The immune response and maternal antibody interference to a heterologous H1N1 swine influenza virus infection following vaccination

This study investigated the efficacy of a bivalent swine influenza virus (SIV) vaccine in piglets challenged with a heterologous H1N1 SIV isolate. The ability of maternally derived antibodies (MDA) to provide protection against a heterologous challenge and the impact MDA have on vaccine efficacy were also evaluated. Forty-eight MDA(+) pigs and 48 MDA(-) pigs were assigned to 8 different groups. Vaccinated pigs received two doses of a bivalent SIV vaccine at 3 and 5 weeks of age. The infected pigs were challenged at 7 weeks of age with an H1N1 SIV strain heterologous to the H1N1 vaccine strain. Clinical signs, rectal temperature, macroscopic and microscopic lesions, virus excretion, serum and local antibody responses, and influenza-specific T-cell responses were measured. The bivalent SIV vaccine induced a high serum hemagglutination-inhibition (HI) antibody titer against the vaccine virus, but antibodies cross-reacted at a lower level to the challenge virus. This study determined that low serum HI antibodies to a challenge virus induced by vaccination with a heterologous virus provided protection demonstrated by clinical protection and reduced pneumonia and viral excretion. The vaccine was able to prime the local SIV-specific antibody response in the lower respiratory tract as well as inducing a systemic SIV-specific memory T-cell response. MDA alone were capable of suppressing fever subsequent to infection, but other parameters showed reduced protection against infection compared to vaccination. The presence of MDA at vaccination negatively impacted vaccine efficacy as fever and clinical signs were prolonged, and unexpectedly, SIV-induced pneumonia was increased compared to pigs vaccinated in the absence of MDA. MDA also suppressed the serum antibody response and the induction of SIV-specific memory T-cells following vaccination. The results of this study question the effectiveness of the current practice of generating increased MDA levels through sow vaccination in protecting piglets against disease.     

IgG from acutely infected cats blocks mucosal feline immunodeficiency virus infection

We have previously shown an absence of detectable systemic or local infection in cats exposed to an infectious (100 TCID(50)) feline immunodeficiency virus (FIV) plasma inoculum via either the rectal or vaginal mucosa. In contrast, this same plasma inoculum was infectious via parenteral inoculation. Moreover an equivalent dose of cell-free tissue culture-origin virus inoculum infected 100% of cats by either the rectal or vaginal exposure route. To evaluate this phenomena, we used a tissue culture system to identify a heat-stable factor in the plasma of cats acutely (3 weeks) infected with FIV that blocked infection of naive peripheral blood mononuclear cells (PBMC) by either cell-free or cell-associated FIV in vitro. A single application of as little as a 1:200 dilution of either heparinized or Alsevier's anticoagulated plasma effectively inhibited production of FIV p26 in culture over a 21-day co-culture period. Depletion of antibody using a protein A column abrogated the inhibitory effect of FIV plasma against in vitro FIV infection. Co-inoculation of heat-inactivated plasma with 400 TCID(50) FIV-B-2542 cell-free supernatant virus onto the vaginal mucosa of two cats resulted in complete inhibition of infection in one cat and increased time to infection in the second. Thus, antibody found in the plasma of cats acutely infected with FIV blocks cell-associated and cell-free infection, inhibits virus production in previously infected cells, and reduces mucosal transmission efficiency in vivo. Extrapolation may help explain the relatively inefficient mucosal transmission of human immunodeficiency virus-1 (HIV) and other lentiviruses.     

In vivo CXCR4 expression, lymphoid cell phenotype, and feline immunodeficiency virus infection

Primary isolates of feline immunodeficiency virus (FIV) appear to require binding to CD134 in conjunction with CXCR4(X4) to infect IL-2-dependent T-cell-derived cells in culture. However, much less is known about the role of X4 for the infection of cells in vivo. To investigate the correlation between X4 expression and FIV infection in cats acutely infected with FIV-C-Pgmr we used high-speed fluorescence-activated cell sorting and realtime PCR to co-analyze cell phenotypes from lymph node, thymus, bone marrow and blood for FIV infection and X4 expression. X4 expression was greatest in lymph node, both in frequency and in mean fluorescence intensity. The thymus demonstrated a higher proviral burden in X4+ thymic T cells (14% in X4+ thymic T cells and 7% in X4− cells) whereas, proviral loads were similar between X4+ and X4− cell populations in all other tissues examined. Assuming a minimum of one proviral copy per cell, a maximum of 50% of FIV-positive cells were X4+. The highest fraction of FIV-infected X4− cells was present in bone marrow. Regardless of X4 status, proviral loads were higher in lymph node and blood T cells than in B cells. These studies provide both a positive association between X4 expression and FIV infection and introduce the probability that X4-independent infection occurs in other target cells in vivo.     

Phytoplankton community structure and the drawdown of nutrients and CO2 in the southern ocean

Data from recent oceanographic cruises show that phytoplankton community structure in the Ross Sea is related to mixed layer depth. Diatoms dominate in highly stratified waters, whereas Phaeocystis antarctica assemblages dominate where waters are more deeply mixed. The drawdown of both carbon dioxide (CO2) and nitrate per mole of phosphate and the rate of new production by diatoms are much lower than that measured for P. antarctica. Consequently, the capacity of the biological community to draw down atmospheric CO2 and transport it to the deep ocean could diminish dramatically if predicted increases in upper ocean stratification due to climate warming should occur.     

Causes of death in sheep exported live by sea

Post-mortem examinations were conducted on 950 dead and terminally ill sheep during assembly for export and during transport by sea from Fremantle, Western Australia to various Middle East ports. Causes of death were grouped into 5 major categories; inanition (deaths associated with reduced feed intake, including hypocalcaemia and hypomagnesaemia), salmonellosis (enteric and septicaemic), trauma, diseases associated with excessive feed intake (lactic acidosis and enterotoxaemia) and miscellaneous diseases (mostly of farm origin). During assembly the causes of death were salmonellosis 53.4%, miscellaneous diseases 23.8%, trauma 12.6%, inanition 10.2%, acidosis 3.9%, enterotoxaemia 3.4% and no diagnosis was made in 3.4%. During shipping the causes of death in defined populations of sheep in 5 voyages were; inanition 43.4%, salmonellosis 20.2%, trauma 10.6%, miscellaneous diseases 5.9%, enterotoxaemia 1.0% and no diagnosis was made in 19.0%. The range of mortality rates per 10,000 sheep at risk for the first 11 days at sea in 5 voyages were inanition 52.6 to 76.7, salmonellosis 7.8 to 109.8, trauma 2.1 to 17.1, miscellaneous diseases 5.9 to 17.1 and enterotoxaemia nil to 10.3.     

Primary cardiac granular cell tumor in a dog

The histological, histochemical, and ultrastructural features of a granular cell tumor in the wall of the right atrium of the heart in a nine-year-old dog are described. The histologic appearance of the mass varied from areas of spindle-shaped cells to sheets of globoid cells with foamy granular cytoplasm. The globoid neoplastic cells contained numerous cytoplasmic granules which were variably positive to periodic acid-Schiff staining, with and without disastase digestion. Ultrastructurally, the globoid cells had numerous various-sized, heterogeneous lysosomes with pleomorphic content. A granular cell tumor originating in the heart has not been reported previously in animals. The support for a neural origin of these tumors by the recent identification of several nervous tissue specific proteins in their granular cells is discussed.