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Immunization of mice against Fusobacterium necrophorum infection by perenteral or oral administration of vaccine.

Immunization of mice against Fusobacterium necrophorum infection was attempted by using 3 vaccination procedures: (1) intraperitoneal (IP) injection of F necrophorum cells in saline solution, (2) IP injection of cells with added aluminum hydroxide adjuvant, and (3) feeding of a powdered mouse diet containing lyophilized cells. One or 2 weekly IP injections of the bacteria cells (in saline solution) for 3, 6, or 12 weeks resulted in protection of 48.7% to 64.5% of the mice against challenge exposure. Of the 2 control groups (given saline solution only), 100% and 97.4% became infected. Weekly IP injections of bacterial cells in an aluminum hydroxide adjuvant for 3, 6, or 12 weeks resulted in protectivity of 54.1% to 77.5%. Of the control mice (given adjuvant only), 97.5% became infected. Bacterial cells fed to mice at a dose level of 1.5 mg (dry weight)/g of powdered diet for 30 days (4 or 5g of diet each day) resulted in only a delay in the mean time of death as compared with the rapid death of the control mice. The feeding dose of 0.15 mg of cells/g of diet did not delay the mean time of death.

Adjuvants, Immunologic

Failure to induce in rabbits effective immunity to a mixed infection of Fusobacterium necrophorum and Corynebacterium pyogenes with a combined bacterin.

Failure to induce in rabbits effective immunity to a mixed infection of Fusobacterium necrophorum and Corynebacterium pyogenes with a combined bacterin. Onderstepoort Journal of Veterinary Research, 44 (4), 253--2;6 (1977). Rabbits were immunized with alum-precipitated, oil adjuvant and an untreated bacterin composed of F. necrophorum and C. pyogenes. Immunized rabbits were challenged intradermally with a mixture of F. necrophorum and C. pyrogenes. Immunized rabbits were challenged intradermally with a mixture of F. necorphorum and C. pyrogenes. Initially a low level of initial transient resistance could be demonstrated but a solid immunity could not be established.

Animals

Evaluation of experimentally induced Fusobacterium necrophorum infections in mice.

Two strains of mice, Swiss Webster and DBA/2Cr, were injected intraperitoneally or intravenously with varying dosages of Fusobacterium necrophorum. The ability to eliminate the infection was assessed by quantitative enumeration of the organisms present in the blood, liver, and spleen, Three- to 4-week-old DBA/2Cr mice were highly resistant to both routes of injection. The intraperitoneal injection of older mice failed to demonstrate a dose-effect relationship whereas an intravenous injection of as few as 10(4) cells of F. necrophorum produced progressively necrotic leg abscesses, apparently involving the lymphonodus ischiadicus which filters the site of injection. Mortality was increased with sensitization by a previous sublethal injection. Also, an ethanol-killed cell vaccine delayed the onset of lethal infection, whereas repeated sublethal live cell injections provided nonspecific protection since mice vaccinated with the growth medium were equally protected. The development of leg abscesses after intravenous injection visibly demonstrated the pathogenicity of F. necrophorum and may provide a suitable model for the evaluation of vaccines and the effectiveness of antibiotics.

Age Factors

Hepatic lesions and bacterial changes in mice during infection of Fusobacterium necrophorum.

Liver abscesses were induced in male albino mice within 1 week after intraperitoneal inoculation of viable Fusobacterium necrophorum LA19 culture. Fusobacteremia was transitory and reached a peak 2 h after inoculation then sharply declined until its disappearance 24 h post inoculation. By contrast, the number of fusobacteria in the liver increased rapidly during the first 4 h post inoculation and continued to do so less rapidly until the last sampling time (48 h post inoculation). There were small or large areas of necrosis, usually surrounded by inflammatory cells, small focal accumulations of lymphocytes, plasma cells, and macrophages in areas of parenchyma with no degenerations, generalized proliferation of Kupffer cells, and a few accumulations of fibrin and leukocytes on the surface. Ultrathin sections of infected liver tissues reveled both intact and partially degraded F. necrophorum cells enclosed in phagocytic and digestive vacuoles of mononuclear cells, The results indicate that macrophages play a key role in the pathogenesis of liver abscesses.

Animals

Effects of minocycline and other antibiotics on Fusobacterium necrophorum infections in mice.

Several antibiotics were evaluated in model infections produced in mice with each of two strains of Fusobacterium necrophorum. In one model, local abscesses occurred at the site of subcutaneous injection; in another intra-abdominal abscesses were produced when the organisms were injected into the peritoneal cavity. Treatment with effective antibiotics prevented the formation of abscesses or minimized the size of the lesions. Several treatment schedules were used. Minocycline was the most active antibiotic of the seven agents tested against both strains and in both models. Clindamycin was equal to minocycline against one strain with certain multiple dose treatment schedules and less active with others. Protective effects in mice were achieved with serum levels of minocycline and clindamycin that appear to be clinically achievable. Doxycycline was less active than minocycline, and tetracycline was relatively ineffective, as were cephalexin, ampicillin and penicillin G.

Animals

Fusobacterium necrophorum infection in mice as a model for the study of liver abscess formation and induction of immunity.

A mouse model is described in which intraperitoneal injection of Fusobacterium necrophorum results in chronic liver abscesses. Viable bacterial counts from mouse lung, liver, and spleen were obtained after whole organ homogenization. From 2 h to 5 days postchallenge, liver was found to contain more bacteria than lung on a per gram basis. Bacterial counts from liver and spleen were about the same during the first 8 h; thereafter liver was found to contain more bacteria. By day 13, though bacterial counts were equivalent in the three organs, abscesses were only observed in liver. This predilection for the liver may be due to a nutritional and/or microenvironmental factor(s). Blood cultures of infected mice revealed a general lack of bacteremia. Extended immunization with formalin-killed cells was found to protect mice against F. necrophorum infection.

Animals

A simple method for rapid identification of Sphaerophorus necrophorus isolates.

A hemagglutination inhibition test for the rapid identification of Sphaerophorus necrophorus is described. Erythrocytes from six species of animals were tested and human cells were found to be the best agglutination indicators. Antiserum prepared in rabbits was found to be specific for S. necrophorus hemagglutinins when tested against 20 isolates of S. necrophorus and 117 other bacteria belonging to 22 genera. The possibility of using a hemagglutination inhibition test for the detection of bovine necrobacillosis was explored.

Animals

Pediatric osteomyelitis: III. anaerobic microorganisms.

Primary osteomyelitis consequent to obligate anaerobic microorganisms represents an infrequently encountered type of infection in pediatric patients. Unlike osteomyelitis caused by more common microorganisms such as Staphylococcus, children with osseous lesions due to anaerobic microorganisms are frequently minimally symptomatic and rarely present the classic signs of fulminant osteomyelitis. Radiographically, the lesions may mimic malignant osseous tumors. Fastidious microbiologic analysis of the material obtained at surgery is necessary to isolate obligate anaerobes. Basic treatment, comprising surgical drainage and appropriate antimicrobial agents, does not differ from that for osteomyelitis caused by aerobic or by facultative anaerobic microorganisms.

Adolescent

Clindamycin and gentamicin for aerobic and anaerobic sepsis.

Thirty-eight adult patients with serious pleuropulmonary, soft-tissue, bone, and intra-abdominal infections caused by combinations of aerobic, facultative, and anaerobic bacteria were treated with parenterally given clindamycin phosphate and gentamicin sulfate and surgery when appropriate. Nine had associated bacteremia. In 29, infections failed to respond to other therapeutic regimens, which included penicillins, cephalosporins, aminoglycosides, and chloramphenicol. Results with clindamycin and gentamicin were excellent and were attributed primarily to the activity of clindamycin against anaerobes, particularly Bacteroides fragilis. Serum concentrations of clindamycin surpassed by manyfold the minimal inhibitory concentrations (MICs) for anaerobes. Serum concentrations of gentamicin did not consistently surpass the MICs for Enterobacteriaceae and Pseudomonas aeruginosa, although those organisms were consistently gentamicinsusceptible by disk diffusion susceptibility tests. Persistent colonization with Enterobacteriaceae, P aeruginosa, enterococci, or Candida were common, and occasionally they were significant in prolonging the clinical courses of patients with extensive infections.

Adolescent