Bacterial Enteritis Research Articles

Faecal S100A12 as a non-invasive marker distinguishing inflammatory bowel disease from irritable bowel syndrome

Objective:S100A12 is a pro-inflammatory protein that is secreted by granulocytes. S100A12 serum levels increase during inflammatory bowel disease (IBD). We performed the first study analysing faecal S100A12 in adults with...

The Role of Mast Cells in Bacterial Enteritis

Considering that the intestinal lumen is home to greater than 400 commensal bacterial species, it is curious that the mucosal immune system can detect the presence of pathogens among benign flora. The rapid and potent response of the innate immune cells ensures that virulent organisms are contained to the intestine, although this reaction can also damage surrounding tissue if not kept in balance. The work by Feng et al1 in this issue of The American Journal of Pathology demonstrates that mast cells are involved in the inflammatory reaction to intestinal pathogens and that mast cell products released during degranulation may be the cause of intestinal damage due to infection. Several innate immune cell types reside in the intestinal lamina propria, including mast cells, dendritic cells, and macrophages. Within the intestine, mast cells are found in the mucosal and submucosal layer and can release a variety of bioactive proteins that can directly affect ion secretion (leading to diarrhea) and epithelial barrier function (leading to bacterial translocation). Although it is well documented that mast cell activation contributes to secretory diarrhea and colitis, it is still unclear how mast cells are triggered by microbial products to cause pathology. The observations presented here by Feng et al1 demonstrate that Toll-like receptor (TLR)2 on mast cells is responsible for diarrhea caused by Staphylococcus aureus. This work is a culmination of past studies demonstrating that mast cell products affect intestinal physiology and that mast cells are an important part of the innate immune response to bacterial infection.

Rifaximin Does Not Induce Toxin Production or Phage-Mediated Lysis of Shiga Toxin-Producing Escherichia coli

Diarrhea in children is often caused by enteropathogen infections that might benefit from early empirical antibiotic therapy. However, when the definition of the pathogen requires sophisticated laboratory studies, the etiology of enteritis is not known early in illness. Empirical therapy may be dangerous if the child is infected with a Shiga toxin-producing Escherichia coli (STEC) strain because antimicrobials may increase Shiga toxin (Stx) release, resulting in increased risk of microangiopathic hemolytic anemia with acute renal failure (hemolytic-uremic syndrome [HUS]) and death. There is a need for antimicrobials that would be effective against multiple bacterial enteropathogens yet not induce Stx release or increase the risk of HUS. Rifaximin has been evaluated in adults for treatment of bacterial enteritis and has a good record for safety and efficacy, but it has not been evaluated extensively in children with gastroenteritis. We therefore evaluated rifaximin's potential for phage induction, drug-induced bacteriolysis, and toxin release in 57 STEC strains (26 O157 and 31 non-O157 strains). Growth in ciprofloxacin, a known Stx phage inducer, caused bacteriolysis and release of toxin in 25/26 (96%) O157 strains and 15/31 (48%) non-O157 strains. In contrast, rifaximin did not induce phage replication or lysis in any strain. Toxin release in the presence of rifaximin was not different from release in the absence of antibiotic. Rifaximin, unlike many antibiotics used to treat pediatric gastroenteritis, does not induce phage-mediated bacteriolysis and Stx release.

Alternatively activated macrophages in intestinal helminth infection: Effects on concurrent bacterial enteritis

Alternatively activated macrophages in intestinal helminth infection: Effects on concurrent bacterial enteritis

Knockout mutagenesis of thekpsEgene ofCampylobacter jejuni81116 and its involvement in bacterium–host interactions

Campylobacter jejuni is a common cause of bacterial enteritis. The surface capsular polysaccharides are important for this bacterium to survive in the environment, but little is known about their involvement in bacterium-host interactions. This study showed that the C. jejuni capsular polysaccharides play an important role in adherence to and invasion of human embryonic epithelial cells. However, no significant role of capsular polysaccharides was shown in colonization of the chicken gut.

SGLT‐1‐mediated glucose uptake protects intestinal epithelial cells against LPS‐induced apoptosis and barrier defects: a novel cellular rescue mechanism?

Excessive apoptosis induced by enteric microbes leads to epithelial barrier defects. This mechanism has been implicated in the pathogenesis of inflammatory bowel diseases (IBD) and bacterial enteritis. The sodium-dependent glucose cotransporter (SGLT-1) is responsible for active glucose uptake in enterocytes. The aim was to investigate the effects of SGLT-1 glucose uptake on enterocyte apoptosis and barrier defects induced by bacterial lipopolysaccharide (LPS). SGLT-1-transfected Caco-2 cells were treated with LPS (50 mug/mL) in low (5 mM) or high (25 mM) glucose media. LPS in low glucose induced caspase-3 cleavage, DNA fragmentation, and increased paracellular permeability to dextran in epithelial cells. These phenomena were significantly attenuated in high glucose. LPS increased SGLT-1 activity in high, but not low glucose media. Addition of phloridzin, which competitively binds to SGLT-1, inhibited the cytoprotection mediated by high glucose. Western blot showed that LPS in high glucose increased the levels of anti-apoptotic Bcl-2 and Bcl-X(L,) and did not change proapoptotic Bax. Differential extraction of membranous vs. cytosolic cell components demonstrated that high glucose inhibits mitochondrial cytochrome c translocation to cytosol. Collectively, SGLT-1-mediated glucose uptake increases anti-apoptotic proteins, and protects enterocytes from LPS-induced apoptosis and barrier defects. The understanding of this novel glucose-mediated rescue mechanism may lead to therapeutic interventions for various enteric diseases.

Manifestations of Clostridium perfringens and related bacterial enteritides in broiler chickens

Well known as the cause of necrotic enteritis, C. perfringens (CP) is now recognized as causing a spectrum of effects including subclinical infection, mild disease with focal intestinal necrosis, diarrhoeal illness and liver disease, as well as the classic form of acute fulminant necrotizing enteritis. The mild and subclinical forms of infection appear to be widespread, and, possibly increasing in incidence. Furthermore, bacterial enteritis is increasingly being recognized less as an invasion by pathogenic organisms per se and more as an expression of the normal process by which the intestinal bacterial population changes overtime in response to changes in the intestinal environment. Such shifts in enteric bacterial populations have been referred to as dysbacteriosis. Management of the microbial ecology of the intestinal tract is therefore an important element of preventing disease, enhancing performance, and preventing foodborne illness. Diagnosis of emerging forms of bacterial enteritis including CP infection can be challenging and involves a comprehensive analysis of flock history and condemnation records, clinical signs, gross and histopathology, bacterial culture and empirical response to treatment, augmented by molecular techniques where available. Control measures are at present based on extensions of validated approaches to the control of the classical form of the disease: managing known risk factors for necrotic enteritis (coccidiosis, diet and litter quality) and the use of approved antimicrobial agents with proven efficacy against CP.

Three cases of cardiac complications associated with Campylobacter jejuni infection and review of the literature

Presented here are three cases of acute cardiac disease (myocarditis, myopericarditis, and acute atrial fibrillation) associated with Campylobacter jejuni infection, followed by a review of the corresponding literature. Since Campylobacter jejuni is the most common cause of human bacterial enteritis in developed countries, these cases emphasize the importance of keeping cardiac complications in mind when treating patients with acute gastroenteritis due to this pathogen.

Lymphoproliferative Erkrankungen nach Nierentransplantation

A 31-year-old male patient was referred because of a worsening graft function 56 months after an allogenic kidney transplantation for interstitial nephritis. He had complained about diffuse abdominal pain and watery diarrhea during the preceding week. Correction of volume status did not result in an improvement of kidney function. Bacterial or viral enteritis could be excluded as well as a mucosa-associated lymphatic tissue lymphoma (MALT-lymphoma). Shortly thereafter, the patient developed a subileus. Kidney biopsy showed a low degree nephrosclerosis and some interstitial fibrosis, but no signs of rejection. The abdominal CT scan showed enlarged lymph nodes partially obstructing the intestinal lumen. Histology showed an EBV-negative, highly aggressive B-blastic lymphoma. EBV-negative post-transplant lymphoproliferative disease (PTLD). Because of the advanced lymphoma stage immunosuppressive therapy was reduced and immunochemotherapy according to the CHOP-protocol (cyclophosphamide, doxorubicin, vincristine, prednisone) in combination with rituximab (R-CHOP) was started. After 4 chemotherapy cycles the patient was in complete remission and another 2 therapy cycles were given for consolidation. The patient remained free of disease during the actual follow-up of 8 months. PTLD can present with unspecific abdominal symptoms including diarrhea and with signs of graft dysfunction.

Dyspepsia and Irritable Bowel Syndrome After a Salmonella Gastroenteritis Outbreak: One-Year Follow-up Cohort Study

It has been reported that some patients develop functional digestive disorders, particularly irritable bowel syndrome (IBS), after acute gastroenteritis (AGE). However, the presence of dyspepsia has not been specifically addressed. We prospectively evaluated development of dyspepsia and IBS during a 1-year follow-up in a cohort of adult patients affected by a Salmonella enteritidis AGE outbreak. Questionnaires were sent to 1878 potential participants at baseline and 3, 6, and 12 months; 677 had experienced a Salmonella enteritidis AGE on June 23, 2002, and 1201 had not (randomly selected controls, matched for village of residence, age, and sex). At 12 months, 271 patients and 335 controls returned the questionnaires. Data permitted the establishment of dyspepsia and IBS diagnosis by Rome II criteria. Before the AGE outbreak, the prevalence of dyspepsia was similar in cases and controls (2.5% vs 3.8%); the prevalence of IBS was also similar (2.9% vs 2.3%). At 3, 6, and 12 months, the prevalence of both dyspepsia and IBS had increased significantly in exposed compared with unexposed subjects. Overlap between dyspepsia and IBS was frequent. At 1 year, the relative risk for development of dyspepsia was 5.2 (95% confidence interval, 2.7-9.8) and for IBS was 7.8 (95% confidence interval, 3.1-19.7). Prolonged abdominal pain and vomiting during AGE were positive predictors of dyspepsia. No predictive factors for IBS were found. Salmonella gastroenteritis is a significant risk factor not only for IBS but also for dyspepsia; at 1 year of follow-up, 1 in 7 and 1 in 10 subjects developed dyspepsia or IBS, respectively.

Campylobacter

Species within the genus, Campylobacter, have emerged over the last three decades as significant clinical pathogens, particularly of human public health concern, where the majority of acute bacterial enteritis in the Western world is due to these organisms. Of particular concern are the species, C. jejuni and C. coli, which are responsible for most of these gastrointestinal-related infections. Although these organisms have already emerged as causative agents of zoonoses, several aspects of their epidemiology and pathophysiology are only beginning to emerge. Trends in increasing antibiotic resistance are beginning to emerge with oral antibiotics, which may be the drug of choice for when it is necessary to intervene chemotherapeutically. This review wishes to examine (i) emerging clinical aspects of the disease, such as Guillain Barre syndrome (GBS), (ii) the association between these organisms and poultry as a natural host, (iii) environmental aspects of Campylobacter epidemiology, (iv) the emergence of atypical campylobacters (v) emerging trends in antibiotic resistance, (vi) adoption of modern methods for the detection of campylobacters.

Immunopathology of giardiasis: the role of lymphocytes in intestinal epithelial injury and malfunction

T lymphocyte-mediated pathogenesis is common to a variety of enteropathies, including giardiasis, cryptosporidiosis, bacterial enteritis, celiac's disease, food anaphylaxis, and Crohn's disease. In giardiasis as well as in these other disorders, a diffuse loss of microvillous brush border, combined or not with villus atrophy, is responsible for disaccharidase insufficiencies and malabsorption of electrolytes, nutrients, and water, which ultimately cause diarrheal symptoms. Other mucosal changes may include crypt hyperplasia and increased infiltration of intra-epithelial lymphocytes. Recent studies using models of giardiasis have shed new light on the immune regulation of these abnormalities. Indeed, experiments using an athymic mouse model of infection have found that these epithelial injuries were T cell-dependent. Findings from further research indicate that that the loss of brush border surface area, reduced disaccharidase activities, and increase crypt-villus ratios are mediated by CD8+ T cells, whereas both CD8+ and CD4+ small mesenteric lymph node T cells regulate the influx of intra-epithelial lymphocytes. Future investigations need to characterize the CD8+ T cell signaling cascades that ultimately lead to epithelial injury and malfunction in giardiasis and other malabsorptive disorders of the intestine.

Increased erythromycin resistance in clinical Campylobacter in Northern Ireland—an update

Sir, Thermophilic campylobacters, particularly Campylobacter jejuni, Campylobacter coli and Campylobacter lari, continue to remain the most common cause of acute bacterial enteritis in Northern Ireland, with ,743 laboratory reports per annum (equating to circa 44 cases per 100 000 population) and where the trend has been decreasing since 2000 (Figure 1). Previously, we have reported trends in antibiotic susceptibility in these organisms for the period 1980–2000. However, since 1999, we have noted a trend in increasing resistance (0.4%–11.3%) to erythromycin in isolates obtained from clinical faecal material. Human isolates were obtained from faecal specimens submitted to the Northern Ireland Public Health Laboratory for routine analysis from general practioners in the community, as well as from hospital wards over the period 2001–2003 (n 1⁄4 703). Isolates were obtained by direct selective plating onto Preston’s selective agar and incubated at 428C for 48 h. Antibiotic susceptibility studies were performed at 378C for human isolates by the standard disc diffusion. The following antibiotic agents were employed at the given disc concentrations: penicillin (2mg), cefalexin (30mg), erythromycin (15mg), chloramphenicol (10mg), gentamicin (10mg), tetracycline (10mg) and ciprofloxacin (1mg), as previously described. With the exception of erythromycin, susceptibility to the other antibiotics has remained relatively static over this period, most notably in relation to resistance to ciprofloxacin (13%). It is especially noteworthy that ciprofloxacin susceptibility has remained stable despite the widespread prescription of quinolone antibiotics. However, from 1999, there has been an increasing trend in erythromycin resistance, rising to 11.3% resistance in 2002, as shown in Figure 1. In concert with this, there has been a concurrent rise in erythromycin resistance in isolates originating from poultry in Northern Ireland, rising to 15.3% resistance in 2002 (Figure 1), and where there has been no other marked increased in antibiotic resistance levels in poultry isolates, [2003 data; tetracycline (16.4%); chloramphenicol (5.5%); nalidixic acid (3.8%); gentamicin (0%)]. Such patterns are in contrast with those reported for the USA, Pakistan and the Republic of Ireland, where rates of erythromycin resistance in clinical campylobacters remain unchanged at ,2%. Although the number of laboratory reports of clinical Campylobacter has been decreasing in Northern Ireland, on average, 9.4% per annum since 2000, the frequency of erythromycinresistant isolates has been increasing, to a maximum value of 11.3% resistance, as was recorded in 2002. Although antibiotic therapy is not normally given for this usually self-resolving infection, where antibiotic intervention is required, oral erythromycin is the first-line treatment. Therefore, any increase in resistance levels to the first-line treatment option is worrying and necessitates an exploration of the potential sources of acquisition of such resistant organisms in the local food chain. However, it is important to note that all clinical isolates remain susceptible to gentamicin. Concurrent with a rise in the resistance levels in human faecal isolates, there has been a rise in resistant rates in campylobacters originating from poultry, suggesting a possible association between the poultry and human isolates. The presence of macrolide resistance in poultry isolates in Northern Ireland is in contrast to other countries, where such data are available, including Russia, where Stern et al. recently described erythromycin resistance in poultry to be , 1%. Alternatively, it has been reported previously that the local pig population harbours a high-level resistant C. coli phenotype, which may be the cause of this increase in the frequency of human erythromycin-resistant campylobacters. In the previous study by Moore et al., these workers demonstrated the presence of C. coli isolates taken from pigs at slaughter, where the MIC of erythromycin was . 500 mg/L. Indeed, this high-level erythromycin resistance observation in C. coli originating from pigs is not unique to Northern Ireland, as similar observations have been made in North America.

Interferon-γ Down-regulates Adenosine 2b Receptor-mediated Signaling and Short Circuit Current in the Intestinal Epithelia by Inhibiting the Expression of Adenylate Cyclase

Adenosine is an endogenous signaling molecule that is highly up-regulated in inflammatory states. Adenosine acts through the A2b receptor, a G protein-coupled receptor that couples positively to Galpha(s) and activates adenylate cyclase. This leads to cAMP-mediated electrogenic chloride secretion in intestinal epithelia. To better understand the regulation of the A2b receptor in intestinal epithelia, we studied the effects of interferon-gamma (IFN-gamma), a potent immunomodulatory cytokine, in the T84 cell line. Pretreatment of cells with 500 units/ml IFN-gamma for 12 h inhibited an adenosine-induced short circuit current (Isc) without affecting the transepithelial resistance. Under these conditions, IFN-gamma did not inhibit the protein expression or membrane recruitment of the A2b receptor, shown to be essential for its function. Interestingly, IFN-gamma inhibited cAMP levels as well as its downstream signaling pathway as shown by the inhibition of adenosine-induced phosphorylation of cAMP response element-binding protein and protein kinase A activity. Similar studies with forskolin, a direct activator of adenylate cyclase, also demonstrated inhibition of cAMP and its downstream response by IFN-gamma. However, IFN-gamma did not affect secretory responses to the calcium-dependent secretagogue carbachol or cAMP analog 8-bromo-cAMP, indicating that normal secretory responses to adequate second messengers in IFN-gamma-treated cells are achievable. Moreover, IFN-gamma inhibited the expression of adenylate cyclase isoforms 5 and 7. In conclusion, we demonstrate that IFN-gamma down-regulates adenosine-mediated signaling possibly through the direct inhibition of adenylate cyclase expression. We propose that IFN-gamma may acutely affect global cAMP-mediated responses in the intestinal epithelia, thereby decreasing secretory responses, which may consequently aggravate inflammatory processes.

P0728 CLINICAL OUTCOMES OF CHILDREN WITH ACUTE ABDOMINAL PAIN IN OUTPATIENTS: ANALYSIS OF RISK FACTORS OF HIGH RISK ETIOLOGIES

Introduction: Acute abdominal pain in children presents a diagnostic dilemma. Although many cases are benign, some require a rapid diagnosis and treatment in order to minimize morbidity. The clinical outcomes of children presenting with acute abdominal pain in a outpatients clinic were determined, and the risk factors of the high risk etiologies were analyzed. Methods: Between January 2002 and June 2002, data from 244 consecutive patients, aged 1 to 13 years, in a pediatric gastroenterology outpatient visit with acute nontraumatic abdominal pain was reviewed. Abdominal ultrasonography was performed in all patients after receiving parental consent. The high risk etiologies were defined as a surgical or medical emergency. The nine risk factors were analyzed; a sick appearance, the symptom duration, the vomiting intensity, the diarrhea intensity, fever, nocturnal pain, colic pain, periodic pain, and localized pain. Results: Of the 244 patients, the six most prevalent final diagnoses were mesenteric adenitis (16.3%), an uncertain etiology (11.8%), pharyngitis (9.4%), constipation (9.0%), pneumonia (8.6%), and bacterial enteritis (6.5%). Approximately 14.8% of the patients were identified as having high risk etiologies and a surgical emergency occurred in 5.7%. The six most prevalent high risk etiologies were intussusception (4.1%), appendicitis (2.9%), hemorrhagic gastritis (2.0%), paralytic ileus (1.6%), hydronephrosis (1.2%), and allergic purpura (0.8%). The high risk factors were 8 with the exception of fever (P <0.05); a sick appearance (odds ratio [OR],4.93), a symptom duration > 72 hours (OR,4.49), a vomiting intensity > 3/day (OR,7.85), a diarrhea intensity > 3/day (OR,3.85), nocturnal pain (OR,4.72), colic pain (OR,4.03), periodic pain (OR,3.37), and localized pain (OR,2.85). Multiple logistic regression analysis showed that the independent predictors of high risks were a symptom duration > 72 hours (OR,1.68) and a vomiting intensity > 3/day (OR,2.44). Multiple logistic regression analysis also showed that with the exception of constipation, the independent predictors were a sick appearance (OR,2.69), a symptom duration > 72 hours (OR,1.53), a vomiting intensity > 3/day (OR,2.07), and localized pain (OR,3.65). Conclusion: The incidence of high risk etiologies in children with acute abdominal pain in pediatric gastroenterology outpatients is approximately 15%, and 6% of cases involve a surgical emergency. The independent predictors of a high risk are a symptom duration > 72 hours and a vomiting intensity > 3/day. With the exception of constipation, a sick appearance and localized pain are also independent predictors of a high risk.

P0539 COMPARISON OF DRUG RESISTANCE RATE OF ANTIBIOTICS USING IN PEDIATRIC BACTERIAL ENTEROCOLITIS-THREE YEARS EXPERIENCES AT A MEDICAL CENTER IN HUALIEN

Introduction: As we know, most of us, would used SMX-TMP ot treat bacterial enteritis patient emperically. But recently, we found the shigella became highly resistance of SMX-TMP. We analysis the resistance of shigella and salmonella to traditional use antibiotics of our patient. Methods: From January 1999 to December 2001,patients who had bacterial enterocolitis at Tzu-Chi general hospital were enrolled. Stool culture were obtained from these patients. Sensitivity about ampicillin, SMX-TMP, chloramphenicol, ciprofloxacin, cefotaxime and Ceftriaxone were done. Results: 1999 Jan to 2001 Dec, we collected 34 shigella B patients and 96 shigella D patients, 113 salmonella. We use Chi-Square to evaluate confidence level. As shigella B, susceptability of ampicillin and SMX-TMP were 2.94% and 11.76%, P value=0.163. As shigella D, susceptability of ampicillin and SMX-TMP were 78.13% and 0.00%, P value=0.001. All shigellosis summary, susceptability of ampicillin and SMX-TMP were 58.46% and 3.08%, P value=0.001. As salmonella, susceptability of ampicillin and SMX-TMP were 46.90% and 76.99%, P value=0.001. Total summary, shigellosis and salmonellosis, susceptability of ampicillin and SMX-TMP sensitive were 53.09% and 37.45%, P value=0.001. Conclusion: According to susceptability of bacterial enterocolitis, ampicillin would be more appropreate than SMX-TMP (53.09% vs 37.45%) as empiric antibiotics. On the other word, 3rd generational cephalosporins (ceftriaxone or cefotaxime) all are more sensitive compared to SMX-TMP (93.00% vs 37.45%) and appropriate as the choice of empiric antibiotics for treating severe bacterial enterocolitis. Ciprofloxacin may cause cartilage destruction in anamial model, it would not use in children. We suggestted use ampicillin as the choice of empiric antibiotics for treating bacterial ente rocolitis, instead of SMX-TMP. Ampicillin or third generation cephalosporin may be more appropriate to SMX-TMP as the choice of empiric antibiotics for treating bacterial enterocolitis.

Species identification by genotyping and determination of antibiotic resistance in Campylobacter jejuni and Campylobacter coli from humans and chickens in Sweden

Campylobacter is today the most common cause of human bacterial enteritis in Sweden, as well as in most other industrialized countries. Common sources of infection are undercooked chicken meat, unpasteurized milk and contaminated drinking water. One aim with our present study was to identify the species Campylobacter jejuni and Campylobacter coli strains from humans and chickens using a polymerase chain reaction/restriction enzyme analysis (PCR/REA) method, as well as traditional hippurate hydrolysis test. Another aim was to investigate the antibiotic resistance pattern of the human domestic C. jejuni/ C. coli isolates from infected patients and isolates from healthy Swedish chicken, as well as isolates from humans infected abroad. If discrimination between C. jejuni and C. coli was based on testing for hippurate hydrolysis, 95% of the human domestic strains and 88% of the chicken strains were identified as C. jejuni. Based on genotyping by PCR/REA, 100% of the human domestic strains and 98% of the chicken strains were attributed to C. jejuni. The E-test and disc diffusion methods were used for phenotypic antibiotic resistance studies. The two methods gave similar results. Most Swedish C. jejuni/ C. coli isolates both from humans and chickens were sensitive to doxycycline and erythromycin, which are antibiotics used to treat human infection. Only 7% of the human domestic strains and 2% of the chicken strains were resistant to the quinolones tested. As a comparison, more than 94% of strains isolated from travelers to Asia and southern Europe showed antibiotic resistance to one or more drugs.

Enteritis-Associated Myocarditis

We describe two cases in which myocarditis was associated with a prodromal diarrhoeal illness as a result of bacterial enteritis. Both cases were associated with elevated troponin T and chest pain mimicking myocardial infarction.

Genetic characterization and antibiotic resistance of Campylobacter jejuni isolated from meats, water, and humans in Sweden.

The incidence of Campylobacter jejuni has increased during the last decade, and today it is the leading cause of bacterial enteritis in most developed countries. Still, there is a lack of knowledge about infection routes and to what extent identified sources are responsible for spreading the bacterium to humans. The major objective of this work was to explore the genetic similarity between C. jejuni isolated from different sources. C. jejuni isolated from patients (n = 95), five types of meat (n = 71), and raw water (n = 11) during the year 2000 were subtyped by pulsed-field gel electrophoresis (PFGE). The pulsotypes obtained after digestion with SmaI revealed not only that C. jejuni is genetically diverse but also that specific pulsotypes occur frequently. Five clusters comprising 88 of the 162 SmaI-digested isolates were obtained. After digestion with KpnI most isolates in four of the five clusters were still indistinguishable, while the fifth cluster was strongly dissolved. The clusters comprised high frequencies of human and meat isolates, while only one of nine water isolates belonged to a cluster. The largest cluster comprised 21 human isolates, one raw water isolate, and seven chicken meat isolates, originating from at least six different broiler flocks. Low frequencies of antibiotic resistance were revealed when the meat and water isolates were tested for sensitivity to six antibiotics. Interestingly, the five isolates resistant to quinolones displayed similar or identical pulsotypes. The results showed that PFGE has proved useful in identifying clones and will be used in future work focusing on identification and eradication of the major reservoirs for common clones.

Characterization of antimicrobial resistant Salmonella Kinshasa from dairy calves in Texas

To determine the prevalence of antimicrobial resistance among Salmonella isolated from a central Texas dairy calf farm that raises animals for dairy-beef production. Salmonella isolates collected from 50 faecal samples were characterized for susceptibility to 20 antimicrobial agents. Seventy per cent of the faecal samples (35 of 50) tested positive for Salmonella, and high rates of resistance to the following drugs that are commonly used for treatment of bacterial enteritis in livestock were observed: ampicillin (88%), apramycin (83%), neomycin (86%), spectinomycin (91%) and oxytetracycline (90%). No resistance to the fluoroquinolone antibiotics was observed. The most prevalent Salmonella serotype was Kinshasha (22 of 35 samples), followed by Agona (4 of 35), Newport (3 of 35), Infantis (2 of 35), Montevideo (2 of 35), Lille (1 of 35) and Newington (1 of 35). The Kinshasa, Agona, Newport and Infantis serotypes all displayed resistance to ampicillin, chloramphenicol, streptomycin, sulphamethoxazole and tetracycline, and the penta-resistance phenotype was transferable to an Escherichia coli recipient strain. Multi-drug resistant Salmonella in dairy calves pose a costly animal health problem and a potential risk to the public health. This study emphasizes the need for alternative, non-antimicrobial intervention strategies for the control of zoonotic pathogens.