Pecan nut germination — A review for the nursery industry

The shell of the pecan nut is freely permeable to water and gases, but retards germination by mechanically restricting growth of the radicle. This mechanical effect, which is pronounced at 20°C, can be overcome by germinating nuts between 30° and 35°C. Cool, moist stratification can substitute for the high-temperature germination-requirement in that following stratification nuts germinate equally well at 20°, 25° and 30°C. During stratification or incubation at high temperature, cytokinin and gibberellin levels increase in the embryo. This increase in endogenous promoter levels is closely correlated with the digestion of food reserves necessary for the resumption of embryo growth.     

The effect of DD and dazomet treatments on nematode populations at various depths in the soil and on the transmission of soil-borne tobacco rattle virus to gladiolus

The relation between log dosage of DD injected at 15 cm depth or of dazomet applied to the soil surface (all in November 1971) and probit mortality ofRotylenchus and trichodorids in the top 20 cm of a field on sandy soil was found to be linear. Dosage increase efficiencies of both chemicals against both nematode species were medium to high. Superficial application of dazomet was very effective against the nematodes that would have survived if only a low dosage of DD had been injected at 15 cm depth. Injection of 40 ml or 80 ml DD per m² at 15 cm depth killed all nematodes between 20 cm and 60 cm deep. Gladiolus planted in the spring of 1972 grew better, flowered earlier and produced more weight of corms on treated than on untreated plots. The poor growth on the untreated plots cannot be ascribed to direct damage by nematodes or to the effect of TRV transmitted to the plants by the viruliferous trichodorids occurring in these plots in high densities. Symptoms of TRV infection in plants grown in 1973 from the corms harvested in the 1972 experimental field showed that only DD treatments had reduced the rate of TRV transmission considerably. However, even the highest dosages of DD had only reduced it from 26% (on untreated plots) to about 8%. Most probably, this residual TRV infection was due to transmission by trichodorids that had survived in soil layers below 60 cm depth. Therefore, soil treatment with nematicides, cannot prevent TRV transmission to gladiolus sufficiently where viruliferous trichodorids occur at great depths, as is the case in many sandy soils having a low water table.     

Severity of E. coli mastitis is mainly determined by cow factors

Intramammary infections of dairy cows with Gram-positive bacteria such as Staphylococcus aureus (major cause of mastitis) have received a lot of attention because of their major economic impact on the dairy farm through production losses induced by an increase in somatic cell count. Management strategies, including greater awareness for efficient milking and hygienic measures, have limited the spread of Gram-positive bacteria and resulted in a significant decrease of proportion of S. aureus isolates and subclinical mastitis worldwide. Other organisms such as coliform subspecies and Streptococcus uberis, both environmental bacteria that cause clinical mastitis, have received less attention. Escherichia coli causes inflammation of the mammary gland in dairy cows around parturition and during early lactation with striking local and sometimes severe systemic clinical symptoms. This disease affects many high producing cows in dairy herds and may cause several cases of death per year in the most severe cases. It is well known that bacterial, cow and environmental factors are interdependent and influence mastitis susceptibility. Many studies, executed during the last decade, indicate that the severity of E. coli mastitis is mainly determined by cow factors rather than by E. coli pathogenicity. During E. coli mastitis, the host defense status is a cardinal factor determining the outcome of the disease. Today, we know that the neutrophil is a key factor in the cows' defense against intramammary infection with E. coli. Effective elimination of the pathogen by neutrophils is important for the resolution of infection and the outcome of E. coli mastitis. This review is a compilation of some major findings over the last 15 years concerning mainly host factors that modulate and influence neutrophil function and the mammary inflammatory reaction. The individual chapters address: virulence factors of E. coli strains, how neutrophils kill E. coli, connection between endotoxins, tumor necrosis factor-alpha and nitric oxide, severity classification of E. coli mastitis, lifespan of neutrophils, host factors that influence severity, tissue damage and production loss.     

Myxozoans infecting the sharptooth catfish, Clarias gariepinus in the Okavango River and Delta, Botswana, including descriptions of two new species, Henneguya samochimensis sp. n. and Myxobolus gariepinus sp. n

During a recent investigation of parasites infecting fishes from the Okavango River and Delta, Botswana (southern Africa) fourteen sharptooth catfish, Clarias gariepinus (Burchell, 1822) (Siluriformes: Clariidae) were examined for the presence of myxozoan infections. Results revealed the presence of two species of the genus Henneguya Thélohan, 1895 and one species of the genus Myxobolus Bütschli, 1882 infecting this fish host. Two of the sampled fish exhibited large plasmodia of Henneguya suprabranchiae Landsberg, 1987 in the cartilage of the accessory breathing organ, another two individuals were infected with H. samochimensis sp. n. plasmodia in the gills and another three individuals revealed an infection with Myxobolus gariepinus sp. n. plasmodia in the ovaries.     

Growth performance of pigs fed diets with and without tylosin phosphate supplementation and reared in a biosecure all-in all-out housing system

Three hundred and eighty-four pigs, mean initial live weight of 20.8 kg, were assigned randomly to groups of 24 (12 females, 12 castrated males). Each group was randomly assigned to 1 of 2 dietary treatments consisting of the same commercial barley-based diet, with or without the addition of tylosin phosphate. The barn where the animals were housed operates as an all-in all-out facility, and all pigs arrived on the same day as part of a group of 960 pigs. No new pigs were introduced into the facility during the period of this trial and pigs were sent to market over a 4-week period upon achieving a live weight of 110 kg. The pigs were weighed at the beginning of the trial and when they left the facility for slaughter. Feed consumption and incidence of disease, mortality, or both were recorded daily. At slaughter, carcass backfat depth over the last rib, 6.5 cm ventral to the dorsal midline (P-2 site); loin depth; carcass weight; predicted lean yield; and grade index were recorded. The sow herd supplying pigs to the unit was known to be free of the major swine diseases such as swine influenza, mycoplasma pneumonia, porcine reproductive and respiratory syndrome (PRRS), necroproliferative enteritis, and ascarids. A strict biosecurity protocol was employed to minimize the risk of introducing disease organisms into the unit. Prior to this study, no subtherapeutic antibiotics had been used in this facility. Tylosin phosphate supplementation had no significant effect on final weight, days on test, total gain, and daily gain. In both treatments, the pigs reached a mean market weight of 110.2 kg within 94.1 days, resulting in daily gains of the order of 950 grams per day. Due to the design of the trial, it was difficult to measure significant feed consumption effects. Feed consumption and conversion appeared to be similar for pigs in both treatment groups. At slaughter, tylosin phosphate supplementation appeared to significantly increase lean muscle content of the carcass as measured by loin muscle depth (P = 0.04). Mortality rates and the number of underweight pigs sent to market were low for this trial. Mortality was similar for both treatments; however, more of the control pigs than of the tylosin phosphate fed pigs were underweight when sent to market. From the results of this study, it appears that pigs of fast growing genotypes fed adequate diets and housed in a biosecure environment do not require dietary tylosin phosphate supplementation in order to maximize growth. There is some indication that tylosin phosphate supplementation may improve lean content of the carcass in pigs housed in such an environment.