A Survey of Phytophthora spp. in Midwest Nurseries, Greenhouses, and Landscapes.

A survey of nurseries, greenhouses, and landscapes was conducted from 2006 to 2008 in order to determine the prevalence and diversity of Phytophthora spp. From sites in Iowa, Michigan, Ohio, and, predominantly, Indiana, 121 Phytophthora isolates were obtained from 1,657 host samples spanning 32 host genera. Based on sequence of the internal transcribed spacer (ITS) region of the ribosomal DNA, 11 Phytophthora spp. and two hybrid species were identified. A majority of the isolates were P. citricola (35.9%) or P. citrophthora (27.4%). Six isolates were confirmed as hybrids (four of P. cactorum × hedraiandra and two of P. nicotianae × cactorum) by cloning and sequencing the ITS region. Three P. cactorum × hedraiandra isolates were obtained from the same site, from three Rhododendron spp., which are known hosts to the parental species. The fourth isolate, however, was recovered out of a different location in a Dicentra sp., which is not a known host to either parental species, suggesting an expansion of host range of the hybrid isolate as compared with either parental species.

First Report of Bacterial Wilt in Mandevilla (= Dipladenia) splendens 'Red Riding Hood' in the United States Caused by Ralstonia solanacearum Biovar 3.

In November of 2007, 6-inch rooted cuttings of Mandevilla (= Dipladenia) splendens 'Red Riding Hood' were submitted from a greenhouse in Indiana to the Purdue Plant and Pest Diagnostic Lab. Plants exhibited leaf dieback, wilting, and reduced top growth. Microscopic observation revealed no fungal structures within the roots, stems, and leaves; however bacterial streaming was observed from the cut edge of stem and root tissue using ×100 magnification with phase contrast. A Ralstonia solanacearum ImmunoStrip test (Agdia Inc., Elkhart, IN) was used to determine that the samples (roots and stem) were positive for R. solanacearum, the causal agent of southern wilt. A bacterial suspension was prepared from infected tissue and streaked onto King's Medium B (KB). Gram-negative, nonfluorescent, oxidase-positive bacteria were consistently isolated from the diseased tissues and determined as R. solanacearum by BIOLOG (Hayward, CA) carbohydrate utilization. A culture of R. solanacearum and infected plant material were submitted to USDA APHIS PPQ as per select agent protocol. (3) CPHST NPGBL generated pure cultures and together with submitted plant materials they tested positive for R. solanacearum using Agdia ImmunoStrips. Culture and plant material tested positive for R. solanacearum and negative for biovar 2 using the Fegan conventional PCR (1) and the Central Science Lab (CSL, York, UK) real-time PCR (4). Pure cultures were determined to be negative for biovar 2 but positive for biovar 3 using the biovar carbohydrate utilization plate assay (2). On the basis of these results, the bacteria were identified as R. solanacearum biovar 3 and not as the select agent R. solanacearum race 3 biovar 2. Koch's postulates confirmed pathogenicity of the isolated bacteria on tomato, a susceptible host. Three 6-week-old plants were mechanically inoculated with a bacterial suspension of approximately 1 × 108 CFU/ml prepared from cultures grown on KB for 2 days at 28°C. Inoculum (0.1ml of bacterial suspension) was injected into stem axils with a 22-gauge hypodermic needle. Three 6-week-old control plants were inoculated with sterile water. Plants were kept at 24°C with supplemental 400W high-pressure sodium light. Within 5 days, all three inoculated plants exhibited wilt symptoms. No symptoms were observed in control plants. Bacteria were reisolated from symptomatic plants on KB medium as described above, and gram negative, nonfluorescent, oxidase-positive bacteria were obtained. Reisolated strains were identical to R. solanacearum using BIOLOG carbohydrate utilization testing, confirming the causal agent of the disease. Personal correspondence with other diagnosticians also confirms the presence of R. solanacearum biovar 3 in Mandevilla in Ohio, Michigan, and Minnesota. To our knowledge, this is the first documented report in the world of R. solanacearum biovar 3 on Mandevilla. References: (1) M. Fegan et al. Page 34 in: Bacterial Wilt Disease Molecular and Ecological Aspects. P. Prior et al., eds. INRA Editions-Springer. Verlag, Germany, 1998. (2) E. R. French et al. Fitopatologia 30:126, 1995. (3) USDA/APHIS/PPQ New Pest Response Guidelines. Ralstonia Solanacearum race3 biovar 2, from http://www.aphis.usda.gov/import_export/plants/manuals/emergency/ downloads/nprg-ralstonia.pdf , retrieved May 2008. (4) S. A. Weller et al. Appl Environ. Microbiol. 7:2853, 2000.

First Report of Black Leg of Hydroponic Basil in the United States Caused by Plectosporium tabacinum.

During August 2007 and again in January 2008, compact sweet basil (Ocimum basilicum 'Genovese') plants grown hydroponically in Indiana displayed dark, irregular, stem lesions extending 2 to 3 cm above the interface of the nutrient solution. These necrotic stem lesions (black leg), observed on 20 to 30% of the basil plants caused very weak, brittle stems so that they could not be marketed fresh. Although no wilting was noted, reduced plant height was observed. Similar symptoms of blackleg and poor growth have been reported from Italy on greenhouse-grown basil infected with Microdochium tabacinum (1,2). Diseased plant samples were sent to diagnostic clinics at Purdue University and the University of Massachusetts. Stem samples were surface sterilized and plated on potato dextrose agar (PDA) acidified with 1 ml of 85% lactic acid per liter as well as onto one-quarter-strength PDA. A fungus morphologically consistent with Plectosporium tabacinum (van Beyma) M.E. Palm, W. Gams, & H.I. Nirenberg (synonyms M. tabacinum (von Arx, 1984) and Fusarium tabacinum (Gams & Gerlagh, 1968) (3) was cultured from the basil stems and identified as P. tabacinum by R. Wick. Cultures sent to J. McKemy and J. Bischof (USDA/APHIS/PPQ) and W. Elmer (Connecticut Agricultural Experiment Station) also were identified as P. tabacinum. Amplification of the 323-bp internal transcribed spacer (ITS) region (ITS1, 5.8S rRNA gene, ITS2) and subsequent BLAST alignments of the resulting sequence indicated a 98% match for Plectosphaerella cucumerina (anamorph P. tabacinum) (GenBank Accession No. U17399; MIDI Inc., Newark, DE). Inoculations were performed on basil plants grown in peat-based soilless medium in a greenhouse for 6 weeks. Immediately before inoculation, the roots were washed with tap water to remove the peat-based medium. A single basil plant was placed in each of eight, 125-ml Erlenmeyer flasks. Four flasks were filled with 100 ml of deionized water as negative controls and four were filled with a 1 × 106 CFU/ml water suspension of P. tabacinum so that the liquid reached the crown of the basil plant. Basil plants in the Erlenmeyer flasks were incubated on a laboratory bench at 23°C. After 24 h, the solutions in all flasks were discarded and each flask and root system was rinsed three times with deionized water. The plants were then incubated in deionized water on the laboratory bench for four to five additional days. Within 4 days, dark brown-to-black stem lesions similar to those observed originally on basil plants in the hydroponic production greenhouse developed on the plants at the water interface and extended up the stem. Lesions extended a mean of 22 mm above the water level on inoculated plants. Control plants remained symptomless. P. tabacinum was recovered from symptomatic tissue of inoculated plants to complete Koch's postulates. The experiment was repeated several times with similar results. Further evidence of pathogenicity was obtained by stem inoculation of basil plants growing in a soilless medium. These data indicate that P. tabacinum was the causal agent of the symptoms observed on the hydroponic basil. To our knowledge, this is the first report of P. tabacinum causing 'black leg' and reduced growth on basil in the United States and the first report in the world of P. tabacinum on hydroponic basil. References: (1) A. Garibaldi et al. Plant Dis. 81:124.1997. (2) A. Matta. Riv. Patol. Veg. Ser. IV 14:119, 1978. (3) M. Palm et al. Mycologia. 87:397.1995.

First Report of Goss's Bacterial Wilt and Leaf Blight on Corn Caused by Clavibacter michiganensis subsp. nebraskensis in Indiana.

In August of 2008, leaves of hybrid corn (Zea mays L.) and popcorn from Pulaski and Jasper counties in northwest Indiana were submitted to the Purdue Plant and Pest Diagnostic Lab with symptoms characteristic of a bacterial disease. Symptomatic leaves had large, tan-to-gray necrotic lesions with dark freckling present within the lesions. Shiny bacterial exudate was present on the surface of many of the lesions. Microscopic observation revealed no fungal structures within the lesions, and bacterial streaming was observed from the cut edge of symptomatic tissue under ×100 magnification with phase contrast. A commercially available ELISA test (Agdia Inc., Elkhart, IN) determined that samples were negative for Pantoea stewartii, the causal agent of Stewart's bacterial leaf blight and wilt. A bacterial suspension was prepared from symptomatic tissue and streaked onto King's B medium and subcultured on semiselective CNS medium (1,2). Axenic, peach-colored colonies present on the CNS medium tested gram positive with a KOH test. Analysis of fatty acid methyl esters (MIDI Inc, Newark, DE) indicated that the strain was very similar (0.611) to Clavibacter michiganensis. Amplification of the 500-bp 16S rRNA region of the bacterial gene and subsequent BLAST alignments of the resulting sequence indicated a 99% match for C. michiganensis subsp. nebraskensis (GenBank Accession Nos. AM410697 and U09763; D16S2 gene bacterial library, version 2.10; MIDI Inc,). Koch's postulates were used to confirm pathogenicity of the isolated bacteria on corn inbred B73. Eighteen plants were mechanically inoculated at growth stage V1 to V2 with a bacterial suspension of approximately 1 × 108 CFU/ml prepared from cultures grown on CNS for 10 days at 28°C (2). Inoculum was rubbed onto leaves dusted with Carborundum and 0.1 ml of the bacterial suspension was injected into stems with a hypodermic needle. Nine control plants were inoculated with sterile water. Plants were kept at greenhouse conditions (24°C) with supplemental 400W high-pressure sodium light. Within 5 to 8 days, leaves and stems of all 18 inoculated plants developed water-soaked, necrotic lesions. No symptoms were observed in control plants. Bacteria were reisolated from symptomatic plants on CNS medium as described above, and gram-positive colonies were obtained. Reisolated strains were identical to C. michiganensis subsp. nebraskensis by D16S2 DNA sequence analysis, confirming the causal agent of the disease. Disease incidence in affected fields ranged from 20 to 60% and significant yield loss was reported. This confirmation is of regulatory importance because of potential export restrictions of Indiana-grown seed corn and popcorn to select countries. To our knowledge, this is the first report of Goss's bacterial wilt and leaf blight on corn in Indiana. References: (1) D. C. Gross and A. K. Vidaver. Phytopathology 69:82, 1979. (2) L. M. Shepherd. M.S. thesis. Iowa State University. Ames, 1999.

[Spontaneous renal angiomyolipoma rupture. Rare differential diagnosis of renal ruptures]. / Spontane Nierenruptur bei Angiomyolipom. Seltene Differentialdiagnose bei Nierenrupturen.

Spontaneous renal rupture is a rare but nevertheless life-threatening complication in cases of benign and malignant space-occupying lesions in the kidneys. A precise preoperative differentiation often turns out to be difficult because of the formation of a hematoma. We report on a 50-year-old female patient with a retroperitoneal hematoma due to a spontaneous renal rupture for which an angiomyolipoma could only by diagnosed after the nephrectomy with histological work-up. In search of the cause, sonography, abdominal computed tomography, and digital subtraction angiography were conducted, which could provide findings suggestive of a space-occupying lesion, but because of the distinct hemorrhagic infarction could not determine whether it was benign or malignant. As shown in this case, when the radiological result is ambiguous, renal exposure is indicated from both a diagnostic and therapeutic standpoint.

First Report of Gray Leaf Spot on Perennial Ryegrass in Indiana.

Pyricularia grisea, the causal agent of gray leaf spot on turfgrass, was isolated from symptomatic perennial ryegrass (Lolium perenne) leaves collected from a golf course in north-central Indiana in August 1999. Gray leaf spot is an emerging threat to stands of perennial ryegrass in the mid-Atlantic and Midwestern United States (1). Symptoms were first evident in taller (6 cm) mown, rough areas surrounding golf course fairways. Field symptoms included diffuse patches (1 to 4 m in diameter) of thin, yellow-tan turf. Within larger affected areas, some of the turf was dead and matted. Close inspection revealed the presence of typical tan-gray lesions with brown margins and fish hook-like distortion of infected leaf blade tips. Incubation of affected turf in a saturated environment at 23°C for 16 h resulted in production of numerous three-celled, pear-shaped conidia characteristic of those produced by P. grisea. A pure culture of the isolate was grown on V8-juice agar in darkness at 29°C. After 10 days, the culture was exposed to continuous light for 4 days at 23°C to induce sporulation. Conidia were washed from the colony surface with sterile distilled water. Two-week-old perennial ryegrass plants in 8-cm-diameter pots were inoculated with the conidial suspension. Typical gray leaf spot symptoms resulted after incubation of inoculated plants at 27°C for 72 h in a saturated atmosphere. Uninoculated control plants exposed to the same environmental conditions remained healthy. This is the first report of gray leaf spot on perennial ryegrass in Indiana. Reference: (1) P. J. Landschoot and B. F. Hoyland. Plant Dis. 76:1280, 1992.

[Primary amyloidosis of the lung]. / Primäre Amyloidose der Lunge.

We report on a female patient of 66 years of age in whom primary nodular amyloidosis of the lung was diagnosed on the basis of a chance radiological finding. Based on this case report we discuss the pathophysiology, diagnosis and clinical findings of pulmonary amyloidosis.

One-week low-dose triple therapy for the eradication of Helicobacter pylori infection.

OBJECTIVE: To evaluate the efficacy and safety of two 1-week low-dose triple therapy regimens for the treatment of Helicobacter pylori infection. PATIENTS AND METHODS: Eighty patients with H. pylori infection and peptic ulcer disease (n = 64) or functional dyspepsia (n = 16), with similar demographic and clinical characteristics, were treated for 1 week with either omeprazole 20 mg once in the morning and clarithromycin 250 mg and metronidazole 400 mg twice daily (OCM; n = 40) or with omeprazole 20 mg once in the morning and clarithromycin 250 mg and tetracycline 500 mg twice daily (OCT; n = 40). H. pylori infection was assessed by urease test, culture and histology performed before and 4 (or more) weeks after cessation of the eradication therapy. RESULTS: H. pylori infection was treated successfully in 38 out of 40 patients by OCM and in 26 out of 40 patients by OCT (95 versus 65%, respectively; P = 0.0015). The OCM regimen was well tolerated in all patients except for one who complained of epigastric pain. Three patients on the OCT regimen reported side effects (abdominal pain, diarrhoea, pruritus), two of whom discontinued the study medication after 1 day. CONCLUSIONS: The 1-week low-dose triple therapy comprising omeprazole, clarithromycin and metronidazole was highly effective in eradicating H. pylori and was well tolerated. The replacement of metronidazole by tetracycline resulted in a significant decrease in the eradication rate.

[The modified 13C-urea breath test in the diagnosis of Helicobacter pylori colonization of the gastric mucosa]. / Modifizierter 13C-Harnstoff-Atemtest in der Diagnostik der Helicobacter-pylori-Besiedlung der gastralen Mucosa.

The value of a modified 13C-urea breath test for the detection of Helicobacter pylori was analysed in a prospective study of 50 consecutive patients (28 women, 22 men, aged 20-90 years) with unknown Helicobacter pylori status about to undergo upper intestinal endoscopy. Four biopsies each were obtained in each patient from the antrum and the body of the stomach and examined for Helicobacter pylori infection of the gastric mucosa histologically (haematoxylin-eosin and Giemsa stain), with the rapid urease test and by culture. The patients then underwent a modified 13C-urea breath test. Results were positive histologically and(or) by culture in 29 patients, while the breath test was positive in 28 (sensitivity 96.3%). The breath test was falsely positive in two (specificity 91.3%). The biopsy urease test had a sensitivity of 96.3% with a 100% specificity. These results demonstrate that the modified 13C-urea breath test is a simple and accurate way of demonstrating Helicobacter pylori infection, equal in diagnostic value to the biopsy urease test.

Intravenous omeprazole/amoxicillin and omeprazole pretreatment in Helicobacter pylori-positive acute peptide ulcer bleeding. A pilot study.

BACKGROUND: The aims of this study were to evaluate a Helicobacter pylori eradication schedule for H. pylori-positive gastroduodenal ulcer bleeding, which could be commenced intravenously after endoscopic diagnosis, and to assess the effect of omeprazole pretreatment on bacterial eradication. METHODS: In a prospective study 20 consecutive patients with H. pylori-positive acute peptide ulcer bleeding, who were managed conservatively including endoscopic injection therapy, were treated with a 2-week regimen consisting of either 40 mg omeprazole three times daily (with the exception of the loading dose of 80 mg) and 2 g amoxicillin three times daily intravenously for 3 days and 20 mg omeprazole twice daily and 1 g amoxicillin twice daily orally for 11 days (n = 10) or only with 40 mg omeprazole three times daily (with the exception of the loading dose of 80 mg) intravenously for 3 days and 20 mg omeprazole twice daily and 1 g amoxicillin twice daily orally for 11 days (n = 10). Subsequently, both groups received 20 mg omeprazole twice daily orally for 4 weeks. RESULTS: H. pylori eradication, defined as negative bacterial findings in urease test, culture and histology, or 13C-urea breath test at least 4 weeks after cessation of omeprazole medication, was achieved in 100% (10/10) of patients in the first group but only in 30% (3/10) of patients in the second group (p < 0.01). Ulcer healing was endoscopically confirmed in all but one patient in the second group. CONCLUSIONS: For the first time a promising concept for H. pylori eradication in H. pylori-positive ulcer bleeding is available by using a combined intravenous and oral omeprazole/amoxicillin therapy, which can be started intravenously immediately after an emergency upper GI endoscopy. In addition, these data imply that omeprazole pretreatment may not be wise when H. pylori eradication is attempted.

Medium- and high-dose omeprazole plus amoxicillin for eradication of Helicobacter pylori in duodenal ulcer disease.

The purpose of the present study was to investigate the Helicobacter pylori eradication potency of combined amoxicillin-omeprazole treatment in patients with duodenal ulcer disease and to compare the efficacy of two omeprazole and amoxicillin doses concerning H. pylori eradication, ulcer healing, pain relief, and safety. Ninety patients with active H. pylori-positive (culture and/or histology) duodenal ulcer disease were randomly treated with either omeprazole 20 mg twice a day plus amoxicillin 1 g twice a day (group I, N = 30), omeprazole 40 mg twice a day plus amoxicillin 1 g twice a day (group II, N = 30), or omeprazole 40 mg twice a day plus amoxicillin 1 g three times a day (group III, N = 30) over two weeks, followed by ranitidine at bedtime for another four weeks. The overall proportion of H. pylori eradication was 83% and of ulcer healing 92% without statistically significant differences between the study groups. Complete pain relief occurred after a median of one day in all groups. Six patients complained of side effects during the therapy phase, which led to therapy discontinuation in one female patient. In conclusion, omeprazole plus amoxicillin is a highly effective and well-tolerated therapy regimen to eradicate H. pylori in duodenal ulcer disease. In addition, the results suggest that there is no clear dose-response relation between the dosages of omeprazole and amoxicillin used in this study on the one hand and the H. pylori eradication rates on the other.

Effective treatment after failure of omeprazole plus amoxycillin to eradicate Helicobacter pylori infection in peptic ulcer disease.

METHODS: Fifty patients with relapsing or complicated Helicobacter pylori positive duodenal (n = 41) or gastric ulcer disease (n = 9) and failure of a combined treatment with omeprazole plus amoxycillin to eradicate H. pylori infection were re-treated with either oral triple therapy (bismuth subsalicylate, metronidazole, tetracycline) plus ranitidine [group I: n = 22] or high-dose omeprazole (40 mg b.d. to t.d.s.) plus amoxycillin (1 g t.d.s.) [group II: n = 28]. RESULTS: Patients of group I and II had similar demographic and clinical characteristics. The overall proportion of eradication of H. pylori infection was 81.8% in group I and 78.6% in group II (P = N.S.) as judged from negative bacterial findings by means of an urease test, specific culture and histology after modified Giemsa stain. Ulcer healing was observed in all patients after a maximum duration of 10 weeks. Ten patients on triple therapy and only one patient on omeprazole plus amoxycillin (45.5% vs. 3.6%; P < 0.001) complained of side effects without necessity of discontinuation of the study medication in either group. Twenty patients (group I: n = 10; group II: n = 10) with relapsing duodenal ulcer disease and successful cure were prospectively followed for one year without any evidence of ulcer relapse or H. pylori re-infection. CONCLUSION: Oral triple therapy plus ranitidine or high-dose omeprazole plus amoxycillin remain highly effective in eradicating H. pylori infection in patients with peptic ulcer disease and treatment failure of omeprazole/amoxycillin, but the omeprazole enhanced antibiotic monotherapy seems to be superior with regard to side effects. Thus, high-dose omeprazole/amoxycillin is recommended as the treatment of first choice in these selected patients. Triple therapy should be reserved for patients intolerant of amoxycillin.

[Pneumatosis cystoides intestinalis: associated diseases, morphology and presumed pathogenesis]. / Pneumatosis cystoides intestinalis: assoziierte Erkrankungen, Morphologie und mutmassliche Pathogenese.

Based on six cases, the clinical presentation, morphology and presumable pathogenesis of pneumatosis cystoides intestinalis (PCI) are discussed. As a rule PCI is not a disease in its own right, but a complication of very different, in part extraintestinal diseases. These can be subsumed in three groups. Group 1 includes patients with PCI as a complication of lung disease and initially normal intestinal status. The patients in group 2 develop pneumatosis on the grounds of intestinal disease secondary to primary extraintestinal or generalized disease. In group 3 pneumatosis develops as a complication of primary gastrointestinal disease.

Medium- or high-dose omeprazole plus amoxicillin eradicates Helicobacter pylori in gastric ulcer disease.

OBJECTIVE: To compare the efficacy of two omeprazole/amoxicillin regimens concerning Helicobacter pylori eradication, ulcer healing, pain relief, and safety in patients with gastric ulcer disease. METHODS: In a prospective, single-blind, single-center study, 70 patients with active, H. pylori-positive (histology and/or culture) gastric ulcers were randomly treated with either omeprazole 20 mg b.i.d. plus amoxicillin 1 g b.i.d. (group I; n = 35) or with omeprazole 40 mg b.i.d. plus amoxicillin 1 g b.i.d. over 2 wk, followed by full dose ranitidine for another 4 wk. Patients were investigated clinically and endoscopically prior to treatment and after 6 wk, including the assessment of H. pylori status by means of urease test, specific culture, and histology. RESULTS: Patients of group I and II had similar demographic and clinical characteristics. Three patients were lost to follow-up. The overall proportion of H. pylori eradication was 88.1% (group I, 91.2%; group II, 84.8%, p = NS). The ulcer healing rate was 79.1% after 6 wk, 92.5% after 10 wk, and 100% after 6 months, without a statistically significant difference between the study groups. Complete pain relief occurred after a median of 2 days (group I) and 1.5 days (group II, p = NS), respectively. Six patients (9.0%) complained of side effects that led to discontinuation of amoxicillin treatment in three patients (4.5%). CONCLUSIONS: Omeprazole plus amoxicillin is a highly effective and well-tolerated therapy regimen to eradicate H. pylori from the gastric mucosa of patients with gastric ulcer disease. In addition, the results clearly suggest that medium- and high-dose omeprazole schedules are equally effective with regard to bacterial eradication, ulcer healing, pain relief, and safety in gastric ulcers. Thus, medium- and not high-dose omeprazole plus amoxicillin should be the treatment regimen of first choice to eradicate H. pylori in gastric ulcer disease.

Methylation sensitivity of the enhancer from the human papillomavirus type 16.

The human papillomavirus type 16 is associated with anogenital cancer. Transcription of the viral transforming genes E6 and E7 is under the control of an epithelial cell type-specific enhancer. In the enhancer core, we have identified a regulatory element that is recognized by a novel nuclear factor named MSPF (methylation-sensitive papillomavirus transcription factor). Mutating the MSPF binding site strongly affects the enhancer activity. The MSPF recognition sequence 5'-ATGCGNNNNCGCCT-3' contains two CpG dinucleotides, potential targets for 5-cytidine methylation. DNA recognition by MSPF is strictly methylation-sensitive, since introduction of 5-methylcytidine into either CpG abolishes complex formation. Moreover, CpG methylation of the MSPF binding site suppresses the activity of the enhancer and of the MSPF enhanson subfragment in vivo. In the cervical carcinoma cell line CaSki, which has integrated multiple transcriptionally inactive human papilloma virus 16 genomes, a few of the viral genomes are methylated at the MSPF binding site. These findings suggest that viral transcription can be suppressed by methylation of the regulatory region, an event that prevents binding of the cellular transcription factor MSPF.

[Omeprazole modified antibiotic therapy of Helicobacter pylori infection: can clarithromycin be replaced by roxithromycin?]. / Omeprazol modifizierte antibiotische Therapie der Helicobacter pylori-Infektion: Kann Clarithromycin durch Roxithromycin ersetzt werden?

Thirty-five consecutive patients (median age: 50 years, 17 men and 18 women) suffering from Helicobacter pylori associated peptic ulcer disease (duodenal ulcer: n = 15, gastric ulcer: n = 13) or severe functional dyspepsia (n = 7) were enrolled in a two-center clinical trial and treated with omeprazole 20 mg bid preprandially and roxithromycin 300 mg bid postprandially over two weeks. After cessation of the study medication, ulcer patients received a full dose H2-blocker treatment up to the final examination four weeks later. All patients completed the trial without contravening the protocol. Side effects were not recorded. The overall proportion of cure of Helicobacter pylori-infection was 29% (10 out of 35 patients) without statistically significant difference between the two participating centers (center I: 7 out of 20 patients [35%], center II: 3 out of 15 patients [20%]; p = 0.33). We conclude from our results that omeprazole plus roxithromycin is an ineffective treatment schedule with regard to cure of H.pylori-infection in patients with peptic ulcer disease or dyspepsia.

Gastric antral vascular ectasia: a case report of a 10 year follow-up with special consideration of histopathological aspects.

The diagnosis of gastric antral vascular ectasia (GAVE) was made in a 67 year old patient with a ten year course of the disease, which was characterized by non-ulcerous dyspeptic symptoms in its early phase. The patient was treated successfully by antrectomy. The morphologic findings in the biopsy material ten to eight years before the operation corresponded with those of gastritis type C. The highly characteristic morphologic findings of sinusoidal capillary ectasia and multiple vascular thromboses appeared only in later biopsies taken during the work-up for iron deficiency anemia. The cause of the mucosal alterations was an acquired submucosal vascular anomaly (malformation).

Medium-term results of oral and intravenous omeprazole/amoxicillin Helicobacter pylori eradication therapy.

OBJECTIVES: The aim of the present study was to examine the effect of the application route of the antibiotic amoxicillin in Helicobacter pylori eradication, using omeprazole/amoxicillin. METHODS: In a prospective medium-term study, 31 patients with H. pylori-positive gastroduodenal ulcer disease were treated with a 14-day course of 20 mg omeprazole bid orally, combined with either 1 g amoxicillin tid intravenously (n = 15) or 500 mg amoxicillin six times daily orally (n = 16). RESULTS: H. pylori eradication, defined as negative bacterial findings in urease test, culture, and histology at least 4 wk after cessation of study medication, was achieved in 93% (14/15) of the patients in the first group and in 91% (11/12) of the patients in the second group. To obtain medium-term results, patients in whom H. pylori had been successfully eradicated were investigated with a 13C-urea breath test at least 6 months later. Medium-term eradication rates of 91% (10/11 patients) in the first and 100% (10/10 patients) in the second group were observed. CONCLUSIONS: In view of the equally high eradication rates obtained by a 14-day course of intravenously administered amoxicillin and an oral therapy of the same length and dosage, during the necessary induction of luminal hypoacidity by the proton pump inhibitor omeprazole, we conclude that the route of administration of amoxicillin does not play a decisive role in bacterial eradication.

Amoxicillin plus omeprazole versus triple therapy for eradication of Helicobacter pylori in duodenal ulcer disease: a prospective, randomized, and controlled study.

Treatment with amoxicillin and omeprazole resulted in encouraging Helicobacter pylori eradication rates in pilot studies that included medium term follow up. These results were evaluated in a prospective, randomised and controlled study. Forty patients with active duodenal ulcer disease and H pylori colonisation of the gastric mucosa were randomly assigned to receive either omeprazole (20 mg twice daily) and amoxicillin suspension (500 mg four times daily) for two weeks (group I) or bismuth subsalicylate (600 mg three times daily), metronidazole (400 mg three times daily), tetracycline (500 mg three times daily), and ranitidine (300 mg in the evening) for two weeks (group II). Study medication was followed in both groups by a four week treatment course with 300 mg ranitidine up to the final examination. One patient from each group was lost to follow up. H pylori was eradicated in 78.9% of group I and 84.2% of group II (p = 1.00). All ulcers in patients on omeprazole plus amoxicillin healed but in the triple treatment group four patients had residual peptic lesions after six weeks (ulcer healing rate: 78.9%, p = 0.11). Complete pain relief occurred after a median duration of 1 day in group I and of 6 days in group II (p = 0.03). There were no major complications in either group but minor side effects were more frequently recorded in patients on triple therapy (63.2% v 15.8%, p < 0.01). In conclusion, two weeks of treatment with omeprazole plus amoxicillin is as good as triple therapy plus ranitidine in eradicating H pylori but seems better with regard to safety, pain relief, and ulcer healing. Thus, amoxicillin plus omeprazole should be recommended as the treatment of choice in eradicating H pylori in patients with duodenal ulcer disease.