If a Baby Have C Difficile for 7 Days Is That Dangerous
Pediatr Gastroenterol Hepatol Nutr. 2014 Jun; 17(2): lxxx–84.
Clostridium difficile in Children: To Care for or Not to Treat?
Jung Ok Shim
Segmentation of Pediatric Gastroenterology, Hepatology, and Diet, Section of Pediatrics, Korea University Guro Hospital, Korea University College of Medicine, Korea.
Received 2014 Jun xiii; Accepted 2014 Jun 26.
Abstract
Clostridium difficile infection has been increasing since 2000 in children and in adults. Frequent antibiotics use, comorbidity, and the development of hypervirulent strains have increased the take chances of infection. Despite the high carriage rates of C. difficile, infants rarely develop clinical infection. Discontinuing antibiotics and supportive management usually leads to resolution of illness. Antibiotics employ should be stratified depending on the patient'southward age and severity of the disease.
Keywords: Clostridium difficile, Child, Anti-bacterial agents
EPIDEMIOLOGY AND PATHOGENESIS
Clostridium difficile is a gram-positive, spore forming bacterium usually spread through the fecal-oral route. It is non-invasive and presentation rages from asymptomatic carriage, to mild diarrhea, colitis, or pseudomembranous colitis acquired past production of toxin A and B. C. difficile infection (CDI) is defined as the astute onset of diarrhea with documented toxigenic C. difficile or its toxin and no other cause for diarrhea. CDI increases morbidity and mortality, particularly in hospitalized patients. CDI has been increasing since 2000 in both hospitalized patients and the general customs in Asia, Europe, and North America. In developed patients, CDI increased 4-fold in Canada [1]. In Korea, the prevalence was 1.7 per i,000 hospitalized adult patients in 2004 and two.vii per one,000 hospitalized adult patients in 2008 [2]. In pediatric patients, the Usa Healthcare Cost and Utilization Projection Kids' Inpatient Database (HCUP-KID) reported 0.two% cases in hospitalized pediatric patients, and a significant increase from three,565 cases in 1997 to 7,779 cases in 2006 [iii].
The increase in CDI incidence is thought to be multifactorial, including increased antibiotic use such as cephalosporins and quinolone, an increasing elderly patient population, and the development of hypervirulent strains of C. difficile [iv]. C. difficile colonizes in the intestine subsequently disruption of normal intestinal microbiota. Frequent use of antibiotics increases the risk of colonization and toxin production by two-16 fold [5]. Astringent CDI is associated with hypervirulent strains such as ribotype 027, North American pulsed-field gel electrophoresis blazon ane (NAP1), and restriction endonuclease analysis B1. The NAP1 strain produces approximately twenty-fold higher levels of toxins A and B due to a deletion in the toxin regulatory cistron, tcdC [6]. Severe CDI outbreaks have been reported in Western countries, Japan and Korea. A fluoroquinolone-resistant strain of C. difficile (B1/NAP1/027) has been predominantly associated with these outbreaks [seven]. In 2008, European multicountry surveillance attributed iv.1 per 10,000 patient-days per infirmary to CDI, and identified 65 different ribotypes. Of the cases analyzed, 22% of patients had died and C. difficile contributed at to the lowest degree in part to forty% of deaths. Infection past polymerase chain reaction-ribotypes is associated with complicated disease outcome [8].
In 2010, the Society for Healthcare Epidemiology of America and the Infectious Diseases Society of America published clinical guidelines for CDI in adults [9]. They recommended metronidazole in mild to moderate disease, and vancomycin as a first-line therapy in severe disease. However, there are thin data and guidelines for treatment of pediatric CDI.
CHARACTERISTICS OF CLOSTRIDIUM DIFFICILE IN CHILDREN
While the incidence of CDI in children also has been increasing, the severity of cases has not increased. In sharp contrast to developed data, HCUP-Kid information reported no significant positive trends in mortality, rate of colectomy, or hospital days [3]. The percent of NAP1 in pediatric CDI was 19.four% in a report [10], compared to more 50% in adults. The relatively low incidence of hypervirulent strains might explain the observation that severe cases in children have non increased. On the other paw, asymptomatic colonization of C. difficile is mutual in early infancy, and it often occurs in the first week of life. The carrier charge per unit is reported to exist ane% to 84% in healthy newborns and infants [11,12], but information technology decreases to less than v% by 8 years of age. The most likely source in infants is from ecology contamination rather than directly maternal infant transmission. Chang et al. [xiii] reported that the toxin positivity charge per unit is significantly higher in the infants with persistent C. difficile colonization than in those with transient colonization (66.7% vs. 24.5%, p=0.001). Sectional chest-milk feeding decreases the risk of persistent colonization compared to formula or mixed feeding. The susceptibility to C. difficile colonization might be because of the immaturity of the intestine and lack of protective abdominal microbiota [xi]. Despite the loftier carriage rates, infants rarely develop clinical infection. The mechanisms for the resistance of infants to CDI are thought to be related to the immunoglobulin fractions of breast milk that inhibit the bounden of toxin A to its abdominal receptor, and absenteeism in the newborn gut of the intestinal receptor that binds C. difficile toxin A [eleven,xiv]. Take a chance factors of CDI in children are previous antibiotics use, and predisposing comorbidities. A recent study of pediatric CDI cases reported 92% of children with previous antibiotics utilise, 60% with immunosuppressive handling, 39% with a malignancy or organ transplantation, and thirteen% with inflammatory bowel disease [fifteen]. While previous proton pump inhibitor use is known to be associated with CDI in adults [xvi], the association with CDI in children is non established.
DIAGNOSIS OF CDI IN CHILDREN
Guidelines for diagnosis recommend that only stools from patients with diarrhea should be tested for C. difficile and tests for cure should not be performed [1]. Endoscopic examination is not unremarkably recommended except in special cases. Toxigenic cultures and cytotoxin assays are the gold standard for CDI diagnosis. Nucleic acid distension tests for toxin genes are superior to the toxin A and B enzyme immunoassay (Environmental impact assessment) tests. Although the Eia examination is highly specific, it is not highly sensitive in adults. C. difficile culture is not recommended because only the toxigenic organisms cause illness. Use of Environmental impact assessment in pediatric patients showed like results, although, Toltzis et al. [17] reported a positive predictive value of 64% in children. Children with fake-positive Eia results were significantly younger than those with true-positive tests. El Feghaly et al. [xv] reported that 24% of children with CDI had a concomitant viral co-infection and reported that norovirus genogroup 2 was the most mutual virus. Detection of C. difficile toxin in stool may non be the causative agent in children with diarrhea, peculiarly in young children. Stool examination for C. difficile in infants should be express.
Treatment
The apply of antibiotics is not recommended in case of asymptomatic colonization with C. difficile. Eradication of C. difficile was attempted in one hospital to eliminate a potential reservoir for nosocomial outbreaks, but metronidazole was ineffective and vancomycin was but of temporary outcome [eighteen].
General considerations for handling of children with CDI include correction of fluid and electrolyte imbalances in addition to examination of the patient'due south medical record for whatever history of antibiotics and proton pump inhibitor utilise. Opiates for pain control increase risk of ileus or toxic megacolon. Antimotility agents such equally loperamide should be avoided.
The treatment of CDI in children is based on data from clinical trials in adults. Mild to moderate disease is defined as diarrhea (<6 stools/mean solar day) without signs of systemic toxicity. Fever is commonly absent. Severe colitis is defined equally frequent diarrhea (>6 stools/day) with astringent abdominal pain and fever. Marked leukocytosis and azotemia may exist observed. Children with fulminant colitis bear witness the virtually extreme manifestations such as hypotension, rise lactic acid levels, shock, and complete ileus or toxic megacolon. For children with moderate or severe affliction, data-supported empirical antibiotic treatment should be started as shortly as the diagnosis of CDI is suspected. Oral metronidazole at 30 mg/kg/day in 4 divided doses for ten-14 days is recommended in mild-to-moderate disease. For severe colitis, oral vancomycin at 40 mg/kg/day in 4 divided doses for 10-14 days is recommended. If necessary, subsequent adjuvant therapy with intravenous metronidazole and vancomycin retentiveness enema (adult dose 0.5-ane.0 thou in 100 mL of normal saline every 4-12 hours) may be considered [xix].
In adult patients, metronidazole and vancomycin showed an initial high cure rate of 76-90% in 2007 [20]. Since then, the rate of treatment failure and illness relapse with the use of metronidazole has increased. NAP1 isolates may have reduced susceptibility to metronidazole [7]. Jardin et al. [21] compared treatment patterns and issue of adult patients earlier and after implementation of severity-based CDI guidelines. After implementation of guidelines, the use of oral vancomycin was increased and the increased use was associated with decreased rates of refractory CDI.
Based on recent observational data, 53-63% of children with CDI are treated with metronidazole, and utilize of oral vancomycin in children varies from 3.5-thirty% [xix]. In a recent study, 27% of children with CDI were not treated with antibiotics, and the bulk (42%) were treated with metronidazole, though 74% of children had astringent colitis [22]. The American Association of Pediatrics recommends discontinuation of antibiotics as the first step in treating CDI, which may suffice in nigh instances [23]. Algorithm for CDI in children is suggested in Fig. 1.
Algorithm for management of children with unexplained diarrhea suspected Clostridium difficile infection.
Probiotics could be started with antibiotic therapy to prevent antibiotic-associated diarrhea in children. The use of high-dose probiotics (5 billion CFU/twenty-four hour period) appears to exist constructive with the number needed to treat to prevent 1 case of diarrhea of 7 (95% confidence interval, 6-ten) [24]. Studies of the effect of probiotics in the treatment of CDI are limited. In recurrent or astringent CDI, fecal microbiota transplantation might be constructive. Donor-acquired feces are implanted into the alimentary canal of the patient via a nasoduodenal catheters, retention enema, duodenoscopy or colonoscopy. van Nood et al. [25] reported 81% resolution of recurrent CDI subsequently the first infusion of feces in a minor group of patients. Normal bowel flora serve as a defence mechanism against pathogenic organisms and may outcome in the emptying of C. difficile spores.
Determination
Cases of CDI in children are dissimilar from those in adults. Despite the high carriage rates of C. difficile, infants rarely develop clinical infection. Antibiotics should exist stratified depending on the patient's age and case severity. Genetic epidemiology of hypervirulent strains may be helpful in pediatric patients with CDI.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107224/
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