Answer to Question 2

Acinetobacter is a Gram-negative coccobacillus that has emerged from being an organism of questionable pathogenicity to an infectious agent of importance in hospitals worldwide. The organism has the ability to accumulate diverse mechanisms of resistance, leading to the emergence of strains that are resistant to all commercially available antibiotics.

The epidemiology of Acinetobacter infections is broad and includes hospital-acquired infection, community-acquired infections in tropical environments, and infections that occur in the setting of wars and natural disasters. Some strains can survive environmental desiccation for months, a characteristic that promotes transmission through fomite contamination in hospitals.

Health care-associated infections tend to occur in debilitated patients in intensive care units (among both children and adults) and among residents of long-term care facilities (particularly facilities caring for ventilator-dependent patients). Additional risk factors include recent surgery, central vascular catheterization, tracheostomy, mechanical ventilation, enteral feedings, and treatment with third generation cephalosporin, fluoroquinolone, or carbapenem antibiotics.

More than 30 different species belonging to the genus Acinetobacter have been identified. Most of these species are environmental organisms and have not been associated with human disease. A. baumanii, A. calcoaceticus and A. lwoffi are the species most frequently reported in the clinical literature.

A number of factors contribute to Acinetobacter virulence:

• The organism can survive under dry and iron-deficient conditions for long periods.
• Approximately one-third of strains produce a polysaccharide capsule that works with the cell wall liposaccharide to prevent complement activation. The capsule may also delay phagocytosis.
• Colonization in the lung is facilitated by the ability of Acinetobacter species to adhere to human bronchial epithelial cells using fimbriae. In addition, colonization of environmental surfaces is promoted by adhesion via pili and the subsequent formation of biofilms.

Hospital-acquired pneumonia and bloodstream infections are the most common infections associated with Acinetobacter. These Acinetobacter infections are associated with high mortality rates, partly because of prevalent comorbid conditions. Other less common infections include meningitis, wound or surgical site infections, and urinary tract infections.

The diagnosis of Acinetobacter infection is made by the growth of Acinetobacter from a patient specimen (e.g., sputum, blood, cerebrospinal fluid) in the setting of other clinical findings that suggest an infection at that site. Acinetobacter can colonize skin, wounds, and the respiratory and gastrointestinal tracts. It is important but may be difficult to distinguish between colonization and true infection, particularly since many infections occur in the setting of colonization.

Acinetobacter endocarditis:
Acinetobacter species are a rare cause of infective endocarditis in native and prosthetic heart valves. In a study of 171 patients with prosthetic heart valve endocarditis resulting from nosocomial bacteremia, two cases were attributable to Acinetobacter. Acinetobacter endocarditis is characterized by an acute onset with an aggressive course. Mortality tends to be higher in the setting of native valve endocarditis than prosthetic valve endocarditis, likely because of the low index of suspicion leading to delayed treatment in such cases.

Blood cultures now grew Stenotrophomonas maltophila, sensitive to trimetroprim/sulfamethoxazole. This was most likely due to the selection pressure created by long term meropenem exposure as Stenotrophomonas is intrinsically resistant to carbapenems. Meropenem was discontinued because there was clinical improvement related to the IE and repeated TOE showed resolution of the AV ring abscess. She was commenced on high dose trimetroprim/sulfamethoxazole for 14 days.

Question 3: What is the clinical significance of Stenotrophomonas maltophila and when do we treat?

Answer to Question 4

Routine antimicrobial prophylaxis for bacterial endocarditis is not recommended in most women with valvular heart disease during pregnancy and delivery. However, the 2008 American College of Cardiology/American Heart Association guidelines for the management of adults with congenital heart disease suggests that in select high-risk patients, such as those with prosthetic heart valves, it is reasonable to consider antibiotic prophylaxis before vaginal delivery at the time of membrane rupture. Antibiotic prophylaxis to reduce the risk of postpartum endometritis is routinely given prior to all cesarean deliveries, and will provide protection against endocarditis as well.

The AHA guidelines state that a very small number of infective endocarditis are prevented by antimicrobial prophylaxis following dental procedures and should be given only in high risk patients eg those with prosthetic valves. Procedures include those involving manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa. Prophylaxis is not routinely recommended for patients undergoing a genitourinary or gastrointestinal tract procedure.

Please refer to reference 7 for further information.

Question 5: What is the role of Antimicrobial stewardship and the Microbiology laboratory in such patients?