Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (482 page)

Klein JO. Danger ahead: politics intrude in Infectious Diseases Society of America Guideline for Lyme disease.
Clin Infect Dis.
2008;47:1197–1199.

Kuehnert MJ, Doyle TJ, Hill HA, et al. Clinical features that discriminate inhalational anthrax from other acute respiratory illnesses.
Clin Infect Dis.
2003;36:328–336.

Maragakis LL, Perl TM.
Acinetobacter baumannii
: epidemiology, antimicrobial resistance, and treatment options.
Clin Infect Dis.
2008;46:1254–1263.

Mundy LM, Sahm DF, Gilmore M. Relationships between enterococcal virulence and antimicrobial resistance.
Clin Microbiol Rev.
2000;13:513–522.

Munoz-Price LS, Weinstein RA.
Acinetobacter
infection.
N Engl J Med.
2008;358: 1271–1281.

Newman LM, Moran JS, Workowski KA. Update on the management of gonorrhea in adults in the United States.
Clin Infect Dis.
2007;44:S84–S101.

Parola P, Paddock CD, Raoult D. Tick-borne rickettsioses around the world: emerging diseases challenging old concepts.
Clin Microbiol Rev.
2005;18:719–756.

Parola P, Raoult D. Ticks and tickborne bacterial diseases in humans: an emerging infectious threat.
Clin Infect Dis.
2001;32:897–928.

Peterson LR, Robicsek A. Does my patient have
Clostridium difficile
infection?
Ann Intern Med.
2009;151:176–179.

Reimer LG. Q Fever.
Clin Microbiol Rev.
1993;6:193–198.

Rosenstein NE, Perkins BA, Stephens DS, et al. Meningococcal disease.
N Engl J Med.
2001;344:1378–1388.

Swartz MN. Recognition and management of anthrax—an update.
N Engl J Med.
2001;345:1621–1626.

Swindells J, Brenwald N, Reading N, et al. Evaluation of diagnostic tests for
Clostridium difficile
infection.
J Clin Microbiol.
2010;48:606–608.

Waites KB, Katz B, Schelonka RL. Mycoplasmas and ureaplasmas as neonatal pathogens.
Clin Microbiol Rev.
2005;18:757–789.

Waites KB, Talkington DF.
Mycoplasma pneumoniae
and its role as a human pathogen.
Clin Microbiol Rev.
2004;17:697–728.

Walker DH. Rickettsiae and rickettsial infections: the current state of knowledge.
Clin Infect Dis.
2007;45:S39–S44.

Weinstein A. Laboratory testing for Lyme disease: time for a change?
Clin Infect Dis.
2008;47:196–197.

Winn WC Jr, Allen SD, Janda WM, et al. Gram positive cocci, part I: staphylococci and related gram-positive cocci. In:
Koneman’s Color Atlas and Textbook of Diagnostic Microbiology
, 6th ed. Baltimore, MD and Philadelphia, PA: Lippincott Williams & Wilkins; 2006.

Wormser GP. Discovery of new infectious diseases—
Bartonella
species.
N Engl J Med.
2007;356:2346–2347.

   
INFECTIOUS DISEASES CAUSED BY ACID-FAST BACTERIAL PATHOGENS (AFB)

The organisms in this group contain mycolic acids in their cell walls, which renders the cells relatively resistant to both staining and destaining. Therefore, special techniques are used for direct visual detection of these organisms in specimens.
Mycobacterium
species, in general, are resistant to strong decolorization procedures with acid–alcohol.
Nocardia
and
Rhodococcus
species have a lower cell wall mycolic acid content and are acid-fast only when weaker decolorizing procedures are used.

Diseases caused by organisms in this group are usually diagnosed by isolation in culture. Specialized culture procedures are required, with prolonged incubation. Because of the slow growth rate of many isolates, molecular methods are increasingly used for direct detection and speciation of isolates. Tests that measure a patient’s cellular immune response (e.g., TSTs and IGRA tests) may be used to screen for TB; serologic testing is not otherwise useful for diagnosis. See Chapter
17
, Infectious Disease Assays for information about AFB culture and staining, and IGRA screening tests.

MYCOBACTERIUM TUBERCULOSIS

See Chapter
13
, Respiratory, Metabolic, and Acid–Base Disorders.

NOCARDIA
INFECTION

   Definition

Nocardiosis describes infections caused by species of the genus
Nocardia
. These bacteria are aerobic gram-positive organisms that form delicate filaments that show branching and fragmentation.
Nocardia
species are widely distributed in nature worldwide and are involved in the decay of organic material. Human infections are usually seen in patients with immunocompromising or debilitating underlying medical conditions. Pulmonary infections acquired by inhalation, or cutaneous infections acquired by direct or traumatic inoculation, represent most primary infections. Local spread and systemic dissemination are common.
Nocardia
have tropism for the CNS. Recurrent or progressive infection may occur despite appropriate antimicrobial therapy.
Nocardia asteroides
is the most common species associated with invasive human infections.
Nocardia brasiliensis
is predominantly associated with cutaneous infections.

   Who Should Be Suspected?

These organisms have a low intrinsic virulence; infection most commonly occurs in immunocompromised patients, but no underlying condition is found in 10–20% of patients. Factors that increase the risk of nocardiosis include AIDS, alcoholism, chronic lung disease, DM, glucocorticoid therapy, malignancy, and solid organ or hematopoietic stem cell transplantation.

   Laboratory Findings

Direct stain
: Gram positive or gram variable; modified acid-fast positive.

Culture
: Most nonselective media for bacterial, fungal, and mycobacterial isolation will support the growth of
Nocardia
but may require up to 6-week incubation for isolation. Noninvasively obtained specimens may be inadequate for sensitive detection of nocardiae. Sputum is positive in only 30% of cases of pulmonary infection. Blood culture is rarely positive. All patients with nocardiosis should be evaluated for possible disseminated, including CNS, infection.

Susceptibility
: Sulfonamides, including TMP/SMX, are considered the drug of choice of nocardiosis because of the low rate of resistance and extensive clinical experience. Susceptibility testing is recommended, however, for life-threatening infections and for patients allergic to sulfa drugs.

RAPIDLY GROWING MYCOBACTERIA

   Definition

Rapidly growing mycobacteria (RGM) are widely distributed in environmental water sources, dust, and soil. Although exposure to these organisms is common, disease is uncommon because of their low intrinsic pathogenicity in normal hosts. RGM produce mature colonies within 7 days after subculture. The clinical significance of culture isolates must be interpreted carefully to rule out contamination. Factors to be considered include site, quantity of growth, number of positive cultures, and signs of inflammation and host immune status.

   Significant Species