The influence of social cues on timing of animal migrations.

Animal migration plays a central role in many ecological and evolutionary processes, yet migratory populations worldwide are increasingly threatened. Adjusting migration timing to match ecosystem phenology is key to survival in dynamic and changing ecosystems, especially in an era of human-induced rapid environmental change. Social cues are increasingly recognized as major components of migratory behaviour, yet a comprehensive understanding of how social cues influence the timing of animal migrations remains elusive. Here, we introduce a framework for assessing the role that social cues, ranging from explicit (for example, active cueing) to implicit (for example, competition), play in animals' temporal migration decisions across a range of scales. By applying this theoretical lens to a systematic review of published literature, we show that a broad range of social cues frequently mediate migration timing at a range of temporal scales and across highly diverse migratory taxa. We further highlight that while rarely documented, several social cue mechanisms (for example, social learning and density dependency) play important adaptive roles in matching migration timing with ecosystem dynamics. Thus, social cues play a fundamental role in migration timing, with potentially widespread ecological consequences and implications for the conservation of migratory species. Furthermore, our analysis establishes a theoretical basis on which to evaluate future findings on the role of both conspecific and interspecific social cues in this intersection of behavioural ecology and global change biology.

Effects of the collagenolytic cell wall component of Fusobacterium necrophorum subsp. necrophorum on bovine hepatocytes.

The effects of the collagenolytic cell wall component (CCWC) of Fusobacterium necrophorum subsp. necrophorum on bovine hepatic cell and cytoskeletons were investigated. Scanning electron microscopy (SEM) demonstrated that CCWC damaged the cell surfaces, forming tiny holes on the cell membranes. Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) profiles revealed that CCWC degraded bovine cytokeratin and vimentin and by indirect fluorescent antibody (IFA) method, it was shown that CCWC caused the deformation of hepatocellular vimentin. This suggested that CCWC contributes to bovine hepatic injury and it may be as important pathogenic factor in the development of bovine hepatic abscesses.

Attempts to separate female Ascaris suum antigen and to investigate its partial characterization.

The location and separation of Ascaris suum antigen for serological testing was investigated. The antigenic constituent was rich in the ovary of the adult worm and was obtained by dialysis with 50% ammonium sulphate saturated solution. Sodium dodecyl sulphate polyacrylamide gel electrophoresis and immunoblotting analysis demonstrated that the heat labile antigenic preparation showed one major and seven faint bands. The major band seemed also to be a glycoprotein. The sera from pigs with/without hepatic milk spot showed relatively high precipitation titres, while, those from the specific pathogen free pigs manifested low titres.

Collagenolytic activity of a cell wall preparation from Fusobacterium necrophorum subsp. necrophorum.

A collagenolytic preparation of Fusobacterium necrophorum subsp. necrophorum was derived from the bacterial cell. It was further treated for gel permeation with Toyopearl HW 50, followed by Sepharose 4B column chromatography. In sodium dodecyl sulphate polyacrylamide gel electrophoresis, the final preparation exhibited one definite band and at least one faint band. It was inactivated completely by adjusting the pH to 4.0 or by heating at 80 degrees C for 30 min.

Adherence of Fusobacterium necrophorum subsp. necrophorum to ruminal cells derived from bovine rumenitis.

Fusobacterium necrophorum subsp. necrophorum strain VPI 2891 was shown to adhere to the surfaces of ruminal cells derived from bovine rumenitis. The strain also attached to bovine type 1 collagen. Treatment of the bacterium with antiserum to bacterial cells reduced attachment. The bacterial attachment was also markedly reduced when the ruminal cells had been pretreated with anticollagen serum. Fluorescence specific for the collagen was demonstrated on the surface of bovine tissue affected with rumenitis. These findings suggest that F. necrophorum subsp. necrophorum strain VPI 2891 adheres to the ruminal cells derived from rumenitis tissue and that the attachment may be mediated by cellular collagen.

Effects of Fusobacterium necrophorum subspecies necrophorum on extracellular matrix of tissue-cultured bovine kidney cells.

The effects of Fusobacterium necrophorum subsp. necrophorum on the extracellular matrix were investigated. The toxic preparation from the culture induced reduction in the number of tissue-cultured bovine kidney cells. The exposed cells often manifested partial loss of cytoplasm and were morphologically irregular. Scanning electron microscopy demonstrated partial loss of the microvilli on the exposed cells and roughness of the cell surfaces. Finally, sodium dodecyl sulphate polyacrylamide gel electrophoresis profiles revealed complete degradation of bovine collagen type 1 after treatment with the toxic preparation. This degradation was inhibited by the addition of homologous antiserum. These findings indicate that the degradation may contribute to the establishment of the infection caused by F.n. subsp. necrophorum.

Fusobacterium necrophorum haemolysin stimulates motility of ileal longitudinal smooth muscle of the guinea-pig.

Fusobacterium necrophorum haemolysin (0.5-3.1 mg protein/mL) dose-dependently induced contractions of the isolated ileal longitudinal smooth muscle of the guinea-pig. The haemolysin (3.1 mg protein/mL) -induced maximum contraction of 75% of the response to 60 mM K+ declined within 17 min and the muscles then demonstrated rhythmic contractions. Tetrodotoxin (3.1 x 10(-6) M) had no effect on the contraction due to the haemolysin. After incubation in Ca(2+)-free medium, the ileal response to the haemolysin was lost. Verapamil, a Ca2+ channel blocker, dose-dependently inhibited the contraction to the haemolysin. The rabbit anti-serum against F. necrophorum haemolysin inhibited the haemolysin-induced contraction of ileal muscle. The bacterial haemagglutinin and the lipopolysaccharide had no effect on the response of ileal muscle. These findings suggest that the haemolysin-induced direct stimulation of ileal motility dependant on Ca2+ influx will increase the probability of contact of F. necrophorum and ileal mucosa and could increase the chances of colonization for F. necrophorum.

Adherence of Fusobacterium necrophorum subspecies necrophorum to different animal cells.

The adherence of Fusobacterium necrophorum subsp. necrophorum to the surfaces of animal cells was studied in order to elucidate the differences between the bacterial appearance in clinical specimens from various animals. The bacterial cells had a strong affinity for murine and rabbit cheek cell surfaces. The bacterium showed a moderate affinity for goat cells, whereas it adhered not so well to canine, feline, human or porcine cells. Treatment of the bacterial cells with haemagglutinin antiserum prior to the binding assay reduced the degree of attachment to murine and rabbit cells. Scanning electron microscopy revealed that the adherent fusobacteria often penetrated into murine and rabbit cell membranes. These observations indicate that the bacterial attachment contributes to the establishment of the infection in mice and rabbits. It is suggested that the weak binding ability resulted in a low incidence of the bacterium in canine, feline and porcine lesions.

Actin degradation concomitant with Fusobacterium necrophorum subsp. necrophorum adhesion to bovine portal cells.

The effects of Fusobacterium necrophorum subsp. necrophorum on cellular actin were investigated using tissue-cultured bovine portal cells. Fluorescence studies revealed the appearance of intense fluorescent spots on the cellular actin and the spots increased in a time dependent manner. Sodium dodecyl sulphate polyacrylamide gel electrophoresis profiles manifested partial or complete degradation of actin preparation after treatment with the bacterial cells. These findings suggest that the bacterial cell wall may contribute to the degradation of the cellular actin during the initial stage of the infection caused by F. necrophorum subsp. necrophorum.

Detection of cytotoxic effects of Clostridium novyi type A on bovine kidney cells.

The cytotoxic effects of a toxic preparation from Clostridium novyi type A were demonstrated on tissue-cultured bovine kidney cells. The cytotoxic response was dose-dependent and could be neutralized by homologous antiserum. Scanning electron microscopy revealed damaged kidney cell surfaces. These findings indicated that the cytotoxicity may contribute to the formation of the foci in bovine tissue during an infection with C. novyi.

Location of haemagglutinin in bacterial cells of Fusobacterium necrophorum subsp. necrophorum.

The location of haemagglutinin (HA) of Fusobacterium necrophorum subsp. necrophorum VPI 2891 strain was investigated by immunofluorescence, confocal laser scan microscopy and immunoelectron microscopy. The immunofluorescence study demonstrated the fluorescence specific for the HA on the bacterial cells and confocal laser scan microscopy indicated similar fluorescence around the cross section of the bacterial cell. The immunoelectron microscopic study also revealed that the protein A-gold conjugates were located around the bacterial surfaces. These findings suggest that HA is one of the components of the cell surfaces of F. necrophorum subsp, necrophorum.

Cloning and sequencing of the genome of chicken anaemia virus (CAV) TK-5803 strain and comparison with other CAV strains.

The complete genomic sequence of chicken anaemia virus (CAV) TK-5803 strain was determined. Comparisons of sequence data showed 37 nucleotide differences between TK-5803 and Cux-1, 38 nucleotide differences between TK-5803 and 26P4, and 48 nucleotide differences between TK-5803 and 82-2. There were 65 nucleotide differences in the largest open reading frame (ORF3) between TK-5803 and one Australian isolate. Base changes introduced amino acid changes at 6 positions in the C-terminal half of VP3, at 4 positions in the C-terminal quarter of VP2 and at 17 positions in VP1 among the strains. These indicate that the N-terminal half of VP3 and the N-terminal three quarter of VP2 are well conserved, and might sustain essential function of these proteins. The amino acid changes in VP1 which is thought to be the capsid protein may influence the antigenic character of different VP1s.

Factors affecting induction of neurological disorders in mice by paralysis-inducing Friend-related PVC viruses.

Our previous studies showed that the passage of the Friend virus complex through rats generated variant MuLVs, designated PVC111, PVC211, PVC321 and PVC441, that induced neurological disorders associated with tremor and paralysis. In this study, we tested the pathogenicity of four different PVC viruses in mice. Although histopathological studies revealed spongiform degeneration in the spinal cords of NFS mice infected with each PVC virus, only PVC441 frequently induced tremor and paralysis. After a long latency, all of these viruses induced leukemia associated with severe anemia. Further studies with PVC441 revealed dose- and age-dependence for tremor induction. In contrast to NFS mice, BALB/c, DBA/2 and C57BL/6 mice infected with PVC441 virus showed no neurological symptoms, although the virus could be isolated from the tissues of central nervous system. Despite the absence of neurological symptoms, a high degree of neuronal degeneration in the lumbar spinal cord was found in PVC441-infected BALB/c mice. A low degree of neuronal degeneration was found in PVC441-infected DBA/2 or C57BL/6 mice. Genetic crosses of these resistant mice with susceptible NFS mice indicated that resistance to tremor induction by PVC441 was dominant in all mouse strains and suggested that various host genes may control the susceptibility of mice to tremor induction by PVC441 virus.

Isolation of obligate and facultative anaerobic bacteria from feline subcutaneous abscesses.

A total of 113 specimens collected from purulent skin lesions of household cats was examined bacteriologically. Ninety seven isolates obtained from 74 specimens (65.5%). Of these, 11 specimens (9.7%) contained obligate anaerobes only, 18 specimens (15.9%) yielded both obligate and facultative anaerobes. In the obligate anaerobes detected, genus Fusobacterium was the most frequently observed and F. nucleatum was most common species. Pasteurella multocida was the facultative anaerobe which was most frequently detected.

Use of enzyme-linked-immunosorbent assay for detection of IgG and IgM antibodies to Fusobacterium necrophorum in cattle.

An enzyme-linked-immunosorbent assay (ELISA) with HCl heat-extracted antigen of Fusobacterium necrophorum was conducted to detect specific immunoglobulins G and M in infected cattle. The ELISA revealed an increase (> 0.40) in specific IgG in most of the animals with hepatic abscesses but not that in specific IgM. All the lesions were positive for F. necrophorum. These findings indicated that the ELISA for immunoglobulin G detection may prove to be a useful tool for predictive serodiagnosis of F. necrophorum infection in cattle.

Biphasic immune responses of cats under controlled infection with a feline enteric coronavirus-79-1683 strain.

Kittens inoculated orally with 10(2) PFU of feline enteric coronavirus developed no antibody to the virus despite the repeated challenges. However, they developed antibody for a long period with 5 x 10(3)-1.6 x 10(5) (mean 3 x 10(4)) and with 2.5 x 10(3)-2 x 10(4) (mean 6 x 10(3)) immunoperoxidase antibody titer when they were challenged with 10(5) and 10(3) PFU of virus following previous challenges, respectively. Viremia was found when kittens were inoculated with 10(5) PFU of virus, but not with 10(3) PFU of virus. The dose of 10(3) PFU of virus seemed to be a lower limit to establish infection. These results indicate that local infection induces a low antibody response and systemic infection induces a high antibody response.

Dermonecrotic activity of a cell wall preparation from Fusobacterium necrophorum.

A cell wall preparation of Fusobacterium necrophorum induced haemorrhagic necrosis in the skins of guinea pigs and rabbits. Effects in mice and rats were weak or absent. The toxic activity of the cell wall preparation was not reduced by heat treatment. A dermonecrotic toxin was isolated from the cell wall preparation with sodium dodecylsulphate and concentrated by precipitation with ethanol. A preparation of the bacterial cytoplasm from Fus. necrophorum induced mainly erythema.

Detection and partial characterization of Pasteurella multocida found in feline skin lesions.

Pasteurella multocida was isolated from 21 of 105 purulent skin lesions in household cats. The bacterium was in pure culture in nine specimens and predominant in six specimens. Its viable counts were 10(2) to 10(7) colony forming units/ml. Of 21 isolates of P. multocida, seventeen were considered to be capsular type A. The predominant capsular and somatic type was the serotype A:3,4. Inoculation of the filter-sterilized supernatants of the isolates induced an erythematous response in guinea pig skins. These findings suggest that P. multocida is a candidate as a pathogen of feline skin lesions and the erythema-inducing activity of the bacterium may participate in the formation of skin lesions in household cats.

Local skin reaction in mice and guinea pigs induced by a single intradermal inoculation of Fusobacterium necrophorum lipopolysaccharide.

Dermal responses induced by Fusobacterium necrophorum strain VPI 2891 lipopolysaccharide (LPS) were studied using mice and guinea pigs. In ddY mice, the LPS elicited inflammatory, haemorrhagic lesions and an increase in local vascular permeability 24 h postinjection. Of the mouse strains, C3H/HeJ mice were less sensitive. The LPS induced erythema and haemorrhagic responses in guinea pig skin 24 h postinoculation. These responses were dose-dependent. The intensity of dermal inflammation-inducing activity of F. necrophorum LPS was similar to that of Escherichia coli strain 055:B5 LPS, but weaker than that of Salmonella typhimurium LPS. These findings suggest that the fusobacterial LPS may play an important role in contributing to produce the initial lesions in the bacterial infection.