> >Has anybody ever heard of a stool culture for E coli being divided into: > >-Adherence >-Enteroinvasive >-Labile Toxin >-Verotoxin > >I had a 10 month old who's diarrhea finally resolved after about 10 days, >but a few days later the culture I'd sent off the previous week came back >positive for >E coli - Adherence, negative for the other three categories. The local GI >consultant had never heard of a culture being reported this way. >Any input would be greatly appreciated. > >Michael Sachs, M.D. >General Pediatrician Hey, I was able to scan, copy, and paste the child's actual lab report into this posting so you can see (if you have a lot of time on your hands) what I was trying to interpret. There may be some bizarre looking words after the OCR but hopefully it'll come out fairly readable. Here goes: TEST NAME IN RANGE OUT OF RANGE REFERENCE UNITS ROTAVIRUS,STOOL - SPECIALTY ROTAVIRUS, STOOL NOT DETECTED NOT DETECTED SP E.COLI STOOL SCREEN - MRL SOURCE ML STOOL ADIIERENCE POSITIVE (1) ML ENTEROINVASIVE NEGATIVE (2) ML LABILE TOXIN NEGATIVE (3) ML VEROTOXIN NEGATIVE (4) ML STOOL CULTURE STATUS FINAL RESULT NO SALMONELLA, SHIGELLA, VIBRIO, STAPH AUREUS OR CAMPYLOBACTER ISOLATED. NORMAL FLORA PRESENT. MICROSCOPIC ONLY, MISC. SOURCE STOOL RESULT NO LEUKOCYTES SEEN. Footnotes: (1) ADHERENCE: ENTEROPATHOGENIC E. COLI (EPEC) IS A DISTINCT CATEGORY OF DIARRHEAGENIC E. COLI THAT DOES NOT PRODUCE ST OR LT AND DOES NOT MANIFEST SHTGELLA-LIKE INVASIVENESS. THESE ORGANISMS EXHIBIT A CHARACTERISTIC ATTACHMENT TO EPITHELIAL CELLS WITH THE FORMATION OF MICROCOLONIES; THIS PROPERTY IS MEDIATED BY EPEC ADHERENCE FACTOR PLASMIOS. CLINICALLY, EPEC ILLNESS IS CHARACTERIZED BY FEVER, MALAISE, VOMITING AND DIARRHEAE WITH PROMINENT AMOUNTS OF MUCUS BUT WITHOUT GROSS BLOOD. THERE IS AMPLE EVIDENCE THAT HEP-2 CELL ADHERENCE AMONG STRAINS IS A MARKER OF VIRULENCE FOR HUMANS. DIFFERENT PATTERNS OF ADHERENCE DESCRIBED ARE DIFFUSE ADHERENCE, LOCALIZED ADHERENCE AND AGGREGATE. (2) ENTEROINVASIVE: THE TERM ENTEROINVASIVE E. COLI (EIEC) IS USED TO DIFFERENTIATE A SMALL NUMBER OF E. COLI BIOSEROTYPES THAT CAN INVADE THE INTESTINAL MUCOSA AND CAUSE A DYSENTERY-LIKE SYNDROME SIMILAR TO SHIGELLOSIS. THESE ORGANISMS INVADE HELN CELLS, n VIRULENCE FACTOR WHICH IS ENCODED BY A PLASMID. EIEC HAVE A PREDILECTION FOR COLONIC MUCOSA CAUSING AN ILLNESS MARKED BY FEVER, SEVERE ABDOMINAL CRAMPS, MALAISE, TOXEMIA, AND OCCASIONAL EARLY WATERY DIARRHEA FOLLOWD BY GROSS DYSENTERY CONSISTING OF SCANTY STOOLS OF BLOOD AND MUCUS. (3) LABILE TOXIN: ETEC ENTEROTOXIGENIC E. COLI PRODUCE DIARRHEA BY CHOLERA-LIKE OR OTHER ENTEROTOXINS. IT IS THE AGENT MOST FREQUENTLY RESPONSIBLE FOR TRAVELER'S DIARRHEA. ETEC INFECTION IS ACQUIRED BY INGESTING CONTAMIUNATED FOOD OR WATER. THE BACTERIA COLONIZE THE PROXIMAL SMALL INTESTINE, WHERE THEY ELABORATE HEAT-LIABLE ENTEROTOXIN (LT) OR HEAT-STABLE ENTEROTOXTN (ST). THE CLINICAL FEATURES OF ETEC INFECTION ARE WATERY DIARRHEA, NAUSEA, ABDOMINAL CRAMPS AND LOW-GRNDE FEVER. (4) VERO: VEROTOXIN PRODUCING E. COLI (VTEC) WAS RECENTLY RECOGNIZED AS THE CAUSE OF MULTIPLE OUTBREAKS OF HEMORRHAGIC COLITIS, HEMOLYTIC UREMIC SYNDROME, AND DIARRHEA IN NURSING HOMES, DAY CARE CENTERS, SCHOOLS AND THE COMMUNITY. THESE E. COLI WERE FIRST RECOGNIZED TO BE SEROTYPE 0157:H7, HOWEVER OTHER SEROTYPES HAVE BEEN REPORTED TO PRODUCE VEROTOXINS. TIIEY ELADORATE PIIAGE-ENCODED POTENT CYTOTOXINS ACTIVE ON HELA AND VERO CELLS. ONE OF THESE TOXINS, APPARENTLY IS IDENTICAL TO A PROTENT CYTOTOXIN - NEUROTOXIN - ENTEROTOXIN, PRODUCED BY S. DYSENTERIAE TYPE 1 (SHIGA TOXIN). MANY STRAINS ELABORATE A SECOND POTENT CYTOTOXIN (VEROTOXIN 2).