Studies were conducted to determine the effects of dietary protein restriction on the humoral immunity (HI) and cell-mediated immunity (CMI) of chickens. New Hampshire chickens were separated into two dietary treatment groups: basal, containing 3,200 kcal/kg and 21% protein; or protein restricted (PR), containing 3,200 kcal/kg and 7% protein. In studies involving HI, half of the birds in each dietary treatment were vaccinated against fowl cholera at 4 and 8 wk of age. Blood samples were collected weekly beginning at 4 wk of age. Overall, unvaccinated birds had lower titers than vaccinated birds and PR groups generally showed lower titers than basal groups. All birds were challenged by palatine cleft inoculation of live, virulent Strain X-73 of Pasteurella multocida. The vaccinated PR group survived live challenge as well as the vaccinated basal group, but all unvaccinated birds died as a result of the challenge, regardless of antibody titer. In studies involving CMI, half of the birds in each dietary treatment were vaccinated at 5 wk of age. At 2 to 3 wk postvaccination, representative birds from each treatment were bled for total and differential blood counts. Also, birds were sacrificed and spleen cells collected. Cells were cultured in Roswell Park Memorial Institute (RPMI) medium with phytohemagglutinin-M (PHA-M), sonicated P. multocida (X-73), or RPMI only.(ABSTRACT TRUNCATED AT 250 WORDS)

Coccidia were recovered from a field outbreak in commercially raised Japanese quail from South Carolina. After propagation in unmedicated quail, the culture was identified as a mixture of approximately 65% Eimeria uzura, 33% E. tsunodai, and 2% E. taldykurganica. Several pure cultures of E. uzura were obtained by single oocyst isolation. A micropyle was not present in all oocysts; thus, it is not a reliable taxonomic characteristic for identification of E. uzura. Neither the mixed culture nor the E. uzura isolates were infective for Bobwhite quail, Chukar partridge, pheasants, chickens, or turkeys. Seventeen-day-old quail were inoculated with various doses of sporulated oocysts ranging from 5 x 10(2) to 5 x 10(5) of the mixed culture and 1 x 10(3) to 1 x 10(6) of E. uzura. The rate of weight gain was depressed at 3 or 4 days postinoculation (DPT) with as few as 5 x 10(2) oocysts/quail of the mixed culture. As few as 1 x 10(3) oocysts of E. uzura produced a weight loss. Some individual quail had depressed packed cell volume and plasma pigment compared with levels in the uninoculated controls. Plasma protein was not affected. Young quail (3 days old at inoculation) were more susceptible than 17-day-old quail. Infection did not adversely affect body weights of adult quail, although egg production was reduced. Mortality was seen only with the mixed culture (100 and 8% in 3- and 17-day-old quail given 5 x 10(5) oocysts, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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The characteristics of two clinical isolates of HSV-1 obtained from an oral (424) and an anal (490) lesion were compared with the highly passaged KOS strain. In contrast to KOS, the clinical isolates produced small plaques, were more cell-associated and the predominant viral glycoprotein species for gC and gD in infected cell lysates was the precursor, high mannose glycoform. Total virus production in Vero cells was equivalent for the three virus strains in one-step growths. Pulse-chase studies of glycoprotein C processing showed a reduction in rate at 7.5 h post infection and a significant block in processing at 10.5 h post infection for 424 and 490 but not KOS. Similar results were obtained for gD. The significant reduction in glycoprotein processing for 424 and 490 suggests a block in transport of viral glycoproteins or virions to and through the Golgi apparatus. Extracellular virions and the cell surface, prior to cell lysis, contained the processed gC glycoform suggesting a competent cellular glycan processing system. Upon co-infection of 424 or 490 with KOS or a gC- KOS strain, gC was processed to levels equivalent to KOS indicating that 424 and 490 are not inhibitory but that an activity(s) encoded by KOS facilitates maturation of gC from 424 and 490. Unlike KOS infected Vero cells, virion-containing vacuoles were observed in the cytoplasm at 12 h p.i. and extracellular virions were concentrated at cell-cell junctions of 424 or 490 infected cells but not in the perinuclear region. These results suggest that intracellular transport of viral glycoproteins and virions in 424 and 490 infected cells is different from KOS infected cells. The reduced level of viral glycoprotein maturation, virus release, cell surface presence and presence of virions at cell-cell junctions are consistent with small plaque production in tissue culture cells.