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• W2230276076 abstract "Original ArticlesCampylobacter Jejuni Enterocolitis in Neonates AKM Harunur Rashid, MRCP (UK), DCH Hussein Salman, MD Mohamed Istiaque Hussain, and MBBS Saad Mohammed Al-HadlaqFacharzt AKM Harunur Rashid Address reprint requests and correspondence to Dr. Rashid: P.O. Box 59046, Riyadh 11525, Saudi Arabia. From the Department of Pediatrics, Suleimania Children's Hospital, Riyadh. Search for more papers by this author , Hussein Salman From the Department of Pediatrics, Suleimania Children's Hospital, Riyadh. Search for more papers by this author , Mohamed Istiaque Hussain From the Department of Pediatrics, Suleimania Children's Hospital, Riyadh. Search for more papers by this author , and Saad Mohammed Al-Hadlaq From the Department of Pediatrics, Suleimania Children's Hospital, Riyadh. Search for more papers by this author Published Online:1 Mar 1993https://doi.org/10.5144/0256-4947.1993.166SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutAbstractCampylobacter jejuni is one of the leading bacterial pathogens causing acute gastroenteritis in children. Only a few cases have been described in the world literature about neonatal enterocolitis due to campylobacter and none from Saudi Arabia. We describe six cases of neonatal enterocolitis due to this organism isolated during the period from September 1989 -January 1991 at Suleimania Children's Hospital, Riyadh, Saudi Arabia. All of the patients presented with diarrhea; duration ranging from 1-20 days. Three patients had blood and two had mucus in their stool. In contrast to the findings of other investigators, five neonates presented with fever. One neonate was treated with erythromycin, another received augmentin, and two received other antibiotics because of suspected sepsis. In one patient, previous antibiotics were discontinued and erythromycin was added and two received no antibiotics. Campylobacter infection should be suspected in any neonate presenting with diarrhea accompanied by mucus and blood in the stool.IntroductionSince 1977 [1], campylobacter fetus ss jejuni has been recognized as a leading bacterial enteropathogen causing gastroenteritis in humans. In 1979 [2], this came into focus as a pediatric enteropathogen. Campylobacter can be cultured from 3-11% of patients with diarrhea. This is a recovery rate comparable to or exceeding that of Shigella or Salmonella species [3]. Only a few cases have been reported in the world literature [4–8], with no literature originating from Saudi Arabia or any Middle Eastern country. We have identified six cases of neonatal campylobacter enterocolitis at Suleimania Children's Hospital in Riyadh, Saudi Arabia from September 1989 - January 1991. We describe the clinical features and other findings of these neonates.MATERIAL AND METHODSStool specimens of neonates admitted in the hospital with diarrhea were cultured for campylobacter in addition to other common enteropathogens as a routine. Specimens were plated on selective campylobacter agar media that contained 5% sheep erythrocytes, vancomycin, polymyxin, cephalothin, and amphotericin B (Campy-5) prepared by Saudi Prepared Media Ltd., Riyadh. Campylobacter agar plates were incubated at 42-43°C in 5% O2, 10-12% CO2 in anaerobic jars with commercial gas generating system (BBL, Gaspak Anaerobic System), examined at 24, 48, and 72 h. Cultures were confirmed later for campylobacter jejuni by colony character, gram staining, and biochemical characteristics [9]. Sensitivity to antibiotics was tested by disc diffusion method.We reviewed the medical records of neonates admitted to the hospital whose stool cultures yielded campylobacter jejuni. Findings were tabulated for the presence of fever, vomiting, signs of dehydration, information about diarrhea, complete blood count, serum electrolytes, blood urea nitrogen, creatinine, and results of blood and spinal fluid cultures, if performed.RESULTSAll six neonates were delivered vaginally at term without any perinatal problems. Three were Saudi and the remaining three neonates, non-Saudi. Age on presentation ranged from 17-27 days. Age at onset of diarrhea was 5-26 days (Table 1); five were female, two neonates (Cases 2 and 3) vomited for 3 and 14 days, respectively, 2-3 times per day. Three neonates had bloody (Cases 1,4, and 5), two had mucoid (Cases 3 and 6), and one neonate presented with watery stools. On presentation, the duration of diarrhea was 1-20 days with a frequency ranging from 5-12 times a day. Two neonates had mild dehydration and the remaining neonates were well hydrated. Four presented with temperatures ranging between 37.5-38.5°C, one had a temperature of 39°C and one neonate was afebrile. Within 24 h of admission, fever subsided in all the neonates. None had abdominal distention, two looked ill (Cases 2 and 3), and one neonate had impetigo (Case 3). Three patients (Cases 2, 5, and 6) were irritable on admission. Body weight ranged from 2.8 to 4.5 kg and mean was 3.87 kg. Three children were fed breast milk since birth, two were on bottle feeding, one was on the breast and artificial feeding.Table 1. Clinical and laboratory features of six neonates with campylobacter gastroenteritis.Table 1. Clinical and laboratory features of six neonates with campylobacter gastroenteritis.InvestigationsLumbar puncture was performed in two (Cases 2 and 3), and spinal fluid examination was normal. Blood was cultured in two (Cases 2 and 3), which yielded no growth. Serum electrolytes, blood urea nitrogen, and creatinine were performed in all neonates. One had hypernatremic dehydration with prerenal failure (Case 2). The child was fed on concentrated artificial milk powder and improved with conservative treatment.Peripheral WBC counts were performed on all. WBC count ranged from 7.6xl09/L - 17.6xl09/L, neutrophil count 20-65%, lymphocytes 27-83%, monocytes 1-6%, blood urea nitrogen 1.2-10.2 mmol/L, and creatinine 37-44 umol/L.Culture sensitivity report revealed campylobacter jejuni was sensitive in all the cases to erythromycin, augmentin, gentamicin, and nalidixic acid, but resistant in all to trimethoprim + cotrimoxazole. Ampicillin was sensitive to all except in one patient (Case 3).TreatmentOne neonate, (Case 4), received oral rehydration solution (ORS) and the remaining received parenteral fluid (IVF). All patients were discharged home following improvement; hospital stay was 3-14 days. Two neonates (Cases 4 and 6) did not receive any antibiotics. Diarrhea improved after two days in both patients who were later discharged with follow-up advice. Culture reports were available after discharge but the patients were lost to follow up. Erythromycin and augmentin were administered for two neonates (Cases 1 and 5) on the fourth and second day of hospitalization, respectively, upon the arrival of the stool culture report. Diarrhea improved in Case 1 on the third day, one day prior to administering erythromycin and the baby was discharged on the following day. In Case 5, diarrhea stopped on the third day, one day after the initiation of augmentin and the baby was discharged the following day. Ampicillin with gentamicin and cloxacillin with cefuroxime were administered in Cases 2 and 3, respectively, on admission because of suspected neonatal sepsis. Septic screening was carried out on both patients which was found to be negative. Campylobacter isolated from Case 2 was sensitive to both ampicillin and gentamicin and they were continued for nine days, at which time the diarrhea improved after two days. Repeated stool culture on the sixth day of admission was negative for campylobacter or any other bacterial enteropathogens.A stool culture report on Case 3 was obtained two days later. With this, erythromycin was added on the third day and cloxacillin and cefuroxime were discontinued. Erythromycin syrup was administered for seven days, but the diarrhea continued for 11 days. A stool culture was repeated nine days after starting erythromycin and was negative. The patient was discharged home on the 14th day in good condition. Stool specimens of parents and siblings were not screened for campylobacter. During this study period, campylobacter was cultured from stools of neonates with diarrhea more often than either Salmonella or Shigella. No secondary case was reported in our nursery.DISCUSSIONCampylobacter has been known to cause perinatal infection in humans for a long period of time. In 1979, Torphy and Bond [10] reported on 12 neonates with campylobacter infection. Two of the newborns had bloody diarrhea [10]. Since then, Karmali and Tan described one neonate in 1980 [4], and in 1981, Anders et al, [5]. reported eight cases of neonatal gastroenteritis due to campylobacter fetus ss jejuni infection. In 1977 a brief epidemiologic report from Britain described nine neonates with gastroenteritis without providing a detailed report [11]. Four additional cases of neonatal enterocolitis were described in a neonatal unit in 1984 by Karmali et al [7]. In 1985, Young et al [8], reported on three cases. This was also described in premature babies [12,13]. Thus far, we know of no cases having been reported from Saudi Arabia or any Middle Eastern country.In contrast to the findings of previous reports [7, 14, 15], 5/6 of our neonates were febrile. Two babies had mild dehydration which may have contributed to the pyrexia. Older children may have associated fever which has been documented in previous studies [15,16] and may even present with convulsions [17]. None had abdominal distention. Monocyte count ranged from 0-6%. We did not encounter any cases involving meningitis or septicemia due to campylobacter jejuni during this period, although they have been recorded in earlier reports [18–21]. Campylobacter may frequently be associated with diarrhea in immunodeficient children [22]. Cases involving severe arthritis with campylobacter were also reported [23].The transmission of campylobacter is through the fecal-oral route or person-to-person contact. Natural reservoirs of campylobacter include: surface water, wild and domestic animals including fowl, cattle, dogs, and cats [24]; outbreaks associated with raw milk and drinking water have also been reported [25–27]. In this study we did not try to look for the source of campylobacter and route of transmission. Erythromycin is regarded as the drug of choice since Vanhoof's report in 1980 [28]. Salazar-Lindo et al [29] demonstrated that erythromycin shortens the duration of diarrhea if started early in the treatment plan. It also appears from other studies that erythromycin decreases the fecal excretion time for campylobacter [30,31]. This may be important from an epidemiological point of view in decreasing intrafamilial spread [15]. We treated one neonate with erythromycin after receiving a stool culture sensitivity report when his diarrhea had already improved. We treated another neonate with augmentin (amoxicillin + clavulinic acid) as it is also a satisfactory regime in our experience at Suleimania Children's Hospital. We did not encounter any resistance to this drug for this organism. Although erythromycin is the preferred drug for campylobacter jejuni enterocolitis, resistance has been reported which reached 13.4% in Taiwan [32].We conclude that campylobacter jejuni should be sought in stool specimens of newborns with diarrhea, particularly if the diarrhea is bloody or mucoid. The neonates may present with or without fever. To learn more about the risks of severe enterocolitis, bacteremic complications or secondary spread in nurseries, further studies should be conducted on infected neonates. Additional studies are required to be conducted in a prospective fashion in this part of the world in order to understand the epidemiological factors related to campylobacter infection during the perinatal period.ARTICLE REFERENCES:1. Skirrow MB. 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Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 13, Issue 2March 1993 Metrics History Accepted20 July 1992Published online1 March 1993 ACKNOWLEDGMENTWe would like to thank Dr. Sami Mohammed Abdul Alim for helping us to isolate campylobacter and other enteropathogens and Lydia D. Medenilla for typing the manuscript.InformationCopyright © 1993, Annals of Saudi MedicinePDF download" @default.
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