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By Carol A. Kemper, MD, FACP
Helicobacter and Your Gallbladder
Source: Silva CP, et al. J Clin Microbiol. 2003;41:5615-5618.
Various Helicobacter spp. have been associated with hepatobiliary diseases in animals, including dogs, sheep, hamsters, and mice. In humans, H pylori has been isolated from the bile, liver, and biliary epithelium, raising questions about a possible association of H pylori and biliary disease. Silva and associates investigated the presence of Helicobacter spp., using PCR, in the gallbladder epithelium and bile from patients (n = 46) with cholecystitis and/or cholelithiasis undergoing cholecystectomy, compared with a control group (n = 18) largely composed of liver transplant patients and patients undergoing surgery for obesity. Cholecystitis was confirmed on histopathological specimens from 28 (55%) patients. Of these, tests for Helicobacter DNA were positive in 15 (50%) gallbladder tissue samples and 7 (23%) bile specimens. Inflammation of gallbladder mucosa was visualized in 94% vs 37% of Helicobacter DNA-positive vs DNA-negative specimens, respectively. However, despite attempts to culture Helicobacter organisms for up to 3 weeks, none was isolated, although 80% of patients had received pre-operative antimicrobacterials.
In univariate analysis, cholelithiasis was significantly associated with older age, female gender, and the presence of Helicobacter DNA in the gallbladder epithelium (no association was found with the presence of Helicobacter in bile). After adjusting for age, there was a strong statistically significant relationship between Helicobacter DNA found in gallbladder tissue and histological evidence of cholecystitis (P = .002). This data convincingly suggest that H pylori may play a significant role in the pathogenesis of gallbladder disease. It remains to be explained why women are at greater risk for cholecystitis, although I’m unaware of data suggesting a gender difference in the frequency of infection with H pylori.
Warning: Can Gardening be Hazardous to Your Health?
Source: ProMED-Mail Post. December 29, 2003; December 30, 2003; and January 3, 2004. www.promedmail.org.
Additional cases of an unusual species of legionellosis related to exposure to contaminated potting soil continue to be reported in Australia and New Zealand. Five new cases of pneumonia due to Legionella longbeachae occurred in December in Australia; 4 of the victims had recently used potting mixes made in that country. At least 49 cases of this type of pneumonia were reported to health authorities in Australia last year, including 2 deaths, plus additional cases in New Zealand. L longbeachae can be found in potting mixes, mulches, composts, and soils and has been previously linked to human disease in California, Oregon, and Washington, as well as in Japan. Symptoms occur within 2-10 days of exposure and range from mild cough, headache, muscle aches, and diarrhea to potentially fatal pneumonia.
Gardeners are advised to use caution when using potting mixes. Open bags outdoors or in a well-ventilated room, wear a mask and gloves, moisten the contents of the bag to limit dust before use, and wash hands thoroughly when done.
Sylvester Shares His Salmonella
Source: ProMED-Mail Post. February 2, 2004. www.promedmail.org.
A few years ago, we reported in this column the occurrence of human infection from E coli 0157 from exposure to a pet dog fed undercooked hamburger meat.
The Idaho Humane Society in Boise has similarly been linked to 10 cases of human Salmonella infection, which has been traced back to cats and kittens housed at the facility. The health epidemiologist tracking the cases was quoted as saying that "18% of the cat population has Salmonella at any given time." Although this figure seems alarmingly high (especially to a cat owner), it is probably dependent on a number of factors, especially living circumstances and diet. Stray cats (and by extension, cats that spend a good deal of time outdoors) are more likely to be infected with Salmonella, where their diets may consist of birds, small snakes, and lizards, compared with their indoor counterparts. Dogs and cats fed raw or undercooked eggs or chicken may also be at risk for Salmonella, which spreads to their owners.
Combination Therapy for Bacterial Endocarditis
Source: Le T, Bayer AS. Clin Infect Dis. 2003;36:615-621.
This succinct article nicely summarizes the evidenced-based recommendations for combination antimicrobial therapy for infective endocarditis (IE) due to common pathogens, including newer data and recommendations. Le and Bayer make the point that, despite advances in echocardiography, surgical techniques, and newer antimicrobials, mortality rates due to IE from viridans streptococci, staphylococci, and enterococci are still in the range of 4-16%, 25-47%, and 15-25%, respectively. Mortality rates for prosthetic valve IE (PVE) may be higher. These figures are likely to worsen with the increasing frequency of penicillin-, aminoglycoside-, and vancomycin-resistant enterococci, and methicillin-resistant staphylococci. Most available synergy data are limited, except for EI due to Enterococcus, although there is still no universally accepted methodology for demonstrating in vitro synergy.
For aminoglycoside-sensitive strains, clinical data suggest that shorter courses of aminoglycoside (2 weeks) may preserve clinical efficacy (~81%) and limit toxicity, especially in older patients. Reducing the time interval between each aminoglycoside dose reduces in vivo efficacy. Maintaining sustained penicillin (or ampicillin) concentrations plus the use of either 3 mg/mL or 5 mg/mL of gentamicin was synergistic, thereby limiting nephrotoxicity. For aminoglycoside-resistant strains, several in vitro and in vivo studies have demonstrated an enhanced bactericidal synergistic effect with combinations of ampicillin and third-generation cephalosporins. Using a combination of ampicillin and cefotaxime, MICs for 48 of 50 strains of high-level aminoglycoside-resistant enterococci were reduced from 0.25-1.0 to 0.01-0.25. Similar results using this combination were obtained in a rabbit aortic valve model, although only when lower levels of amoxicillin were used. Combined imipenem-imipenem was bactericidal in vivo against vancomycin-aminoglycoside-resistant strains. Ampicillin-ceftriaxone combinations were synergistically effective but again only at lower levels of ampicillin. However, the dose of ceftriaxone used was quite high (4 gm/d), in order to ensure sustained high levels.
Combination of cell wall active agents with either rifampin and/or aminoglycoside may be synergistic, although the mechanism is poorly defined, the data are somewhat conflicting, and, in some circumstances, the addition of rifampin may be antagonistic. However, clinical data in PVE (most of which was due to CNS) suggest that the addition of rifampin and/or aminoglycoside to either vancomycin or a cell wall active agent improves efficacy. Using vancomycin alone, clinical cures were ~81% but increased to 90% with the addition of rifampin and/or an aminoglycoside. In PVE due to high-level aminoglycoside-oxacillin-resistant isolates of CNS, a combination of vancomycin, gentamicin, and rifampin was synergistic against 7 of 10 isolates.
Viridans Group Streptococcus
For penicillin-susceptible isolates, the addition of streptomycin was not found to be better than PCN G or ceftriaxone alone. A number of studies have confirmed that short courses of aminoglycosides (2 weeks) allows the reduction in total therapy from 4-6 weeks to 2 weeks. A recent study found that a 2-week course of ceftriaxone plus once-daily gentamicin was similar to a 4-week course of ceftriaxone alone (clinical cures ~96%). The dose of gentamicin (~3 mg/kg) needed for synergy is less than that required for Gram-negative infection. The recommendations for penicillin-resistant VGS strains (MIC to PCN > 0.1 to < 0.5 mcg/mL) remain 2 weeks of combined gentamicin plus PCN G or ampicillin, followed by 2 weeks of PCN G or ampicillin alone. For those strains with an MIC to PCN > 0.5 mcg/mL, > 4 weeks of combined PCN G or ampicillin plus gentamicin should be used, similar to that recommended for Enterococcus. However, clinicians should be aware that there are no good clinical trial data to support these recommendations.
Dr. Kemper, Clinical Associate Professor of Medicine, Stanford University, Division of Infectious Diseases; Santa Clara Valley Medical Center, is Associate Editor of Infectious Disease Alert.