5B 14 BF 1298 PO SRILA AS Vol. 14 No. 12, 2012 4F 12 A (Chin J Contemp Petite Dec. 2012 TO + MG ROEFE KNBR Ais tH BORE ILA HEE NOE 9S 31. Bil hs HE 3 BT RR AEE RR RR CRM ERM BFR ILS Ba ALA, ae BM 325027) (CHE) AY ACHR BCE LTE BOR AYR AUR AS a ELS EDDIE SEER, 7 IAB TT REAR. FRR AHTE 10 AE 31 LEE LIRA RSE AOISPRRERETT EBUEEADT. IR WRR UA BERRA Me RAIL MEE ES I SH AE 17 Bl BRB 8 i DEBUT BE 2 i FOC AREA 2 1 RTBETE 1) CRP FBG 30 BH, ch 97% . AA 14 BAR BLBL Je 12 BAC SEAPIET: 5 BH). 2007 ~ 2011 FEA MEA ANY HE LY RE RES Sk EST BGI 50% VA be BG F 2001 ~2006 4F, 2007 ~ 2011 F748) B-PBEIBETIE ( ESBLs ) BRIBE HH 39 57% , THF 2001 ~ 2006 4 Ae Hy 7 ESBLs BK. BAC PALABRA MBA RAMSAR BUS. CRP AAR ASME. AE AS RT WE EA BE, ESBLs BR EAE I CoB PIL BLS , 2012, 14 ( 12) :910 -912] (3 SB HD] ACRE RRR AURA BPEL CRRSES] 512.3 [SCMRARIRAB] A [3CHMT] 1008 -8830( 2012) 12 -0910 -03 Clinical analysis of 31 cases of neonatal purulent meningitis caused by Escherichia coli ZHU Min-Li, MAI Jing-Yun, ZHU Jiang-Hu, LIN Zhen-Lang. Department of Neonatology, Yuying Children's Hospital of Wenzhou Medical College, Wenzhou, Zhejiang 325027, China (Lin Z-L, Email; linzhenlang@ hotmail. com) Abstract; Objective Neonatal purulent meningitis is a severe infection responsible for high mortality and disabling sequelae. Escherichia coli is the main pathogen of neonatal purulent meningitis. This study explored the clinical characteristics and antibiotic resistance of Escherichia coli-induced neonatal meningitis. Methods A retrospective chart review was performed. A total of 31 cases of neonatal purulent meningitis caused by Escherichia coli were identified in the neonatal intensive care unit between January 1, 2001 and December 31, 2011. The clinical characteristics and antibiotic sensitivity test results were analyzed. Results Fever, poor feeding, lethargy and seimre were common clinical signs of neonatal purulent meningitis caused by Escherichia coli. Acute complications mainly included hyponatremia (17 cases) , hydrocephalus (8 cases) , subdural collection (2 cases) , ventricultis (2 cases) and cerebral infarction (1 case). Thirty neonates (97% ) had increased CRP levels. Of the 31 patients, 14 cases were cured and 12 had adverse outcomes (5 patients died during hospitalization ). Escherichia coli strains were resistant (> 50%) to commonly used penicillins and cephalosporins between 2007 and 2011, presenting significantly higher resistance rates than between 2001 and 2006. ‘The detection rate of extended spectrum f-lactamases(ESBLs )-producing strains between 2007 and 2011 increased significantly compared with between 2001 and 2006 (57% vs 0). Conclusions The clinical manifestations of neonatal purulent meningitis caused by Escherichia coli are non-specific. The outcome is poor. Monitoring of CRP levels is valuable for the early diagnosis of neonatal purulent meningitis. The antimicrobial resistance rates of Escherichia coli are increasing, especially to cephalosporins. ‘The percentage of ESBLs-producing strains is increasing over the years. [Chin J Contemp Pediatr, 2012, 14(12) :910 -912] Key words; Purulent meningitis; Escherichia coli; Newbom ‘Bie SLAC GR ASB oe ILE CSOSA ALAA UR A HERA. BO RRR eet || Sone") ARIA TBA ILM AORTA OE. TUERSRIDI ERA ACHR ISRAEL MODESEAR aT ABO (etl 981 }2012 -06 -20; (em ap 01 07-20 tHE! Gaereat ote EEEBEIO 910+14 5 1H 2012 12 i PO SRILA AS Chin J Canton Petr Vol. 14 No. 12 Dee. 2012 KERRGAMRAMBGER RES, MERCH 4 JL Bei 10 AFIS 31 BART JL ARs HEIR RES DR 2 BE FR EAT BE ST, VAS IR BIB 1 BRS 11 HRT 2001 4E.1 9 2011 4E 12 ABER LEEW WR AILA BR BBR BIL 31 Fl, Bw RE Has (1) ABA LAR AT A JL He FRBSR (2) BAPE BE BR AE EAT A CE PRATER ; (3 ) IR FE BL A BME BI FEA Rae. 12 ik SY 31 GTA: JL i HR As A EAB LB RA TKERERDGSRRRA RA ARE EERIE EET. 1.3 Site JE SPSS 17.0 StiP eCPM BGR MEAT SITS BT, TBO ABR = PRMEZE (% + 5) FAR TL BERL FAR ( % ) FEAR , WUT AGE AY OBER Ay? HP <0.05 HRRARTFEEX. 2 BR 2.1 ARR FE 10 ER BERL JL BE LACHER KR 269 Gil, FERS BLE FE PAE IAG A 102 GF, LA KR HBR ABS, 3 31 Gi, PH 19 Ge 12 Bi); APL 6 Bil (BAR HH AE EL 1 Bl), BAL 25 Bil, PHAR 267 +22 d PYAR LAE 2956 + 127 go SORT AM <7 d 8 GHP <3 d 3 Gil) ,8 ~ 28 d 23 Bij, BEBE AE 25 Bi, BAAS RRR hh AE 6 Gil BATE 26 i), BET 5 Bil. WMTATT :22 BEAD FAA BRAS HE BSS USS FA RPMI | MALAKGARER, AAR PRG SRA IGE SARA RK, RYO PHAM NHE RIA. 31 BIBIL PIR 14 Gi) (45% ) SFE 5 B(16% ) AR BRB 12 Bi)(39% ) FEHR ESP RAEBGNAT 7 BIEL 5 Bi. 2.2 RRR IGPREABERA (29 i] 94% ) , >We RABEL (23 Hi, TAG ) RIZE (21 Gil 68% ) BARAK (18 Gil, 58% ) & Fc 18 PVDRBRAB ILA , LAZE AEE RSE (10 Bi]) « AAR MRR 8 Gi ( APRS 6 Fi), HABE BES Bl) A ILIR 3 HI BFR 3 Bil, BEI 3 HI BE FREY 2 Gil, PRERRRIN2 fi, ATUL BIR A HE ER ARABS | Fl. SHIRE 4 Bi) CAAGEIGTE 2 6), FERED ME 1 G,21-= HS FEL Bil). FAA MLE 17 Bil BK 8 Bi ACER "PRE 6 OF] SATU 5 Bi), SEAS TAGE 3 Hi), BEBE FR 2 Bil HE RR 2 Bi), PAH tn 2 Bi, BBE, 1 Bie 2.3 RSE SPALL ALG 23 (74% ); FAMAH > 20 x 10°/L 11 Bi), AAA <5 x 10°/L 3 Bil, th Jv# < 100 x 10°/L5 fl, C BR 1M BE FH ( > 10 mg/L) 30 Hi (97% ) FLFR >50 mg/L %25 fi, > 100 mg/L # 13 Hi, AAA C ROE AAA IE RY 1 Ol. BaP BEES: SIL 40 ~ 14400 x 10°71, HRP LS 0.03 ~ 0. 93, EAI 0. 19 ~ 30 e/L, ALM 97 ~ 122 mmol/L. HLS 378 FA HE 27 Bil, BBA HOLS FE BH 10 Goi ( SEF 3 i MIE FR BE) , BLK IEE HORE FE PRES 1 Gi), 2007 ~ 2011 4E =a i B-A BRR ES CESBLs) BPR RE 39 57% , THT 2001 ~2006 AEE i7* ESBLs BAPE. 2.4 Bea R 2001 ~ 2006 4F AHS BAM HS FA Ae ES SARRAIAZ 5 1H 2007 ~ 2011 AERA BT A RRA Ke RA BIH BB ( > 50% ) . RH 1. Rl AANMRE LC RMRAA BRO fies (91%) 2001 ~2006 AF 2007 ~2011 48? 3/1030) 97R0(45) 0.625 ono) oo), = s/0(s0) 18/2186) 6.871 o7o(0)—2/20(10) 1.071 o70(0) —13/21(62) 10.661 ono(0) —2n(s7) 9.323 ono(o) 12137) 9.323 on0(0) —2n(s7) 9.323 ono(o) 1237) 9.323 ono) ono) = 0760) 120(55) 5.720 0710) 20110) 0.756 070) 1719(5) 0.388, oa) 080) = Pt EKER TRE ato FADE um SUT 8 BE Sen Ea Ae ud RTA HME SURI Olle5B 14 BF 1298 PO SRILA AS Vol. 14 No. 12, 2012 4F 12 A (hin J Contemp Pent Dec. 2012 BFC DRA RAIS MAS ORT 3 Wt BAY fhe BAR, RP RR 72) LACH BU BUS XE, JOR FIRM BS ER, B RARE ALIL ‘ACE BE SB RS A RA WO, ERE wR ASA LARA ATR TET RE, BA LRA BA ILE SH RACER , ROE 10 EMER LET GRATE ICR IR TL IE Z. ADR BABA LAG RA RAEN SHE, WRIA DOL UIBAL LIMBE RTA TLR 2 BB PILFEB ADP ( BAPE BLE HAO 5} BJs 30°? Jd. 327°), JE 1 REAL ARIE) RAR OT SRA. PERRIN EI HSL, HR RASHEED LE, SIEM AOD, 2 DAS. ASE, AES RL 74% , TAG C SRM a SF BE Us 97% , FEF > 100 mg/L. #13 Bl HABA 250 me/L, AML C RE AX AMBRE MVOMI. Hemmati 9 3B VON C BLT AER IN BAS BC BO ML I VARY C RIM AT ALE SEAR, th SEAR ACEI FH OIF RE UK ATE FEAR LOR 55% A CA A, 7 I EL BEE SUA RCN OS Le ALE EL nM, SRAM I, MLE S RARE. SAE LAC ERR ea RAV 8 5 Be, (EU SEL, Tc ABBR TROL. ARISE 3 iL SDA te, MOAR TERED A SEP 1 GUILA BE 551 UOTE 2 4 SER. BRE SEBEL EE (OVE Dy aa AJL A A, WTO ANSE RRR IE RULE ee LAL ELA AE ea WBA ARETE. BOR EE Dy BEER S61 PRES WCIE 18 A, DET OR 2 UES I ERAT, RTE BET - SEES, AIR AS ALERT ILRI Pw HE BE FRB, SPURT BG TBS HEE FBO BE, ALSEMAER”. AHRPAERE ERY AR SRT UE, SOIR SCARRING ERE AO ASI EER. PG RAM B-PABAT LS WT E PUGET ESBLs, B-ARBAT RAW TES AB PARA ESBLs BAAR SA. SARE RMB tRAG HH 2007 ~ 2011 4F4ABE 2001 ~ 2006 SEL RT SE BRGMGE BE LAB SAAS REAM KRE—-RABAR. BHb,2007 ~ 2011 4E #817* ESBLs BHPR(57% ) BE 2001 ~ 2006 4F 4H (0) BA BAB SARA BN KH RR A PAF DNA ABR Ae ASS He HR 2 MH] EER STE ESBLs AK. ARIA AIRE BS ESBLs HER SL RAMA, MBS EAD 5b MAALARBS OURS F BH 7K LD SL ARR , (LBA YRS HEA TYGER B LANE. a PR ESS DRO BE BIL. —B RAGA ABA, EARP ESBLs BRR 7 (SEF Sk FALE AG, 3k Fa HS F* ESBLs BERRY AY ULMER. IBY, HT ESBLs BRAT JBORLSy SEAR FAL BB PR A FSH, PR — ESBLs SRM 995 Oi, IZ Be Bat FRB BS HH SE A, EEBEA™ ESBLs BIPRESTRAT. [e * x m] in BE, Foie, TA, TAK, EER. 156 HURT IL ACRE PIR BRIBED I). “PR HZ ,2007 , 6(2) 117-119. RES Bibs RAD, Bie LCR A REA SEE RB HEAL). SAVER, 2008 36 (5) :334-337, (2 [3] Gaschignard J, Levy C, Romain 0, Cohen R, Bingen E., Aujard Y, etal. Neonatal Bacterial Meningitis; 444 cases in 7 years J] Pediat Infect Dis J, 2011, 30(3) : 212217. (4) REF MR, RL, AS, BRR. 176 LMA ER SPL]. ELAR ILA 2009, 11 (5) 407-409. RAC ARRAN. ILC PRD SESH LI). FBLA ,2009,24(4) .217-219. Hemmati F, Pishva N. C-reactive protein as an indicator of aque- ductal gliosis and hydrocephsly innconatal meningitis{ J]. Singa- pore Med J, 2008, 496); e163. BO, HR FIBA. i ILA MLE RT APSE IS ‘ees LS). PE JLAL Se, 2008 ,23 5) 261-264, {s. (6] 07 CRI ERE) 912+