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[The "diseased" or "dead" guillemots (Uria aalge), three-toed gulls (Rissa tridactyla), silver gulls (Larus argentatus) and laughing gulls (Larus ridibundus) found in the area of the German Bay, 1982-1985].

Between 1982 and 1985 the cadavers of 50 Guillemots (Uria aalge), 41 Kittiwakes (Rissa tridactyla), 26 Herring Gulls (Larus argentatus) and 34 Black-headed Gulls (Larus ridibundus) were examined pathological, bacteriological and virological. The probable cause of death was established. Parasitosis were particularly prevalent in Herring Gulls (49%), where the main infection--as in Black-headed Gulls--was with Cestoides. In Kittiwakes and Guillemots mainly Spiruroideae were recorded. The commonest bacterium isolated in organs and intestinal tract was Escherichia coli, followed by Aeromonas hydrophila and Clostridium perfringens. Salmonella were found in the organs of 5% and in the intestinal tract of 3% of the birds. The species of Salmonella most frequently isolated was Salmonella typhimurium varieties copenhagen. Also recorded were Yersinia intermedia Serovar 0:17 (1x), Pseudomonas spp. (2x), bacteria of the Haemophilus-Pasteurella-Actinobacillus group (1x), Pasteurella multocida (2x), Moraxella septicaemiae (1x), Campylobacter spec. (1x), Mycoplasma spec. (6x), DNase positive Staphylococcus spec. (4x) and Streptococcus spec. (6x). Less in evidence among the birds examined were fungus diseases with Aspergillus spec. (4x) and Blastomyces spec. (4x). As for viruses one Guillemot was found to have an Adenovirus and another one to have a Paramyxovirus. From one of the Herring Gulls there also was isolated a Paramyxovirus, from a second one to a Reovirus. Three other species isolated have get to be identified. The chief cause of sickness and death in the Guillemots was oil-contamination. The majority of the examined Kittiwakes and Herring Gulls were victims of pathogenic agents. Many of the Black-headed Gulls died through traumata as gunshots or road traffic etc. In order to establish the causes of sickness and death in seabirds and to ascertain the importance of the various species as possible carriers of infectious diseases, a systematic series of investigation will be necessary. Without this it will not be possible to assess their epidemiological relevance for other wild birds, domestic poultry and humans.

Animals↗

Multiple evolutionary origins of the fungus causing Panama disease of banana: concordant evidence from nuclear and mitochondrial gene genealogies.

Panama disease of banana, caused by the fungus Fusarium oxysporum f. sp. cubense, is a serious constraint both to the commercial production of banana and cultivation for subsistence agriculture. Previous work has indicated that F. oxysporum f. sp. cubense consists of several clonal lineages that may be genetically distant. In this study we tested whether lineages of the Panama disease pathogen have a monophyletic origin by comparing DNA sequences of nuclear and mitochondrial genes. DNA sequences were obtained for translation elongation factor 1alpha and the mitochondrial small subunit ribosomal RNA genes for F. oxysporum strains from banana, pathogenic strains from other hosts and putatively nonpathogenic isolates of F. oxysporum. Cladograms for the two genes were highly concordant and a partition-homogeneity test indicated the two datasets could be combined. The tree inferred from the combined dataset resolved five lineages corresponding to "F. oxysporum f. sp. cubense" with a large dichotomy between two taxa represented by strains most commonly isolated from bananas with Panama disease. The results also demonstrate that the latter two taxa have significantly different chromosome numbers. F. oxysporum isolates collected as nonpathogenic or pathogenic to other hosts that have very similar or identical elongation factor 1alpha and mitochondrial small subunit genotypes as banana pathogens were shown to cause little or no disease on banana. Taken together, these results indicate Panama disease of banana is caused by fungi with independent evolutionary origins.

Base Sequence↗

Molecular characterization of a partitivirus from Ophiostoma himal-ulmi.

The complete nucleotide sequences of two double-stranded (ds) RNA molecules, S1 (1,744 bp) and S2 (1,567 bp), isolated from an isolate HP62 of the Himalayan Dutch elm disease fungus, Ophiostoma himal-ulmi, were determined. RNA S1 had the potential to encode a protein, P1, of 539 amino acids (62.7 kDa), which contained sequence motifs characteristic of RNA-dependent RNA polymerases (RdRps). A database search showed that P1 was closely related to RdRps of members of the genus Partitivirus in the family Partitiviridae. RNA S2 had the potential to encode a protein, P2, of 430 amino acids (46.3 kDa), which was related to capsid proteins of members of the genus Partitivirus. Virus particles isolated from isolate HP62 were shown to be isometric with a diameter of 30 nm, and to contain dsRNAs S1 and S2 and a single capsid protein of 46 kDa. N-terminal sequencing of tryptic peptides derived from the capsid protein proved unequivocally that it is encoded by RNA S2 and corresponds to protein P2. It is concluded that O. himal-ulmi isolate HP62 contains a new member of the genus Partitivirus, which is designated Ophiostoma partitivirus 1. A phylogenetic tree of RdRps of members of the family Partitiviridae showed that there are least two RdRp lineages of viruses currently classified in the genus Partitivirus. One of these lineages contained viruses with fungal hosts and viruses with plant hosts, raising the possibility of horizontal transmission of partitiviruses between plants and fungi. The partitivirus RdRp and capsid proteins appear to have evolved in parallel with the capsid proteins evolving much faster than the RdRps.

Amino Acid Sequence↗

Sequence of RNA-dependent RNA polymerase genes provides evidence for three more distinct mitoviruses in Ophiostoma novo-ulmi isolate Ld.

Three of the twelve double-stranded (ds) RNAs, dsRNAs 1a, 1b and 3b, which are located in the mitochondria of a diseased isolate, Ld, of the Dutch elm disease fungus, Ophiostoma novo-ulmi have been cDNA cloned and sequenced. Examination of the sequences of the RdRp genes predicted from the nucleotide sequences of the three dsRNAs suggest that they constitute the genome of three new mitoviruses.

Amino Acid Sequence↗

Refinement of physiological roles for cerato-ulmin by analogy with other hydrophobins.

Cerato-ulmin, a hydrophobic protein produced by the Dutch elm disease fungus Ophiostoma ulmi, is toxic to susceptible elms. The physiological role of this protein may be related to its location on hyphal surfaces. Cerato-ulmin is a member of the hydrophobins, proteins used in the formation of structures involved in asexual reproduction (sporulation and conidiation).

Allergens↗

Action of aluminum, novel TPC1-type channel inhibitor, against salicylate-induced and cold-shock-induced calcium influx in tobacco BY-2 cells.

Previously, effect of Al ions on calcium signaling was assessed in tobacco cells expressing a Ca2+-monitoring luminescent protein, aequorin and a newly isolated putative plant Ca2+ channel protein from Arabidopsis thaliana, AtTPC1 (two-pore channel 1). TPC1 channels were shown to be the only channel known to be sensitive to Al and they are responsive to reactive oxygen species and cryptogein, a fungal elicitor protein. Thus, involvement of TPC1 channels in calcium signaling leading to development of plant defense mechanism has been suggested. Then, the use of Al as a specific inhibitor of TPC1-type plant calcium channels has been proposed. Here, using transgenic tobacco BY-2 cells expressing aequorin, we report on the evidence in support of the involvement of Al-sensitive signaling pathway requiring TPC1-type channel-dependent Ca2+ influx in response to salicylic acid, a key plant defense-inducing agent, but not to an elicitor prepared from the cell wall of rice blast disease fungus Magnaporthe grisea. In addition, involvement of Al-sensitive Ca2+ channels in response to cold shock was also tested. The data suggested that the elicitor used here induces the Ca2+ influx via Al-insensitive path, while salicylic acid and cold-shock-stimulate the influx of Ca2+ via Al-sensitive mechanism.

Aequorin↗

Detection and characterization of the Gloeosporium gloeosporioides growth inhibitory compound iturin A from Bacillus subtilis strain KS03.

The Bacillus subtilis strain KS03 was isolated, and identified as a biological control agent that inhibits the anthracnose disease fungus Gloeosporium gloeosporioides. The antifungal compound was purified from its culture broth through butanol extraction, diethylaminoethyl (DEAE) Sepharose CL-6B chromatography, and preparative thin layer chromatography. Tandem mass spectrometric analyses (MS/MS), with matrix-assisted laser desorption ionization (MALDI) time-of-fight/time-of-flight (TOF/TOF) mass spectrometry, showed that the antifungal compound was iturin A, a cyclic lipopeptide antibiotic. The major compound, with a molecular mass of 1042 Da, was identified as iturin A(2).

Anti-Bacterial Agents↗

Medical treatment of allergic fungal sinusitis.

LEARNING OBJECTIVES: This review of allergic fungal sinusitis (AFS) will enable the reader to (1) differentiate AFS from the other forms of fungal sinusitis, (2) understand AFS pathophysiology, (3) recognize AFS clinical presentation, (4) prepare an effective treatment and follow-up strategy, and (5) avoid diagnostic and treatment pitfalls. DATA SOURCES: All English language MEDLINE articles that cross-referenced allergy, fungal, and sinusitis from 1983-present. Other MESH words referenced included: antibodies, fungal; fungus diseases; IgE; spores, fungal; rhinosinusitis. Additional referenced articles, published abstracts, and conference proceedings were also utilized. STUDY SELECTION: All case reports, studies, and review articles. RESULTS: Allergic fungal sinusitis is a distinct form of non-invasive fungal sinusitis. It is under-diagnosed, and incidence varies by region. Dematiaceous fungi predominate. In the southwestern United States, Bipolaris spicifera is the most common cause. Patients present with nasal polyps, rhinosinusitis, and occasionally proptosis. CT scans show hypertrophic sinusitis and often hyperattenuating allergic mucin within the sinus cavities. Extra-sinus extension of disease is common. Surgical histopathology shows eosinophilic-lymphocytic mucosal inflammation and inspissated allergic mucin containing non-invasive fungal hyphae. All patients are atopic and have positive allergy skin tests to the AFS organism. Total serum IgE levels are usually elevated. AFS immunopathophysiology is analogous to allergic bronchopulmonary aspergillosis. Treatment requires surgery, postoperative oral corticosteroids (OCS), and aggressive allergy management including allergen immunotherapy. Oral corticosteroids reduce disease activity and forestall the need for recurrent sinus surgery. Postoperative changes in total serum IgE mirror the clinical status and may predict disease recurrence. Patients should be cooperatively followed by the medical specialist and surgeon because early sinus surgery for recurrence, together with aggressive medical management, gives the best outcome. CONCLUSIONS: Allergic fungal sinusitis is a new allergic disorder with recognizable clinical and histopathologic findings. Treatment requires aggressive allergy management, postoperative OCS, monitoring of total serum IgE, and medical/surgical co-management.

Aspergillosis↗

Two ascomycete classes based on fruiting-body characters and ribosomal DNA sequence.

Traditional fruiting body-based classification of ascomycetes has been under attack for 2 decades. Fruiting-body types can converge, and few researchers now assume that either the closed fruiting bodies (cleistothecia) characterizing the class Plectomycetes or the flask-shaped fruiting bodies (perithecia) characterizing the class Pyrenomycetes are stable, unifying characters. Unless we identify characters uniting major ascomycete groups, orders of ascomycetes remain narrowly defined, and supraordinal classification is impossible. We sequenced both strands of 18s rDNA from nine ascomycete fungi, adding three sequences from GenBank into our analysis. The phylogeny, inferred from 162 informative sites in 1,700 bp of DNA sequence data and using yeast as an outgroup, divided the fungi into two groups correlating well both with fruiting-body type and with the traditional classes Plectomycetes and Pyrenomycetes. Each group received strong statistical support. Genera producing cleistothecia, such as Talaromyces (with a Penicillium asexual state) and the human pathogen Ajellomyces capsulatus (causing histoplasmosis), fall within the plectomycete group. Plectomycetes also includes Eremascus albus and the bee pathogen Ascosphaera apis, although both lack typical fruiting bodies. The Dutch elm disease fungus groups with pyrenomycetes such as Neurospora, in spite of its confusing mixture of class-level characters.

Ascomycota↗