Enteroviruses (primary coxsackle A and B and, less frequently, echoviruses) Adenoviruses Influenza viruses BACTERIA (RELATIVELY UNCOMMON) Mycoplasma pneumoniae Chlamydia trachomatis Mycobacterium tuberculosis Staphylococcus aureus Streptococcus pneumoniae Enterobacteriaceae and other gram-negative bacilli FUNGI (RELATIVELY UNCOMMON) Coccidioides immitis Aspergillus spp. Candida spp. Cryptococcus neoformans Histoplasma capsulatum PARASITES (RELATIVELY UNCOMMON) Entamoeba histolytica Toxoplasma gondii

Myocarditis (inflammation of the heart muscle itself) may accompany pericarditis. The pathogenesis of disease involves the host inflammatory response contributing to fluid buildup and cell and tissue damage. The most common etiologic agents of pericarditis and myocarditis are listed in Box 61-1. Other bacteria/fungi, and parasitic agents have been recovered from pericardial effusions, and therefore all agents should be sought.

Patients who develop pericarditis resulting from agents other than viruses are often compromised in some way. An example is infective endocarditis, in which a myocardial abscess develops and then ruptures into the pericardial space.

Joint Fluid

Infectious arthritis may involve any joint in the body. Infection of the joint usually occurs secondary to hematogenous spread of bacteria or, less often, fungi, or as a direct extension of infection of the bone. It may also occur after injection of material, especially corticosteroids, into joints or after insertion of prosthetic material (e.g., total hip replacement). Although infectious arthritis usually occurs at only one site (monoarticular), a preexisting bacteremia or fungemia may seed more than one joint to establish polyarticular infection, particularly when multiple joints are diseased, such as in rheumatoid arthritis. Knees and hips are the most frequently affected joints.

In addition to active infections associated with viable microorganisms within the joint, sterile, self-limited arthritis caused by antigen-antibody interactions may follow an episode of infection, such as meningococcal meningitis. When an etiologic agent cannot be isolated from an inflamed joint fluid specimen, either the absence of viable agents or inadequate transport or culturing procedures can be blamed. For example, even under the best circumstances, BorreJia burgdorferi is isolated from the joints of fewer than 20% of patients with Lyme disease. Nonspecific test results, such as increased white blood cell count, decreased glucose, or elevated protein, may seem to implicate an infectious agent but are not conclusive. A role has been postulated for the persistence of bacterial L-forms (cell-wall-deficient forms) in joint fluid after systemic infection, but such theories have not been proved.

Overall Staphylococcus aureus is the most common etiologic agent of septic arthritis, accounting for approximately 70% of all such infections. In adults younger than 30 years of age, however, Neisseria gonorrhoeae is isolated most frequentiy. Haemophilus influenzae has been the most common agent of bacteremia in children younger than 2 years of age, and consequendy it has been the most frequent cause of infectious arthritis in these patients, followed by S. aureus. The widespread use of H. influenzae type B vaccine should contribute to a change in this pattern. Streptococci, including groups A (Streptococcus pyogenes) and B (Streptococcus agalactiae), pneumocood, and viridans streptococci, are prominent among bacterial agents associated with infectious arthritis in patients of all ages. Among anaerobic bacteria, Baderoides, including B. fragilis, may be recovered, as may Fusobacterium necrophorum, which usually involves more than one joint in the course of sepsis. Among people living in certain endemic areas of the United States and Europe, infectious arthritis is a prominent feature of Lyme disease. Some of the more frequendy encountered etiologic agents of infectious arthritis are listed in Box 61-2.

These agents act to stimulate a host inflammatory response, which is initially responsible for the pathology of the infection. Arthritis is also a symptom associated with infectious diseases caused by certain agents, such as Neisseria meningitidis, group A streptococci (rheumatic fever), and Streptobacillus moniliformis, in which the agent cannot be recovered from joint fluid. Presumably, antigen-antibody complexes formed during active infection accumulate in a joint, initiating an inflammatory response that is responsible for the ensuing damage.

Infections in prosthetic joints are usually associated with somewhat different etiologic agents than those in natural joints. After insertion of the prosthesis, organisms that gained access during the surgical procedure slowly multiply until they reach a critical mass and produce a host response. This may occur long after the initial surgery; approximately half of all prosthetic joint infections occur more than 1 year after surgery.

BOX 61-2 Must Frequently Encountered Etiologic Agents of Infectious Arthritis



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