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PubMed2004

The participation of nitric oxide in peritoneal exudate cell cytotoxicity of mice by Fusobacterium nucleatum.

Previously we reported that mice infected recurrently with live Fusobacterium nucleatum(Fn) synthesize a significant amount of NO between 12 hr and 24 hr after Fn injection. Fn is a gram-negative rod periodontal pathogen. NO could not be induced by heat-killed Fn or in untreated mice. This NO, derived from the iNOS after infection of live Fn, was not involved in the Fn reduction because Fn clearance occurs within 6 hr. We investigated in this study whether this NO was involved in cytotoxicity in peritoneal exudate cells (PEC) in vivo. The mice were divided into two groups: those treated with live Fn (immune) and those left untreated (normal). PEC number, NO production, detection of apoptosis or death cells, and lactate dehydrogenase (LDH) release activity after injection of live Fn were compared in these groups. In the immune group, the increase of the total cell numbers caused by an increase in neutrophils, a significant NO production only after injection of live Fn at 24 hr and identification of iNOS positive macrophages were confirmed. The apoptotic rate was very low and did not increase at 24 hr in vivo. Therefore, apoptosis was seldom relevant to the NO. In the immune group, LDH activity was remarkable high at 24 hr, and dead cells and macrophages phagocytizing cell fragments increased at the same time. Pretreatment of L NMMA, an inhibitor of iNOS, suppressed LDH activity and cell death. Therefore, the NO derived from the iNOS is involved in the cytotoxicity. These results suggest that NO may contribute to the inflammatory response during Fn infection in periodontitis.

Animals↗

PubMed1990

Fusobacterium necrophorum hemolysin in bovine hepatic abscess.

An immunofluorescence study was made on bovine hepatic abscess containing Fusobacterium necrophorum predominantly. The abscess section stained with anti F. necrophorum hemolysin serum demonstrated fluorescence which formed irregular and granular shapes. Actinomyces pyogenes isolates from the abscess were not stained with the serum. These findings suggest that the bacterial hemolysin contributes to the formation of the hepatic abscess during an infection with F. necrophorum.

Animals↗

PubMed1990

Necrobacillosis--primary anaerobic septicaemia due to Fusobacterium necrophorum.

Necrobacillosis is a severe septicaemic illness caused by an anaerobic Gram-negative bacillus, Fusobacterium necrophorum. It occurs predominantly in young people and is characterised by oropharyngeal infection and subsequent metastatic complications, frequently involving the lungs and/or large joints. We report four recent cases in previously healthy young men, describing the clinical features of the disease (including autopsy findings), and the problems associated with diagnosis and treatment.

Adolescent↗

PubMed2000

Isolation and characterization of a human neutrophil aggregation defective mutant of Fusobacterium nucleatum.

Fusobacterium nucleatum is known to adhere to human polymorphonuclear neutrophils (PMNs) and cause them to aggregate. In this study, we isolated a spontaneously occurring aggregation defective (AGG(-)) mutant and this mutant will be used for future study of the interactions between this bacterium and human PMN. Genomic DNA fingerprinting by random-primed polymerase chain reaction method revealed a difference between the parent strain and the AGG(-) mutant. This mutant also showed an altered phenotype in both microbicidal and phagocytic assays, suggesting that the bacterial factor involved in the aggregation may also be very important for the phagocytosis and, subsequently, the killing by human PMNs. Further study of this mutant may help to clarify the molecular mechanisms of the interaction between this pathogen and human PMNs.

Bacterial Adhesion↗

PubMed1985

Cultural characteristics and virulence of strains of Fusobacterium necrophorum isolated from the feet of cattle and sheep.

Sixty-one isolates of Fusobacterium necrophorum were recovered for study. Thirty-one were obtained from lesions of foot abscess in cattle (25) and sheep (6), 28 were from interdigital lesions in cattle and 2 were from the normal interdigital skin of cattle. The majority of isolates from lesions of foot abscess were virulent, belonged to biotype AB (Fievez 1963), produced flat, irregular shaped, greyish colonies and haemolysis on blood agar, and grew as turbid filamentous suspensions in liquid media. They produced a soluble exotoxin, a leucocidin, and were pathogenic for cattle and mice. Virulent isolates also produced a haemolysin which most readily lysed bovine, equine and chicken erythrocytes; those from sheep were less susceptible while those of rabbit and pig were the most resistant. Isolates recovered from lesions of the feet not classified as foot abscess and from clinically normal feet were predominantly of the B biotype and caused few experimental lesions, produced convex, round, yellow colonies, flocculated and sedimented while growing in liquid medium and produced little or no haemolysin or leucocidin. Routine differentiation between virulent and non-virulent bovine isolates of F. necrophorum could be achieved by assessing the colour, morphology, and degree of haemolytic activity of colonies grown on blood agar.

Abscess↗

PubMed1985

The role of Fusobacterium necrophorum and Bacteroides melaninogenicus in the aetiology of interdigital necrobacillosis in cattle.

When cultures of known pathogenic strains of Fusobacterium necrophorum, isolated either from cattle or sheep were injected through the interdigital skin of cattle typical lesions of interdigital necrobacillosis were produced. The inclusion of Bacteroides melaninogenicus in the inoculum did not appear to contribute to the development of lesions.

Abscess↗

PubMed2005

Genetic determinant of intrinsic quinolone resistance in Fusobacterium canifelinum.

Fourteen fluoroquinolone-resistant fusobacterial strains, originating from cats or dogs, were characterized by sequencing of the 16S-23S and 16S rRNA genes and DNA-DNA hybridization and were described as a new species, Fusobacterium canifelinum. All of the strains are intrinsically resistant (MIC, >4 g/ml) to levofloxacin and other fluoroquinolones. Compared to the quinolone resistance-determining region (gyrA) of the susceptible relative F. nucleatum, we found that Ser79 was replaced with leucine and Gly83 was replaced with arginine.

Amino Acid Sequence↗

PubMed1974

Chemotherapy of an experimental Fusobacterium (Sphaerophorus) necrophorum infection in mice.

An experimental animal model for testing antibiotics in vivo against Fusobacterium (Sphaerophorus) necrophorum has been developed. It incorporates the subcutaneous injection of the bacteria into mice followed by intraperitoneal administration of the antibiotic at 24, 48, 72, and 96 h. Mean effective dose values are based on the number of survivors 21 days after challenge. Tetracycline was the most effective drug tested, with a mean effective dose of 5.0 mg/kg, compared with mean effective dose values of 11.1 for clindamycin, 11.8 for penicillin-G, and 52.9 for lincomycin.

Animals↗

PubMed1997

Ribotyping to compare Fusobacterium necrophorum isolates from bovine liver abscesses, ruminal walls, and ruminal contents.

Restriction fragment length polymorphism analysis of rRNA genes was employed to genetically compare Fusobacterium necrophorum subsp. necrophorum and F. necrophorum subsp. funduliforme isolates from multiple abscesses of the same liver and isolates from liver abscesses, the ruminal wall, and ruminal contents from the same animal. Four livers with multiple abscesses and samples of ruminal contents, ruminal walls, and liver abscesses were collected from 11 cattle at slaughter. F. necrophorum was isolated from all liver abscesses, nine ruminal walls, and six ruminal content samples. Chromosomal DNA of the isolates was extracted and single or double digested with restriction endonucleases (EcoRI, EcoRV, SalI, and HaeIII); then restriction fragments were hybridized with a digoxigenin-labeled cDNA probe transcribed from a mixture of 16S and 23S rRNAs from Escherichia coli. EcoRI alone or in combination with EcoRV yielded the most discriminating ribopatterns for comparison. Within the subspecies multiple isolates from the same liver were indistinguishable based on the ribopattern obtained with EcoRI. The hybridization patterns of liver abscess isolates were concordant with those of the corresponding isolates from ruminal walls in eight of nine sets of samples. None of the six ruminal content isolates matched either the liver abscess isolates or the ruminal wall isolates. The genetic similarity between the isolates from liver abscesses and ruminal walls supports the hypothesis that F. necrophorum isolates of liver abscesses originate from the rumen.

Animal Feed↗

PubMed1996

Taxonomy, biology, and periodontal aspects of Fusobacterium nucleatum.

The pathogenic potential of Fusobacterium nucleatum and its significance in the development of periodontal diseases, as well as in infections in other organs, have gained new interest for several reasons. First, this bacterium has the potential to be pathogenic because of its number and frequency in periodontal lesions, its production of tissue irritants, its synergism with other bacteria in mixed infections, and its ability to form aggregates with other suspected pathogens in periodontal disease and thus act as a bridge between early and late colonizers on the tooth surface. Second, of the microbial species that are statistically associated with periodontal disease, F. nucleatum is the most common in clinical infections of other body sites. Third, during the past few years, new techniques have made it possible to obtain more information about F. nucleatum on the genetic level, thereby also gaining better knowledge of the structure and functions of the outer membrane proteins (OMPs). OMPs are of great interest with respect to coaggregation, cell nutrition, and antibiotic susceptibility. This review covers what is known to date about F. nucleatum in general, such as taxonomy and biology, with special emphasis on its pathogenic potential. Its possible relationship to other periodontal bacteria in the development of periodontal diseases and the possible roles played by OMPs are considered.

Amino Acid Sequence↗

PubMed1977

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↗

PubMed1984

Monocyte suppression of Fusobacterium nucleatum-induced human polyclonal B-lymphocyte activation.

Previous studies reported that Fusobacterium nucleatum induced polyclonal B-lymphocyte activation (PBA) as determined by immunoglobulin M production in cultures of human peripheral blood mononuclear cells. However, the PBA response was greatly enhanced when the cells were depleted of esterase-positive, adherent cells (i.e., monocytes). The purpose of this study was to confirm and further examine the suppression of F. nucleatum-induced PBA (F. nucleatum-PBA) by blood monocytes. For comparison, PBA induced by pokeweed mitogen (PWM-PBA), which is enhanced by monocytes, was assessed in some experiments. We found the removal of monocytes from unfractionated cells by (i) Sephadex G-10, (ii) anti-monocyte specific OM-1 monoclonal antibody plus complement, or (iii) L-leucine methyl ester, a compound which selectively kills lysosome-rich cells, resulted in a population of cells responsive to F. nucleatum-PBA and unresponsive to PWM-PBA. The addition of double adherence-purified monocytes (greater than 85% esterase-positive cells), particularly in concentrations of greater than 10%, to lymphocytes depleted of monocytes by G-10, OM-1, or L-leucine methyl ester treatments, suppressed F. nucleatum-PBA and enhanced PWM-PBA. Monocytes also suppressed a mixture of isolated T and B cells combined in a T/B cell ratio of 3:1, which is an optimal ratio for F. nucleatum-PBA. Allogeneic monocytes suppressed F. nucleatum-PBA, although at low numbers these cells were not as suppressive as autologous monocytes. Heating at 56 degrees C for 15 min, sonicating, or freeze-thawing the monocyte preparations resulted in an abrogation of monocyte-induced suppression of F. nucleatum-PBA. Kinetic studies in which fresh monocytes were added daily to lymphocytes stimulated with F. nucleatum or PWM showed that the monocytes must be added within the first 2 days of culture to suppress F. nucleatum-PBA or enhance PWM-PBA. Monocytes incubated with F. nucleatum for 48 h released into the culture medium a soluble factor that suppressed F. nucleatum-PBA. The results from this study demonstrate a potent mechanism by which the host might prevent exaggerated nonspecific immunoglobulin responses when exposed to PBA-inducing concentrations of F. nucleatum. On the other hand, the induction of suppressive monocytes (or monocyte-mediated suppressive factors) by interaction with F. nucleatum might result in the inhibition of host protective immune reactions.

Antibody Formation↗

PubMed1996

Mixed infection with Porphyromonas gingivalis and Fusobacterium nucleatum in a murine lesion model: potential synergistic effects on virulence.

These studies determined the characteristics of tissue destruction in a murine abscess model elicited by mixed infection with the periodontopathogens Fusobacterium nucleatum and Porphyromonas gingivalis. The interbacterial effects of this synergism, the kinetics of the relationship of the bacterial interaction, and the characteristics of the bacteria required for the tissue destruction were studied. Infection of mice with P. gingivalis and F. nucleatum strains elicited lesions of various sizes as a function of infective dose. Primary infection with F. nucleatum plus P. gingivalis at various ratios (i.e., <1:1) resulted in a significantly greater lesion size (P < 0.001) compared with that resulting from primary infection with P. gingivalis alone. At F. nucleatum/P. gingivalis ratios of > or = 1:1, spreading lesion formation and progression were significantly (P < 0.001) decreased, suggesting that bacterial interaction (i.e., coaggregation) may have inhibited the spread of the P. gingivalis infection to a site distant from the initial injection. Infection with F. nucleatum and P. gingivalis simultaneously (at different sites) or F. nucleatum administered within 4 h prior to or 1 h following P. gingivalis infection significantly enhanced the ability of P. gingivalis to form large phlegmonous lesions. Chemical inhibition of the P. gingivalis trypsin-like protease activity or the use of a trypsin-negative P. gingivalis strain abrogated tissue destruction either alone or in combination with F. nucleatum. Therefore, it was possible to examine aspects of virulence of these pathogens in a murine lesion model by either altering bacterial ratios, manipulating the time of infection, or targeting vital bacterial virulence factors.

Animals↗

PubMed2004

Fusobacterium nucleatum induces premature and term stillbirths in pregnant mice: implication of oral bacteria in preterm birth.

Fusobacterium nucleatum is a gram-negative anaerobe ubiquitous to the oral cavity. It is associated with periodontal disease. It is also associated with preterm birth and has been isolated from the amniotic fluid, placenta, and chorioamnionic membranes of women delivering prematurely. Periodontal disease is a newly recognized risk factor for preterm birth. This study examined the possible mechanism underlying the link between these two diseases. F. nucleatum strains isolated from amniotic fluids and placentas along with those isolated from orally related sources invaded both epithelial and endothelial cells. The invasive ability may enable F. nucleatum to colonize and infect the pregnant uterus. Transient bacteremia caused by periodontal infection may facilitate bacterial transmission from the oral cavity to the uterus. To test this hypothesis, we intravenously injected F. nucleatum into pregnant CF-1 mice. The injection resulted in premature delivery, stillbirths, and nonsustained live births. The bacterial infection was restricted inside the uterus, without spreading systemically. F. nucleatum was first detected in the blood vessels in murine placentas. Invasion of the endothelial cells lining the blood vessels was observed. The bacteria then crossed the endothelium, proliferated in surrounding tissues, and finally spread to the amniotic fluid. The pattern of infection paralleled that in humans. This study represents the first evidence that F. nucleatum may be transmitted hematogenously to the placenta and cause adverse pregnancy outcomes. The results strengthen the link between periodontal disease and preterm birth. Our study also indicates that invasion may be an important virulence mechanism for F. nucleatum to infect the placenta.

Amniotic Fluid↗

PubMed2006

Fusobacterium nucleatum transports noninvasive Streptococcus cristatus into human epithelial cells.

Analysis of human buccal epithelial cells frequently reveals an intracellular polymicrobial consortium of bacteria. Although several oral bacteria have been demonstrated to invade cultured epithelial cells, several others appear unable to internalize. We hypothesized that normally noninvasive bacteria may gain entry into epithelial cells via adhesion to invasive bacteria. Fusobacterium nucleatum is capable of binding to and invading oral epithelial cells. By contrast, Streptococcus cristatus binds weakly to host cells and is not internalized. F. nucleatum and S. cristatus coaggregate strongly via an arginine-sensitive interaction. Coincubation of KB or TERT-2 epithelial cells with equal numbers of F. nucleatum and S. cristatus bacteria led to significantly increased numbers of adherent and internalized streptococci. F. nucleatum also promoted invasion of KB cells by other oral streptococci and Actinomyces naeslundii. Dissection of fusobacterial or streptococcal adhesive interactions by using sugars, amino acids, or antibodies demonstrated that this phenomenon is due to direct attachment of S. cristatus to adherent and invading F. nucleatum. Inhibition of F. nucleatum host cell attachment and invasion with galactose, or fusobacterial-streptococcal coaggregation by the arginine homologue l-canavanine, abrogated the increased S. cristatus adhesion to, and invasion of, host cells. In addition, polyclonal antibodies to F. nucleatum, which inhibited fusobacterial attachment to both KB cells and S. cristatus, significantly decreased invasion by both species. Similar decreases were obtained when epithelial cells were pretreated with cytochalasin D, staurosporine, or cycloheximide. These studies indicate that F. nucleatum may facilitate the colonization of epithelial cells by bacteria unable to adhere or invade directly.

Bacterial Adhesion↗

PubMed1985

Aggregation of platelets by Fusobacterium necrophorum.

Broth cultures and washed cells of 13 of 24 bovine isolates of Fusobacterium necrophorum aggregated human platelets in platelet-rich plasma. The cell-free culture fluid was inactive. Bacteria stored at 4 degrees C in saline remained active for at least 3 months, but they did not release activity into the storage solution. Aggregation typically began within 1 min after the addition of 10(3) bacteria to 10(3) platelets was complete within 5.5 min. Assays for cytosolic lactic dehydrogenase revealed that platelet lysis did not occur. The release of [14C]serotonin from platelets preincubated with this amine accompanied aggregation, indicating that this was a typical aggregation-degranulation reaction. Platelet aggregation was inhibited by EDTA (88% at 2.0 mM), aspirin (75% inhibition at 1.0 mM), and quinacrine (80% inhibition at 0.25 mM). Thus the reaction was an ion-dependent, cyclooxygenase-sensitive event. Gel-filtered platelets were less sensitive to aggregation than were platelets in plasma, but this sensitivity was fully restored by the addition of plasma and partially restored with fibrinogen. Biotyping of the cultures revealed that none of the avirulent, B-type strains of F. necrophorum could aggregate platelets, whereas 13 of 16 virulent A type strains were positive. These results suggest that platelet aggregation by F. necrophorum is related to the virulence of this organism.

Aspirin↗

PubMed1992

Cellular fatty acids in Fusobacterium species as a tool for identification.

Identification of fusobacteria from clinical specimens currently requires analysis of metabolic end products by gas-liquid chromatography in addition to certain biochemical and enzymatic tests because of the relative biochemical inactivity of these bacteria. Even the finding of pointed, thin gram-negative cells on Gram-stained slides can no longer be relied on for identification of Fusobacterium nucleatum, since at least four other species of fusobacteria have been seen to exhibit similar morphology. We examined 46 clinical isolates and six American Type Culture Collection type strains of fusobacteria by conventional methods and by the Microbial ID Systems MIDI software package for analyzing cellular fatty acid patterns measured by capillary column gas-liquid chromatography. Distinctive patterns of major fatty acids could be used to reliably identify most clinical isolates to the species level. The MIDI system identified 89% of the isolates correctly and provides an alternative to conventional methods.

Bacterial Typing Techniques↗

PubMed1993

Polymerase chain reaction-amplified nonradioactive probes for identification of Fusobacterium nucleatum.

A polymerase chain reaction probe with 100% sequence identity to 120 deoxyribonucleotides of Fusobacterium nucleatum Fev1, coding for a part of the 40-kDa major outer membrane protein, was labeled with the steroid hapten digoxigenin. The probe was compared with various degenerate oligonucleotide probes and found to tolerate much more stringent washing conditions. It was therefore superior in distinguishing, by means of Southern blots and slot blots, F. nucleatum from other oral gram-negative bacteria in the periodontal pocket and from other fusobacterial species and in distinguishing among different strains of F. nucleatum. F. periodonticum was found to be more similar to F. nucleatum than the other fusobacterial species tested.

Blotting, Southern↗