Dermal necrosis caused by Pasteurella multocida infection in turkeys.

Severe dermal necrosis caused by Pasteurella multocida Serotype 1 was diagnosed in three dressed turkey carcasses and two live turkeys from a commercial flock. The dressed carcasses were among several condemned at a processing plant. The isolate, P. multocida Serotype 1, produced progressive dermal necrosis when experimentally inoculated into injured skin of turkeys. The organism was reisolated from the dermal lesions. The turkey houses were found to be infested by mice; the skin injury and infection with P. multocida probably originated from mouse bites.

Reticuloendotheliosis in breeder turkeys.

Reticuloendotheliosis virus (REV) was isolated at 21 weeks from a flock of breeder turkeys with lymphoid neoplasms. Except for about 2% mortality due to tumors mainly between 20 and 30 weeks of age, the livability and egg production of the flock were normal. Egg transmission as a source of infection seemed unlikely, because no REV antibodies or production problems were observed in two sister flocks (hatchmates) and in three progeny flocks, and because eggs obtained from the breeder flock at 45 weeks lacked REV group-specific antigen and produced poults negative for REV infection. The virus isolate, designated REV strain 339, produced an acute neoplastic disease when inoculated into young chickens.

Outbreaks of fowl cholera in quail.

Acute fowl cholera causing high mortality was diagnosed in three flocks of quail, one involving pharaoh quail (Coturnix coturnix) and two involving bobwhite quail (Colinus virginianus). The causative organism, Pasteurella multocida, was identified as type 3.

Isolation of avian influenza virus in Texas.

An avian influenza virus with surface antigens similar to those of fowl plague virus (Hav 1 Nav 2) was isolated in 1979 from 2 commercial turkey flocks in Central Texas. Two flocks in contact with these infected flocks developed clinical signs, gross lesions, and seroconversion but yielded no virus. This was the first recorded incidence of clinical avian influenza in Texas turkeys and only the second time that an agent with these surface antigens was isolated from turkeys in U.S.

Rotavirus antibody in chickens as measured by enzyme-linked immunosorbent blocking assay.

The antibody titer of 202 chickens to SA-11 rotavirus was determined by enzyme-linked immunosorbent blocking assay. The chickens were from 15 separate flocks on six farms. The titer was detectable (1:18 or greater dilution) in 43% of the chickens. The wide variation in infection rate between flocks on individual farms (0% to 90%) indicated there is probably not significant transmission of the virus between flocks on the farm. Significant differences in numbers of serotest-positive birds were found between separate farms, possibly reflecting different management practices.

Experimental induction of hemorrhagic-aplastic anemia in chickens. II. Serum protein changes.

The serologic response of chickens to infectious bursal disease virus (IBDV) and inclusion body hepatitis virus (IBHV) was analyzed. Inoculation at one day old with either IBDV or IBHV significantly (P less than 0.05) reduced levels of serum gamma-globulins at 4 weeks postinoculation. This response was not elicited by inoculation of IBDV together with IBHV. Birds with experimentally induced or naturally occurring hemorrhagic anemia syndrome (HAS) had serum proteins quantitatively and qualitatively changed from those of controls. Serum protein profiles did not coincide, however, in experimentally infected and naturally infected chickens. Among naturally infected chickens, those that were IBHV-positive upon culture had significantly (P less than 0.05) lower hematocrit values.

Cooperative state-federal turkey ornithosis task force, Texas, 1974.

Ornithosis was suggested by a routine analysis of tissue specimens from Texas turkey flocks submitted to the Texas A&M University Poultry Disease Laboratory at Gonzales on April 30, 1974, and of subsequent specimens from four additional flocks. Subsequently, illness in humans at turkey processing plants in Texas, Nebraska, and Missouri, implicating turkeys from Texas, was confirmed as ornithosis in July 1974; and, associated with this outbreak, ornithosis was suspected as the cause of the death of one human. Action was taken by state and federal poultry disease control and inspection officials, public health agencies, and the turkey industry in Texas.

Characterization of the mRNA of influenza virus.

The kinetics of the appearance of influenza mRNA, the distribution of mRNA between free and membrane-associated polyribosomes, its poly(A) content, and the extent to which the genome was transcribed into mRNA early in infection were determined. Polyribosomes were prepared from influenza virus-infected cells labeled for 30-min periods at various times after infection with [3H]uridine. Most of the 3H-labeled RNA extracted from these polyribosomes sedimented as a heterogeneous 8S to 20S peak in sucrose gradients, and it was largely complementary to virion RNA. By the following criteria, the complementary RNA had properties normally ascribed to mRNA: (i) it labeled rapidly with [3H]uridine; (ii) after glutaraldelyde treatment, it banded with polyribosomes in CsCl density gradients; and (iii) it contained poly(A). In chick cells at 37 C, virus mRNA was first detectable at 45 min postinfection and reached its maximal rate of appearance at 2 to 2.5 h postinfection. The free and membrane-bound polyribosomes of infected cells were separated and were found to contain the same classes of mRNA. There was no absolute segregation of mRNA sequences into either polyribosome class although each probably contained distinct ratios of the different mRNA's. From 45 min postinfection onwards, both membrane-bound and free polysomal poly(A)-containing RNA contained sequences complementary to at least 80% of the genome RNA, whereas poly(A)-minus RNA contained sequences complementary to 90 to 100% of the genome. There was no evidence for the temporal control of transcription of influenza mRNA. At 31 C, when virus development was slowed relative to 37 C,complementary RNA first appeared at 1 h postinfection. At this time, total polysomal RNA contained sequences complementary to the whole genome.