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Staphylcoccus spp. and Streptococcus spp. can also infect and cause inflammation in the tissues surrounding the heart, a condition called acute pericarditis . Pericarditis is marked by chest pain, difficulty breathing, and a dry cough. In most cases, pericarditis is self-limiting and clinical intervention is not necessary. Diagnosis is made with the aid of a chest radiograph, electrocardiogram, echocardiogram, aspirate of pericardial fluid, or biopsy of pericardium. Antibacterial medications may be prescribed for infections associated with pericarditis; however, pericarditis can also be caused other pathogens, including viruses (e.g., echovirus, influenza virus), fungi (e.g., Histoplasma spp., Coccidioides spp.), and eukaryotic parasites (e.g., Toxoplasma spp.).

a heart with subacute bacterial endocarditis. There are thick, swollen strands in the heart. There are also large lumpy structures at the ends of the chordae tendinae.
The heart of an individual who had subacute bacterial endocarditis of the mitral valve. Bacterial vegetations are visible on the valve tissues. (credit: modification of work by Centers for Disease Control and Prevention)
  • Compare acute and subacute bacterial endocarditis.

Gas gangrene

Traumatic injuries or certain medical conditions, such as diabetes, can cause damage to blood vessels that interrupts blood flow to a region of the body. When blood flow is interrupted, tissues begin to die, creating an anaerobic environment in which anaerobic bacteria can thrive. This condition is called ischemia . Endospores of the anaerobic bacterium Clostridium perfringens (along with a number of other Clostridium spp. from the gut) can readily germinate in ischemic tissues and colonize the anaerobic tissues.

The resulting infection, called gas gangrene , is characterized by rapidly spreading myonecrosis (death of muscle tissue). The patient experiences a sudden onset of excruciating pain at the infection site and the rapid development of a foul-smelling wound containing gas bubbles and a thin, yellowish discharge tinged with a small amount of blood. As the infection progresses, edema and cutaneous blisters containing bluish-purple fluid form. The infected tissue becomes liquefied and begins sloughing off. The margin between necrotic and healthy tissue often advances several inches per hour even with antibiotic therapy. Septic shock and organ failure frequently accompany gas gangrene; when patients develop sepsis, the mortality rate is greater than 50%.

α-Toxin and theta (θ) toxin are the major virulence factors of C. perfringens implicated in gas gangrene. α-Toxin is a lipase responsible for breaking down cell membranes; it also causes the formation of thrombi (blood clots) in blood vessels, contributing to the spread of ischemia. θ-Toxin forms pores in the patient’s cell membranes, causing cell lysis. The gas associated with gas gangrene is produced by Clostridium ’s fermentation of butyric acid, which produces hydrogen and carbon dioxide that are released as the bacteria multiply, forming pockets of gas in tissues ( [link] ).

Gas gangrene is initially diagnosed based on the presence of the clinical signs and symptoms described earlier in this section. Diagnosis can be confirmed through Gram stain and anaerobic cultivation of wound exudate (drainage) and tissue samples on blood agar. Treatment typically involves surgical debridement of any necrotic tissue; advanced cases may require amputation . Surgeons may also use vacuum-assisted closure (VAC) , a surgical technique in which vacuum-assisted drainage is used to remove blood or serous fluid from a wound or surgical site to speed recovery. The most common antibiotic treatments include penicillin G and clindamycin . Some cases are also treated with hyperbaric oxygen therapy because Clostridium spp. are incapable of surviving in oxygen-rich environments.

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Source:  OpenStax, Microbiology. OpenStax CNX. Nov 01, 2016 Download for free at http://cnx.org/content/col12087/1.4
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