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PubMed2003

Increased diagnosis of Lemierre syndrome and other Fusobacterium necrophorum infections at a Children's Hospital.

OBJECTIVE: To assess the apparent increase in the diagnosis of Lemierre syndrome (LS) and other Fusobacterium necrophorum infections at a large children's hospital. Infections with F necrophorum ranged from peritonsillar abscess to potentially fatal LS. LS is an oropharyngeal infection characterized by septic thrombophlebitis of head and neck veins, complicated by dissemination of septic emboli to pulmonary and systemic sites. METHODS: Review of the medical and laboratory records was conducted of all patients who were seen at or admitted to the Children's Hospital of Wisconsin with the diagnosis of LS and/or isolation of F necrophorum from a clinical specimen between January 1995 and January 2002. RESULTS: During the 7-year period of the study, there was an increase in the isolation of F necrophorum from patients who were seen at Children's Hospital of Wisconsin, as well as the number of cases of LS. There was 1 isolation of F necrophorum from clinical specimens per year from 1996 to 1999, which increased to 10 isolates of the organism from January 2000 to January 2002. During the most recent period, January 2001-January 2002, 5 cases of LS were diagnosed, a distinctive entity not recognized previously at the institution. CONCLUSIONS: The cause for the recent increase in the number of serious infections caused by F necrophorum infection diagnosed at our institution is unclear but does not seem to be related to changes in microbiologic techniques or patient demography. We speculate that it could be attributable, in part, to alterations in antibiotic usage patterns in our region. Clinicians need to be aware of the increasing clinical importance of F necrophorum infections and the life-threatening nature of LS.

Adolescent↗
PubMed1977

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↗
PubMed2002

[Retrospective analysis of Fusobacterium associated infections; experience at Aomori Prefectural Hospital with 108 cases from 1995 to 1999].

We experienced 108 cases of Fusobacterium associated infections, including otolaryngeal, oral, pleuropulmonary, intraabdominal, skin and soft tissue infections, at Aomori Prefectural Hospital during The 5 year-period from 1995 to 1999. A total of 433 organisms, included 113 Fusobacterium spp. (80 Fusobacterium nucleatum, 18 Fusobaterium necrophorum, 5 Fusobacterium varium, 4 Fusobacterium mortiferum, 6 Fusobacterium spp.), were recovered with an average of 4.0 organisms per case of the 108 cases, 68% were mixed aerobic and anaerobic and yielded 185 anaerobic bacteria (2.5 per case) and 137 aerobic bacteria (1.9 per case) with an average of 4.4 per case. The remaining 32% were purely anaerobic and yielded 111 organisms with an average of 3.2 per case, Prevotella spp., Bacteroides fragilis group, Streptococcus milleri group, Enterobacteriaceae, Peptostreptococcus spp. Staphylococcus spp. were most frequently coisolated with Fusobacterium spp.

Adult↗
PubMed1991

Further observations on enhancement of the infectivity of Fusobacterium necrophorum by other bacteria.

It had already been shown with a single virulent strain (A42) of Fusobacterium necrophorum that suspension of the fusobacteria in sub-lethal doses of broth cultures of other bacteria reduced the minimum infective dose (greater than 10(6) organisms) for mice by subcutaneous inoculation, sometimes to less than 10 organisms. The present study extended the known range of bacteria with strong infectivity-enhancing properties to include Bacillus cereus, Klebsiella oxytoca and Staphylococcus aureus; and those with weaker effect to include Bacillus subtilis, 'Bacteroides melaninogenicus', Clostridium sporogenes, Pasteurella haemolytica, and Proteus mirabilis. The study also showed that five further virulent strains of F. necrophorum closely resembled A42 in respect of striking susceptibility to infectivity enhancement by Escherichia coli. Actinomyces (Corynebacterium) pyogenes and S. aureus. One further strain (A6) of F. necrophorum resembled A42 in respect of strong infectivity enhancement by A. pyogenes, S. aureus, B. cereus and K. oxytoca but differed from it and the other five strains in being only slightly affected by E. coli. This work was a necessary prelude to the development of a method, based on infectivity enhancement, for the detection and isolation of F. necrophorum present in small numbers in heavily contaminated material such as faeces.

Actinomycosis↗
PubMed2005

Molecular diagnosis of Fusobacterium necrophorum infection (Lemierre's syndrome).

Presented here is the case of a 27-year-old male with atypical features of Lemierre's syndrome in which a definitive diagnosis was achieved using molecular methods. While routine investigations, including bacterial cultures, were unhelpful, two real-time PCR assays demonstrated Fusobacterium necrophorum-specific DNA in aspirates from brain and renal abscesses. This is the first report demonstrating that a laboratory diagnosis can be made using molecular methods in suspected cases of Lemierre's syndrome. Use of these methods can thus resolve diagnostic confusion, prevent unnecessary investigation, and direct specific antimicrobial treatment.

Adult↗
PubMed2005

Fusobacterium necrophorum infection associated with portal vein thrombosis.

This report describes a patient without obvious upper respiratory tract or gastrointestinal infection who developed portal vein thrombosis secondary to Fusobacterium necrophorum septicaemia. The patient responded well to systemic antibiotic therapy. The implications of F. necrophorum infection caudal to the head are discussed.

Anti-Bacterial Agents↗
PubMed2004

Fibrinonecrotic rhinitis caused by a concurrent infection of Fusobacterium necrophorum and Arcanobacterium pyogenes in a cow.

An 8 year-old cow showing severe dyspnea and nasal mucosal necrosis immediately after parturition was subjected to pathological examination. The principal lesions were fibrinonecrotic rhinitis, necrotic bronchopneumonia and renal infarction. Fusobacterium necrophorum biotype A and Arcanobacterium pyogenes antigens were detected in the nasal and pulmonary lesions. These results suggest that the lesions were caused by a concurrent infection of the detected bacteria and that the pulmonary lesions were caused by the aspiration of infectious materials from the nasal ones. Mucosal coagulative necroses observed as the initial lesions in rhinitis were frequently associated with multiple thrombosis. The findings might suggest that thrombosis played an important role in the development of the nasal lesions.

Actinomycetaceae↗
PubMed2005

Human infections with Fusobacterium necrophorum.

Fusobacterium necrophorum is a Gram-negative anaerobic bacillus that can be a primary pathogen causing either localised abscesses and throat infections or systemic life-threatening disease. Systemic infections due to F. necrophorum are referred to as either Lemierre's disease/syndrome, post-anginal sepsis or necrobacillosis, but in the context of this mini-review, all are included under the umbrella term of 'invasive F. necrophorum disease' (IFND). Although IFND has been well documented for over a century, it is quite a rare condition and modern-day clinicians of various medical disciplines are frequently unaware of this organism and the severity of symptoms that it can cause. IFND classically occurs in previously healthy young people although the factors that trigger the invasive process are not fully understood. There are countless descriptive case histories and small series of cases of IFND disease in the literature and although commonly referred to as a 'forgotten' disease, in truth, it is probably best described as a repeatedly 'discovered' disease, as it may not always be included in medical curricula, and neither is it mentioned in some major medical textbooks. There is some evidence that IFND may be on the increase, particularly in the UK. The potential reasons for this are considered in this review along with an historical overview, and updates on disease incidence, patient demography, pathogenesis and laboratory diagnosis.

Adolescent↗
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↗
PubMed1989

Enhancement of the infectivity of Fusobacterium necrophorum by other bacteria.

Necrobacillosis is caused by Fusobacterium necrophorum (FN), but other organisms are often present in the lesions. Their possible role was studied in experiments made with a virulent FN strain which, by itself, produced fatal necrobacillosis in mice provided that large doses (greater than 10(6) organisms, subcutaneously) were given. Mice were inoculated subcutaneously with FN suspended in sub-lethal doses (0.1 ml) of undiluted or diluted broth cultures of other bacteria. Undiluted culture of a strain of Escherichia coli reduced the infective dose of FN to less than 10 organisms; in the necrobacillosis lesions that developed, fusobacteria greatly outnumbered E. coli. A heat-killed preparation or sterile filtrate of E. coli culture had little if any effect on FN. Citrobacter freundii and comparatively small numbers of Corynebacterium (Actinomyces) pyogenes produced effects similar to that of E. coli. An alpha-haemolytic streptococcus, Pseudomonas aeruginosa, Bacteroides fragilis and Fusobacterium nucleatum also enhanced the infectivity of FN, though less strikingly than E. coli. FN increased the persistence in vivo of the alpha-haemolytic streptococcus and B. fragilis, and enabled the latter to multiply profusely.

Animals↗
PubMed2005

Fusobacterium necrophorum infections in animals: pathogenesis and pathogenic mechanisms.

Fusobacterium necrophorum, a Gram-negative, non-spore-forming anaerobe, is a normal inhabitant of the alimentary tract of animals and humans. Two subspecies of F. necrophorum, subsp. necrophorum (biotype A) and subsp. funduliforme (biotype B), have been recognized, that differ morphologically, biochemically, and biologically. The subsp. necrophorum is more virulent and is isolated more frequently from infections than the subsp. funduliforme. The organism is an opportunistic pathogen that causes numerous necrotic conditions (necrobacillosis), either specific or non-specific infections, in a variety of animals. Of these, bovine liver abscesses and foot rot are of significant concern to the cattle industry. Liver abscesses arise with the organisms that inhabit the rumen gaining entry into the portal circulation, and are often secondary to ruminal acidosis and rumenitis complex in grain-fed cattle. Foot rot is the major cause of lameness in dairy and beef cattle. The pathogenic mechanism of F. necrophorum is complex and not well defined. Several toxins or secreted products, such as leukotoxin, endotoxin, hemolysin, hemagglutinin, proteases, and adhesin, etc., have been implicated as virulence factors. The major virulence factor appears to be leukotoxin, a secreted protein of high molecular weight, active specifically against leukocytes from ruminants. The complete nucleotide sequence of the leukotoxin operon of F. necrophorum has been determined. The operon consists of three genes (lktBAC) of which the second gene (lktA) is the leukotoxin structural gene. The leukotoxin appears to be a novel protein and does not share sequence similarity with any other leukotoxin. F. necrophorum is also a human pathogen and the human strains appear to be different from the strains involved in animal infections.

Journal Article↗
PubMed2000

Endotoxin-triggered haematological interactions in Fusobacterium necrophorum infections.

The haematological mechanisms in the course of liver abscess formation were evaluated. They were examined by employing viable cells of Fusobacterium necrophorum subsp. necrophorum and Fusobacterium necrophorum subsp. funduliforme in comparison with their endotoxins. Whole cell infection with F.n. necrophorum led to neutrophilia and to a concomitant monocytosis in parallel with those responses induced by the in vivo injection of its endotoxin. Viable infection with F.n. funduliforme was characterized by a sustained endotoxin-related monocytosis against neutropenia. The stimulatory impact of endotoxin on monocytes when released from a viable F.n. funduliforme infection suggested an inherently peculiar mechanism which differed from the induction of both neutrophilia and monocytosis when F.n. funduliforme endotoxin was administered alone. The neutrophilic inducing capacity of the F.n. necrophorum endotoxin was equally illustrated by its positive chemotactic effect on polymorphonuclear neutrophils in vitro. The data presented here emphasize the virulence of F.n. necrophorum viewed in reference to changes in leucocyte trafficking and as complemented by a relatively high endotoxin content.

Animals↗
PubMed2002

Fusobacterium necrophorum infections in England and Wales 1990-2000.

In response to a marked increase in both the number of Fusobacterium necrophorum bacteraemia reports to the PHLS Communicable Disease Surveillance Centre and the number of F. necrophorum isolates referred to the PHLS Anaerobe Reference Unit in 1999, the data from both sources on F. necrophorum infections were reviewed for the decade 1990-2000. There were 208 reports of F. necrophorum bacteraemia (average 19/year; range 14-34/year) with a peak in incidence in the late winter months; 68% were from male patients and the peak age range was 16-23 years. Of 205 referred isolates of F. necrophorum, 122 (59%) were from blood cultures and these represented 58% of the bacteraemia reports; the others were from brain and soft tissue abscesses, pleural and joint fluids, eyes, ears and lymphatic tissue. The average number of referrals was 19/year (range 9-37/year). The peak year for bacteraemia reports (34) and isolate referrals (37) was 1999; this increase was not sustained in 2000. All isolates were susceptible to metronidazole, but 2% were resistant to penicillin and 15% to erythromycin. F. necrophorum continues to be a regular but uncommon cause of bacteraemia and metastatic abscesses following an acute sore throat, especially in young, otherwise healthy adults.

Abscess↗
PubMed1977

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↗
PubMed2005

Efficacy of vaccination against Fusobacterium necrophorum infection for control of liver abscesses and footrot in feedlot cattle in western Canada.

A randomized and blinded field trial was carried out to evaluate the efficacy of a Fusobacterium necrophorum bacterin for control of liver abscesses and footrot under commercial feedlot conditions in western Canada. Half of the vaccinated and half of the unvaccinated control animals had ad libitum access to a forage-based (ALF) growing diet. The other half of each group was limit-fed a grain-based (LFG) growing diet. The overall prevalence of A and A+ liver abscesses in this trial was 16.7%. A strong association was found between diet group and presence of A or A+ liver abscessation at slaughter. Diet group modified the effect of vaccination on the prevalence of liver abscesses at slaughter, and on the incidence of footrot during the feeding period. The odds that a vaccinated animal in the ALF group would have an A or A+ liver abscess at slaughter were less than 1/3 the odds that an unvaccinated animal in the same diet group would have an A or A+ liver abscess at slaughter (OR = 0.27, [95% CI: 0.07 to 1.02], P = 0.05). The overall incidence of footrot in this trial was 6.5%. The odds that a vaccinated animal in the ALF group would be treated for footrot were less than 1/5 the odds that an unvaccinated animal in the same group would be treated for foot-rot (OR = 0.18, [95% CI: 0.04 to 0.82], P = 0.03). Within the LFG group there were no differences between vaccinated and unvaccinated animals in the odds of an animal being treated for footrot, or in the odds of having an A or A+ liver abscess score at slaughter. This trial suggests that vaccination against F. necrophorum infection may have applications to decrease the prevalence of severe liver abscesses at slaughter and decrease footrot treatments in certain diet situations.

Animals↗
PubMed1975

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↗