A previously undescribed virus disease of lettuce, for which the name lettuce necrotic yellows is proposed, occurs in epiphytotic proportions in Victoria and, to a similar or lesser extent, in parts of Queensland, New South Wales, and South Australia.Infected plants are extremely chlorotic and have a flattened appearance. They exhibit varying degrees of flaccidity and necrosis, and the mortality rate may be high. Chronically affected survivors have small, slightly distorted, but otherwise normal heart leaves. The tomato spotted wilt virus, which causes an almost identical disease in lettuce, lacks the "recovery" phase.The virus was sap-transmissible from infected lettuce or sowthistle (Sonchus oleraceus L.) to several indicator species, but not to lettuce or sowthistle. Lettuce has been infected on a few occasions with inoculum from Nicotiana glutinosa L. There is no evidence that the virus is transmitted through lettuce or sowthistle seed.The virus was inactivated in N. glutinosa sap between 52 and 5 4 T , was relatively short-lived in vitro (1-8 hr), and its dilution end-point was close to lop2.Symptoms are described on known experimental hosts, including N. glutinosa, petunia, and spinach, that are regarded as the best differential indicators.Several lettuce-infesting insects-thrips (Thrips tabaci Lind. and Frankliniella schultzei (Tryb.)), leafhoppers (Orosius argentatus Evans), and aphids (Myzus persicae (Sulz.) and Macrosiphum eiiphovbiae (Thos.))-failed to transmit the virus from infected lettuce or sowthistle.Transmission was achieved with the aphid Hyperomyzus lactucae (L.) bred on infected sowthistle, the only known source in Victoria of both the vector and the virus.The virus persisted through a moult of the vector, and thus the mode of transmission is of the circulative type. H. lactucae has not previously been recognized as a vector of a "circulative" virus.It is considered unlikely that lettuce necrotic yellows virus is indigenous to Australia, because sowthistle, the only known natural host of both the virus and the vector, is an introduced species.

An investigation since 1949 of viruses of the citrus tristeza complex indicated that the association of virulent, yellows, and tristeza-inducing viruses with orange and mandarin and that of avirulent types with grapefruit, lemon, and sour orange is a general but not absolute rule, as some exceptions were noted. Attempts to separate yellows and non-yellows components from a virulent isolate, by applying short and long feed techniques to the vector aphid, Toxoptera citricidus Kirk., were unsuccessful. A comparison of the vector efficiency of 12 clonal lines of T. citricidus aphids revealed different transfer characteristics between clones. However, transmission results from two experiments were inconclusive. Cross-protection experiments were conducted over an 11 year period with seedling trees of grapefruit and sweet and sour orange seedling combinations. In these, mild isolates from grapefruit and lemon differed considerably in initial protective ability. Over a long period, however, even a strain of low initial protective ability exerted a considerable influence, as determined by tree growth. The virulent challenge virus used in these experiments retained its yellows- and tristeza-inducing ability when it was the sole inoculant, but not in trees previously inoculated with a mild isolate. The results of transmission and cross-protection tests are interpreted as evidence that viruses of the tristeza complex are related entities, varying in virulence but rarely if ever existing as pure strains. An explanation of host-reaction phenomena in terms of the combined effect of host selectivity of strains and mutual interference between tristeza variants is discussed.

Fusarium avenaceum (Corda ex. Fr.) Sacc. was detected for the first time on seed of strand medic (M. littoralis Rhode), lucerne (M. sativa L.), white clover (T. repens L.) and strawberry clover (T. fragiferum L.). The percentage of seed infected was 24% on medic seed, 2–3% on strawberry clover, 2–6% on white clover, and 10–14% on lucerne, compared with 1–42% on subterranean clover seed. The majority of infected seed lines were grown in the main seed-producing areas of Victoria. F. arthrosporioides Sherb., F. equiseti (Corda) Sacc., F, acuminatum Ellis & Everhart and F. culmorum (W. G. Sm.) Sacc. were isolated from subterranean clover seed for the first time, comprising between 1 and 8% of Fusarium spp. isolates, while F. oxysporum (Schlecht) and F. avenaceum comprised the remaining 55% and 35% of isolates respectively. In laboratory tests, isolates of F. avenaceum from each seed host were all strongly pathogenic on roots of subterranean clover, but there was no evidence of pathogenicity by other Fusarium spp. F. oxysporum had no effect on the severity of root rot disease either alone or in combination with F. avenaceum.

Broad bean wilt virus has been transmitted experimentally by the green peach aphid, Myzus persicae (Sulz.), by using short feed techniques as applied to non-persistent viruses. A comparative study of transmission was made between this aphid and the aphids Aphis craccivora Koch and Macrosiphum euphorbiae (Thos.). After short (10–15 sec), naturally terminated access probes on low concentration virus source plants, and successive single probe transfers, starved pairs of M. persicae aphids infected 27 of 110 plants inoculated in two experiments, whereas A. craccivora failed to infect any test plants. In comparisons between individual starved aphids given single access and transmission probes on high concentration virus source plants, the infection rate for M. persicae approximately trebled those of A. craccivora and M. euphorbiae. Differences in transmission ability were generally more pronounced when aphids probed low concentration virus source plants. Groups of 10 M. persicae were able to transmit after a 24 hr access to a high concentration virus source plant, but less efficiently than after single access probes on the same plant. The virus was not retained by the aphid after an additional 24 hr period on healthy broad beans. A. craccivora failed to transmit after a 24 hr exposure to the same source. The experimental results provide an explanation of the manner of field spread of the virus, and of the control obtained by regulation of sowing time. They also demonstrate that broad bean wilt is a typical non-persistent virus, apparently unrelated to other viruses which infect broad bean.

In two controlled experiments conducted in 1960 and 1961 respectively, the ability of recognized root pathogens to induce premature ripening ("deadheads") of wheat was compared with that of the barley yellow dwarf virus, a hitherto uninvestigated factor in this regard. In both experiments the heads of virus-infected plants ripened earlier than those of plants inoculated with fungal pathogens, and grain in heads which were not completely sterile was extremely shrivelled. However, it was impossible to decide by visual observation when normal ripening commenced. To overcome this difficulty a formula for the classification of prematurely ripened heads, on a weight per floret basis, was used for the statistical analysis of the results. On this quantitative basis it was found that the virus significantly reduced the yield of grain (l% level), but there was no interaction between the virus and any of the root-rot fungi. The fungus, Rhizoctonia solani, Kuehn, also significantly reduced the yield in both experiments (5% level) and Fusarium culmorum (W.G.Sm.) Sacc. caused a reduction (5% level) in the 1960 experiment. There was a significant interaction (5% level) between these fungi in the 1961 experiment. The fungi Ophiobolus graminis Sacc., Helminthosporium sativum Pamm., King & Bakke, and Curvularia ramosa (Bainer) Boed., did not significantly reduce grain yield in either experiment. All fungi were recovered, but to a varying degree, from the roots of inoculated plants.