Stephen A. Chartrand

Colonization with penicillin-resistant Streptococcus pneumoniae in a child-care center

We obtained nasopharyngeal cultures for Streptococcus pneumoniae from 54 children ages 2 to 24 months attending an Omaha child-care center (CCC) in April 1994. Thirty-two (59%) of the 54 children were colonized with S. pneumoniae belonging to serotypes 23, 19, 6 and 11. Seventeen (53%) of the pneumococcal isolates were highly resistant to penicillin (minimal inhibitory concentration ≥2.0 mUg/ml; HR-SP) and 7 (22%) were intermediately resistant to penicillin (0.12 ≤minimal inhibitory concentration ≤ 1.0 mUg/ml; IR-SP). Within each pneumococcal capsular serotype, there were 1 to 3 DNA subtypes based on pulsed field gel electrophoresis analysis. A single pulsed field gel electrophoresis strain predominated in most CCC rooms, suggesting horizontal transmission among cohorted children. Nasopharyngeal cultures obtained 4 months later revealed similar S. pneumoniae colonization rates (28 of 52, 54%); however, only 2 (7%) of 28 isolates were HR-SP and 11 (39%) were IR-SP. Colonization with resistant pneumococci persisted after 4 months in 4 (12%) of 34 children cultured on both occasions. Antibiotic use by attendees had decreased notably between the two sampling periods, suggesting that selective pressure within the CCC might contribute to seasonal variation in colonization rates with HR-SP and IR-SP. We conclude that multiple genetic clones of penicillin-resistant pneumococci can occur simultaneously in a single CCC, especially during periods of heavy antibiotic selection pressure. However, individual clones of penicillin-resistant S. pneumoniae may be spread

Hydrocephalus complicating lymphocytic choriomeningitis virus infection

Lymphocytic choriomeningitis virus (LCMV) disease is a human zoonotic infection acquired by contact with infected mice, hamsters or their excreta.1 The reported spectrum of LCMV-associated central nervous system (CNS) disease ranges from mild aseptic meningitis to fatal meningoencephalitis. Hydrocephalus is a rare CNS complication of viral infections but there have been a few reports of LCMV causing acquired and congenital hydrocephalus.2–5 We believe this complication may not be so rare and report two cases of LCMV-associated hydrocephalus identified within a 12-month period. The first case is a child with transient hydrocephalus complicating LCMV meningitis and the second case is a full term infant born with congenital hydrocephalus and severe chorioretinitis. To our knowledge this is the first case of congenital hydrocephalus caused by LCMV reported in the United States.

Antibiotic-resistant, gram-negative bacillary infections

Summary Compared with their gram-positive brethren, gram-negative bacteria have evolved an exceedingly complex anatomy and physiology in order to adapt and survive in the rather harsh environment of the gastrointestinal tract. Not surprisingly, they also have adopted an intricate, highly integrated, and broad repertoire of antibiotic resistance tactics, many of which build on mechanisms inherently present in the organism. The bacterium can regulate normal nutrient channels to block access of the antibiotic and then upregulate an already functioning efflux system to pump right back out those invaders that slip through the first line of defense. The gram-negative bacteria efficiently line up their assault weaponry (beta-lactamases) in the confines of the periplasmic space “killing field” to destroy those invaders who persist in the assault. If the enemy manages to penetrate the inner realm (cytoplasm), the organism still can disarm the invader by intercepting and inactivating the incoming missiles with modifying enzymes. If all else fails, the organism effectively can camouflage the target, redeploy the supply lines (alternate pathways), or just produce more targets. We just now are beginning to appreciate how superbly organized, integrated, and efficient this defense system really is. Future research must be directed not at bigger and more powerful versions of our current artillery. Researchers must be creative in order to exploit our new understanding of the mechanisms of resistance. Potential strategies might include altering porin proteins to allow increased diffusion of antibiotics, inactivation of efflux systems, and inactivation of inactivating enzymes, among others. In the meantime, it is clear that all resistance strategies in bacteria occur in response to the overuse of antimicrobials in the environment. Clinicians can join in the war against resistance by using this weaponry discretely and aiming it accurately.

Activity of faropenem against resistant isolates of Streptococcus pneumoniae

An in vitro study of the activity of 9 agents against 181 US pediatric isolates of Streptococcus pneumoniae identified imipenem and faropenem as the most active agents. Overall, faropenem was the most potent oral agent inhibiting 98% of isolates at 1 microg/mL.

Activity of oral agents against pediatric isolates of Streptococcus pneumoniae

An in vitro study of the activity of 10 oral agents against 153 pediatric isolates of Streptococcus pneumoniae identified moxifloxacin and levofloxacin as the most active agents regardless of penicillin or macrolide susceptibility. Moxifloxacin inhibited all strains at 0.25 microg/ml and was 8- to 16-fold more potent than levofloxacin.

Antibiotic resistance in pediatric respiratory tract pathogens

Antibiotic resistance in pediatric respiratory pathogens is now widespread, primarily because of overuse of these agents in the community. Twenty to sixty percent of pediatric Streptococcus pneumoniae isolates are nonsusceptible to penicillin (MIC90 > 0.1 mg/L), although most are in the intermediately resistant category and remain susceptible to amoxicillin. Forty to sixty percent of nontypeable Haemophilus influenzae and greater than 95 percent of Moraxella catarrhalis produce β-lactamase. Penicillin resistance has not been documented in Streptococcus pyogenes , but macrolide resistance is common when these drugs are overused in the community. Penicillin-resistant meningococci are rare in the United States. More accurate diagnosis and judicious use of antibiotics are critical to prevent further spread of these resistant organisms.