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PubMed1977

Necrotizing enterocolitis after cardiac surgery: a local ischemic lesion?.

Necrotizing enterocolitis continues to be a perplexing problem in the newborn and, in particular, the premature. Its pathogenesis is controversial, although there are well established clinical risk factors. Three patients had necrotizing enterocolitis while under close clinical observation and monitoring, despite the fact that these patients were not at high risk for necrotizing enterocolitis. All three had necrotizing enterocolitis after hypothermia and total circulatory arrest--a complication which until now has not been reported. Because of the close monitoring, these patients provide a unique clinical setting which eliminates most of the etiologic factors that have been implicated in the pathogenesis of necrotizing enterocolitis. The onset of necrotizing enterocolitis shortly after total circulatory arrest and the selective ischemic organ damage observed suggest local perfusion inadequacy. The authors postulate that splanchnic vasoconstriction as a result of marked sympathetic stimulation contributes to this local ischemia and subsequent necrotizing enterocolitis.

Cardiac Surgical Procedures↗

PubMed1999

Mucoid presentation of acute enterocolitis in children: a hospital-based case-control study.

A hospital-based case-control study was carried out to clarify the characteristics of mucoid presentation of acute enterocolitis in children. One hundred sixty-eight cases of acute mucoid enterocolitis (study population) were compared with 200 cases of watery diarrhoea and 118 cases of blood dysentery (control groups) on the basis of clinical characteristics and findings on stool examination. Study and control groups were comparable with respect to age, body weight and nutritional status. There was no significant difference in clinical characteristics (duration of diarrhoea, stool frequency, presence of vomiting, fever and dehydration) between patients suffering from mucoid enterocolitis and blood dysentery. However, watery diarrhoea patients had significantly high frequencies of vomiting (p=0.00001) and dehydration (p=0.00001). High numbers of microscopic red blood cells (mean +/- SD: 40.8 +/- 16.8) and white blood cells (40.6 +/- 18.0) were present in faecal samples of the patients with mucoid enterocolitis, which is indicative of infection caused by enteroinvasive enteropathogens. Shigella was a commonly identified enteropathogen in patients with mucoid enterocolitis (40.5%) and in patients with dysentery (46.6%), with no statistically significant difference (p = 0.30). Isolation of Salmonella was statistically similar in study and control groups. However, Entamoeba histolytica was detected in significantly high frequency in patients with mucoid enterocolitis as compared to the patients with dysentery (p = 0.0004) and watery diarrhoea (p = 0.00004). Our results indicate that mucoid enterocolitis patients are infected with enteroinvasive enteropathogens, and that stool examination is useful in establishing the aetiological diagnosis.

Acute Disease↗

PubMed1998

Double blind, randomised, placebo controlled study of oral vancomycin in prevention of necrotising enterocolitis in preterm, very low birthweight infants.

AIMS: To evaluate the effectiveness of oral vancomycin in the prophylaxis of necrotising enterocolitis in preterm, very low birthweight infants. METHODS: A prospective, double blind, randomised, placebo controlled study in a tertiary referral centre of a university teaching hospital was conducted on 140 very low birthweight infants consecutively admitted to the neonatal unit. The babies were randomly allocated to receive oral vancomycin (15 mg/kg every 8 hours for 7 days) or an equivalent volume of placebo solution. Prophylaxis was started 24 hours before the start of oral feeds. All suspected cases of necrotising enterocolitis were investigated with a full sepsis screen and serial abdominal radiographs. Necrotising enterocolitis was diagnosed and staged according to modified Bell's criteria. RESULTS: Nine of 71 infants receiving oral vancomycin and 19 of 69 infants receiving the placebo solution developed necrotising enterocolitis (p = 0.035). Infants with necrotising enterocolitis were associated with a significant increase in mortality (p = 0.026) and longer duration of hospital stay (p = 0.002). CONCLUSIONS: Prophylactic oral vancomycin conferred protection against necrotising enterocolitis in preterm, very low birthweight infants and was associated with a 50% reduction in the incidence. However, widespread implementation of this preventive measure is not recommended, as it would only be effective in necrotising enterocolitis caused by Gram positive organisms and could increase the danger of the emergence of vancomycin resistant or dependent organisms. Its use should be restricted to a high prevalence nursery for a short and well defined period in a selected group of high risk patients.

Administration, Oral↗

PubMed2006

Prevention of necrotizing enterocolitis in preterm infants: a 20-year experience.

OBJECTIVE: Diet, indomethacin, and early use of dexamethasone have been implicated as possible causes of necrotizing enterocolitis and intestinal perforation. Because we seldom prescribe indomethacin or early dexamethasone therapy and we follow a special dietary regimen that provides late-onset, slow, continuous drip enteral feeding, we reviewed our 20 years of experience for the incidence of necrotizing enterocolitis and bowel perforation. METHODS: We reviewed data on all 1239 very low birth weight infants (501-1500 g) admitted to our level III unit over a period of 20 years (1986-2005), for morphologic parameters, necrotizing enterocolitis, bowel perforation, use of the late-onset, slow, continuous drip protocol, and indomethacin therapy. Outcome data were also compared with Vermont Oxford Network data for the last 4 years. RESULTS: In 20 years, 1158 infants received the late-onset, slow, continuous drip feeding protocol (group I), whereas 81 infants had either a change in dietary regimen, use of indomethacin, or early use of dexamethasone (group II). The rate of necrotizing enterocolitis in group I of 0.4% was significantly lower than that in group II of 6%. Group I, in comparison with the Vermont Oxford Network, had significantly lower rates of necrotizing enterocolitis (0.4% vs 5.9%), surgical necrotizing enterocolitis (0.4% vs 3.1%), and bowel perforation (0.35% vs 2.2%). CONCLUSIONS: Our 20-year experience with 1239 very low birth weight infants suggests strongly that the late-onset, slow, continuous drip feeding protocol and avoidance of indomethacin and early dexamethasone treatment contribute to the prevention of necrotizing enterocolitis.

Dexamethasone↗

PubMed2003

Short-term ceftriaxone therapy for treatment of severe non-typhoidal Salmonella enterocolitis.

AIM: To evaluate the clinical efficacy of a short-course ceftriaxone therapy in the treatment of paediatric patients with severe non-typhoidal Salmonella enterocolitis. METHODS: During a 1 y period, all paediatric patients who were suspected having Salmonella enterocolitis by the presentation of bloody and/or mucoid diarrhoea with or without fever were eligible for the study. Patients with either negative stool cultures or bacteraemia were excluded. Severe enterocolitis was defined as a bloody and/or mucoid diarrhoea associated with high fever persisting for longer than 48 h and signs of moderate or severe dehydration. The patients with severe enterocolitis were assigned to treatment with ceftriaxone (50 mg kg(-1) d(-1)) for 3-5 d, while the rest were given supportive treatment only. Before treatment all study patients received blood testing for white blood cell (WBC) count, C-reactive protein (CRP) level and blood culture. The duration of the fevers was recorded. Patients were followed up after clinical recovery for the possibility of relapse. RESULTS: Seventy-three patients with culture-confirmed Salmonella enterocolitis without bacteraemia were analysed. The duration of fever was longer in severe cases who were treated with ceftriaxone than those who were not. However, rapid defervescene was found after short-course ceftriaxone therapy in those patients with severe enterocolitis. CRP was significantly higher in severe cases. There was no significant difference in the WBC count between the two groups of patients. No relapse was found in these patients. CONCLUSION: High CRP, prolonged high fever and signs of moderate or severe dehydration appear appropriate to define severe cases of Salmonella enterocolitis. Short-course ceftriaxone therapy is clinically beneficial to these patients. Neither clinical nor microbiological relapse was seen after therapy.

Anti-Bacterial Agents↗

PubMed1971

Ischaemic enterocolitis: an expression of the intravascular coagulation syndrome.

In 20 cases of ischaemic enterocolitis unassociated with lesions of major vessels, fresh thrombi were found in the small vessels of the bowel wall and were widespread in other tissues. The capillaries of the renal glomeruli and vessels in the lung were the commonest sites. Pseudo-membranous enterocolitis is shown to be an early or more slowly evolving but identical entity to other forms of so-called ischaemic enterocolitis. This is a condition which includes ischaemic enterocolitis, postoperative enterocolitis, necrotizing enterocolitis, and probably some cases of clostridial and staphylococcal enterocolitis. It is due to an episode of intravascular coagulation occurring principally in the gut wall but also elsewhere.

Adult↗

PubMed1987

Enhanced urinary immunoreactive thromboxane in neonatal necrotizing enterocolitis. A diagnostic indicator of thrombotic activity.

Urinary thromboxane B2 levels increased threefold to 20-fold in infants with neonatal necrotizing enterocolitis compared with healthy infants and infants with benign causes of heme-positive stools. Increased urinary thromboxane B2 levels were detected coincidently with the initial signs of necrotizing enterocolitis, and values paralleled the course of the illness. Infants with serious illnesses other than necrotizing enterocolitis had increased urinary thromboxane B2 levels but with lower values than those of infants with necrotizing enterocolitis. Indomethacin therapy appeared to reduce urinary thromboxane B2 levels and reduce their usefulness as a marker of illness. Another product of platelet activation, beta-thromboglobulin, was increased in the urine of infants with necrotizing enterocolitis. Decreased platelet counts in infants with necrotizing enterocolitis correlated inversely with urinary thromboxane. Results of beta-thromboglobulin and platelet studies are consistent with the concept that platelet consumption due to ischemic thrombosis was the source of enhanced thromboxane excretion.

Enterocolitis, Pseudomembranous↗

PubMed2001

Oral immunoglobulin for preventing necrotizing enterocolitis in preterm and low birth-weight neonates.

BACKGROUND: Necrotizing enterocolitis (NEC) is the most common emergency of the gastrointestinal tract occurring in the neonatal period. There have been published reports which suggest that oral immunoglobulins IgA and IgG produce an immunoprotective effect in the gastrointestinal mucosa. This systematic review was undertaken to clarify the issue. OBJECTIVES: To assess whether oral immunoglobulin administered to preterm and low birth-weight neonates reduces the incidence of necrotizing enterocolitis without adverse effects. SEARCH STRATEGY: The databases MEDLINE, CINAHL, Embase and the Cochrane Controlled Trials Register were searched. The text words 'necrotising enterocolitis OR necrotizing enterocolitis' AND 'immunoglobulin' with constraints 'neonate OR infant' were used. Proceedings of the Perinatal Society of Australia and New Zealand were hand searched. The computer neonatal discussion site 'Nicu Net' was also used. Additionally, all references in the identified trials were checked and authors were contacted to request any additional published or unpublished data. SELECTION CRITERIA: All randomized or quasi-randomized controlled trials where oral immunoglobulins were used as prophylaxis against necrotizing enterocolitis in preterm (<37 weeks gestation) and/or low birth-weight (<2500 gms) neonates. DATA COLLECTION AND ANALYSIS: The procedures of the Cochrane Neonatal Review Group (CNRG) were used. The two reviewers independently assessed the trials for their methodological quality and subsequent inclusion in the review. Relative risk (RR), risk difference (RD), and number needed to treat (NNT) were used in the analysis. MAIN RESULTS: Five studies on oral immunoglobulin for the prevention of necrotizing enterocolitis were identified of which three met the inclusion criteria. In this review of the three eligible trials (including a total of 2095 neonates) the oral administration of IgG or an IgG/IgA combination did not result in a significant reduction in the incidence of definite NEC [RR 0.84 (95% CI 0.57, 1.25), RD -0.01 (95% CI -0.03, 0.01)], suspected NEC [RR 0.69 (95% CI 0.42, 1.13), RD -0.01 (95% CI -0.03, 0.00)], need for surgery [RR 0.21 (95% CI 0.02, 1.75), RD -0.03 (95% CI -0.06, 0.00)] or death from NEC [RR 1.10 (95% CI 0.47, 2.59), RD 0.00 (95% CI -0.01, 0.01)]. REVIEWER'S CONCLUSIONS: Based on the available trials, the evidence does not support the administration of oral immunoglobulin for the prevention of NEC. There are no randomised controlled trials of oral IgA alone for the prevention of NEC.

Administration, Oral↗

PubMed1999

Cytomegaloviral enterocolitis: clinical associations and outcome.

PURPOSE: Cytomegaloviral enterocolitis is an uncommon disorder that can complicate inflammatory bowel disease. It is more common in patients with acquired immunodeficiency syndrome and can occur in patients on immunosuppressive therapy for autoimmune or inflammatory diseases and in allograft recipients. Mortality rates of up to 71 percent have been reported for cytomegaloviral enterocolitis. The aims of this study were 1) to identify the presentation, underlying medical conditions, treatment, and outcome of patients with cytomegaloviral enterocolitis and 2) to determine the prevalence of this infection in patients undergoing intestinal resection for inflammatory bowel disease. METHODS: A retrospective chart review of patients with pathologic evidence of cytomegaloviral enterocolitis from 1985 through 1996 was performed. To determine the prevalence of this condition, the hospital discharge database was searched for the diagnoses of ulcerative colitis and Crohn's disease in patients who underwent bowel resection. RESULTS: 93 patients (mean age, 44 years; 66 percent males) had cytomegaloviral infection in the small intestine (n = 6), large intestine (n = 86), or appendix (n = 1). Patients with acquired immunodeficiency syndrome (n = 42), with ulcerative colitis (n = 11), with Crohn's disease (n = 11), receiving organ transplant (n = 12), receiving bone marrow transplant (n = 8), and in other immunosuppressed states (n = 11) comprised this study. Seventeen patients (18 percent) underwent intestinal resection, and the remaining 76 patients were treated medically. Abdominal pain (77 vs. 37 percent; P < 0.01) and gastrointestinal bleeding (65 vs. 34 percent; P < 0.05) were more common presenting symptoms in patients who required resection than patients in the medically managed group. Mortality was 17.6 percent in the surgically managed group and 14.5 percent in the patients who were managed medically. The median duration of ulcerative colitis in patients with coexisting cytomegaloviral infection was 12 months. The prevalence of cytomegaloviral enterocolitis was 4.6 percent in patients with ulcerative colitis and 0.8 percent in patients with Crohn's disease. CONCLUSIONS: These data suggest that cytomegaloviral infection more frequently complicates ulcerative colitis than Crohn's disease. Furthermore, a short and fulminant course of ulcerative colitis may indicate coexisting cytomegaloviral infection. The overall low mortality in this retrospective study suggests that aggressive medical and surgical treatment improves survival in patients with cytomegaloviral enterocolitis.

Acquired Immunodeficiency Syndrome↗

PubMed1984

Hexosaminidase: a biochemical marker for necrotizing enterocolitis in the preterm infant.

To evaluate hexosaminidase as a biochemical marker for the early detection of necrotizing enterocolitis in preterm infants, 33 preterm infants without necrotizing enterocolitis and 18 preterm infants with necrotizing enterocolitis had hexosaminidase activity measured during the course of their hospitalization. Although hexosaminidase activity could not identify those preterm infants with necrotizing enterocolitis who had impending perforation, the data strongly suggest that measurements of serum hexosaminidase activity may provide an early biochemical indication of the presence of necrotizing enterocolitis in the preterm infant. Hopefully, early detection of necrotizing enterocolitis in these infants will reduce the morbidity and mortality of this disease.

Clinical Enzyme Tests↗

PubMed2005

Necrotizing enterocolitis increases the bone resorption in premature infants.

BACKGROUND: Necrotizing enterocolitis is a common neonatal gastrointestinal disease that affects approximately 10% of premature infants less than 1500 g. The average mortality is 20-40% and survivors may present with diarrhea or malabsorption, intestinal strictures and fistulas, feeding abnormalities and failure to thrive. It is not clear whether the higher incidence of this gastrointestinal disease in premature infants contributes to the risk of osteopenia of prematurity. AIM: To examine bone turnover state in premature infants who had a necrotizing enterocolitis attack during postnatal period. STUDY DESIGN AND SUBJECTS: We examine the bone turnover markers in infants with necrotizing enterocolitis and compare them with infants with sepsis. Forty-one premature infants participated in the study and were divided into three groups. In group I, there were 14 premature infants who developed necrotizing enterocolitis with negative blood culture during their hospitalization. In group II, there were 12 premature infants who developed sepsis during their hospitalization. Age-matched 15 premature infants who were given parenteral nutrition served as control group (group III). Blood samples and 6-h urine samples were obtained for bone turnover markers and calcium, phosphorous, creatinine and 25-hydroxy vitamin D between the day 20 and 25. Bone osteoblastic activity was assessed by measurement of serum osteocalcin. Bone resorption was assessed by measurement of serum levels of beta-CrossLaps and urinary deoxypyridinoline. RESULTS: There were no significant differences in bone osteoblastic activity among the groups, but bone resorption markers were significantly higher in infants with necrotizing enterocolitis compared to other groups (p < 0.016). CONCLUSION: Necrotizing enterocolitis increases the bone resorption in premature infants. It may be related with reduced glucagon like peptide-2 levels, a new intestinal hormone that is primary secreted from distal small intestine.

Amino Acids↗

PubMed1986

Ischemic enterocolitis as a complication of Hirschsprung's disease.

Enterocolitis is a recognized complication of Hirschsprung's disease. However, little distinction has been made in the literature between inflammatory enterocolitis and ischemic (necrotizing) enterocolitis when seen with Hirschsprung's disease. We report on four cases of ischemic enterocolitis complicating Hirschsprung's disease. The characteristics of ischemic enterocolitis are compared to those of inflammatory enterocolitis.

Enterocolitis, Pseudomembranous↗

PubMed1998

Turnover of radioactive mucin precursors in the colon of patients with Hirschsprung's disease correlates with the development of enterocolitis.

BACKGROUND/PURPOSE: Mucin glycoproteins (mucins) in the colonic mucus gel layer interact with pathogens performing protective functions by a variety of mechanisms. It is recognised that patients with Hirschsprung's disease (HD) are prone to episodes of enterocolitis even after corrective surgery, the aetiology of which is poorly understood. The authors correlated the turnover of radioactive mucin precursors in organ culture of the proximal ganglionated colon at the time of pull-through with the development of postoperative enterocolitis. METHODS: The colonic mucins in the retained proximal ganglionated colon of nine HD patients at the time of pull-through were studied. Organ culture of intact mucosa was performed with radioactive mucin precursors 35S-sulphate and 3H-glucosamine. Mucins in the secretions and epithelial cells were then purified by gel filtration. Turnover of the isotopes was determined by relating radioactivity to tissue DNA content. These patients were followed up prospectively for a mean duration of 30.8 months. The patients were assigned to one of two groups according to the criteria of requiring hospital admission for enterocolitis during this period. There were five patients in the group that remained well after corrective surgery and four in the group that developed entercolitis. The turnover values of both radioisotopes were analysed for differences in the two groups of patients. RESULTS: Patients in the enterocolitis group had a median value for turnover of 331 dpm/microg DNA, and the group that was well had a median value of 2044 dpm/microg DNA. These differences were statistically significant (Mann-Whitney, P = .037). CONCLUSIONS: A reduced turnover of mucins as shown by incorporation of radioactive precursors will give rise to a defective colonic mucus-defensive barrier. It can be inferred that the lower the turnover, the more prone a patient is to postoperative enterocolitis. It is therefore possible that organ culture with radioactive mucin precursors of the proximal ganglionated mucosa performed at the time of pull-through has a predictive value in the development of postoperative enterocolitis.

Colon↗

PubMed1990

Role of platelet activating factor and tumor necrosis factor-alpha in neonatal necrotizing enterocolitis.

Because previous investigations have suggested that platelet activating factor and tumor necrosis factor-alpha (TNF-alpha) are important mediators of experimental necrotizing enterocolitis in the rat, we measured platelet activating factor, acetylhydrolase (the platelet activating factor breakdown enzyme), and TNF-alpha in the plasma of 12 human neonates with necrotizing enterocolitis and eight age-matched control subjects with similar gestational ages, postnatal ages, and weights. Almost all patients with necrotizing enterocolitis had elevated plasma platelet activating factor values (18.1 +/- 3.6 ng/ml vs. 3.1 +/- 0.9 ng/ml in control subjects, p less than 0.01). Plasma acetylhydrolase activity was lower in patients than in control subjects (10.6 +/- 0.7 nmol/ml/min vs 23.0 +/- 1.4 nmol/ml/min, p less than 0.01). Plasma TNF-alpha concentration was significantly elevated in patients with necrotizing enterocolitis (136 +/- 75 U/ml vs 1.5 +/- 0.8 U/ml, p less than 0.05), although the individual variation was high. There was no correlation between individual TNF-alpha and platelet activating factor levels. We conclude that platelet activating factor and TNF-alpha are elevated in patients with necrotizing enterocolitis and that suppressed platelet activating factor degradation contributes to the increased platelet activating factor levels; platelet activating factor and TNF-alpha may contribute to the pathophysiology of necrotizing enterocolitis.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed1986

Staphylococcus epidermidis-associated enterocolitis.

Nineteen infants (mean +/- SD gestational age 30 +/- 2 weeks, birth weight 1.28 +/- 0.53 kg) with Staphylococcus epidermidis bacteremia were found on retrospective chart review to have had signs and symptoms of acute enterocolitis. This S. epidermidis-associated enterocolitis constituted 37% of the 51 cases of enterocolitis and 23% of the 81 cases of S. epidermidis sepsis during the study period. S. epidermidis-associated enterocolitis was relatively mild compared with other forms of enterocolitis. Although abdominal radiographs showed markedly abnormal bowel gas patterns with distended bowel loops and bowel wall edema, only one infant had pneumatosis intestinalis and none had portal venous or free intraperitoneal gas. Only three infants had neutropenia, and five had thrombocytopenia. None of these infants required surgical intervention. Although bloody stools often persisted for weeks, none of the neonates had prolonged feeding intolerance or development of a stricture. We conclude that S. epidermidis infection is commonly associated with a mild form of enterocolitis in the neonate and that this association should be considered when selecting antibiotics for therapy.

Enterocolitis↗

PubMed1979

Neonatal necrotizing enterocolitis: implications for an infectious disease.

There is a broad spectrum of presentations and severity of necrotizing enterocolitis. Because it may have several different causes, ncerotizing enterocolitis may be a syndrome rather than a specific disease. The triad of formula feeding, intestinal ischemia, and bacterial growth may be part of the pathogenesis of necrotizing enterocolitis. Bacteria are of central importance for the production of pneumatosis, a prerequisite of which is formula feeding. Bacteria may also contribute to the intestinal injury seen after ischemia. However, the disease in the low risk patient seen during an epidemic associated with a single organism is probably caused by a primary gastrointestinal infection. On the other hand, in the stressed newborn infant with mucosal injury the presence of the appropriate bacteria may be all that is needed to initiate the chain of events leading to necrotizing enterocolitis. Figure 2 illustrates the importance of bacteria in all the causes proposed to be involved in the pathogenesis of necrotizing enterocolitis. Whether bacteria are primary or secondary agents, necrotizing enterocolitis should always be approached therapeutically as an infectious disease.

Bacterial Infections↗

PubMed2001

Enteral human IgG for prevention of necrotising enterocolitis: a placebo-controlled, randomised trial.

BACKGROUND: Neonatal necrotising enterocolitis is a serious, commonly fatal disease in premature neonates. Although feeding with expressed breast milk and other good nursery practices are partly protective, preventive measures are needed. Treating neonates enterally with a mixture of human IgA and IgG, prepared from donated blood, has been claimed to protect against necrotising enterocolitis. However, no IgA preparation is available in Australia. Our aim, therefore, was to identify whether or not enteral IgG could prevent the disorder. METHODS: We did a multicentre, double-blind, placebo- controlled trial. We randomly assigned 768 infants to receive human IgG 1200 mg/kg daily, and 761 to receive placebo, for up to 28 days. Treatment began at the same time as enteral feeding. The primary outcome measure was the proportion of infants who developed definite necrotising enterocolitis during the trial, and any deaths that resulted from the disorder in the treatment and placebo groups. Analysis was on an intention-to-treat basis. FINDINGS: 43 infants developed definite necrotising enterocolitis in the IgG group, ten of whom died. In the placebo group, 41 infants contracted the disorder and six died (p=0.47). 25 infants on IgG and 36 on placebo had suspect necrotising enterocolitis (p=0.14). INTERPRETATION: Supplementation of enteral feeds with human IgG does not reduce necrotising enterocolitis.

Double-Blind Method↗

PubMed2000

Clostridial enterocolitis.

Equine clostridial enterocolitis is being recognized with increasing frequency. It has been identified in foals with diarrhea, antibiotic-associated enterocolitis, or nosocomial enterocolitis. The sporadic occurrence of clostridial enterocolitis, the variety of types of clostridia involved, and the difficulty of experimentally reproducing the disease suggest that it is a poorly defined multifactorial syndrome. The risk factors associated with susceptibility to colonization and progressive infection are largely based on anecdotal observations and extrapolation from human studies. Quantitative studies are needed to decipher the complex interactions between host and indigenous microflora that provide for and maintain a healthy colonization resistance environment. It seems that such studies might be more beneficial in furthering our understanding of the pathogenesis of clostridial enterocolitis than attempting to implicate another agent or toxin as the sole cause of the disease in equids. Treatment protocols that interrupt the pathogenesis of the disease need to be devised and critically evaluated to complement the present protocols emphasizing supportive care. Perhaps it is time to consider clostridial enterocolitis as yet another consequence of the use of antimicrobials analogous to the selective pressures that result in the emergence of multiple drug-resistant pathogens.

Animals↗