Authors: Mary A. Williamson Mt(ascp) Phd,L. Michael Snyder Md
Meningitis
: CNS infection with
S. aureus
may occur in traumatic or surgical wounds, by hematogenous spread from other primary site of infection, or contamination of an intraventricular pressure monitoring device or other foreign body. Signs and symptoms are similar to those caused by other pathogens.
Toxic shock syndrome (TSS)
: This syndrome is caused by the action of TSS toxin-1 (or related toxin), a pyrogenic superantigen elaborated by a colonizing strain of
S. aureus
. Note that several other species, like group A
Streptococcus
, may elaborate similar toxins that produce an identical clinical presentation. Patients present acutely with vascular congestion, increased permeability of capillaries, and decreased vascular resistance. Hypotension and tissue hypoxia develop as a consequence of the loss of the intravascular blood volume. ARDS and DIC are common complications in patients with severe disease. Staphylococcal TSS is defined by fever >38.9°C, diffuse macular rash, desquamation, and hypotension (systolic blood pressure ≤90 mm Hg for adults).
Diagnosis is possible when signs and symptoms of disease are seen in three organ systems (muscular, GI, liver, bone marrow, CNS, kidney, skin/mucous membranes). TSS is probable when five organ systems are involved and confirmed if all six organ systems are affected.
Laboratory Findings
Direct detection
: In pyogenic infections, Gram stain usually demonstrates many GPCs in clusters, with a brisk PMN response.
Culture
:
Staphylococcus aureus
grows on standard media after overnight incubation. In patients with bacteremia, the persistence of positive blood cultures at 72–96 hours after the initiation of appropriate antimicrobial therapy is a predictor of a complicated recovery course and predicts the need for prolonged treatment.
Susceptibility testing
: Should be performed on significant
S. aureus
isolates because resistance to primary therapeutic agents is common; resistance or intermediate susceptibility to vancomycin is uncommon but has been well documented.
STENOTROPHOMONAS MALTOPHILIA
INFECTION
Definition
Stenotrophomonas maltophilia
is a commonly isolated glucose nonfermenting GNB in clinical laboratories. Organisms may colonize a variety of hospital and environmental sources, which serve as the reservoir for human colonization and infection.
Who Should Be Suspected?
Stenotrophomonas maltophilia
infections have been reported for all organ systems; however, most infections occur in patients with some type of innate or acquired immune defect. Isolates from patient specimens must be carefully evaluated for clinical significance because
S. maltophilia
may be isolated at a component of endogenous or contaminating flora. True
S. maltophilia
infection is associated with increased mortality. Typical syndromes include the following:
Lower respiratory tract infection
:
Stenotrophomonas maltophilia
is most commonly isolated from respiratory specimens and may cause approximately 5% of nosocomial pneumonias, especially in intubated patients with significant prior exposure to broad-spectrum antibiotics.
Bacteremia
:
Stenotrophomonas maltophilia
bacteremia is most commonly nosocomial, caused by indwelling catheter or other site of primary infection.
Wound infections
:
Stenotrophomonas maltophilia
is a relatively common cause of traumatic wound and soft tissue infections. Metastatic cellulitis has been described in oncology patients with neutropenia.
Laboratory Findings
Culture
:
S. maltophilia
grows well on routine laboratory media after overnight incubation.
Susceptibility
: With few exceptions, penicillins (including beta-lactam/betalactamase combinations), cephalosporins, quinolones, and aminoglycosides are ineffective for
S. maltophilia
infections. TMP/SMX is the treatment of choice; alternative agents include ceftazidime, chloramphenicol, levofloxacin, minocycline, or ticarcillin–clavulanate.
STREPTOCOCCUS AGALACTIAE
(GROUP B) INFECTION
Definition