Open access peer-reviewed chapter

Bacterial Skin Abscess

Written By

Mohammed Malih Radhi, Fatima Malik AL-Rubea, Nada Khazal Kadhim Hindi and Rusull Hamza Kh. AL-Jubori

Submitted: 27 October 2019 Reviewed: 07 February 2020 Published: 10 April 2020

DOI: 10.5772/intechopen.91657

From the Edited Volume

Insights Into Drug Resistance in Staphylococcus aureus

Edited by Amjad Aqib

Chapter metrics overview

712 Chapter Downloads

View Full Metrics


Patients with skin and soft tissue infections may appear with the abscess. Erroneous diagnosis of these entities is common, and should carefully consider the possible alternative diagnoses. Risk for developing skin abscess factors includes disruption of the skin barrier, edema, venous insufficiency, and immune suppression. However, healthy individuals who have no risk factors may also develop these diseases. The most common microbiologic cause of abscess, a commonly group Streptococcus or Streptococcus pyogenes; Staphylococcus aureus (including methicillin-resistant strains) is a notable but less common cause. The most common microbiologic cause of skin abscess is S. aureus; a skin abscess can be caused by more than one pathogen. The diagnosis is based on skin abscess usually on the clinical manifestations. It must be subject to patients with disposable abscess incision and drainage, with a test of culture and susceptibility of materials wet. There is no justification for the blood of patients in the cultures of the abovementioned circumstances. It can be a useful radiographic examination to determine whether the skin abscess is present (via ultrasound) to distinguish cellulitis from osteomyelitis (via magnetic resonance imaging). There may be a justification for radiological assessment in patients with immune suppression, diabetes, venous insufficiency, or lymphedema in patients with persistent symptoms of systemic lymphatic obstruction.


  • bacteria
  • skin
  • abscess
  • S. aureus

1. Introduction

1.1 Bacterial skin abscess

The most common cause of abscess skin is Staphylococcus aureus (either methicillin or midwife to methicillin. Staphylococcus aureus aureus), occurring in up to 75% of cases; many patients infected with MRSA do not have risk factors [1, 2, 3]. It can be caused by skin abscess more than one pathogens [4]. The isolation of multiple objects (including S. aureus CT with Gram-negative bacilli and anaerobes) are more common in patients with skin abscess, which includes the surrounding areas of oral or anal or vaginal [5]. Organisms live by mouth, including anaerobic, you see most often among drug users by intravenous. Include unusual causes of skin abscess such as fungus pneumococcus and Streptococcus. Most cysts are caused by infection. However, it can occur in a sterile abscesses put irritants injected. Examples include (especially those drugs Injected that depend on oil), which may not be fully absorbed and remain at the injection site, causing local irritation. Cysts can be transformed into a sterile solid during solid lesions scars [5].


2. Original of abscess

The abscess arise in many tissues and organs of the body, the most important of which are subcutaneous tissue, lymph nodes, soft and adipose tissue around the anus, and breasts in pregnant or lactating women and at the root of the teeth. Cysts can also arise in internal organs such as the liver, lung, brain, kidney and appendix. The abscess has spread significantly in recent years [6]. And the risk factor has been more than 65% including the use of intravenous drugs. In 2005, Dermatology departments received more than 3.2 million people with abscess in the United States [7], while in Australia, about 13,000 patients were hospitalized [8]. Cysts arise in many tissues and organs of the body, the most important of which are subcutaneous tissues (then they are superficially dimple or deep), such as liver, lung, brain abscess, kidney, and appendix. The most important complication is the spread of the abscess (pus) to neighboring tissues by means of treatment tools, which may sometimes cause the death of these tissues (gangrene). Acute inflammation of the abscess originates from the entry of pus bacteria into the affected organ or tissue. Surface cysts are swollen red and painful, accompanied by high fever and pulse [9]. The abscess can also be fatal in rare cases, such as when it is in an area where pressure on vital organs such as the trachea in the case of abscess in the neck area. If the abscess is superficial, it will fluctuate during palpation due to the movement of pus inside. A contributing factor to the formation of an abscess in addition to the use of intravenous drugs [10]. An unconfirmed study suggests that the presence of previous cases of hernia of the vertebrae or any imbalance thereof [11]. While the main cause is pathogenic bacteria, fungi or parasites, the most common cause is methicillin-resistant Staphylococcus aureus in the United States and other parts of the world [6]. Staphylococcus aureus causes subdural abscesses and parasites to cause abscess, especially in developing countries [12].


3. Epidemiology of skin abscesses

Because of changing the display skin abscess, it was difficult to assess the incidence and prevalence. The incidence of skin abscess is 24.6 per 1000 people per year [13]. Because the majority of the ski abscess tends to melt within 7–10 days, the estimate variable spread significantly. Among patients in hospitals, the rate of prevalence ranges from abscess skiing 7–10% [14, 15]. Among all patients infected in hospitals only infections, skin abscess plays a more important role. Emergency care center, an outlying ski, is the third most common diagnoses after chest pain and asthma [16]. There is an increase in the prevalence rate of men (60–70% of all cases) and patients aged between 45 and 64 years old. It managed approximately 70–75% of all cases in the outpatient setting [13, 16]. With many cases of skin abscess involving the lower leg area (7.9–11). In general, the incidence of benign tumors complex is low (Arasepelas 0.09 per 1000 people per year; inflammation of the lymphatic vessels is 0.16% of all cases of inflammation of cellular tissue and the lymphatic vessels. 16 per 1000 people per year and fasciitis necrotizing 0.04 per 1000 person-years) [13].

The real spread of abscess skin infection is unknown because the light is usually self-occurrence and patients seeking medical care. However, often they face skin abscess in the outpatient and inpatient. According to national statistics for 2011 regarding the cost of health care project and use, skin abscess rate led to 3.4 million visits to the emergency department, or 2.6% of the total emergency department visits, with 13.9% of visits have led to hospitalization [17].

They have caused the infection, skin and soft tissue as well as the case of 500,000 outside the hospital, or 1.4% of total departures, with an average length of stay of 3.7 days and an average cost of $ 18.299 per case. These figures are on the rise due to the prevalence of Staphylococcus aureus resistant to methicillin-associated Balmethycelin in the past decade [18, 19, 20, 21].

A recent prospective study showed that one out of every 5 patients provide primary care clinic for skin abscess caused by Staphylococcus aureus resistant to methicillin (MRSA) require additional interventions at a cost of approximately $ 2000 per patient [22].


4. Risks factors of skin abscesses

The presence of specific risk factors may stimulate the skin abscess, may impose pathogens, disease course and respond to specific treatments. It did not prove the existence of risk factors for the development of skin abscess associated with the seriousness of the disease [23]. It can be organized into two categories of risk factors. First, there are factors associated with the patient, which may provide for the disease or the effects of predictive. Risk factors in this category include serious diseases and the age of the elderly and the situation that suffers from a lack of human immunodeficiency virus and diseases of the liver, kidney and vascular insufficiency (especially the lymphatic or venous) [24]. Since it turns out that the lower part of the leg is more places of infection transmitted through sexual contact common, studies have described risk associated with the patient’s infection due to these factors [25]. It was able to determine the likelihood of skin abscess in the lower limbs based on the presence of Staphylococcus aureus and/or beta-hemolytic Streptococcus in the toe box, erosion or leg ulcers, and/or eradication of the former esophagus. These factors independently associated with the development of skin abscess in the lower leg. In the same population group, if the bacteria found in the toes are absent, the presence of the pedal palm has the ability to moderate predictive secretion of the skin. Moreover, the multiple risk factors associated with the patient may be associated with a poor prognosis of the disease faster, and the development of slow recovery and the causes of the most resistant diseases. Must take into account the specific risk factors (renal failure or chronic kidney, spleen deficiency, immune status, vascular insufficiency or neuropathy) when determining the severity of the disease [26].

Observed factors associated with skin abscess are often among middle-aged adults and older. Erysipelas occurs in young children and the elderly [13].

It includes predisposing factors associated with the risk of skin abscess are:

  1. Disable the skin barrier due to trauma (such as corrosion, penetrating wound, pressure ulcers, venous leg ulcers, insect bite, injecting drug use).

  2. Inflammation of the skin (such as eczema, psoriasis and radiation therapy).

  3. Edema due to poor lymphatic drainage.

  4. Edema due to venous insufficiency.

  5. Obesity.

  6. Immune suppression (such as diabetes or infection with HIV) disease.

  7. Skin breaks between these fingers may not be clinically.

  8. Dermatitis pre-existing (such as foot frond, herpes, varicella) [27].

Also, acute bacterial skin infections occur when exposure to the risk of loss of skin integrity e.g high bacteria in pregnancy skin or the availability of food bacterial, or excess moisture in the skin, or lack of blood supply, or immune suppression, or a damaged cornea layer. Poor hygiene and the exchange of personal things, physical contact, and crowded living conditions facilitate the spread of infectious diseases. Vascular diseases, peripheral diseases and skin pre-existing increase the risk of acid cellulose. Usually leads to diabetes, a diabetes which is controlled by a bad foot injury. Cause painful events such as wounds, biting and drug abuse by injection injuries increase the risk of skin infections and cysts. The risk of infection on surgical-site support is in the process category, where clean and smaller operations are at the risk of contaminated infections and high-risk operations have a higher risk of injury [28].

Colonization with Staphylococcus aureus and Streptococcus in the front lines on the skin increases the risk of skin abscess. Considered skin contact to the skin through exercise and attendance in day care or school and live in a place nearby (such as military barracks) risk factors for CAMRSA skin abscess [29].


5. Bacterial invasion of the skin

For as long as microorganisms that colonize the skin of importance to skin diseases and microbiology; I have been collecting our knowledge of these organisms live accurate until recently through the existing studies on the culture. Historically, it is Staphylococcus aureus and other Staphylococcus aureus negative coagulation as the primary bacterial colonies of the skin. Other microorganisms that are generally regarded as skin colonizers include coryneforms of the phylum Actinobacteria (the genera Corynebacterium, Propionibacterium and Brevibacterium) and the genus Micrococcus. Gram-negative bacteria, with the exception of some Acinetobacter spp., are generally not isolated from the skin, but are thought to arise in cultures owing to contamination from the gastrointestinal tract [30].

It was isolated from non-bacterial microorganisms from the skin. Fungal species are the most common Malassezia spp., which is particularly widespread in the fatty areas. Considered mite Demodex (such as Demodex follicle and Demodex brevis), a microscopic arthropods, part of the natural skin flora. They feed on mites Demodex sebum and be more prevalent after puberty, preferring to colonize the oily areas of the face. Demodex mites may also feed on epithelial cells lining the unit sunscreens space, or even other organisms (such as acne Brobbeoneptariom) that live in the same place. It is not the role of the experimental study of viruses, and is limited research on the molecular and microbiological methods available for the identification and characterization of viruses [31].

Historically, culture-based approach is the standard to describe the microbial diversity. It is now clear that only a minority of bacteria able to thrive in isolation [32]. Choose mainly culture-based laboratory techniques “herbs”: species that thrive under conditions typical nutritional and physiological use of diagnostic microbiology laboratories. This is not necessarily the most abundant organisms in society. This bias is particularly evident when trying to isolate the organisms living in micro skin, which adapted to the nature of cold, dry and acidic environment. Moreover, the hair follicles and sebaceous glands are an oxygen-free environment and are home to the anaerobic microorganisms. Isolate the problem especially anaerobic using routine methods based on culture. These are often slow-growing organisms and require special conditions for growth and during the transfer and processing of samples [33, 34].

The development of molecular techniques to identify and quantify microorganisms has revolutionized our view of the world Microbial. Characterization of genetic diversity of bacterial depends on the sequence of genes for RNA ribosomal 16S, found in all bacteria and analyzes antique, but not in eukaryotes. Genes rRNA contain 16S in highly variable regions of certain types, which allows the classification of classification, and the spaces reserved for the one who, operating Xaah molecular site linking the primers PCR. The emergence of new sequencing technologies (such as pyrosequencing) is to increase productivity significantly while reducing the cost of sequencing. More importantly, the living organism culture does not need to determine the sequence of its kind by 16S rRNA [35].

The skin is the largest organ in the human body, colonized by a variety of tiny, mostly harmless organisms or even beneficial to their hosts. Colonialism is the motivation behind the surface of the skin environment, which is highly variable depending on the site topography, and host factors internal factors, the external environment. The responses can be innate immune and lead to a modified adaptive skin microorganisms in the skin, but microorganisms are also working to educate the immune system. Molecular road development has led to the identification of microorganisms to see the emerging skin bacteria resident are very diverse and variable. The improved understanding of the microbes in the skin is necessary to gain insight into the involvement of microbes in human skin disorders and to enable new methods for therapeutic drugs antimicrobial and antimicrobial therapy [36].

The main barrier against microbial invasion is the skin. It interacts continuously with the external environment, a colonizer with a variety of microbes. The vast majority of plants colony consists of bacteria. To help organize the distribution of plants, one that divides the body into two halves at the waist. The usual things that colonizes the skin above the waist are usually positive types of Gram such as Staphylococcus epidermidis, Corynebacterium species, S. aureus and Streptococcus pyogenes [37].

Staphylococcus aureus and Corynebacterium spp. It is the most abundant organisms that colonize humid areas, consistent with the data culture that indicate that these organisms prefer high humidity areas. These include navel wet sites (navel), and the basement axillary, and wrinkling inguinal (side thigh) and wrinkling brigades (the upper part of the fold between the buttocks), insole foot, hole popliteal (behind the knee) and the pit antecubital (elbow inner). Staphylococcus aureus occupies air position on the skin and may use urea in the race as a source of nitrogen. Insect bacteria are highly sensitive organisms that have slow growth in culture, and such as the role of the skin accurate objects has been appreciated until recently. Treatment of sweat by bacteria and Staphylococcus (along with the minute in the basement of underarm living organisms), resulting in a transient characteristic odor associated with sweating in humans [38].

On the other hand, the typical living organisms colonize the skin below the waist Gram-positive and Gram-negative. It is expected that this will be a minor near the anal area difference. Attracted intestinal species, such as the intestinal bacteria, to this region of the skin so-called “Fecal Crust” [36].

Normal distribution pattern consists of the largest population areas in the armpit and groin and thigh, where there is moisture level higher. Microflora tend to fill the upper layer of the cornea and parts of the hair follicles. Specific microbes tend to colonize the anatomical structures based on tropical stimuli and biochemical interactions of the site and the formation of specific tissues of biological membranes. Plants can be significantly by climate group differ, genetics, age, sex, stress, hygiene, nutrition, hospitalization [37].

Skin abscess is the most common manifestations of bacterial infection. Abscess may appear in painful blocks degrade transient without medical intervention, or in severe cases, such as large deep cysts associated with the spread of the blood stream. Although many of the bacteria, causing Gram-positive and Gram-negative cysts, but Staphylococcus aureus, especially MRSA associated with the community, it is the causative agent of the most common. Once configured, it can interfere with pus in the lesion Walled significantly with the activity of antibiotics to the extent this makes antibiotic treatment effective to some extent when the abscess exceeds a certain size, with the emergence of the problem of additional scarring. In the case of EBioMedicine [39].

Hancock and his colleagues have positive peptide targeted basically describing the formation of cysts. Developed peptides screen anti-biofilm. In the laboratory, which prevent or eliminate biofilms formed by bacteria both Gram-positive and Gram-negative. In non-vertebrate models of infection P. aeruginosa, boosted the survival of the host [40].

The main question that arises from the study is the relationship between the strict response and abscess formation. It was responsible for the formation mechanisms kharaj an important topic for research in this field aureus. While some defense mechanisms for stress, such as reducing metals and oxidative stress and nitric, appear to have a role in the ability of S. aureus to form abscesses, the stringent response in this context has not been clarified yet. It is likely to be the primary contact due to the direct impact of the stringent response CodY regulator. CodY has proven that it affects the severity of the disease in many animal models by changing the expression of the organizers of key, such as agr (RNAIII and RNAII) and saeR, hemolysins (hla), leukocidins (lukSF), the synthesis of the capsule (icaADBC), as well as genes that show it is important to form an abscess. Expression PSMα, which shows that it prevents installed by DJK-5, independently organized through RSH for CodY. Specific factors that regulate the formation of abscess under the strict response remains identified in Staphylococcus aureus and other microbes [41].

From a clinical perspective, the siege imposed on the composition of the abscess would be a useful assistant to kill pathogens. Often, infected individuals already infected a large abscess requires Tbarva surgically. For those who provide abscesses smaller or in the early stages which are not viable after discharge surgical, antibiotics are used routinely, but may not be enough to stop the progress of formation of abscess, especially if the pathogen offending is relatively resistant to antibiotics. It can be strict inhibition of the response to the formation of mass abscess useful, and will compare the use of helper inhibitors of protein synthesis inhibition in the treatment of inflammatory toxin mediated by poison. Inhibitors will be particularly useful if they also prevent chronic or recurrent cysts including cases related to chronic bacteria gold that are difficult to treat, such as inflammation of the sweat glands Almqih. Future studies will need to prove that the inhibitors are still effective when used with antibiotics effective or marginal [42].

Other Bacteriologic characteristics. In the monomicrobial form, the pathogens are S. pyogenes, S. aureus, V. vulnificus, A. hydrophila, and anaerobic streptococci (i.e., Peptostreptococcus species). Can Staphylococcus aureus and Streptococcus hemolytic occur simultaneously? Most injuries are obtained from the community and there in the limbs, with nearly two-thirds of cases in the lower limbs. There is often an underlying cause, such as diabetes or vascular disease, atherosclerosis or venous insufficiency with edema. Sometimes, chronic vascular ulcers turn into a more intense process. Fasciitis cases of necrotizing that arise after infection varicella or trivial injuries, such as minor scratches and insect bites, always be the result of bacteria S. pyogenes. The mortality rate in this group is high, where close to 50–70% in patients with low blood pressure and organ failure [43].


6. Pathophysiology of abscesses formation

There are other factors, has not yet fully be understood, perhaps play a role. In addition, the large number of organisms found in the abscess, and the presence of an antibiotic inhibitor of enzymes, hostility Anaerobic activity anti-microbial host and defense environment, as well as fibroblasts in the capsule surrounding Boukerg, contributes to the persistence of infection despite antibiotic treatment and the need to exchange. You must remember the contribution of both aerobic and anaerobic organisms in the formation of cysts when one chooses antibiotics to treat such infections [44].


7. Common causes of a skin abscess

When breaking the skin’s natural barrier we have, even from simple shock, or small tears, or infections, bacteria can enter the skin. It can be formed where the abscess is trying to kill your body’s defenses these germs through the inflammatory response (white blood cells = pus). It can cause blockage of sweat or sebaceous gland or hair follicle or the bag to a pre-existing abscess.

Staphylococcus aureus, E. coli, P. aeruginosa, and Streptococcus pyogenes are the most common types of bacteria that cause skin abscesses in the following areas of the body; the head and neck, parties, armpits, trunk.

There are Staphylococcus aureus on the proper surface of the skin. It can cause skin infections, such as skin abscesses and boils, and preferably live in wet areas of the body such as the armpits, groin, and inside the nostrils.

Can some bacteria S. aureus produces a toxin called Panton-Valentine leukocidin (PVL), which kills white cells, causing the body to do more white cells to continue to fight infection.

PVL-positive strains of bacteria are therefore more likely to cause skin infections and abscess. They can also cause more serious conditions:

  • Septicaemia is blood poisoning caused by bacteria multiplying in the blood.

  • Pneumonia is swelling (inflammation) of the lungs caused by an infection. Pus collects in the airways and is coughed up as mucus [45, 46].


8. Types of skin abscesses

  • Impetigo, erysipelas, and cellulitis. Impetigo may be caused by infection with S. aureus and/or S. pyogenes. The decision of how to treat impetigo depends on the number of lesions, their location (face, eyelid, or mouth), and the need to limit spread of infection to others.

The tests antibody conjugate Streptococcus no value in the diagnosis and treatment of herpes, but they provide a useful supporting evidence of infection Streptococcus recent in patients suspected of having inflammation glomerulonephritis after Streptococcus. Anti Alstrptullizin O weak response in patients with herpes Streptococcus [47], Supposed to be fat in the skin working to suppress Alstrptullizin O response, but the levels consistently high DNase B [48].

Because S. aureus currently accounts for most cases of herpes bullosa, as well as for a large part of the non-inflammatory tumor. Complications of herpes retroviruses Streptococcus uncommon, for reasons not yet known, rheumatic fever did not occur after herpes Streptococcus. On the other hand, are skin infections that affect the strains of the renal group “A” of the main Streptococcus previous glomerulonephritis after Streptococcus in many regions of the world. There are no conclusive data indicate that the treatment of the skin Streptococcus pyoderma prevents nephritis, but this treatment is an important measure of a pandemic in the elimination of strains that infect the college community [49].


9. Abscess, cellulitis, and erysipelas

Cause inflammation of the tissue cell may be many of the original skin living organisms or in specific environmental areas. Inflammation associated with cysts usually caused by S. aureus.

9.1 Cellulitis

These terms refer to the spread of skin infections spread, except for infections associated with the well pyogenic inherent, such as skin abscesses and inflammation of the fascia enterocolitis and arthritis Morphological and osteomyelitis. Unfortunately, doctors use the term “cellulitis” and “blush” is inconsistent. For some, it regards the distinction between the two terms deeply inflammation: erysipelas affect the upper dermis, including surface lymphocyte, while the inflammation of the tissue cell includes deep dermis, as well as subcutaneous fat. In practice, it may be difficult to distinguish between inflammation of cellulose and Aloristil clinically, and used some doctors, especially in northern Europe, the term “blush” to describe both infections.

Erysipelas is characterized by clinically from other forms of skin infections following Balmizatan: lesions are raised above the surrounding skin level, and there is a clear line of demarcation between the concerned tissue and tissue is involved [50]. This disorder is more common among infants, young children, and older adults. It is almost always caused by β-hemolytic streptococci (usually group A), but similar lesions can be caused by streptococci from serogroups C or G. Rarely, group B streptococci or S. aureus may be involved. In older reports, erysipelas characteristically involved the butterfly area of the face, but at present, the lower extremities are more frequently affected [51].

With early diagnosis and appropriate treatment, the prognosis is excellent. However, the infection rarely extends to the deeper levels of the skin and soft tissue. Is penicillin, which is given either by intravenous or oral according to clinical severity, is the optimal treatment (A-III). In the case of suspected infection Staphylococcus aureus, you must choose penicillin-resistant semi-industrial penicillinase or cephalosporin of the first generation. (A-III). In multiple prospective randomized trial, the effectiveness of roxithromycin, anti-Maikaroledat, equivalent to those used in penicillin. Resistance between macrolides streptococci group, however, is increasing in the United States [52].

These infections arise when living organisms enter through breakthroughs in skin. Include predisposing factors for these infection cases that make it more fragile or local host defenses skin is less effective, such as obesity and previous skin damage, edema of venous insufficiency or blockage of the lymphatic or other reasons. The origin of the barrier may be inactivated skin is shock, and skin infections previously existing, such as herpes or eczema, ulceration, and networks toe chapped spots or fungal infections, skin and inflammatory diseases, such as eczema. Often, the commas are in a small skin and is clinically moderate. These infections can occur anywhere, but the most common in the lower legs [53].

Include surgical procedures that increase the risk of inflammation of cellulose, which is assumed to be due to the interruption of lymphatic drainage, eradication of venous bile, and the anatomy of the axillary node breast cancer, surgery for diseases of malignant women involving the lymph node dissection, especially when following radiation therapy node of lymph. The radical hysterectomy [54, 55, 56].

Streptococcus responsible in areas of intermittent intra-toe or cracked, underlining the importance of the discovery and treatment of ringworm foot and other causes of toe deformities in these patients. Sometimes, the Streptococcus tank is the anal canal or vagina, especially for the group B Streptococcus, which causes inflammation of the cellular tissue in patients with cancer, former women treated with surgery and radiation therapy. S. aureus less frequent causes inflammation of cellular tissue, and is often associated with penetrating trauma earlier, including the injection sites of drug use illegal [57, 58].

Can many factors other infectious inflammation of the production of cellular tissue, but usually only in special cases. With cat bites or dogs, for example, the administrator would be responsible for the object types Bastorella, especially P. multocida, or Capnocytophaga canimorsus. This may cause inflammation of the cellulose Alheffilh after immersion in fresh water, while the infection after exposure to salt water can arise from species Vibrio, especially V. vulnificus in warm climates. In rare cases, Streptococcus iniae or E. rhusiopathiae may cause infection in persons employed in aquaculture or meatpacking, respectively. Inflammation can occur Salil about the pilgrims caused by Haemophilus influenzae in children. It has been reported diagnostic and therapeutic considerations for these infections by the Committee on Infectious Diseases, American Academy of Pediatrics. In anti-neutropenia, infection may be caused by Pseudomonas aeruginosa or Gram-negative bacilli, and in patients with HIV, may be in charge of the organism is Helicobacter sinaada. From time to time, Alkraatokov neoformans cause inflammation of cellulose in patients with cellular immune deficiency [59, 60].

Due to the low production rate, the blood cultures is not fruitful for the case of typical cases of erysipelas or cellulitis, which were not particularly severe [61]. The aspirations of the needle and skin biopsies also are not necessary in typical cases, which must respond to treatment with antibiotics directed against Streptococcus and Staphylococcus. This may be more useful for patients with diabetes procedures, malignant tumors, and factors to prepare non-regular, such as injury immersion, bites and animals, neutropenia, and immune deficiency [62].

Include diseases that are sometimes confused with acute inflammation of the tissue cell, such as resulting from contact with a skin disease, inflammation of the causes of allergies; gout, with skin inflammation significantly extends beyond the affected joint; herpes zoster. Hardening of the skin of acute fatty, which is inflammation of the lip which occurs mostly in obese women with deficient women phlebitis in the lower limb, causing painful areas, erythematous, thin, warm, non-saturated, and sometimes scaly in the medial leg-like inflammation of cellular tissue [63].

The lifting of the affected area, which is an important aspect and is often overlooked in the treatment, the improvement process accelerates by encouraging the discharge of gravity edema and inflammatory substances. Patients should also receive appropriate treatment for any medical condition may be ripe for infection, such as ringworm foot or venous eczema (“stasis dermatitis”) or shock.

Each bout of cellulitis cause inflammation and lymphatic perhaps some permanent damage. Acute or recurrent seizures may result from inflammation of the tissue cell to lymph edema, which are in some cases large enough to cause the elephant’s disease. Measures to reduce the recurrence of inflammation of the tissue cell treatment maceration between the numbers, maintain skin hydration well emollients to avoid dehydration and cracking, and minimize any essential edema in ways such as raising the upper limb, or compression stockings, or pressure pumps air, and if appropriate, treatment Diuretic. If frequent infections occur despite such measures, prophylactic antibiotics appear reasonable; however, published results demonstrating efficacy have been mixed [64]. Because streptococci cause most recurrent cellulitis, options include monthly intramuscular benzathine penicillin injections of 1.2 MU in adults or oral therapy with twice-daily doses of either 250 mg of erythromycin or 1 g of penicillin V (B-II). An alternative option, but has not been tested, for patients suffering from inflammation of trusted frequent cellulose is an attempt to shorten each episode by providing antibiotics by mouth for them to start treatment as soon as the start of the symptoms of infection. One of the selenium experience by mouth showed a decline in the rate of recurrence of erysipelas in the secondary lymph edema by 80%. This report requires independent confirmation [65].

9.2 Cutaneous abscesses

Skin cysts are collections of pus intradermal skin and deep tissue. Usually red nodules are painful, thin, volatile, often surmounted by a pimple surrounded by the edge of the swelling erythema. Usually multiple microbes skin cysts, and contain bacteria form the regional natural skin flora, and are often combined with living organisms from the adjacent mucous membranes [65]. S. aureus is present, usually one nurse, only ~25% of skin cysts in general. Cysts contain up the skin, which often carry the wrong signs as “fat bags,” usually on the Flora Leather article in the cornea Aljbnah, even when they are not inflamed. The cultures of the inflamed cysts produce the same living organisms, suggesting that inflammation and vomiting occur in reaction to the rupture of the cyst wall and threw its contents into the dermis, instead of infectious complications [66].

9.3 Furuncles and carbuncles

Strangeness (or “boils”) is inflammation of the hair follicles, usually caused by Staphylococcus aureus, extending pus through the dermis to the subcutaneous tissue, where a small abscess is formed. It is therefore different from folliculitis, where inflammation is more superficial and there is pus in the skin. Deer can occur anywhere on the skin hairy. Each lesion consists of dogma Inflammatory and upper blister show which hair. When the infection extends to include several contiguous follicles, and produces a homogeneous mass inflammatory with pus distracted from multiple holes porous, called the beauty of the lesion. Muscles tend to develop on the back of the neck is likely to occur particularly in people with diabetes. For small oven, be moist heat, which seems to enhance drainage, satisfactory. Larger Alorfan require larger and all bony rip Tbarva. Systemic antibiotics are usually not necessary, what inflammation Salil or the surrounding fever did not occur on a large scale (E-III). Cases may occur outbreak of inflammation of the thyroid gland caused by MS (MSSA), and as well as MRSA disease in families and other places that involve personal contact and close (such as prisons), especially when the skin are common injury, such as sports teams or Entertainment groups outdoors. The lack of personal hygiene and insufficient exposure to others injured Balfrt predisposing factors important in these circumstances. In some cases, it may harbor fungus organism and facilitate the transmission. Depending on the individual circumstances, it may require control of outbreaks bathing antibacterial soap, such as chlorhexidine; thorough washing of clothes, towels and clothes family; use separate towels and towels. And try to eliminate the transfer of cluster Meningococcal between the colonists [67].

Some individuals have frequent bouts of injury. Have a few of these people, especially children, host responses methodology is not normal, but for most of them, the only Almahb factor that can be determined is the presence of Staphylococcus aureus in the front openings or sometimes elsewhere, such as perineum [68].

9.3.1 Soft-tissue infections and the evaluation of MRSA infection

The emerging problem is to increase the spread of the skin and soft tissue infections caused by MRSA acquired by the community. Considered MRSA, which is traditionally considered one of the causes of disease-causing diseases, pathogens that occur in the community, and differ from their counterparts in hospitals in several ways [69]. Cause community strains infections in patients who lack the typical risk factors, such as hospitalization or residence in a long-term care facility; often are susceptible to antibiotics, non-lactam, including doxycycline or clindamycin or trimethoprim—sulfamethoxazole or fluoroquinolone or rifampin; genetically, do not appear to be linked to local hospitals and strains contain a cassette-type SCCmec of the fourth type is unusual in Isolates hospital. Finally, community isolates frequently contain genes for Banoudin Valuksidin, which is associated with mild to severe infections in the skin and soft tissue. It occurred because of an outbreak of MRSA isolates acquired from the community between prison inmates and prisons, injecting drug users and the Native American population and gay men and participants in sports Immobilizer children [70]. Thus, recurrent or persistent furuncles and impetigo, particularly in these high-risk groups, that do not respond to oral β-lactam antibiotic therapy are increasingly likely to be caused by MRSA.

9.3.2 Necrotizing skin and soft-tissue infections

Necrotizing fasciitis may be chronic to bacteria and result from Cyclococcus, Pseudomonas, or aqueous Aeromonas. Recently, necrotizing fasciitis has been prescribed in a patient with MRSA infection. Inflammation of multiple necrotic fasciitis may occur microbes after surgery or in patients with peripheral vascular disease, diabetes, ulcers lie down, tears spontaneous mucous in the digestive tract or the digestive system (i.e., Fournier gangrene). As with renal bone necrosis, unless there is gas in the deep tissue often in these mixed infections [71].

Soft and soft tissue infections skin infections differ from light and surface through clinical presentation and common systemic manifestations and treatment strategies [72]. Are often deep and destructive. It is deep because it may involve fascial compartments and/or muscles; it is devastating because it caused great destruction of tissue and can lead to a fatal outcome. These cases are usually an injury “minor,” as it evolves from an initial break in the skin due to trauma or surgery. It can be abnormal (usually containing Streptococcus or Staphylococcus aureus rarely) or multiple microbes (containing plants from mixed bacterial aerobe-anaerobe). In the initial stages, it may be difficult to distinguish between inflammation of the cellular tissue, which must respond to the treatment of anti-microbial alone necrotizing infection that requires surgical intervention. Many of the clinical characteristics indicate a necrotic infection of the skin and deep structures: (1) severe pain and constant; (2) bubbles, concerning the obstruction of blood vessels deep that traverse the fascia or muscle compartments; (3) the skin or bruises necrosis (bruises) that precedes skin necrosis; (4) gas in the soft tissue, detection palpation or photography; (5) edema extends beyond the margin of erythema; (6) skin anesthesia; (7) of systemic toxicity, manifested in fever, leukocytosis, delirium, and renal failure; and (8) rapid deployment, especially during antibiotic treatment. Bubbles alone is not a diagnosis of deep infections, because they also occur with erysipelas, cellulitis, burned skin syndrome, coagulation diffuse into the blood vessels, Volminac Purpura, some toxins (e.g., those associated with bites of spider brown), skin diseases skin.


10. Necrotizing fasciitis

Fasciitis is an infection necrotizing under the skin are relatively rare tracks on the aircraft along the fascia and extends beyond the surface signs of infection, such as erythema and other skin changes [73]. The term fasciitis sometimes leads to the mistaken impression that the muscle fascia or interruption of urine. The most common fascia is superficial fascia, which consists of all the tissues between the skin and the core muscles (i.e., tissue under the skin).

The clinical characteristic feature is the sense of the wooden tissue under the skin. Inflammation of cellular tissue or blush, can seep tissue under the skin and produces. But in the inflammation of the fascia, the tissue implicit fixed, and cannot distinguish blame and vascular aircraft by palpation. It is often possible to note the course of erythema wide in the skin along the infection during its progress in cattle head. If there is an open wound, the examination of the edges with a sharp tool allows an autopsy on ready-to-aircraft vascular surface that exceed the margins of the wound.

11. Anaerobic streptococcal myositis

Streptococcus anaerobic cause more than other Streptococcus aureus infection lazy. Unlike other dead infections, usually associated with muscle injury and aircraft Allvaiah streptococcal anaerobic shock or perform surgery. Incision and drainage necessary. The necrotic tissue and debris eradication but should not remove the inflamed muscles viable, because they can heal and restore function. It must be packed incision with wet bandages. Antibiotic treatment is very effective. All of these organisms susceptible to penicillin or ampicillin, which must be administered in high doses.

12. Pyomyositis

Inflammation of the mouth, which is caused by Staphylococcus aureus essentially, is the presence of pus within individual muscle groups. In some cases, the pulmonary S. or Gram-negative intestinal bacillus is responsible. Because of its geographical distribution, often called the case “orbital inflammation of the pus,” but it is recognized cases increasingly in temperate climates, especially in patients with HIV or diabetes, lack of. Present the results are local pain in a muscular one, muscle cramps, and fever. This disease occurs mostly, but can share any muscle group, including lumbar muscle or trunk muscles. At first, it may not be possible to contact the separate abscess because localized infection deep within the muscles, but the area has a wooden feeling strong is associated with pain and tenderness. In the early stages, you can perform ultrasound imaging or CT scans to distinguish between this entity and deep venous thrombosis. In the most advanced cases, the abscess is swollen and clinically evident. And appropriate antibiotics in addition to the surgical incision and extensive health and sanitation are required for the proper management [74].

13. Synergistic necrotizing cellulitis

This is simply inflammation of the soft tissue enterocolitis, which includes muscle groups in addition to the surface tissue and fascia. The level of participation depends on the depth and levels of tissue affected by the process of origin or pathological process that precedes infection. Predisposing main causes are cysts circular ischemic. Similar recognition and treatment with inflammation of the fascia grunt, but surgical exploration reveals his innermost.

  • Surgical site infections. Include infections of soft tissue surgical those that occur after surgery and those severe enough to require surgical intervention for diagnosis and treatment. Clearly provided the algorithm indicates that the infection site surgical rarely occur during the first 48 h after surgery, usually arise fever during that period of non-infectious causes or unknown.

14. Fournier gangrene

Gas gangrene is a rapidly progressive infection caused by Clostridium perfringens, Clostridium septicum, Clostridium histolyticum, or Clostridium novyi. Severe penetrating trauma or crush injuries associated with interruption of the blood supply are the usual predisposing factors. C. perfringens and C. novyi infections have recently been described among heroin abusers following intracutaneous injection of black tar heroin. C. septicum, a more aerotolerant Clostridium species, may cause spontaneous gas gangrene in patients with colonic lesions (such as those due to diverticular disease), adenocarcinoma, or neutropenia.

This type of inflammation of the soft tissue grunt includes scrotum and penis or vagina and can have a malicious or explosive beginning [75]. The average age of onset is 50 years. Most of the patients suffer from a significant illness, especially diabetes, but 20% of them will not have a clear reason. Most patients initially have an infection around the anus or retroperitoneal spread on aircraft along the fascia to the genitals. Inflammation of the urinary tract, the most common in the event of a narrowing of the urethra, and includes glands around the urethra and extends to the penis and scrotum; or previous trauma to the genital area, allowing the arrival of living organisms to the tissues under the skin.

Infection can start insidious with a separate area of necrosis in the perineum, which is rapidly advancing within 1–2 days with the progress of skin necrosis. In the beginning, it tends to cause surface gangrene, and is limited to the skin and subcutaneous tissue, and extends to the base of the scrotum. Usually save the testicles, glans penis, and the spermatic cord, because they contain a separate blood source. Infection may extend to the perineum and the anterior abdominal wall through the fascia aircraft.

Most of the cases caused by mixed aerobic and anaerobic plants. Often there are types of Staphylococcus aureus bacteria Pseudomonas, usually in a mixed culture, but in some cases, be Staphylococcus aureus is the only pathogen. False is another common object in the mixed culture. As with other infections dead, is the rapid surgical exploration of aggressive and appropriate purification necessary to remove all the dead tissue, while avoiding the deeper structures when possible.

15. Clostridial myonecrosis

Cause gas gangrene Clostridium (e.g., muscular muscle necrosis) significantly from C. perfringens and C. novyi and C. histolyticum and C. septicum. C. perfringens is the most common cause of gas gangrene associated with shocks. Severe pain increasingly begins at the site of infection after 24 h of infection is the first symptom of reliable. The skin may be pale at first, but quickly changed to bronze and then to the red color purple. The area becomes infected tense and smooth, show fluid-filled bubbles blue reddish. There is gas in the tissue, which is detected as crepitus or on the basis of imaging studies, globally present at this late stage. Systemic signs of toxicity, including irregular heartbeats, fever, sweating, develop rapidly, followed by shock and the failure of multiple members.

Both painful gas gangrene and spontaneous are destructive infection requiring accurate intensive care, and support measures, and aggressive surgical revision, and appropriate antibiotics. The role of oxygen therapy high pressure is still unclear. Altemeier and Fullen [76]. It has been reported significant reduction in the mortality rate among patients with gas gangrene using penicillin and tetracycline in addition to aggressive surgery in the absence of high-pressure oxygen. Treatment of experimental gas gangrene proved that tetracycline and clindamycin and chloramphenicol were more effective than penicillin or high-pressure oxygen treatment [77].

16. Clinical manifestations

Abscess clear zones of erythema, edema, and warmth. Evolve as a result of bacteria entering through the breakthroughs in the skin barrier [78]. You can be seen Petechiae and/or bleeding in the skin erythema, and can surface bubbles occur. Fever and other systemic manifestations of infection may also be present. Cysts are always one-sided almost, lower limbs are the most common sites of involvement; bilateral engagement should consider quickly in alternative causes [79].

Cysts deep dermis and subcutaneous fat include; reddish include the upper and lymph dermis surface. Cysts with or without purulent may appear. Erysipelas is grainy [80]. It tends patients with cysts or cellulitis to get more comfortable with the development cycle of topical symptoms over a few days [81].

Patients suffering from erysipelas usually suffer from the emergence of severe symptoms with systemic manifestations, including fever, chills, feeling very upset and headache; these can precede the onset of signs and symptoms of local infections from minutes to hours. In erysipelas, there is a clear demarcation between the involved and associated tissues. There may be raised or erythematous border with central clearing. Classic descriptions of the red leaf notes “butterfly” face involvement. The involvement of the ear (ear tag in Milian) is a distinctive feature of Oryeceblas, because this area does not contain deeper tissues of the skin [82].

Additional features of the abscesses and lymphatic vessels Oristepelas inflammation and enlargement of the regional lymph nodes. Edema surrounding Bbesellat hair may lead to variation in the skin, which creates showing little strength orange peel (“peau d’orange”). This can be seen vesicles bubbles and akimats or Alnchat. Can bleeding skin in the case of a significant inflammation of the skin. Inflammation of the cellular tissue that causes injury and inflammation Alglazi Algrgreeni is an unusual manifestation of inflammation due to cellular Alclaustradia and other anaerobes. It should be the acute manifestations of systemic toxicity with the rapid investigation of additional sources underlying infection [83].

17. Diagnosis of complicated abscess and soft tissues infections

Often begins with a diagnosis of a comprehensive abscesses clinical history and physical examination results, which helps to assess the severity of infection, followed by the study of the living organisms that cause microbearing [84, 85].

Standard procedure is to increase the clinical assessment of laboratory investigations, especially for inpatient. In addition to the patient’s history, should be taken into account relevant risk factors such as frequent entry in the hospital factors, diabetes, neutropenia, wounds sting and animal contact, which may indicate a potential junior responsible for the injury of living organisms [86].

Possible complications associated with cysts such as inflammation of the lymph glands and muscle inflammation and inflammation of the intestine and colon, gangrene, osteomyelitis, bacteremia, endocarditis, blood poisoning or poisoning should be taken into account during the diagnosis. It may indicate a significant increase in the number of white blood cells (or leukopenia) syndrome poisoning, while the levels of creatine kinase high may indicate the presence of muscles selflessly caused by inflammation of the fascia or inflammation of the bowel syndrome and colon [87].

Radiological examination and investigations aid imaging of deep tissue infections to assess the location and size of the infection and any involvement of blood vessels that can guide surgical drainage procedures. Tests must be performed culturing microbiological in all cases to distinguish between abscesses and MRSA infections, non-infectious MRSA, and therefore the revision of the final decision on the management of antibiotics to reduce the risk of treatment failure likely [88].

Diagnosis of skin abscess usually depends on the clinical manifestations. Abscess appears Oristepelas in areas of skin erythema, edema, and warmth. It is raised lesions Erysipelas higher than the surrounding skin with a clear delineation of the level of tissue between the concerned and involved. Skin abscess appears as a painful, volatile, erythematous node, with or without a surrounding abscess.

For laboratory tests are not required for patients with uncomplicated infection in the absence of associated diseases or complications. It must be subject to patients with disposable abscess incision and drainage. Routine culture of materials debrided is not necessary in healthy patients who are not receiving antibiotics [89].

There is no justification for the cultures of abandoned materials and cultures of blood (before the addition of antibiotic treatment) in the following cases [90, 91]:

  • Severe local infection (e.g., extensive cellulitis).

  • Systemic signs of infection (e.g., fever).

  • History of recurrent or multiple abscesses.

  • Failure of initial antibiotic therapy.

  • Extremes of age (young infants or older adults).

  • Presence of underlying comorbidities (lymphedema, malignancy, neutropenia, immunodeficiency, splenectomy, diabetes).

  • Special exposures (animal bite, water-associated injury).

  • Presence of indication for prophylaxis against infective endocarditis.

  • Community patterns of S. aureus susceptibility are unknown or rapidly changing.

Blood cultures are positive in less than 10% of cellulitis cases [92]. There may be a justification for skin biopsy if the diagnosis is uncertain; cultures from samples of skin biopsy result in pathogens in 20–30% of cases. Cultures of healthy skin wipes are not useful and should not be done [93].

It can be useful radiographic examination to determine whether the skin abscess is present (via ultrasound) and to distinguish between cellulitis and osteomyelitis (via magnetic resonance imaging). There may be a justification for radiological assessment in patients with immune suppression, diabetes, venous insufficiency, or lymphedema in patients with persistent symptoms of systemic. Radiological examination cannot reliably distinguish inflammation from Salil fasciitis or gas gangrene Grunt; if there is clinical doubt for these entities, the imaging should not delay surgical intervention [94].

In patients with recurrent cysts, serological tests for drugs Almnhllh blood beta may be a useful diagnostic tool. Assays include the reaction of an anti Alstrptullizin-O (ASO), or test an anti-desoxyribonuclease b (anti-DNA), or anti Alheialoronidaz test (AHT), or antibody test Alstrepettosem [95].

18. Problems related to the emergence of MDR related abscesses and related clinical management issues

Experimental methods are used to treat a range of cysts surgical treatments and antimicrobial support. However, high resistance of microorganisms to the antibiotics [96]. Resistant organisms medicines in particular, may complicate the treatment of cSSTI. Between the organisms of multi-drug resistance, MRSA, enterococci resistant to vancomycin (VRE), and gentle stretching act-lactamase (ESBL)—producing isolates of E. coli and Klebsiella spp. It has the highest incidence of [97]. Strains of CA-MRSA differ genetically apparently from HA-MRSA, and thus involve the risk of more severe infections and ease of transmission of resistance [98].

The presence of Pantone assumed—Valentin Okosidin, Botulinum cellular genes coding in MRSA isolated from infection CA—skin to play an important role in this increased virulence strains associated with tissue necrosis, and necrosis of the severity of the largest local and systemic manifestations [99]. Carrying strains of CA-MRSA is also the genes of chromosome mec (SCCmec) Staphylococcus aureus (types IV and V), which gives resistance to methicillin and antimicrobial agents β currently available and help in the transfer of resistance easily between living organisms. Although MRSA infection was considered, HA mainly, recent evidence has appeared on the emergence of CA-MRSA rapid even in hospitals [100].

19. Surgical methods and supportive care

The secretions of fluid from the abscess and ulcers are the common features of bacterial abscesses. Therefore, aggressive surgical revision dead tissue/infected by using chemical or mechanical methods of preferred whenever possible to stop the spread of infection and promote wound healing. The delay is known in the final revision of the soft tissue infections is considered one of the most important risk factor for death [101]. Implementation of incision and drainage of inflammatory cysts and purulent [102]. Other roads dressing negative pressure, chronic infection or localized large wounds with excessive secretion [103]. Download closure with the help of the vacuum (as a substitute for wound healing), especially for surgical wounds or subsequent surgery deep infections, infections of the blood clotting involving venous blood clots, and vascular compensation cases involving injuries in the vascular arteries. Supportive care, which includes fluid resuscitation, and members of the support, nutritional, and management to maintain oxygen and tissue perfusion important interventions in the clinical outcomes of these patients are considered [104].

20. Treatment of skin abscess

Some small cysts degrade without treatment, up to the point of disposal. Warm compresses help to speed up the process. It referred to as the incision and drainage when there is a great pain, tenderness and swelling. It is not necessary to wait for volatility. Under sterile conditions, local anesthesia either lidocaine or freezing spray is given [105].

Patients suffering from abscesses intravenous anesthesia large and extremely painful and may benefit pain during the exchange. Often enough having one hole tip stripes to open the abscess. After draining the pus, you must examine the cavity or glove full finger scan sites. Optional normal saline irrigation with gauze used to reduce dead space cavity and prevents the formation of vaccines. Usually the valves are removed after 24–48 h. However, the recent data did not prove the effectiveness of routine irrigation or packing. High local temperature may precipitate inflammation decision [106].

Surgical intervention is the main therapeutic method in cases of fasciitis enterocolitis (A-III). However, many cases of inflammation of the fascia Grunt may begin to Kthab descendant, and if you have been identified fasciitis necrotizing early and treated aggressively, it avoids some patients distort surgical procedures. It must be based on the decision of an aggressive surgery to several considerations. First, there is no response to antibiotics after a reasonable experience is the most common indicator. You must be judged to respond to antibiotics by reducing fever and toxicity and lack of progress. Second, deep toxicity, fever, low blood pressure, or skin and soft tissue provided during antibiotic treatment is an indication for surgical intervention. Third, when the local wound necrosis appears in any skin with easy dissecting along the fascia using a blunt tool, you need to make an incision and a more complete discharge. Fourth, any soft tissue infection accompanied by gas in the injured tissue suggests the presence of tissue necrosis requires Tbarva surgically and/or anesthesia.

Most of the patients must come back with rheumatoid fasciitis Grunt to the operating room over the first 24–36 h after the anesthesia process, and then a day until the surgical team finds no further need debridement. Although separate pus is usually absent, these wounds can discharge abundant amounts of tissue fluid. Aggressive management of fluid is necessary assistant.

You must treat inflammation of the fascia Grunt and/or toxic shock conjugate caused by Streptococcus Group A syndrome of streptococci using penicillin and clindamycin (A-II). The rationale for clindamycin in laboratory studies that show both the suppression of toxins and modify the production of cytokines (i.e., TNF), and on animal studies showing the effectiveness of superior versus penicillin, and two studies Rsiditin demonstrating the greater effectiveness of clindamycin for β-antibiotics lactam [107, 108]. You must add penicillin due to increased resistance to Group A Streptococcus conjugate of Macroledat, although it is in the United States, only 0.5% of the Group A drug resistance Almacrolad is also resistant to clindamycin.

Cannot be recommended for sure using of beta globulin (B-II) intravenously in the treatment of toxic shock syndrome conjugate Streptococcus. Although there is sufficient evidence on the role of toxins Streptococcus outside the cellular in shock, organ failure, and the destruction of tissue, containing different sets of IVIG variable amounts of neutralizing antibodies to some of these toxins, and lacked the final clinical data [107]. One of observational studies have shown better results in patients receiving IVIG, but these patients were more likely to undergo surgery and received more than historical control subjects clindamycin [108]. Showed a second study, was a double-blind trial, which placebo-controlled northern Europe, no improvement statistically significant in survival, and specifically for this section, any decrease in due time for the lack of further progress fasciitis necrosis (69 h for IVIG group, compared to 36 h for a placebo) [109]. The results of these studies provide some promise. However, the Committee believes that further studies on the effectiveness of IVIG is necessary before it can make a recommendation on the use of IVIG for the treatment of toxic shock syndrome conjugate Streptococcus.

21. Abscess arises from the body parts

21.1 Dental abscess

In the early seventeenth century, death bonds began in London on account of the causes of death with teeth inserted continuously in the list of the main reasons for the fifth or sixth death [110]. By the twentieth century, it has been recognized the possibility of the spread of dental abscesses and cause acute poisoning leading to death. An audit was conducted at the Hull Royal Hospital between 1999 and 2004, an increase in the number of patients who provide services to oral surgery, face and jaws with teeth rot [111]. In the United States, a large prospective study reported that 13% of adult patients sought treatment for dental pain and infection over 24 months of follow-up [112]. The percentage of abscess dentoalveolar occurred 6.4% among children who attended the dental clinic at the outpatient clinics in Nigeria. In India, dental caries affect 60–65% of the general population [113]. Factors involved in the bacteriological cause abscesses teeth consist of a complex mix of strict anaerobic and anaerobic optional. Derived data sets show cultural and molecular studies that have been identified more than 460 unique bacterial species that belong to 100 genus and 9 species in different types of infections pulposus [114]. Signs and symptoms of acute abscess in the teeth are pain, swelling, and erythema are usually localized infected teeth, although suppuration can spread often to nearby tissues, causing fatal complications. Fever, swelling of the mouth and inside the mouth, erythema, tenderness to palpation significantly. Trismus in addition to any changes in the sound, such as hoarseness and a torrent of saliva should pay the doctor to the state of emergency [115].

21.2 Subcutaneous tissue abscess

Respond to simple infections confined to the skin and underlying soft tissues in general to manage outpatient. Among the common symptoms are simple: cellulitis, erysipelas, herpes, folliculitis, fur, shrimp, cysts, infections and injuries. Include complex injuries that extend to the deep underlying tissue, which include deep cysts, ulcers decubitus, fasciitis grunt, Fournier gangrene, infections of human or animal bite. These infections may appear with the inflammatory response syndrome features or systemic sepsis, and sometimes brain necrosis. Inflammation around the anus, and diabetic foot infections, infections in patients with accompanying diseases, and infections of the causes of resistance diseases also represent a complex inflammatory. The diseases of aging, heart disease, or liver, or diabetes, or weakness, or immune poisoning, or obesity, or arterial venous insufficiency or peripheral lymphatic, and psychological trauma among the risk factors of infection of sexually transmitted. The spread of the disease is more common among military personnel during deployment abroad and athletes participating in the nearby sports. Provide with erythema, warmth, edema, and pain on the affected site. Systemic manifestations of infection may follow, reflect the size of the severity of infection. Lower limbs are the most common [116].

21.3 Lymph node abscess

Found swollen lymph node cervical in many different disciplines of general medicine to specialized disciplines such as ear nose and throat surgery or maxillofacial surgery craniofacial. It causes swelling benign or malignant may be. Swellings or even benign cysts as a result of infection due mostly Staphylococcus aureus and Group A. Rare disease of animal origin also causes swelling of the lymph node is Altolemia disease. This disease shows all over the northern hemisphere, but the proportion of a 1056 case only registered in the EU in 2016 is very low [117]. Francasla Tolensis, one of the causes of Altolemia disease, is Gram-negative bacteria; been described for the first time in 1911 in the United States of America (USA). Bacteria can be divided into four different strains. Sub-species F. tularensis subspecies holarctica spread mostly in Europe, while the sub-species F. tularensis subspecies tularensis exist frequently in North America. Although it is the same bacteria can be identified in more than 250 different animal species, but the exact path of transmission to humans is not yet clear [118]. In order to avoid serious illness and complications, it is necessary to appropriate early treatment after identifying pathogens. Active substances of antibiotics are aminoglycosides and fluoroquinolones and tetracycline and chloramphenicol and rifampicin. It should not be used erythromycin as a representative of Macroledat because of natural resistance, especially for the type of mushroom ring [119].

21.4 Perianal abscess

Cysts around the anus are the most common types of cysts anal. These cysts can cause considerable annoyance to patients. It is located at the edge of the anus, and if left untreated can extend into space ischioanal or space intersphincteric because these areas are continuing with the space around the anus. It can also cause systemic infection if left untreated [120]. The prevalence rate of cysts around the anus and anal cysts, in general, is underestimated, since most patients do not seek medical care, or are refusing as the occasional hemorrhoids. It is estimated that there are approximately 100,000 cases of benign anal disease in general. The average age at presentation is 40 years, and that the male mostly of adults twice the rate of infection than females [121]. Abscess around the anus is an indication of the incision and drainage in a timely manner. Antibiotics management alone is inadequate and inappropriate. Once you make an incision and drainage, there is no need to antibiotics unless management require some use of medical problems. Such cases include valvular heart disease, and patients with immune deficiency, diabetes patients, or in the development of sepsis. Antibiotics are also considered in these patients or cases showing signs of infection or systemic inflammation of the cellular tissue surrounding [122].

21.5 Breast abscess

Breast infections are divided into categories of breastfeeding and non-breastfeeding, or postpartum and non-puerperal. It can be associated with the surface of the skin or underlying lesion. The breast abscesses are more common in lactating women, but they also occur when women are breastfeeding. It is important to rule out more serious diseases such as breast cancer when the patient gets unsatisfactory signs and symptoms of breast abscess. The vast majority of these injuries occur in females, but they can also occur in males. Diagnosis and treatment of breast abscess is not difficult, but there is a high percentage of repetition [123]. Abscesses breast disease is often caused by Staphylococcus aureus and Streptococcus species, it became Staphylococcus aureus resistant MRSA increasingly common. Usually breast abscess is a result of a mixed deciduous plants with bacteria S. aureus and Streptococcus and anaerobic bacteria [124]. Incision and drainage are the standard for the care of breast abscesses. If the patient’s back in a primary care centers by the provider is not satisfied with the implementation of these procedures, the patient may start antibiotics and transmit it to a general surgeon for final treatment. You may be trying to suction the needle abscesses smaller than 3 cm or abscesses milk [125].

21.6 Liver abscess

Liver abscess is a pus-filled mass inside the liver [126]. Common causes are cases of abdominal such as appendicitis or diverticulitis because of the spread of blood through the portal vein. Can also develop liver injury complication [127]. The prognosis has improved for liver abscesses. The mortality rate in-hospital is about 2.5–19%. The elderly, ICU admissions, shock, cancer, fungal infections, cirrhosis, chronic kidney disease, acute respiratory failure, severe disease, or disease of biliary origin have a worse prognosis [128]. Antibiotics: metronidazole fourth and third generation cephalosporin/quinolones, antibiotics and β-lactam, and aminoglycosides effective [129].

21.7 Brain abscess

Cysts inside the skull is a common and serious life-threatening. They include brain abscess and subdural empyema or outside the dura and are classified by location anatomic or the causative agent of the disease. The term brain abscess is used in this article to represent all types of cysts within the skull [130]. Abscess formation may occur after nerve surgery or head trauma. In these cases it is often the cause of the bacterial skin infection by, such as Staphylococcus aureus and S. epidermidis, or negative bacilli Gram. Sinus) it is often caused by Streptococcus species 4 but abscesses Staphylococcus aureus and microbes (including those resulting from the anaerobic Gram-negative bacilli) also occur [131].

21.8 Renal abscess

Renal cysts and the period surrounding the animal are satisfactory entities that are uncommon due to kidney infections or around it. Moreover, it is a challenge for diagnostic physicians. Delays in diagnosis may lead to higher morbidity and mortality rates [132]. With the availability of computerized tomography (CT) and magnetic resonance imaging (MRI) in the diagnosis of renal cysts, the mortality rate dropped to 12% [133]. The mainstay of the treatment of kidney cysts or perineum is adequate drainage system and antibiotics optimal. Include the classic management of kidney cysts surgical exploration, incision and drainage, or the eradication of the kidney. However, the destructive treatment at the beginning of the 1970s appeared, and the trend towards common conservative treatment due to advances in new imaging techniques and antibiotics. It is noticed several reports that small cysts nephrotic effectively treated through antibiotics intravenously.


  1. 1. Stevens D, Bisno A, Chambers H. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clinical Infectious Diseases. 2014;59(3):147-240
  2. 2. Singer A, Talan D. Management of skin abscesses in the era of methicillin-resistant Staphylococcus aureus. The New England Journal of Medicine. 2014;370(23):1039-1099
  3. 3. Demos M, McLeod M, Nouri K. Recurrent furunculosis: A review of the literature. The British Journal of Dermatology. 2012;167(21):725-780
  4. 4. Summanen P, Talan D, Strong C. Bacteriology of skin and soft-tissue infections: Comparison of infections in intravenous drug users and individuals with no history of intravenous drug use. Clinical Infectious Diseases. 1995;20(Suppl 2):279-390
  5. 5. Brook I, Frazier E. Aerobic and anaerobic bacteriology of wounds and cutaneous abscesses. Archives of Surgery. 1990;125(37):1445-1499
  6. 6. Talan JA, David A. Management of skin abscesses in the era of methicillin-resistant Staphylococcus aureus. England Journal of Medicine. 2014;370(11):1039-1047
  7. 7. Singer A, Thode H, Lee C. National epidemiology of cutaneous abscesses: 1996 to 2005. The American Journal of Emergency Medicine. 2009;27(3):289-292
  8. 8. Paterson D. Increases in Australian cutaneous abscess hospitalisations: 1999-2008. Microbiology & Infectious Diseases. 2012;31(1):93-96
  9. 9. United Kingdom National Health Service. Abscess. 2014;32(12):10-30
  10. 10. Kanz G. Diagnostic and treatment options for skin and soft tissue abscesses in injecting drug users with consideration of the natural history and concomitant risk factors. European Journal of Medical Research. 2008;13(9):415-424
  11. 11. John K. Spinal subdural abscess following epidural steroid injection. Journal of Neurosurgery. Spine. 2014;22(1):90-93
  12. 12. Marx D, John A, Marx M. 8th Chapter 137 Rosen’s emergency medicine: Concepts and clinical practice. Skin and Soft Tissue Infections. 2014;43(65):4123-4207
  13. 13. Ellis Simonsen S, van Orman E, Hatch B. Cellulitis incidence in a defined population. Epidemiology and Infection. 2006;134(21):293-299
  14. 14. Vinh D, Embil J. Rapidly progressive soft tissue infections. Lancet Infectious Diseases. 2005;5(31):501-513
  15. 15. Baddour L. Epidemiology, Clinical Features, and Diagnosis of Cellulitis. 2008. Available from:
  16. 16. Eron L, Lipsky B, Low D, Nathwani D, Tice A, Volturo G. Expert panel on managing skin and soft tissue infections. Managing skin and soft tissue infections: Expert panel recommendations on key decision points. The Journal of Antimicrobial Chemotherapy. 2003;52(31):102-202
  17. 17. Dworkin R, Johnson R, Breuer J. Recommendations for the management of herpes zoster. Clinical Infectious Diseases. 2007;44(1):1-26
  18. 18. Merritt C, Haran J, Mintzer J. All purulence is local—Epidemiology and management of skin and soft tissue infections in three urban emergency departments. BMC Emergency Medicine. 2013;13(21):26-43
  19. 19. Talan D, Krishnadasan A, Gorwitz R, EMERGEncy ID Net Study Group. Comparison of Staphylococcus aureus from skin and soft-tissue infections in US emergency department patients, 2004 and 2008. Clinical Infectious Diseases. 2011;53(21):144-149
  20. 20. Edelsberg J, Taneja C, Zervos M. Trends in US hospital admissions for skin and soft tissue infections. Emerging Infectious Diseases. 2009;15(31):1516-1518
  21. 21. Gerber J, Coffin S, Smathers S. Trends in the incidence of methicillin-resistant Staphylococcus aureus infection in children’s hospitals in the United States. Clinical Infectious Diseases. 2009;49(20):65-71
  22. 22. Labreche M, Lee G, Attridge R. Treatment failure and costs in patients with methicillin-resistant Staphylococcus aureus skin and soft tissue infections: A South Texas Ambulatory Research Network (STARNet) study. Journal of the American Board of Family Medicine. 2013;26(98):508-517
  23. 23. Horowitz Y, Sperber A, Almog Y. Gram-negative cellulitis complicating cirrhosis. Mayo Clinic Proceedings. 2004;79(21):247-250
  24. 24. Björnsdóttir S, Gottfredsson M, Thórisdóttir A. Risk factors for acute cellulitis of the lower limb: A prospective case-control study. Clinical Infectious Diseases. 2005;41(21):1416-1422
  25. 25. Stevens D, Bisno A, Chambers H. Infectious Diseases Society of America. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clinical Infectious Diseases. 2005;41(32):1373-1406
  26. 26. Quirke M, Ayoub F, McCabe A. Risk factors for nonpurulent leg cellulitis: A systematic review and meta-analysis. The British Journal of Dermatology. 2017;177(10):382-609
  27. 27. Cohen J. Clinical practice: Herpes zoster. The New England Journal of Medicine. 2013;369(76):255-263
  28. 28. Herman R, Kee V, Moores K. Etiology and treatment of community-associated methicillin-resistant Staphylococcus aureus. American Journal of Health-System Pharmacy. 2008;65(77):219-225
  29. 29. Mansour S, Pletzer D, De La Fuente-Nunez C, Kim P, Cheung G, Joo H, et al. Bacterial abscess formation is controlled by the stringent stress response and can be targeted therapeutically. eBioMedicine. 2016;12(3):219-226
  30. 30. Roth R, James W. Microbial ecology of the skin. Annual Review of Microbiology. 1988;42(22):441-464
  31. 31. Dunbar J, Barns S, Ticknor L, Kuske C. Empirical and theoretical bacterial diversity in four Arizona soils. Applied and Environmental Microbiology. 2002;68(32):3035-3045
  32. 32. Bowler P, Duerden B, Armstrong D. Wound microbiology and associated approaches to wound management. Clinical Microbiology Reviews. 2001;14(76):244-269
  33. 33. Davies C. Use of molecular techniques to study microbial diversity in the skin: Chronic wounds reevaluated. Wound Repair and Regeneration. 2001;9(12):332-340
  34. 34. Hugenholtz P, Pace N. Identifying microbial diversity in the natural environment: A molecular phylogenetic approach. Trends in Biotechnology. 1996;14(7):190-197
  35. 35. Vincent Ki M, Coleman Rotstein M. Bacterial skin and soft tissue infections in adults: A review of their epidemiology, pathogenesis, diagnosis, treatment and site of care. Canadian Journal of Infectious Diseases and Medical Microbiology. 2008;19(2):173-184
  36. 36. Todar K. The Bacterial Flora of Humans. 2008. Available from: http:// [Accessed: 12 February]
  37. 37. Iwase T. Staphylococcus epidermidis esp inhibits Staphylococcus aureus biofilm formation and nasal colonization. Nature. 2010;465(89):346-349
  38. 38. De La Fuente-Nunez C, Reffuveille F, Haney E, Straus S, Hancock R. Broad-spectrum anti-biofilm peptide that targets a cellular stress response. PLoS Pathogens. 2014;32(55):10-213
  39. 39. Geiger T, Francois P, Liebeke M, Fraunholz M, Goerke C, Krismer B, et al. The stringent response of Staphylococcus aureus and its impact on survival after phagocytosis through the induction of intracellular PSMs expression. PLOS Pathogens. 2012;89212:43-124
  40. 40. Steer A, Lamagni T, Curtis N, Carapetis J. Invasive group a streptococcal disease: Epidemiology, pathogenesis and management. Drugs. 2012;72:1213-1227
  41. 41. Chelsom J, Halstensen A, Haga T, Hoiby E. Necrotising fasciitis due to group A streptococci in western Norway: Incidence and clinical features. Lancet. 1994;344(8):1111-1115
  42. 42. Bieluch V, Tally F. Pathophysiology of abscess formation. Clinics in Obstetrics and Gynaecology. 1983;10(1):93-103
  43. 43. Hindi NK. Microbiology for Nurses. 1st ed. Alsadiq Printer; 2018 (Chapter 2)
  44. 44. Hirschmann J. Impetigo: Etiology and therapy. Current Clinical Topics in Infectious Diseases. 2002;22(3):42-51
  45. 45. Darmstadt G, Lane A. Impetigo: An overview. Pediatric Dermatology. 1994;11(12):293-303
  46. 46. Bisno A, Nelson K, Waytz P, Brunt J. Factors influencing serum antibody response in streptococcal pyoderma. Journal of Laboratory and Clinical Medicine. 1973;81(22):410-420
  47. 47. Kaplan E, Wannamaker L. Suppression of the anti-streptolysin O response by cholesterol and by lipid extracts of rabbit skin. The Journal of Experimental Medicine. 1976;144(66):754-767
  48. 48. Demidovich C, Wittler R, Ruff M, Bass J, Browning W. Im-petigo: Current etiology and comparison of penicillin, erythromycin, and cephalexin therapies. American Journal of Diseases of Children. 1990;144(54):1313-1315
  49. 49. Bisno A, Stevens D. Streptococcal infections in skin and soft tissues. New England Journal of Medicine. 1996;334:240-245
  50. 50. Chartier C, Grosshans E. Erysipelas: An update. International Journal of Dermatology. 1996;35:779-781
  51. 51. Weinstein L, Le Frock J. Does antimicrobial therapy of streptococcal pharyngitis or pyoderma alter the risk of glomerulonephritis? The Journal of Infectious Diseases. 1971;124(1):229-231
  52. 52. Dupuy A, Benchikhi H, Roujeau J. Risk factors for erysipelas of the leg (cellulitis): Case-control study. BMJ. 1999;318(212):1591-1594
  53. 53. Dan M, Heller K, Shapira I, Vidne B, Shibolet S. Incidence of ery-sipelas following venectomy for coronary artery bypass surgery. Infection. 1987;15(6):107-108
  54. 54. Baddour L. Breast cellulitis complicating breast conservation therapy. Journal of Internal Medicine. 1999;24(34):5-9
  55. 55. Bouma J, Dankert J. Recurrent acute leg cellulitis in patients after radical vulvectomy. Gynecologic Oncology. 1988;29(21):50-57
  56. 56. Semel J, Goldin H. Association of athlete’s foot with cellulitis of the lower extremities: Diagnostic value of bacterial cultures of ipsi-lateral interdigital space samples. Clinical Infectious Diseases. 1996;23(32):1162-1164
  57. 57. Eriksson B. Anal colonization of group Gb-hemolytic streptococci in relapsing erysipelas of the lower extremity. Clinical Infectious Diseases. 1999;29(21):1319-1320
  58. 58. Committee on Infectious Diseases, American Academy of Pediatrics. Antimicrobial agents and related therapy. In: Pickering LK, editor. Red Book 2003 Report of the Committee on Infectious Diseases. Vol. 4(90). 26th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2003. pp. 693-694
  59. 59. Burman W, Cohn D, Reves R, Wilson M. Multifocal cellulitis and monoarticular arthritis as manifestations of Helicobacter cinaedi bacteremia. Clinical Infectious Diseases. 1995;20(22):564-570
  60. 60. Perl B, Gottehrer N, Raveh D, Schlesinger Y, Rudensky B, Yinnon A. Cost-effectiveness of blood cultures for adult patients with cellulitis. Clinical Infectious Diseases. 1999;29(5):1483-1488
  61. 61. Kielhofner M, Brown B, Dall L. Influence of underlying disease process on the utility of cellulitis needle aspirates. Archives of Internal Medicine. 1988;148(21):2451-2452
  62. 62. Kirsner R, Pardes J, Eaglstein W, Falanga V. The clinical spectrum of lipodermatosclerosis. Journal of the American Academy of Dermatology. 1993;28(11):623-627
  63. 63. Wang J, Liu Y, Cheng D. Role of benzathine penicillin G in prophylaxis for recurrent streptococcal cellulitis of the lower legs. Clinical Infectious Diseases. 1997;25(70):685-689
  64. 64. Kasseroller R. Sodium selenite as prophylaxis against erysipelas in secondary lymphedema. Anticancer Research. 1998;18(212):2227-2230
  65. 65. Diven D, Dozier S, Meyer D, Smith E. Bacteriology of inflamed and uninflamed epidermal inclusion cysts. Archives of Dermatology. 1998;134(217):49-51
  66. 66. Zimakoff J, Rosdahl V, Petersen W, Scheibel J. Recurrent staphylococcal furunculosis in families. Scandinavian Journal of Infectious Disease. 1988;20(3):403-405
  67. 67. Hedstrom S. Recurrent staphylococcal furunculosis: Bacteriological findings and epidemiology in 100 cases. Scandinavian Journal of Infectious Diseases. 1981;13(9):115-119
  68. 68. Ma X, Ito T, Tiensasitorn C. Novel type of staphylococcal cassette chromosome mec identified in community-acquired methi-cillin-resistant Staphylococcus aureus strains. Antimicrobial Agents and Chemotherapy. 2002;46(21):1147-1152
  69. 69. Centers for Disease Control and Prevention. Outbreaks of community-associated methicillin-resistant Staphylococcus aureus skin infections—Los Angeles County, California, 2002-2003. MMWR. Morbidity and Mortality Weekly Report. 2003;52(2):88-121
  70. 70. Miller L, Perdreau-Remington F, Rieg G. Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureusin Los Angeles. The New England Journal of Medicine. 2005;352:1445-1453
  71. 71. Lewis R. Necrotizing soft-tissue infections. Infectious Disease Clinics of North America. 1992;6(219):693-703
  72. 72. Giuliano A, Lewis F, Hadley K, Blaisdell F. Bacteriology of necrotizing fasciitis. American Journal of Surgery. 1977;13(4):52-57
  73. 73. Sissolak D, Weir W. Tropical pyomyositis. The Journal of Infection. 1994;29:121-127
  74. 74. Eke N. Fournier’s gangrene: A review of 1726 cases. The British Journal of Surgery. 2000;87:718-728
  75. 75. Altemeier W, Fullen W. Prevention and treatment of gas gangrene. JAMA. 1971;217:806-813
  76. 76. Stevens D, Bryant A, Adams K, Mader J. Evaluation of hyperbaric oxygen therapy for treatment of experimental Clostridium perfringens infection. Clinical Infectious Diseases. 1993;17(51):231-237
  77. 77. Raff A, Kroshinsky D. Cellulitis: A review. JAMA. 2011;316(337):325-453
  78. 78. Ellis H, Simonsen S, van Orman E, Hatch B. Cellulitis incidence in a defined population. Epidemiology and Infection. 2006;134(33):293-321
  79. 79. Liu C, Bayer A, Cosgrove S. Clinical practice guidelines by the infectious diseases society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clinical Infectious Diseases. 2009;52(8):18-98
  80. 80. Stevens D, Bisno A, Chambers H. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clinical Infectious Diseases. 2014;59(7):147-212
  81. 81. Bisno A, Stevens D. Streptococcal infections of skin and soft tissues. The New England Journal of Medicine. 1996;334(99):240-565
  82. 82. Bruun T, Oppegaard O, Hufthammer K. Early response in cellulitis: A prospective study of dynamics and predictors. Clinical Infectious Diseases. 2016;63(34):1034-1112
  83. 83. Eron L. Managing skin and soft tissue infections: Expert panel recommendations on key decision points. The Journal of Antimicrobial Chemotherapy. 2003;98(90001):3-17
  84. 84. Bassetti M, Baguneid M, Bouza E, Dryden M, Nathwani D, Wilcox M. European perspective and update on the management of complicated skin and soft tissue infections due to methicillin-resistant Staphylococcus aureus after more than 10 years of experience with linezolid. Clinical Microbiology and Infection. 2014;20(4):3-18
  85. 85. Zilberberg M, Chaudhari P, Nathanson B. Development and validation of a bedside risk score for MRSA among patients hospitalized with complicated skin and skin structure infections. BMC Infectious Diseases. 2012;12(1):154
  86. 86. Suaya J, Eisenberg D, Fang C, Miller L. Skin and soft tissue infections and associated complications among commercially insured patients aged 0-64 years with and without diabetes in the U.S. PLoS One. 2013;8(4):60057-66809
  87. 87. Fitch M, Manthey D, McGinnis H. Videos in clinical medicine. Abscess incision and drainage. The New England Journal of Medicine. 2007;357(11):20-55
  88. 88. Woo P, Lum P, Wong S. Cellulitis complicating lymphoedema. European Journal of Clinical Microbiology & Infectious Diseases. 2000;19(31):294-319
  89. 89. Peralta G, Padrón E, Roiz M. Risk factors for bacteremia in patients with limb cellulitis. European Journal of Clinical Microbiology & Infectious Diseases. 2006;25(44):619-787
  90. 90. Perl B, Gottehrer N, Raveh D. Cost-effectiveness of blood cultures for adult patients with cellulitis. Clinical Infectious Diseases. 1999;29(43):1483-1534
  91. 91. Torres J, Avalos N, Echols L. Low yield of blood and wound cultures in patients with skin and soft-tissue infections. The American Journal of Emergency Medicine. 2017;350(7):1159-1212
  92. 92. Stamenkovic I, Lew P. Early recognition of potentially fatal necrotizing fasciitis. The use of frozen-section biopsy. New England Journal of Medicine. 1984;310(44):1689-1790
  93. 93. Leppard B, Seal D, Colman G, Hallas G. The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas. The British Journal of Dermatology. 1985;112(55):559-643
  94. 94. Dryden M. Complicated skin and soft tissue infection. The Journal of Antimicrobial Chemotherapy. 2010;65(3):35-44
  95. 95. Moet G, Jones R, Biedenbach D. Contemporary causes of skin and soft tissue infections in North America, Latin America, and Europe: Report from the SENTRY Antimicrobial Surveillance Program (1998-2004). Diagnostic Microbiology and Infectious Disease. 2007;57(1):7-13
  96. 96. Gorwitz R. A review of community-associated methicillin-resistant Staphylococcus aureus skin and soft tissue infections. The Pediatric Infectious Disease Journal. 2008;27(1):1-7
  97. 97. Loewen K, Schreiber Y, Kirlew M. Community-associated methicillin-resistant Staphylococcus aureus infection: Literature review and clinical update. Canadian Family Physician. 2017;63(7):512-520
  98. 98. Katayama Y, Ito T, Hiramatsu K. A new class of genetic element, staphylococcus cassette chromosome mec, encodes methicillin resistance in Staphylococcus aureus. Antimicrobial Agents and Chemotherapy. 2000;44(6):1549-1555
  99. 99. Napolitano L. Severe soft tissue infections. Infectious Disease Clinics of North America. 2009;23(3):571-591
  100. 100. Pan A, Cauda R, Concia E. Consensus document on controversial issues in the treatment of complicated skin and skin-structure infections. International Journal of Infectious Diseases. 2010;14(4):39-53
  101. 101. Kujath P, Kujath C. Complicated skin structure and soft tissue infections—Are we threatened by multi-resistant pathogens? European Journal of Medical Research. 2010;15(12):544-553
  102. 102. Stevens D, Bisno A, Chambers H. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clinical Infectious Diseases. 2014;59(2):10-52
  103. 103. Chinnock B, Hendey G. Irrigation of cutaneous abscesses does not improve treatment success. Annals of Emergency Medicine. 2015;67(3):379-383
  104. 104. O’Malley G, Dominici P, Giraldo P. Routine packing of simple cutaneous abscesses is painful and probably unnecessary. Academic Emergency Medicine. 2009;16(5):470-473
  105. 105. Stevens D. Dilemmas in the treatment of invasive Streptococcus pyogenes infections. Clinical Infectious Diseases. 2003;37(21):341-343
  106. 106. Kaul R, McGeer A, Norrby-Teglund A. Intravenous immuno-globulin therapy for streptococcal toxic shock syndrome: A comparative observational study. Clinical Infectious Diseases. 1999;28:800-807
  107. 107. Darenberg J, Ihendyane N, Sjolin J. Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: A European randomized, double-blind, placebo-controlled trial. Clinical Infectious Diseases. 2003;37(95):333-340
  108. 108. Clarke J. Toothaches and death. Journal of the History of Dentistry. 1999;47(7):11-13
  109. 109. Carter L, Starr D. Alarming increase in dental sepsis. British Dental Journal. 2006;200(4):243-299
  110. 110. Azodo C, Chukwumah N, Ezeja E. Dentoalveolar abscess among children attending a dental clinic in Nigeria. Odonto-stomatologie Tropicale. 2012;35(32):41-46
  111. 111. Kaur J. Dental education and oral health problems in India. Indian Journal of Dental Education. 2009;2(21):167-171
  112. 112. Siqueira J, Rôças I. Diversity of endodontic microbiota revisited. Journal of Dental Research. 2009;88(3):969-981
  113. 113. González-García R, Risco-Rojas R, Román-Romero L, Moreno-García C, López GC. Descending necrotizing mediastinitis following dental extraction. Radiological features and surgical treatment considerations. Journal of Cranio-Maxillofacial Surgery. 2011;39(12):335-339
  114. 114. Hersh A. National trends in ambulatory visits and antibiotic prescribing for skin and soft-tissue infections. Archives of Internal Medicine. 2008;168(14):1585-1591
  115. 115. EFSA. The European Union summary report on trends and sources of zoonoses. Zoonotic agents and food-borne outbreaks in 2016. EFSA Journal. 2017;15(12):5077
  116. 116. Oyston P, Sjostedt A, Titball R. Tularaemia: Bioterrorism defence renews interest in Francisella tularensis. Nature Reviews Microbiology. 2004;2(12):967-978
  117. 117. Tomaso H, Hotzel H, Otto P, Myrtennas K, Forsman M. Antibiotic susceptibility in vitro of Francisella tularensis subsp. holarctica isolates from Germany. Journal of Antimicrobial Chemotherapy. 2017;72(9):2539-2543
  118. 118. Choi Y, Kim D, Lee D, Lee J, Lee E, Lee S, et al. Clinical characteristics and incidence of perianal diseases in patients with ulcerative colitis. Annals of Coloproctology. 2018;34(3):138-143
  119. 119. Amato A, Bottini C, De Nardi P, Giamundo P, Lauretta A, Realis Luc A, et al. Italian society of colorectal surgery. Evaluation and management of perianal abscess and anal fistula: A consensus statement developed by the Italian Society of Colorectal Surgery (SICCR). Techniques in Coloproctology. 2015;19(10):595-606
  120. 120. Nguyen V, Jiang D, Hoffman S, Guntaka S, Mays J, Wang A, et al. Impact of diagnostic delay and associated factors on clinical outcomes in a U.S. inflammatory bowel disease cohort. Inflammatory Bowel Disease. 2017;23(10):1825-1831
  121. 121. Patani N, MacAskill F, Eshelby S, Omar A, Kaura A, Contractor K, et al. Best-practice care pathway for improving management of mastitis and breast abscess. British Journal of Surgery. 2018;105(12):1615-1622
  122. 122. Leung S. Breast pain in lactating mothers. Hong Kong Medical Journal. 2016;22(4):341-346
  123. 123. Rao R, Ludwig K, Bailey L, Berry T, Buras R, Degnim A, et al. Select choices in benign breast disease: An initiative of the American Society of Breast Surgeons for the American Board of Internal Medicine Choosing Wisely® campaign. Annals of Surgical Oncology. 2018;25(10):2795-2800
  124. 124. Liver Abscess Definition in Medical Conditions Dictionary. 2018. Available from: [Accessed: April 11, 2018]
  125. 125. Medline Plus Encyclopedia Pyogenic liver abscess. Skin abscess. Hong Kong Medical Journal. 2012;21(10):323-432
  126. 126. Webb G, Thomas P, Cadman P, Gorard D. Pyogenic liver abscess. Frontline Gastroenterology. 2014;5(1):60-67
  127. 127. Akhondi H, Sabih D. Liver Abscess. Vol. 3(12). StatPearls: StatPearls Publishing; 2019. pp. 431-490
  128. 128. Nicolosi A, Hauser W, Musicco M, Kurland L. Incidence and prognosis of brain abscess in a defined population: Olmsted County, Minnesota, 1935-1981. Neuroepidemiology. 1991;10(34):122-131
  129. 129. Helweg-Larsen J, Astradsson A, Richhall H, Erdal J, Laursen A, Brennum J. Pyogenic brain abscess, a 15 year survey. BMC Infectious Diseases. 2012;12(21):332-400
  130. 130. Yen D, Hu S, Tsai J, Kao W, Chern C, Wang L. Renal abscess: Early diagnosis and treatment. The American Journal of Emergency Medicine. 1999;17:192-197
  131. 131. Meng M, Mario L, McAninch J. Current treatment and outcomes of perinephric abscesses. Journal of Urology. 2002;168(1):1337-1340
  132. 132. Anderson K, McAninch J. Renal abscesses: Classification and review of 40 cases. Urology. 1980;16:333-338
  133. 133. Siegel J, Smith A, Moldwin R. Minimally invasive treatment of renal abscess. Journal of Urology. 1996;155(23):52-55

Written By

Mohammed Malih Radhi, Fatima Malik AL-Rubea, Nada Khazal Kadhim Hindi and Rusull Hamza Kh. AL-Jubori

Submitted: 27 October 2019 Reviewed: 07 February 2020 Published: 10 April 2020