The Health Blog

ACUTE INFECTIOUS DIARRHEAL DISEASES: LABORATORY STUDIESBecause most diarrheal illnesses are self-limited and mild, physicians must use their clinical judgment to determine whether diagnostic testing will be helpful in managing each patient. Laboratory testing may include fecal leukocytes, lactoferrin, routine stool culture, toxin assays, ova and parasites, and specific bacterial cultures or studies, depending on the suspected cause of diarrhea. Laboratory testing should be considered in the following situations:- Inflammatory diarrhea (bloody stools, fever)- Persistent symptoms for more than 3 days- Recent travel- Immunosuppressed host- Nosocomial diarrhea- Potential community outbreak- Potential food-borne outbreak
Fecal Leukocytes and LactoferrinMicroscopic identification of fecal leukocytes or a positive immunoassay for the neutrophil marker lactoferrin can confirm a suspected inflammatory origin. One study found that fecal leukocytes were absent in all cases of viral diarrhea and present in 89% of cases of bacterial diarrhea. Negative results would justify watchful waiting in place of further diagnostic testing that is likely to be unhelpful. Because stool cultures may take several days to grow, stool positive for leukocytes or lactoferrin justifies the use of empiric antibiotics in patients with infectious diarrhea. Physicians should keep in mind that stool tested in cases of diarrhea due to toxin-mediated disease will usually be negative, and suspected cases need a specialized approach. Certain situations mandate that empiric antibiotics be used despite negative fecal leukocytes and lactoferrin, as in traveler’s diarrhea caused by enterotoxogenic E. coli. Lactoferrin may be a more sensitive test, but fresh stool (less than 24 hours old) will increase the sensitivity of fecal leukocytes.
Routine CulturesRoutine stool cultures in most laboratories screen for Salmonella, Shigella, Campylobacter, and, usually, Aeromonas and plesiomonas. Most other bacteria can either be cultured by special requests (Yersinia, Vibrio) or are identified only in research laboratories. The Centers for Disease Control and Prevention recommend special testing for E. coli 0157:H7 in all patients with acute bloody diarrhea or HUS because of public health implications. Other types of enterohemorrhagic E. coli cannot be readily cultured; however, toxin can be detected in stool samples. Routine bacterial stool cultures should not be requested for patients who develop diarrhea after 3 days of hospitalization because studies have shown an extremely low yield. These patients should have stool evaluated for Clostridium difficile toxin with up to three stool specimens for maximal sensitivity.
Ova and ParasitesMicroscopy by trained microbiologists can identify a parasitic origin, and specific immunoflorescent testing is available for Giardia and Cryptosporidium. Testing should be reserved for patients with a longer duration of diarrhea, recent travel to mountainous regions, exposure to infants, and AIDS, and in patients with dysentery who have few fecal leukocytes on fecal examination.*73/348/5*

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EMPIRIC TREATMENT OF ACUTE BACTERIAL MENINGITISAs has been mentioned, antibiotic selection in cases of acute bacterial meningitis is of paramount importance. Since antibodies and complement are lacking in the CSF, allowing for rapid bacterial multiplication, bactericidal antibiotics are needed to sterilize the CSF. Due to the inflammation at the blood-brain barrier, antibiotics can more readily enter the CSF. The chosen antibiotics must have adequate CSF penetration, reach bactericidal concentrations in the CSF, and retain activity in the low pH and high protein environment of infected spinal fluid. To facilitate this, antibiotic dosages used to treat acute bacterial meningitis are generally higher than those used for other infections.The latest data from the Centers for Disease Control and Prevention indicate that almost 20% of clinical isolates of pneumococcus are resistant to penicillin and another 10% display intermediate susceptibility. Moreover, 7.5% of isolates are noted to be resistant to third-generation cephalosporins and another 10% have intermediate resistance. Recommendations have thus evolved to include vancomycin in addition to ceftriaxone or cefotaxime as part of initial empiric therapy.Additionally, given the high prevalence of Listeria infection in people older than 50 years and those with significant comorbidities or immune dysfunction, clinicians should also add ampicillin to their initial empiric coverage. For the population aged 18 to 50 years, both a third-generation cephalosporin and vancomycin should be part of the initial empiric regimen. For patients with a prior neurosurgical procedure, broad empiric coverage is initially recommended with vancomycin and an antipseudomonal cephalosporin such as cefepime.There are cases in which the clinical presentation and CSF indices are consistent with acute bacterial meningitis but Gram stain, CSF cultures, and blood cultures fail to reveal a pathogen. This occurs most often in cases of partial antibiotic treatment. Empiric therapy with a third-generation cephalosporin, vancomycin, and, if indicated, ampicillin, is warranted in these situations as well.Quite frequently, patients are noted to have a true penicillin allergy, which necessitates alterations in first-line therapy. In these situations, empiric therapy should include chloramphenicol with the addition of vancomycin. Combination vancomycin and rifampin may be the best definitive regimen for pneumococcal disease when penicillin is contraindicated. When Listeria is a consideration, trimethoprim-sulfamethoxazole should be added. The necessarily high doses of intravenous antibiotic come with a high fluid load, which may necessitate close attention to volume status in a patient with potential cardiac disease.Once a pathogen is identified, definitive therapy should use the best agents possible. In many cases, desensitization to penicillin may be necessary given the known clinical failures of chloramphenicol for pneumococcus and fears about poor penetration of vancomycin into the CSF.*5/348/5*

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