An exact classification of necrotizing subcutaneous, fascial, and muscle infections is difficult because the distinctions between many of the clinical entities are blurred. Clinical classification is as follows: (1) crepitant anaerobic cellulitis, (2) necrotizing fasciitis, (3) nonclostridial myonecrosis, (4) clostridial myonecrosis, (5) fungal necrotizing cellulitis, and (6) miscellaneous necrotizing infections in the immunocompromised host. These types of infections usually occur in traumatic or surgical wounds or around foreign bodies and in patients who are medically compromised by diabetes mellitus, vascular insufficiency, or both. In the traumatically, surgically, or medically compromised patient, local tissue conditions, hypoxia, and decreased oxidation-reduction potential (Eh) promote the growth of anaerobes. Most necrotizing soft tissue infections have an endogenous anaerobic component. Since anaerobes are the predominant members of the microflora on most mucous membranes, there are many potential pathogens. Hypoxic conditions also allow proliferation of facultative aerobic organisms, since polymorphonuclear leukocytes function poorly under decreased oxygen tensions. The growth of aerobic organisms further lowers the Eh, more fastidious anaerobes become established, and the disease process rapidly accelerates. Show
Discernible quantities of tissue gas are present in most of these infections. Carbon dioxide and water are the natural end products of aerobic metabolism. Carbon dioxide rapidly dissolves in aqueous media and rarely accumulates in tissues. Incomplete oxidation of energy sources by anaerobic and facultative aerobic bacteria can result in the production of gases that are less water soluble and therefore accumulate in tissues. Hydrogen is presumably the major tissue gas in mixed aerobic-anaerobic soft tissue infections. Its presence indicates rapid bacterial multiplication at a low Eh. Clinically, the hallmarks of mixed aerobic-anaerobic soft tissue infections are tissue necrosis, a putrid discharge, gas production, the tendency to burrow through soft tissue and fascial planes, and the absence of classic signs of tissue inflammation. shows the differentiation between the common bacterial necrotizing soft tissue infections. Table 100-2Differentiation of the Common Necrotizing Bacterial Soft Tissue Infection. Crepitant Anaerobic CellulitisNonclostridial and clostridial cellulitides have a similar clinical picture and are discussed together under the term, crepitant anaerobic cellulitis. Crepitant anaerobic cellulitis appears as a necrotic soft tissue infection with abundant connective tissue gas. The condition usually occurs after local trauma in patients with vascular insufficiency of the lower extremities. Multiple aerobic and anaerobic organisms have been isolated, including Bacteroides species, Peptostreptococcus species, Clostridium species, and members of the family Enterobacteriaceae. Crepitant anaerobic cellulitis can be differentiated from more serious soft tissue infections by the abundance of soft tissue gas, lack of marked systemic toxicity, gradual onset, less severe pain, and absence of muscle involvement. Necrotizing FasciitisNecrotizing fasciitis is a relatively rare infection with a high mortality (40 percent). The infection was originally called hemolytic streptococcal gangrene by Meleney in 1924. Although his clinical description was accurate, better culture techniques have demonstrated that organisms other than Streptococcus pyogenes more commonly cause these infections. Clinical manifestations include extensive dissection and necrosis of the superficial and often the deep fascia. The infection undermines adjacent tissue and leads to marked systemic toxicity. Thrombosis of subcutaneous blood vessels leads to necrosis of the overlying skin. Initial local pain is replaced by numbness or analgesia as the infection involves the cutaneous nerves. Most cases of fasciitis follow surgery or minor trauma. The highest incidence is seen in patients with small vessel diseases such as diabetes mellitus. When careful bacteriologic techniques are used, anaerobes, particularly Peptostreptococcus, Bacteroides, and Fusobacterium species, are found in 50 to 60 percent of cases. Aerobic organisms, especially Streptococcus pyogenes, Staphylococcus aureus, and members of the Enterobacteriaceae have also been isolated. Most infections are mixed aerobic-anaerobic infections, but a type of necrotizing fasciitis caused solely by Streptococcus pyogenes has been reported and is referred to by the lay press as “flesh eating bacteria.” Nonclostridial MyonecrosisNonclostridial myonecrosis, called synergistic necrotizing cellulitis by Stone and Martin, is a particularly aggressive soft tissue infection. It is similar to clostridial myonecrosis in that there is widespread involvement of soft tissue with necrosis of muscle tissue and fascia. The prominent involvement of muscle tissue differentiates this infection from necrotizing fasciitis. Subcutaneous tissue and skin are secondarily involved. Clinically, there is exquisite local tenderness, with minimal skin changes, and drainage of foul-smelling “dish-water” pus from small skin surface ulcers. Severe systemic toxicity is found in most patients. Nonclostridial myonecrosis occurs most frequently in the perineal area, as a result of an extension of a perirectal abscess, and in the lower extremities of patients with vascular insufficiency. Multiple organisms have been isolated, including Peptostreptococcus and Bacteroides species and members of the Enterobacteriaceae. Mortality approaches 75 percent. Clostridial MyonecrosisClostridial myonecrosis, or gas gangrene, is a clostridial infection primarily of muscle tissue. Clostridium perfringens is isolated in 90 percent of these infections. Other clostridial species frequently isolated are C novyi (4 percent), C septicum (2 percent), C histolyticum, C fallax, and C bifermentans. Classically, clostridial myonecrosis has an acute presentation and a fulminant clinical course. The infection usually occurs in areas of major trauma or surgery or as a complication of thermal burns. However, it also has been reported following minor trauma, including intravenous administration of drugs, intramuscular injections of epinephrine, insect bites, and nail punctures. Moreover, it may occur in the absence of recent trauma by activation of dormant clostridial spores in old scar tissue. Finally, clostridial myonecrosis may occur in the absence of trauma, by bacteremic spread of the organism from a gastrointestinal or genitourinary site. Clostridium septicum is the major cause of spontaneous, nontraumatic gas gangrene and is often associated with a lesion in the colon such as an adenocarcinoma. Clostridial myonecrosis is diagnosed mainly on a clinical basis. The infection may be so rapidly progressive that any delay in recognition or treatment may be fatal. The onset is sudden, often within 4 to 6 hours after an injury. Sudden, severe pain in the area of infection is an early clinical finding. Early in the course of infection, the skin overlying the wound appears shiny and tense and then becomes dusky. Within hours, the skin color may progress from dusky to a bronze discoloration, which can advance at a rate of 1 inch per hour. Vesicles or hemorrhagic bullae appear near the wound. A thin, brownish, often copious fluid exudes from the wound. Bubbles occasionally appear in the drainage. This exudate has often been described as having a sweet “mousy” odor. Swelling and edema in the area of infection is pronounced. Within hours the skin overlying the lesion can rupture and the muscle herniate. At surgery, the infected muscle is dark red to black, is noncontractile, and does not bleed when cut. Crepitus, although not prominent, is sometimes detected. Radiographs may show tissue gas outlining fascial planes and muscle bundles. The rapid tissue necrosis in clostridial myonecrosis is caused by the clostridial toxins. Clostridial species are capable of producing multiple toxins, each with its own mode of action. Clostridium perfringens produces at least 12 different extracellular toxins. The most common of these, a lecithinase called alpha toxin, is hemolytic, histotoxic, and necrotizing. Other toxins act as collagenases, proteinases, deoxyribonucleases (DNases), fibrinolysins, and hyaluronidases. The systemic toxic reaction cannot be fully explained by a single circulating exotoxin. The “toxic factor” may be produced by interaction of the clostridial toxins with infected tissue. The mortality from clostridial myonecrosis ranges from 15 to 30 percent. Fungal Necrotizing CellulitisPhycomyces and Aspergillus species may cause a gangrenous cellulitis in compromised hosts. The hallmark of these infections is the invasion of blood vessels by hyphae, followed by thrombosis and subsequent necrosis extending to all soft tissue compartments. Spores from these fungi are ubiquitous. The Phycomyces species are characterized by broad-based nonseptate hyphae. Rhizopus, Mucor, and Absidia are the major pathogenic genera within the family Mucoraceae. Serious rhinocerebral, pulmonary, or disseminated infections have been found in patients with diabetes, lymphoma, or leukemia. Phycomycotic gangrenous cellulitis usually occurs in patients with severe burns or diabetes. The characteristic dermal lesion is a black, anesthetic ulcer or an area of necrosis with a purple edematous margin. There is no gas or exudate, and the infection may progress rapidly. Aspergillus species are characterized histologically by branching septate hyphae. These fungi can cause serious pulmonary or disseminated infections in compromised hosts. Aspergillus gangrenous cellulitis may be primary or from a disseminated infection. The dermal lesion is an indurated plaque that leads to a necrotic ulcer. Gas and exudate are not present. What bacteria causes joint infection?A common type of joint infection is caused by Neisseria gonorrhoeae, the sexually transmitted bacteria that cause gonorrhea; this is called a gonococcal joint infection. Joint infection with other types of bacteria, such as Staphylococcus, is called nongonococcal bacterial (septic) arthritis.
What is deep joint infection?A bacterial infection of a joint can cause a severe and potentially destructive form of arthritis, often referred to as septic arthritis. Bacterial joint infections can be caused by a number of different organisms and can occur in both natural and artificial joints (eg, after a knee replacement).
What kind of bacterial infection are you most likely to find deep in the muscle tissue?Pyomyositis is a rare bacterial infection of the muscle that usually results in an abscess. It's most common in your thigh muscles. Pyomyositis can be difficult to diagnose, and symptoms usually include fever and muscle pain.
Which of the following bacteria is the most common cause of all bone and joint infections?Bone and joint infections are usually caused by bacteria called Staphylococcus aureus (or “staph”) and require treatment with antibiotics.
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