A Novel Disease of Big-Leaf Mahogany Caused by Two Fusarium Species in Mexico.

Big-leaf mahogany (Swietenia macrophylla) is valued for its high-quality wood and use in urban landscapes in Mexico. During surveys of mango-producing areas in the central western region of Mexico, symptoms of malformation, the most important disease of mango in the area, were observed on big-leaf mahogany trees. The objectives of this research were to describe this new disease and determine its cause. Symptoms on big-leaf mahogany at four sites in Michoacán, Mexico resembled those of the vegetative phase of mango malformation, including compact, bunched growth of apical and lateral buds, with greatly shortened internodes and small leaves that curved back toward the supporting stem. Of 163 isolates that were recovered from symptomatic tissues, most were identified as Fusarium pseudocircinatum (n = 121) and F. mexicanum (n = 39) using molecular systematic data; two isolates represented unnamed phylospecies within the F. incarnatum-equiseti species complex (FIESC 20-d and FIESC 37-a) and another was in the F. solani species complex (FSSC 25-m). However, only F. mexicanum and F. pseudocircinatum induced malformation symptoms on 14-day-old seedlings of big-leaf mahogany. The results indicate that F. mexicanum and F. pseudocircinatum, previously reported in Mexico as causal agents of mango malformation disease, also affect big-leaf mahogany. This is the first report of this new disease and the first time that F. mexicanum was shown to affect a host other than mango.

Better quality of mother-child interaction at 4 years of age decreases emotional overeating in IUGR girls.

BACKGROUND/OBJECTIVES: While most "fetal programming" area focused on metabolic disease, intrauterine growth restriction (IUGR) is also associated with a preference for less healthy food. Post-natal factors such as strained maternal-child interactions are equally related to obesogenic eating behaviors. We investigated if IUGR and the quality of the mother/child relationship affect emotional overeating in children. SUBJECTS/METHODS: Participants were 196 children from a prospective birth cohort (the MAVAN project). As part of the protocol at 4 years of age, mothers completed the Children Eating Behavior Questionnaire (CEBQ) and mother-child interactions were scored during a structured task. A GLM adjusted for BMI examined the interaction between the "Atmosphere" score (ATM) task, sex and IUGR on the emotional over-eating domain of the CEBQ. RESULTS: There was a significant interaction of BWR vs. sex vs. ATM (P = .02), with no effects of IUGR, sex or ATM. The model was significant for girls with low ATM scores (B = -2.035, P = .014), but not for girls with high (P = 0.94) or boys with high (P = .27) or low (P = .19) ATM scores. Only in IUGR girls, 48 months emotional over-eating correlated with BMI at that age (r = 0.560, P = 0.013) and predicted BMI in the subsequent years (r = 0.654, P = 0.006 at 60 months and r = 0.750, P = 0.005 at 72 months). CONCLUSIONS: IUGR and exposure to a negative emotional atmosphere during maternal-child interactions predicted emotional overeating in girls but not in boys. The quality of mother-infant interaction may be an important target for interventions to prevent emotional overeating and overweight in early development, particularly in girls with a history of IUGR.

First Report of Mango Malformation Disease Caused by Fusarium pseudocircinatum in Mexico.

Mango (Mangifera indica L.) malformation disease (MMD) is one of the most important diseases affecting this crop worldwide, causing severe economic loss due to reduction of yield. After the first report in India in 1891 (3), MMD has spread worldwide to most mango-growing regions. Several species of Fusarium cause the disease, including F. mangiferae in India, Israel, the USA (Florida), Egypt, South Africa, Oman, and elsewhere; F. sterilihyphosum in South Africa and Brazil; F. proliferatum in China; F. mexicanum in Mexico; and recently, F. tupiense in Brazil (1,2,3,4). Besides F. mexicanum, F. pseudocircinatum, not yet reported as a causal agent of MMD, was isolated in Mexico from affected inflorescences and vegetative malformed tissues (4). Symptoms of vegetative malformation caused by F. pseudocircinatum included hypertrophied, tightly bunched young shoots, with swollen apical and lateral buds producing misshapen terminals with shortened internodes and dwarfed leaves. Infected inflorescences of primary or secondary axes on affected panicles were shortened, thickened, and highly branched, while the peduncles became thick, remained green and fleshy, and branches profusely resembled a cauliflower in shape and size (3). Ten isolates of F. pseudocircinatum were recovered from cultivars Ataulfo, Criollo, Haden, and Tommy Atkins in Guerrero, Campeche, and Chiapas states and characterized. Isolates produced mostly 0-septate but occasionally 1- to 3-septate oval, obovoid, or elliptical aerial conidia (0-septate: 4 to 19 [avg. 8.7] × 1.5 to 4 [avg. 2.6] µm) in false heads in the dark and in short false chains under black light, unbranched or sympodially branched prostrate aerial conidiophores producing mono- and polyphialides, and sporodochia with straight or falcate conidia that were mostly 3- to 5-septate, but sometimes up to 7-septate (3-septate: 25 to 58 [avg. 41] × 2 to 3.3 [avg. 2.9] µm; 5-septate: 33.5 to 76.5 [avg. 56.7] × 2.5 to 6 [avg. 3.5] µm). Circinate sterile hyphae were rarely formed. Two representative isolates, NRRL 53570 and 53573, were subjected to multilocus molecular phylogenetic analyses of portions of five genes: nuclear large subunit 28S ribosomal RNA, ß-tubulin, calmodulin, histone H3, and translation elongation factor (TEF)-1α (GenBank GU737456, GU737457, GU737290, GU737291, GU737371, GU737372, GU737425, GU737426, GU737398, and GU737399). Two pathogenicity tests were conducted with NRRL 53570 and 53573 on healthy 2-year-old nucellar seedlings of polyembryonic Criollo; 20 µl conidial suspensions (5 × 106 conidia/ml) of each isolate and water controls were inoculated separately on 15 buds on 3 different trees, as described previously (1). The following conditions were used in experiment 1: 24 to 27°C with light intensity of 16.2 to 19.8 •Mol m-2s-1 in the range of 400 to 700 nm, and photoperiods of 14 h light and 10 h dark. Typical vegetative disease symptoms were discernible in plants inoculated with NRRL 53570 (20%) and 53573 (7%) after 8 months. In experiment 2, after 3 months growth under the above conditions, seedlings were transferred to an outdoor nursery in Iguala, Guerrero. Typical vegetative symptoms of MMD were observed in 86.7 and 13.3% of the buds inoculated with F. pseudocircinatum NRRL 53570 and 53573, respectively, after 9 months. Isolates from typical symptomatic vegetative buds were confirmed as F. pseudocircinatum by sequencing a portion of their TEF-1α gene, thus fulfilling Koch's postulates. This is the first report of F. pseudocircinatum as a causal agent of MMD. References: (1) S. Freeman et al. Phytopathology 89:456, 1999. (2) C. S. Lima et al. Mycologia 104:1408, 2012. (3) W. F. O. Marasas et al. Phytopathology 96:667, 2006. (4) G. Otero-Colina et al. Phytopathology 100:1176, 2010.

First Report of Sexual Reproduction by the Soybean Sudden Death Syndrome Pathogen Fusarium tucumaniae in Nature.

Of the four fusaria that have been shown to cause soybean sudden death syndrome (SDS), field surveys indicate that Fusarium tucumaniae is the most important and genetically diverse SDS pathogen in Argentina. Although none of the SDS fusaria have been shown to produce perithecia in nature, a heterothallic sexual cycle has been demonstrated for F. tucumaniae via laboratory crosses. Herein we report on the discovery of perithecia of F. tucumaniae on soybean in Argentina. Ascospores derived from these perithecia gave rise to colonies that produced sporodochial conidia diagnostic of F. tucumaniae. Sporodochial conidia were longer and narrower than those produced by the other SDS fusaria; these conidia also possessed a diagnostic acuate apical cell and a distinctly foot-shaped basal cell. Sixteen strains derived from single ascospores subjected to a validated multilocus genotyping assay (MLGT) for SDS species determination, together with 16 conidial isolates from two sites where teleomorphs were collected, independently confirmed the morphological identification as F. tucumaniae. This study represents the first authentic report of sexual reproduction by a soybean SDS pathogen in nature.

Recent Outbreak of Soybean Sudden Death Syndrome Caused by Fusarium virguliforme and F. tucumaniae in Argentina.

Sudden death syndrome (SDS) of soybean was detected initially in Argentina during 1991-1992 in the Pampas Region and 1992-1993 in the Northwest Region. The first report of the fulfillment of Koch's postulates of SDS caused by Fusarium solani f. sp. glycines in Argentina was published in 2003 (3). Subsequently, analyses have shown that F. solani f. sp. glycines represents several morphologically and phylogenetically distinct species, including F. tucumaniae in Argentina and F. virguliforme in the United States (1). Isolations were made from plants that exhibited typical SDS symptoms (interveinal foliar chlorosis and necrosis leading to defoliation of the leaflets but not the petioles) from fields in Santa Fe and Buenos Aires provinces in 2001, 2002, and 2003. To determine which species are responsible for SDS in Argentina, cultures of eight slow growing isolates that developed bluish pigmentation and produced abundant macroconidia in sporodochia on potato dextrose agar were subjected to morphological and molecular phylogenetic analyses and pathogenicity tests. Morphological analyses demonstrated that three of the isolates were F. virguliforme and five were F. tucumaniae. Isolates of F. tucumaniae produced long and narrow sporodochial conidia while F. virguliforme produced diagnostic comma-shaped conidia. Molecular phylogenetic analyses of DNA sequences from multiple loci confirmed morphology-based identifications and showed that the soybean SDS pathogen in the United States, F. virguliforme, was also present in Argentina. To our knowledge, this is the first report of F. virguliforme in Argentina and of this pathogen outside the United States. Five isolates of F. tucumaniae and three isolates of F. virguliforme were used for pathogenicity tests. F. virguliforme isolate 171 provided by J. Rupe (University of Arkansas, Fayetteville) was used as a positive control. Soybean cultivars Ripley, RA 702, Pioneer 9492RR, Spencer, and A-6445RG were inoculated with each of the isolates tested in a greenhouse assay using soil infestation and toothpick methods (2). All eight isolates produced typical foliar SDS symptoms 15 to 25 days after inoculation. Severity of foliar symptoms averaged 3.3 for F. virguliforme, 2.6 for F. tucumaniae, and 3.3 for the positive control using a disease severity scale in which 1 = no symptoms and 5 = severely infected or dead plants. Under these conditions, F. virguliforme appeared to be more virulent than F tucumaniae. Noninoculated plants remained symptomless. Koch's postulates were confirmed with soybean cultivars RA 702 and A6445RG. Isolates recovered from symptomatic plants inoculated by the soil infestation and toothpick methods were identical to those used to inoculate the plant. Strains were recovered at frequencies of 100 and 60% from plants inoculated by the toothpick and soil infestation methods, respectively. To our knowledge, this is the first report of the fulfillment of Koch's postulates for F. tucumaniae and F. virguliforme in Argentina. References: (1) T. Aoki et al. Mycologia 95:660, 2003. (2) K. W. Roy et al. Plant Dis. 81:1100, 1997 (3) M. Scandiani et al. Plant Dis. 87:447, 2003.

A randomized study of combined zidovudine-lamivudine versus didanosine monotherapy in children with symptomatic therapy-naive HIV-1 infection. The Pediatric AIDS Clinical Trials Group Protocol 300 Study Team.

OBJECTIVE: The Pediatric AIDS Clinical Trials Group (PACTG) Protocol 300 assessed the clinical efficacy and safety of combination zidovudine/lamivudine (ZDV/3TC) compared with either didanosine (ddI) alone or combination ZDV/ddI. STUDY DESIGN: Children with symptomatic human immunodeficiency virus (HIV) infection, 6 weeks through 15 years of age, were stratified according to age and randomly assigned to receive ddI, ZDV/3TC, or ZDV/ddI. The primary endpoint was time to first progression of HIV disease or death. Enrollment in the ZDV/ddI arm stopped after 11 months on the basis of results of PACTG Protocol 152, but blinded follow-up continued. RESULTS: For the 471 children who could be evaluated, the median age was 2.7 years, median CD4 cell count was 699 cells/mm3, and median log10 HIV RNA was 5.1/mL. Median follow-up was 9.4 months. Patients receiving ZDV/3TC had a lower risk of HIV disease progression or death than those receiving ddI alone (15 vs 38 failures, P = .0006) and a lower risk of death (3 vs 15 deaths, P = .0039). Weight and height growth rates, CD4+ cell counts, and RNA concentrations showed results favoring ZDV/3TC. For patients concurrently randomized to all 3 treatment arms, both ZDV/3TC and ZDV/ddI recipients had lower risk of HIV disease progression than those who received ddI alone (P = .0026 and P = .0045). CONCLUSIONS: Combination therapy with either ZDV/3TC or ZDV/ddI was superior, as determined by clinical and laboratory measures, to monotherapy with ddI.

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.