicate the polarity, and contribute to the interaction with metal ions (21). In addition, the LPS of S. putrefacienspredisposes these bacteria to form biofilms on iron surface, and also enables to use this metal in their metabolic pathways.

solates of S. putrefacienshavethe ability to adhere to human epithelial type 2 cells(HEp-2) (20). Moreover, S. putrefaciensadhere and form biofilms on steel surfaces due to iron reduction (3). Bacterial adhesion ability is a significant problem in food industry, as it causes difficulties in their elimination from the production areas, adversely affects the quality of food, and may lead todiseases in humans. From the perspective of aquaculture, ability of S. putrefaciensto adhere to various tools and equipment at fish farms may be a source of fish infections. Since most bacterial fish pathogens, including S. putrefaciens, are facultative and may cause the diseases when environmental conditionsbecome unfavourable, it poses a serious problem

Another important property of the bacteria is secretion of cytolysins, e.g. haemolysins. Most strains of S. putrefaciensare not able to produce haemolysins (17, 24, 30); however, some isolates show this ability (20, 22, 36, 46), which indicates the diversity of these microorganisms.

Factors determining penetration and proliferation of S. putrefaciens, or tissue damage in the infected organisms have not been described yet. Therefore, potential virulence factors, which include enzymatic activity, cytotoxins secretion, adhesion ability, lipopolysaccharides (LPS), and the presence of siderophores, are analysed in this review.

It should be noted that S. putrefacienscould also be associated with different infections in humans, such as skin and tissue infections, bacteraemia, otitis. Investigations on pathogenic mechanisms of S. putrefaciensinfections are very limited. Enzymatic activity, cytotoxin secretion, adhesion ability, lipopolysaccharide (LPS), and the presence of siderophores are potential virulence factors of S. putrefaciens. Antimicrobial resistance of S. putrefaciensis different and depends on the isolates. In general, these bacteria are sensitive to antimicrobial drugs commonly used in aquaculture.

The rate of biofilm formation and the thickness of the film were not dependent on the availability of carbohydrate (lactate or glucose) or on iron starvation. The number of S. putrefaciens bacteria on the surface was partly influenced by the presence of other bacteria (Pseudomonas fluorescens) which reduced the numbers of S. putrefaciens bacteria in the biofilm. Numbers of bacteria on the surface must be quantified to evaluate the influence of environmental factors on adhesion and biofilm formation.

This Shewanella outbreak had a single-source origin and spread by contact transmission via a contaminated measuring cup. Shewanella species are emerging as potentially serious human pathogens in hospitals and could be included in hospital infection surveillance systems.

The estimated incubation period for Shewanella acquisition was 3-49 days

S. algae or S. putrefaciens was isolated from blood, for 9 (29.0%) of 31 patients who acquired one of the organisms; from bile, for 8 (25.8%), and from ascitic fluid, for 8 (25.8%). The attack rate of this outbreak was 5.8% (31 patients infected or colonized, of 534 potentially exposed on ward

and the pathogenicity of the two species together was 77.4% (24 patients infected, of 31 who acquired the pathogens)

To our knowledge, this is the first report of V. vulnificus andS. putrefaciens as causes of severe suppurative eye infection. Fortu-nately, this infection was limited to the eye.

S. alga causes the most human illnesses and that significant differences exist between these two species regarding resistance to antimicrobial agents, mouse pathogenicity, and certain virulence factors (hemolysis and adhesion).

Pathogenicity studies of mice indicate that S. alga appears to be the more virulent species, possibly due to the production of a hemolytic substance.

In contrast, Shewanella putrefaciens organisms (Gilardi biovars 1 and 3; CDC biotype 1) were more often associated with nonhuman sources (70%)

Published literature on S. putrefaciens, has reported sensitivity to aminoglycosides, fluoroquinolones, third/fourth-generation cephalosporins,

Shewanella putrefaciens is as yet rarely responsible for clinical syndromes in humans

Nevertheless, S. putrefaciens also retains pathogenic potential, mainly under special environmental circumstances. Indeed, most of the reported infections pertained to contact with contaminated waters or injuries or occurrences in which integrity of the skin was compromised to some extent (3, 4, 9, 10, 12); this last issue encompasses also long-term catheters (1). In addition, isolation of S. putrefaciens occurred in polymicrobial infections (3).

Both S. putrefaciens and Shewanella alga are uncommon as isolates from clinical syndromes, their natural habitats being all forms of water, fish, oily foodstuffs, and soils (2, 4, 11)

We report 16 cases of S. putrefaciens infection that occurred at the Veterans General Hospital-Kaohsiung in Taiwan between 1990 and 1995. S. putrefaciens infection was associated with a wide clinical spectrum including bacteremia/septicemia, skin and soft-tissue infection, biliary tract infection, peritonitis, and empyema.

Shewanella putrefaciens keratitis in the lamellar bed 6 years after LASIK.

Shewanella putrefaciens has only been isolated from such clinical materials as various body wounds, feces, conjunctiva, urine, CSF, bile, ascitic fluid, pleural fluid, and stored blood. The major risk factor of S. putrefaciens infection is hepatobiliary disease, peripheral vascular disease, with chronic leg ulcer, poor hygiene, and socioeconomic status. In most cases, the bacteria reside in devitalized tissue or denuded skin and serve as a nidus for opportunistic infection. Soft tissue infections have various clinical manifestations including infected leg ulcer, cellulitis, abscess formation, and wound infection, which are often preceded by chronic ulceration of the lower limb, trauma, burn wound, and seawater exposure.

Campylobacter species also produce the bacterial toxin cytolethal distending toxin (CDT), which produces a cell block at the G2 stage preceding mitosis. CDT inhibits cellular and humoral immunity via destruction of immune response cells and necrosis of epithelial-type cells and fibroblasts involved in the repair of lesions.

Cytotoxin production has been reported in Campylobacter strains from patients with bloody diarrhea

Infection with the organism produces diffuse, bloody, edematous, and exudative enteritis

C jejuni appears to invade and destroy epithelial cells. C jejuni are attracted to mucus and fucose in bile, and the flagella may be important in both chemotaxis and adherence to epithelial cells or mucus. Adherence may also involve lipopolysaccharides or other outer membrane components. Such adherence would promote gut colonization. PEB 1 is a superficial antigen that appears to be a major adhesin and is conserved among C jejuni strains.

Chickens may account for 50-70% of human Campylobacter infections.

Macrolide resistance in Campylobacter is mainly associated with target modification and active efflux [55–59]. Modification of the ribosomal target, leading to macrolide resistance in Campylobacter, can occur either by enzyme-mediated methylation or by point mutation in the 23S rRNA and/or ribosomal proteins L4 and L22

In addition to the mutations in GyrA, the multidrug efflux pump, CmeABC, also contributes to FQ resistance by reducing the accumulation of the agents in Campylobacter cells

In Campylobacter, the resistance to FQs is mainly mediated by point mutations in the quinolone resistance-determining region (QRDR) of DNA gyrase A (GyrA)

Generally, the prevalence of erythromycin resistance among Campylobacter strains (including both C. jejuni and Campylobacter coli) isolated from humans, broilers and cattle in the USA and Canada has been reported at 10% or lowe

19–47% of Campylobacter strains isolated from humans were resistant to ciprofloxacin [

Alternative drugs include tetracyclines and gentamicin, which are used in cases of systemic infection with Campylobacter [5]. However, Campylobacter is increasingly resistant to the clinically important antibiotics and this rising resistance is a concern for public health.

Cefoperazone is added to inhibit many gram-positive and gram-negative organisms, both aerobic and anaerobic. Vancomycin inhibits gram-positive microorganisms. Amphotericin B is incorporated to inhibit the growth of yeast.

Campy CVA is recommended. The use of cefoperazone-containing media, as opposed to cephalothin-containing media, is recommended for the primary isolation of Campylobacter from fecal samples

C. jejuni continues to be the most common enteric pathogen isolated form patients with diarrhea

In Campylobacter, a recurring theme is synergy between antibiotic efflux and a second mechanism.

Azithromycin therapy would be a primary antibiotic choice for Campylobacter infections, when indicated (see Medical Care), [20] with a typical regimen of 500 mg/d for 3 days. However, erythromycin is the classic antibiotic of choice. Its resistance remains low, [21] and it can be used in pregnant women and children

being able to execute N-linked glycosylation of more than 30 proteins related to colonization, adherence, and invasion. Moreover, the flagellum is not only depicted to facilitate motility but as well secretion of Campylobacter invasive antigens (Cia). The only toxin of C. jejuni, the so-called cytolethal distending toxin (CdtA,B,C), seems to be important for cell cycle control and induction of host cell apoptosis and has been recognized as a major pathogenicity-associated factor. In contrast to other diarrhoea-causing bacteria, no other classical virulence factors have yet been identified in C. jejuni.

The bacteria colonize the small and large intestines, causing inflammatory diarrhea with fever. Stools contain leukocytes and blood. The role of toxins in pathogenesis is unclear.

Many types of media have been used to culture C. jejuni. Mueller-Hinton medium, blood agar, Columbia blood agar, and BBL medium are commonly used. However, Mueller Hinton (MH) has the highest recovery rate and is recommended in this unit

C. jejuni is also able to grow in anaerobic conditions.

All Campylobacter species are inherently resistant to vancomycin, rifampin, and trimethoprim.

Erythromycin has once again come to be considered the optimal drug for treatment of Campylobacter infections. Despite decades of use, the rate of resistance of Campylobacter to erythromycin remains quite low. Other advantages of erythromycin include its low cost, safety, ease of administration, and narrow spectrum of activity. Unlike the fluoroquinolones and tetracyclines, erythromycin may be administered safely to children and pregnant women and is less likely than many agents to exert an inhibitory effect on other fecal flora.

However, in the past few years, a rapidly increasing proportion of Campylobacter strains all over the world have been found to be fluoroquinolone-resistant

Maintenance of hydration and electrolyte balance, not antibiotic treatment, is the cornerstone of treatment for Campylobacter

contaminated water, contact with pets (especially birds and cats)

Fecal leukocytes and RBCs are detected in the stools of 75% of infected persons

Clinically, Campylobacter infection is indistinguishable from acute gastrointestinal infections produced by other bacterial pathogens, such as Salmonella, Shigella, and Yersinia species.

They grow best at 42°C. Because most Campylobacter species are resistant to cephalothin (an agent to which most other stool flora are susceptible), the usual method for isolation from stool samples is use of a medium that contains cephalothin.

Campylobacter species are motile by means of unipolar or bipolar flagellae. The organisms grow quite slowly; 72–96 h are required for primary isolation from stool samples

ampylobacter infections were found to cause diarrheal disease >2–7 times as frequently as infections with Salmonella species, Shigella species, or Escherichia coli O157:H7

Obtaining cultures of the organism from stool samples remains the best way to diagnose this infection

Azithromycin and fluoroquinolones (e.g., ciprofloxacin) are commonly used for treatment of these infections, but resistance to fluoroquinolones is common. Antimicrobial susceptibility testing can help guide appropriate therapy.

What are public health agencies doing to prevent or control campylobacteriosis?

Do not drink unpasteurized milk or untreated surface water.

Surface water and mountain streams can become contaminated from infected feces from cows or wild birds.

Most cases of campylobacteriosis are associated with eating raw or undercooked poultry meat or from cross-contamination of other foods by these items. Outbreaks of Campylobacter have most often been associated with unpasteurized dairy products, contaminated water, poultry, and produce. Animals can also be infected, and some people get infected from contact with the stool of an ill dog or cat.

Almost all persons infected with Campylobacter recover without any specific treatment. Patients should drink extra fluids as long as the diarrhea lasts. Antimicrobial therapy is warranted only for patients with severe disease or those at high risk for severe disease

Campylobacter jejuni grows best at 37°C to 42°C, the approximate body temperature of a bird (41°C to 42°C), and seems to be well adapted to birds, who carry it without becoming ill. These bacteria are fragile. They cannot tolerate drying and can be killed by oxygen. They grow only in places with less oxygen than the amount in the atmosphere. Freezing reduces the number of Campylobacter bacteria on raw meat.

The organism is isolated from infants and young adults more frequently than from persons in other age groups and from males more frequently than females.

The diarrhea may be bloody

Most people who become ill with campylobacteriosis get diarrhea, cramping, abdominal pain, and fever within two to five days after exposure to the organism.

nonspore-forming, Gram-negative, microaerophilic, nonfermenting bacterium

The vast majority of cases occur as isolated events, not as part of recognized outbreaks.

Ciprofloxacin, levofloxacin, ofloxacin, sparfloxacin and trovafloxacin have all been shown to inhibit the intracellular growth of L. pneumophila in either guinea pig alveolar macrophages 17,18,19 or HL-60 cells.

In one comparative study of in-vitro, extracellular susceptibility sparfloxacin and trovofloxacin were the most active, ciprofloxacin, levofloxacin, ofloxacin and lomefloxacin were slightly less active, and pefloxacin was the least active. 15 However, all the quinolones tested can be said to have good activity and low MICs (Table). Quinolones readily enter the intracellular compartment.

Within HL-60 cells azithromycin achieves the greatest inhibition of growth of L. pneumophila

Amongst the macrolides most experience has been gained with erythromycin. However, by in-vitro extracellular, testing it is less active than clarithromycin, azithromycin and roxithromycin, although more active than dirithromycin and josamycin (Table). In some comparative studies clarithromycin has been more active than azithromycin

L. pneumophila is a significant human pathogen that lives in amoebae in the environment but may opportunistically infect the alveolar macrophage. To maintain its intracellular lifestyle, Legionella extracts essential iron from the cell, blocks inflammatory responses and manipulates trafficking to avoid fusion with the lysosome.

The Mip protein exhibits activity of a peptidyl prolyl cis trans isomerase (PPIase), an enzyme which is able to bind the immunosuppressant FK506 and is involved in protein folding. The recently cloned major outer membrane protein (MOMP) could play a role in the uptake of legionellae by macrophages.

Many antibiotics are highly effective against Legionella bacteria. The two most potent classes of antibiotic are the macrolides (azithromycin), and the quinolones (ciprofloxacin, levofloxacin, moxifloxacin, gemifloxacin, trovofloxacin). Other agents that have been shown to be effective include tetracycline, doxycycline, minocycline, and trimethoprim/sulfamethoxazole. Erythromycin, the former antibiotic of choice, has been replaced by more potent and less toxic antibiotics.

Abnormal sounds called crackles may be heard when listening to the chest with a stethoscope.

Chest painCough that does not produce much sputum or mucus (dry cough)Coughing up bloodDiarrhea, nausea, vomiting, and abdominal painFever, shaking chillsGeneral discomfort, uneasiness, or ill feeling (malaise)HeadacheJoint painLoss of energyMuscle aches and stiffnessProblems with balanceShortness of breath

Risk factors include:Alcohol abuseCigarette smoking

Culture Clinical and environmental isolates can be compared Detects all species and serogroups Technically difficult Slow (>5 days to grow) Sensitivity highly dependent on technical skill May be affected by antibiotic treatment Requires BCYE agar, which some laboratories may not have readily available

The most commonly used laboratory test for diagnosis is the urinary antigen test, which detects a part of the Legionella bacterium in urine. If the patient has pneumonia and the test is positive, then the patient is considered to have Legionnaires' disease.

Isolation of Legionella from lower respiratory secretions, lung tissue, pleural fluid, or a normally sterile site is confirmatory and an important method for diagnosis.

Patients who have failed outpatient antibiotic therapy for community-acquired pneumonia Patients with severe pneumonia, in particular those requiring intensive care Immunocompromised patients with pneumonia Patients with pneumonia in the setting of a legionellosis outbreak Patients with a travel history (patients that have traveled away from their home within two weeks before the onset of illness)

Urine test Laboratory test that involves taking a sample of sputum (phlegm) or washing from the lung

Legionnaires’ disease can also be associated with other symptoms such as diarrhea, nausea, and confusion

Cough Shortness of breath Fever Muscle aches Headaches

Cooling towers(https://www.cdc.gov/healthywater/other/industrial/cooling_towers.html) (air-conditioning units for large buildings)

People 50 years or older Current or former smokers

In general, people do not spread Legionnaires’ disease and Pontiac fever to other people.

hile Fusobacterium species are generally resistant to vancomycin and susceptible to kanamycin and colistin.

A definition of community extends beyond geography and racial identity, and depends heavily on members’ perceptions of what “the community

CBPR is “a collaborative process that equitably involves all partners in the research process and recognizes the unique strengths that each brings.

Penicillin or ampicillin remains the drug of choice for intrapartum antibiotic prophylaxis for GBS colonization in pregnant women

Resistance genes were detected in 100% of erythromycin-resistant isolates (Table ​(Table1).1). Twelve isolates (6%) were resistant to both erythromycin and clindamycin.

All GBS were susceptible to penicillin and vancomycin, and 30 (15%) were susceptible to tetracycline. Resistance to erythromycin was found in 44 (22%) of the isolates.

During a group B strep test, your health care provider will swab your vagina and rectum and send the samples to a lab for testing. In some cases, you might receive instructions on how to collect the samples yourself. Because you can test positive at certain times and negative at other times, you'll need to repeat the group B strep test each time you're pregnant.

Pneumonia(https://www.cdc.gov/pneumonia/index.html) (lung infection) symptoms include: Fever and chills Cough Rapid breathing or difficulty breathing Chest pain

Vancomycin is in broad clinical use with the main indications including skin and soft tissue infections and osteomyelitis

Vancomycin binds to the d-ala-d-ala moiety of the monomers, subsequently the monomers cross the cell membrane. This complex leads to conformational change that blocks the glycosyltransferase leading to inhibition of the incorporation of the murein monomers to the growing peptidoglycan chain and preventing further transpeptidation with consequent interruption of the cell wall synthesis

inhibit cell wall synthesis in its later stages thus affecting dividing bacteria

Vancomycin remains the first-line agent for methicillin-resistant coagulase-negative and coagulase-positive staphylococcal infections

Vancomycin is effective against most Gram-positive cocci and bacilli with the exception of rare organisms as well as enterococci that became vancomycin resistant, mostly Enterococcus faecium

COAGULASE test which is positive for Staphylococcus aureus (generally accepted criterion for the identification) and negative for all other Staphylococci. Coagulase is an enzyme used by S.aureus to induce coagulation and convert soluble fibrinogen into fibrin which will protect bacteria from the immune system. It is also a clumping factor for bacteria’s coalescence. All other staphylococcus species can be collectively referred to as coagulase-negative staphylococci.

The main criterion for differentiation between Staphylococcus and Streptococcus genera is the catalase test. Staphylococci are catalase positive whereas Streptococci are Catalase negative.

Living in crowded or unsanitary conditions. Outbreaks of MRSA have occurred in military training camps, child care centers and jails.

Warm to the touch Full of pus or other drainage Accompanied by a fever

Wound cultures were monomicrobial for MRSA in 12 patients (86 percent).

Most patients had documented coexisting conditions or risk factors, most commonly current or past injection-drug use (six patients [43 percent]), a seizure disorder (three [21 percent]), diabetes (three [21 percent]), and chronic hepatitis C (three [21 percent]) (Table 1). Four patients (29 percent) had no serious coexisting conditions or risk factors. Four patients (29 percent) were homeless; six patients (43 percent) had been hospitalized within the year before the current admission.

Eleven patients (79 percent) required débridement that was described as either “wide” or “radical,” often with incisions greater than 15 cm, and three required subsequent skin grafting.

Ten of the 14 patients were men (71 percent), and the median age was 46 years (

This finding suggests that necrotizing fasciitis caused by community-associated MRSA has the potential to cause rapidly progressive disease that is clinically indistinguishable from necrotizing fasciitis caused by pathogens such as group A streptococcus. Furthermore, although none of the patients died, serious complications were common, including prolonged stays in the intensive care unit, the need for mechanical ventilation and reconstructive surgery, septic shock, nosocomial infections, and endophthalmitis.

The absence of deaths in our series suggests that necrotizing fasciitis caused by community-associated MRSA may be less virulent than similar infections caused by other organisms. Indeed, the onset of disease in our series was often subacute, with symptoms present an average of 6 days before admission (range, 3 to 21).

To date, MRSA has been reported to be associated with necrotizing fasciitis in only one case of subacute, polymicrobial infection25 and as a monomicrobial cause of an iatrogenic, surgery-associated “necrotizing fasciitis–like” infection and bacteremia.

S. aureus has not been described as a monomicrobial cause of necrotizing fasciitis in major clinical reviews of the topic or in published microbiologic studies of the disease.1

The staphylococcus aureus bacteria that cause MRSA infections can survive for days to weeks on surfaces. MRSA bacteria can live on surfaces for longer than some other bacteria and viruses because they survive better without moisture. Generally, MRSA bacteria survive for longer on hard surfaces than on soft surfaces.

Pocket of infection that forms at the site of injury. Usually filled with pus. Area surrounding the abscess is usually red, painful and swollen and the skin surrounding the abscess can feel warm to the touch.

Usually results from a scrape or cut in the skin which allows bacteria to enter, although no injury may be apparent. Cellulitis can occur anywhere in the body, but most often occurs on the legs or arms. Symptoms include redness, swelling, and pain at the site of infection.

In conclusion, S. aureus is an important pathogen of monomicrobial necrotizing fasciitis, and MRSA has emerged as the predominant causative agent in recent years

Lower limbs and upper limbs are the most commonly involved sites

Of 105 necrotizing fasciitis cases during the study period, 18 were caused by monomicrobial S. aureus infection (17%). The median age was 62 years (range, 12-81 years).

The overall mortality rate was 31%

In 5/13 cases a recent animal-derived trauma could be found. In the other cases the source of the infecting organism was thought to be endogenous (from patients’ own pharyngeal commensal flora) or secondary to contact with secretions of a pet animal.

All the patients had an underlying disease (77 % had cirrhosis) and 2 were receiving chemotherapy for hematologic malignancy.

Transmission by aerosol, fecal-oral, and contact with infected secretions (including venereal transmission) has been reported.