Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “watermelon spot disease”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

6 recordsLinked to original sources
PubMed2026

Host Range and Chemical Control of Cercospora citrullina, the Causal Agent of Watermelon Spot Disease.

This study systematically evaluated cultivation requirements, host range, and chemical control options for Cercospora citrullina causing watermelon spot disease. Among 11 chemically defined media tested, corn meal agar medium supported optimal mycelial growth of C. citrullina, with an average radial growth rate of 56.72 ± 1.45 mm under controlled conditions (25°C, darkness). Host range determination via artificial inoculation of 19 plant species confirmed that the host range of the strain UNL090101 is limited to the Cucurbitaceae species tested, with watermelon (Citrullus lanatus) exhibiting the highest susceptibility, followed by melon (Cucumis melo) and cucumber (Cucumis sativus). Fungicide screening of 17 commercial formulations identified 40% iminoctadine tris (albesilate) WP (EC50 = 2.82 μg·liter-1) and 64% mancozeb + 8% cymoxanil (WS) (EC50 = 48.75 μg·liter-1) as the most effective treatments, achieving control efficacies of 74.47 and 58.62%, respectively. These findings provide actionable guidelines for optimizing crop rotation, intercropping strategies, and fungicide selection in watermelon production systems.

Cercospora citrullina↗
PubMed2004

Gastric antral vascular ectasia (GAVE) syndrome.

Gastric antral vascular ectasia (GAVE) syndrome is an uncommon cause of chronic gastrointestinal bleeding and iron deficiency anaemia. We describe two cases of GAVE, one pernicious anaemia related and the other portal hypertension related. In both the cases, progressive mucosal changes, which lead to development of GAVE, were documented. Those changes were progression of multiple antral erythematous spots into linear configuration and lastly to watermelon stomach. One of the cases was treated with tranexamic acid with good response.

Aged↗
PubMedDate not supplied

[Characterization of Xanthomonas campestris pv. cucurbitae, causal agent of the bacterial spot of squash].

Bacterial leaf spot of squash was characterized for the first time in Argentina. Cultural, physiological, morphological and cross-infection tests on Cucurbitaceae showed that the pathogen was Xanthomonas campestris pv. cucurbitae (Bryan) Dye. The bacterium isolated from winter squash proved pathogenic for pumpkin, winter squash, cucumber and watermelon but no for muskmelon.

Plant Diseases↗
PubMed2001

[A case of gastric antral vascular ectasia (GAVE) with chronic renal failure].

A 76-year-old woman was admitted to our hospital complaining of tarry stool, general fatigue and marked anemia(Hb 5.2 g/dl). Gastric endoscopic findings showed longitudinal red stripes and diffuse erythematous spots, indicating dilated vascular vessels. They resembled the stripes of a watermelon at the gastric antrum. The marked anemia was caused by chronic blood loss from the abnormally dilated mucosal and submucosal capillary veins in the gastric antrum. She was diagnosed as having gastric antral vascular ectasia(GAVE) with chronic renal failure(CRF). The association of GAVE and CRF is considered to be rare according to previous reports in Japan. Endoscopic argon plasma coagulation therapy was performed three times. After therapy, capillary dilatation disappeared, and the marked anemia was greatly improved. Argon plasma coagulation therapy was found to be a safe and effective procedure for this disease. Although GAVE is essentially a benign gastric disease, endoscopic therapy should be the treatment of first choice for this disease.

Aged↗
PubMed2004

An endoscopic study of upper-GI mucosal changes in patients with congestive heart failure.

BACKGROUND: Congestive heart failure results in an increase in systemic venous pressure that is transmitted to the inferior vena cava and to the hepatic veins. This can cause GI vascular and mucosal congestion. The aim of this study was to define upper-GI mucosal changes in patients with congestive heart failure. METHODS: A total of 57 patients with congestive heart failure presenting with GI symptoms underwent upper endoscopy. Echocardiography was performed in all patients to determine the ejection fraction and the degree of tricuspid regurgitation. Transabdominal US was performed to measure the diameters of the hepatic veins, the inferior vena cava, and the portal vein. The presence and the severity of gastropathy and duodenopathy were compared with the parameters relating to severity of cardiac failure. RESULTS: Of the 57 patients studied, gastric mucosal changes were observed in 50 (88%), duodenal mucosal changes in 31 (54%), and esophageal mucosal changes in none. Gastric mucosal changes were the following: mosaic-like pattern (n = 50), punctate spots (n = 34), thickened folds (n = 5), watermelon stomach (n = 3), and telangiectasia (n = 10). Duodenal mucosal changes were the following: mosaic-like pattern (n = 29), thickened folds (n = 8), and telangiectasia (n = 2). Upper-GI symptoms were associated with gastropathy ( p = 0.027) and duodenopathy ( p = 0.003). The presence and the severity of duodenopathy showed a high degree of positive correlation with the presence and the severity of gastropathy (gamma value 0.690; p value <0.001). Patients with gastropathy and duodenopathy had higher mean inferior vena cava and hepatic vein diameters than those without gastropathy and duodenopathy. The severity of duodenopathy but not that of gastropathy was significantly associated with increasing severity of tricuspid regurgitation ( p = 0.001), larger portal vein diameter ( p = 0.02), and lower ejection fraction ( p = 0.008). CONCLUSIONS: Among patients with congestive cardiac failure with GI symptoms, changes of congestive gastropathy are evident in 88% and duodenopathy in 54%. The presence and the severity of duodenopathy was significantly associated with increasing severity of features of congestive heart failure.

Adolescent↗
PubMed2003

Nucleotide sequence and infectious transcripts from a full-length cDNA clone of the carmovirus Melon necrotic spot virus.

We have studied the biological and molecular characteristics of a MNSV isolate collected in Spain (MNSV-Malpha5) and generated a full-length cDNA clone from which infectious RNA transcripts can be produced. The host range of MNSV-Malpha5 appeared to be limited to cucurbits and did not differ from that of MNSV-Dutch [4, 21]. However, differences were observed in the type of symptoms that both isolates could induce. A full-length cDNA of MNSV-Malpha5 was directly amplified by reverse-transcription polymerase chain reaction (RT-PCR) using a 5'-end primer anchoring a T7 RNA promoter sequence and a 3'-end primer, and cloned. Uncapped RNAs transcribed from this cDNA clone were infectious and caused symptoms indistinguishable from those caused by viral RNA when mechanically inoculated onto melon, cucumber or watermelon plants. The complete genome sequence of MNSV-Malpha5 was deduced from the full length cDNA clone. It is 4271 nt long and, similarly to MNSV-Dutch, consists of 5' and 3' untranslated regions (UTRs) and five open reading frames (ORFs) coding for 29, 89, 42 and two small 7 kDa proteins. One notable difference between MNSV-Malpha5 and other sequenced MNSV isolates was found, as for MNSV-Malpha5 the first of the two small ORFs, which are contiguous in the genome, terminates with a genuine stop codon, whereas for MNSV-Dutch and other sequenced MNSV isolates it terminates with an amber codon. This suggested that the putative p14 readthrough protein that could be expressed from the MNSV-Dutch and other MNSV genomes could not be expressed from the MNSV-Malpha5 genome. Also, the nucleotide and amino acid sequences comparisons showed a distant relationship of MNSV-Malpha5 with other known MNSV isolates.

Carmovirus↗