Normally Sterile Body Fluids, Bone and Bone Marrow, and Solid Tissues

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Normally Sterile Body Fluids, Bone and Bone Marrow, and Solid Tissues

Objectives

1. Describe the fine main cavities of the human body; also name the membranes associated with these cavities and state the function of these membranes.

2. Define each of the following body cavity fluids, and explain the diagnostic culture methods for each: pleural fluid, pericardial fluid, peritoneal fluid, joint fluid, and dialysis fluid.

3. Define parietal and visceral pleura.

4. Define cellulitis; name the etiologic agents of this illness, and explain the associated risk factors for the development of disease.

5. Define pleural effusion; explain the difference between exudative pleural effusion and transudative pleural effusion.

6. Explain when a pleural effusion becomes an empyema and what medical condition contributes to the development of an empyema?

7. Define pericarditis and myocarditis; explain the physical conditions that may contribute to the accumulation of pericardial fluid.

8. Define peritonitis and differentiate between primary and secondary peritonitis.

9. Name the etiologic agents most commonly isolated from primary peritonitis cases in children, adults, sexually active females, and immunocompromised patients.

10. Define osteomyelitis; explain how this infection is transmitted, the diagnostic method, and the organisms most frequently responsible for this type of infection.

11. Explain the process for culturing organisms from the following specimens: bone, tissue, and bone marrow.

12. Correlate patient signs and symptoms with laboratory results to identify the etiologic agent associated with the body fluid, bone and bone marrow, and other solid tissue infection.

The human body is divided into five main body cavities: cranial, spinal, thoracic, abdominal, and pelvic. Each cavity is lined with membranes, and within the body wall and these membranes, or between the membranes and organs, are small spaces filled with minute amounts of fluid. The purpose of this fluid is to bathe the organs and membranes, reducing the friction between organs.

Bacteria, fungi, virus, or parasite can invade any body tissue or sterile body fluid site. Although from different areas of the body, all specimens discussed in this chapter are considered normally sterile. Therefore, even one colony of a potentially pathogenic microorganism may be significant. (Refer to Table 5-1 for a quick guide regarding collection, transport, and processing of specimens from sterile body sites.)

Specimens From Sterile Body Sites

Fluids

In response to infection, fluid may accumulate in any body cavity. Infected solid tissue often presents as cellulitis or with abscess formation. Areas of the body from which fluids are typically sent for microbiologic studies (in addition to blood and cerebrospinal fluid [see Chapters 68 and 71]) include those in Table 77-1.

TABLE 77-1

Microbiology Laboratory Body Fluid Collection Sites

Body Area Fluid Name(s)
Thorax Thoracentesis or pleural or empyema fluid
Abdominal cavity Paracentesis or ascitic or peritoneal fluid
Joint Synovial fluid
Pericardium Pericardial fluid

Pleural Fluid

Lining the entire thoracic cavity (see Chapter 69) of the body is a serous membrane called the parietal pleura. Covering the outer surface of the lung is another membrane called the visceral pleura (Figure 77-1). Within the pleural space between the lung and chest wall is a small amount of fluid called pleural fluid that lubricates the surfaces of the pleura (the membranes surrounding the lungs and lining the chest cavity). Normally, equilibrium exists among the pleural membranes, but in certain disease states, such as cardiac, hepatic, or renal disease, excess amounts of this fluid can be produced and accumulates in the pleural space; this is known as a pleural effusion. Pleural effusions can either be exudative or transudative. Exudative pleural effusions are caused by inflammation, infection, and cancer, whereas transudative effusions are due to systemic changes, such as congestive heart failure.

Normal pleural fluid contains few or no cells and has a consistency similar to serum, but with a lower protein count. Pleural fluid containing numerous white blood cells is indicative of infections. Pleural fluid specimens are collected by thoracentesis, a procedure in which a needle is inserted through the chest wall into the pleural space and the excess fluid aspirated. This fluid is then submitted to the laboratory as thoracentesis fluid, pleural fluid, or empyema fluid. The fluid, or effusion, can then be analyzed for cell count, total protein, glucose, lactate dehydrogenase, amylase, cytology, and culture. The total protein and glucose results determine if the effusion is transudate or exudate. The patient’s serum or plasma glucose level is needed to compare with the results indicated in the body fluid. Several characteristics can be used to determine whether a fluid is a transudate or exudate (Table 77-2). When effusions are extremely purulent or full of pus, the effusion is referred to as an empyema. Empyema often arises as a complication of pneumonia, but other infections near the lung (e.g., subdiaphragmatic infection) may seed microorganisms into the pleural cavity. It has been estimated that 50% to 60% of patients develop empyema as a complication of pneumonia.

TABLE 77-2

Pleural Fluid Effusion Characteristics

  Transudate Exudate
Appearance Clear Cloudy
Specific Gravity <1.015 >1.015
Total Protein <3.0 mg/dL >3.0 mg/dL
LD Fluid: Serum Ratio <0.6 >0.6
Cholesterol <60 mg/dL >60 mg/dL
Cholesterol Fluid: Serum Ratio <0.3 >0.3
Bilirubin Fluid:Serum Ratio <0.6 >0.6
Total Protein Fluid: Serum Ratio <0.5 >0.6
White Blood Cells <1000/µL (all white blood cell types, all <50%) >1000/µL
Red Blood Cells <10,000/µL = because of traumatic tap >100,000/µL
Clotting Will not clot May clot

Modified from Strasinger SK, Di Lorenzo MS: Urinalysis and body fluids, ed 5, Philadelphia, 2008, F.A. Davis.

Peritoneal Fluid

The peritoneum is a large, moist, continuous sheet of serous membrane lining the walls of the abdominal-pelvic cavity and the outer coat of the organs contained within the cavity (Figure 77-2). In the abdomen, these two membrane linings are separated by a space called the peritoneal cavity, which contains or abuts the liver, pancreas, spleen, stomach and intestinal tract, bladder, and fallopian tubes and ovaries. The kidneys occupy a retroperitoneal (behind the peritoneum) position. Within the healthy human peritoneal cavity is a small amount of fluid that maintains the surface moisture of the peritoneum. Normal peritoneal fluid may contain as many as 300 white blood cells per milliliter, but the protein content and specific gravity of the fluid are low. During an infectious or inflammatory process, increased amounts of fluid accumulate in the peritoneal cavity, a condition called ascites. Most cases of ascites are due to liver disease, and in severe cases, the abdomen is often distended. The fluid can be collected for testing by paracentesis (the insertion of a needle into the abdomen and removal of fluid). The peritoneal or ascites fluid can then be analyzed for amylase, protein, albumin, cell count, culture, and cytology. Often ascitic fluid contains an increased number of inflammatory cells and an elevated protein level.

Agents of infection gain access to the peritoneum through a perforation of the bowel, through infection within abdominal viscera, by way of the bloodstream, or by external inoculation (as in surgery or trauma). On occasion, as in pelvic inflammatory disease (PID), organisms travel through the natural channels of the fallopian tubes into the peritoneal cavity.

Primary Peritonitis.

Peritonitis results when the peritoneal membrane becomes inflamed and can be either primary or secondary. Primary peritonitis is rare and results when infection spreads from the blood and lymph nodes with no apparent evidence of infection. The organisms likely to be recovered from patient specimens with primary peritonitis vary with the patient’s age. The most common etiologic agents in children are Streptococcus pneumoniae and group A streptococci, Enterobacteriaceae, other gram-negative bacilli, and staphylococci. In adults, Escherichia coli is the most common bacterium, followed by S. pneumoniae and group A streptococci. Polymicrobic peritonitis is unusual in the absence of bowel perforation or rupture. Among sexually active young women, Neisseria gonorrhoeae and Chlamydia trachomatis are common etiologic agents of peritoneal infection, often in the form of a perihepatitis (inflammation of the surface of the liver, called Fitz-Hugh–Curtis syndrome). Tuberculous peritonitis occurs infrequently in the United States and is more likely to be found among individuals that have recently traveled in South America, Southeast Asia, or Africa. Fungal causes of peritonitis are not common, but Candida spp. may be recovered from immunosuppressed patients and patients receiving prolonged antibacterial therapy.

Secondary Peritonitis.

Secondary peritonitis is a complication of a perforated viscus (organ), surgery, traumatic injury, loss of bowel wall integrity following a destructive disease (e.g., ulcerative colitis, ruptured appendix, carcinoma), obstruction, or a preceding infection (liver abscess, salpingitis, septicemia). The nature, location, and etiology of the underlying process govern the agents recovered from peritoneal fluid. With PID as the background, gonococci, anaerobes, or chlamydiae are isolated. With peritonitis or intra-abdominal abscess, anaerobes generally are found in peritoneal fluid, usually together with Enterobacteriaceae and enterococci or other streptococci. In patients whose bowel flora has been altered by antimicrobial agents, more resistant gram-negative bacilli and Staphylococcus aureus may be encountered. Because anaerobes outnumber aerobes in the bowel by 1000-fold, it is not surprising that anaerobic organisms play a prominent role in intra-abdominal infection, perhaps acting synergistically with facultative bacteria. The organisms likely to be recovered include E. coli, the Bacteroides fragilis group, enterococci and other streptococci, Bilophila spp., other anaerobic gram-negative bacilli, anaerobic gram-positive cocci, and clostridia.

Peritoneal Dialysis Fluid

More than 900,000 patients with end-stage renal disease are maintained on continuous ambulatory peritoneal dialysis (CAPD). One in every 10 American adults, totaling more than 20 million, suffer from some type of chronic kidney disease. In this treatment, fluid is injected into the peritoneal cavity and subsequently removed, which allows exchange of salts and water and removal of various wastes in the absence of kidney function. Because the dialysate fluid is injected into the peritoneal cavity via a catheter, the break in the skin barrier places the dialysis patient at significant risk for infection. The average incidence of peritonitis in these patients is up to two episodes per year per patient. Peritonitis is diagnosed by the presence of two of the following: cloudy dialysate, abdominal pain, or a positive culture from dialysate. Although white blood cells are usually plentiful (a value of leukocytes >100/mL is usually indicative of infection), the number of organisms is usually too low for detection on Gram stain of the peritoneal fluid sediment unless a concentrating technique is used; fungi are more readily detected. Many recent studies show that improved sensitivity can be achieved by using automated blood culture systems in which 10 mL of fluid is inoculated into culture bottles.

Most infections originate from the patient’s own skin flora; Staphylococcus epidermidis and S. aureus are the most common etiologic agents, followed by streptococci, aerobic or facultative gram-negative bacilli, Candida spp., Corynebacterium spp., and others. The oxygen content of peritoneal dialysate is usually too high for the development of anaerobic infection. Among the gram-negative bacilli isolated, Pseudomonas spp., Acinetobacter spp., and the Enterobacteriaceae are frequently observed.

Pericardial Fluid

The heart and contiguous major blood vessels are surrounded by the pericardium, a protective tissue. The area between the epicardium, which is the membrane surrounding the heart muscle, and the pericardium is called the pericardial space and normally contains 15 to 20 mL of clear fluid. If an infectious agent is present within the fluid, the pericardium may become distended and tight, and eventually tamponade (interference with cardiac function and circulation) can ensue. Up to 500 mL of fluid can accumulate during infection, which may seriously complicate cardiac function.

Agents of pericarditis (inflammation of the pericardium) are usually viruses, especially Coxsackie virus. Parasites, bacteria, certain fungi, and noninfectious causes are also associated with this disease.

Myocarditis (inflammation of the heart muscle itself) may accompany or follow pericarditis. The pathogenesis of disease involves the host inflammatory response contributing to fluid buildup as well as cell and tissue damage. Common causes of myocarditis include viral infections with Coxsackie virus, echoviruses, or adenovirus. The most common etiologic agents of pericarditis and myocarditis are listed in Box 77-1. Other bacteria, fungi, and parasitic agents have been recovered from pericardial effusions.

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

Joint Fluid

Arthritis is an inflammation in a joint space. 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, 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 a single 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. In bacterial arthritis, the knees and hips are the most commonly affected joints in all age groups.

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 may be the cause. For example, even under the best circumstances, Borrelia 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 indicate that an infectious agent is present but inconclusive.

Overall, Staphylococcus aureus is the most common etiologic agent of septic arthritis, accounting for approximately 70% of infections. In adults younger than 30 years of age, however, Neisseria gonorrhoeae is isolated most frequently. Haemophilus influenzae has been the most common agent of bacteremia in children younger than 2 years of age, and consequently 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), pneumococci, and viridans streptococci, are prominent among bacterial agents associated with infectious arthritis in patients of all ages. Among anaerobic bacteria, Bacteroides, including B. fragilis, may be recovered and 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 associated with Lyme disease. Chronic monoarticular arthritis is frequently due to mycobacteria, Nocardia asteroides, and fungi. Some of the more frequently encountered etiologic agents of infectious arthritis are listed in Box 77-2.

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