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We report a case of Lemierre's syndrome due to Fusobacterium nucleatum in a previously healthy 19-year-old male. This is the first case report of Lemierre's syndrome due to thrombophlebitis of the external jugular vein. The patient had a rapid clinical response to anticoagulation and antibiotics, as supported by anecdotal evidence.
A rare case of a thyroid abscess due to mixed anaerobic flora containing Fusobacterium mortiferum in an immunocompetent patient is described. The patient was successfully treated with immediate surgical intervention and appropriate antimicrobial agents.
BACKGROUND: Bacteria are implicated in certain forms of model chronic colitis but the identity and role of bacteria in human ulcerative colitis (UC) are uncertain. AIMS: To isolate pathogenic bacteria from inflamed mucosa of patients with UC, to examine whether the bacteria have a toxin to Vero cells, and to determine whether the toxin induces UC-like lesions in animals. METHODS: Bacteria were isolated from UC patients and supernatants from cultures were filtered and tested for cytotoxicity to Vero cells. Bacterial cells producing the cytotoxic supernatants were examined by polymerase chain reaction for verotoxin genes. Culture supernatants of cytotoxic strains were examined by high performance liquid chromatography for organic acid concentrations. Mice were given enemas containing organic acid at the mean concentration in the supernatants of cytotoxic strains to ascertain whether colonic lesions appear in UC. RESULTS: Only supernatants from cultures of Fusobacterium varium killed Vero cells. Bacterial cells lacked verotoxin genes. Bacterial culture supernatants contained high concentrations of n-butyric acid and the mean concentration (32 mmol/l) was cytotoxic to Vero cells. Twenty four hours after mice were given enemas containing either butyric acid or F varium culture supernatants, colonic ulcers with crypt abscesses, inflammatory cell infiltration, and apoptotic changes were observed. CONCLUSIONS: Butyric acid in culture supernatants from cultures of F varium caused UC-like lesions in mice. This study indicates that F varium may be one of the elusive pathogenic factors in UC.
A fatal case of meningitis due to Bacteroides fragilis and Fusobacterium necrophorum is reported. This appears to be the first case in which meningitis due to these organisms was not secondary to a disease elsewhere in the body. The organisms are difficult to culture and strict anaerobic methods should be used whenever they are suspected. Intravenous metronidazole is probably the antibiotic of choice.
A 23 year old woman died within six hours of admission from acute disseminated intravascular coagulation. Fusobacterium necrophorum, a Gram negative anaerobic organism, was isolated as a single pathogen from the blood cultures. This association has not previously been reported.
We report the case of a young man with Fusobacterium necrophorum meningitis who developed bilateral carotid artery stenosis associated with thrombosis of the cavernous sinuses. Intraluminal clot was present in the region of the stenoses for which he was anticoagulated. The clinical presentation, problems with diagnosis, the use of anticoagulation and the need for prolonged treatment with metronidazole are discussed.
Wallabies (Macropus rufogriseus) were not appreciably more susceptible than rabbits or mice to Fusobacterium necrophorum, a fact established by the subcutaneous injection of a series of graded doses into animals of each species. The strikingly frequent occurrence of necrobacillosis in captive macropods is therefore not due to a uniquely high susceptibility. A vaccine containing inactivated F necrophorum culture emulsified with Freund's complete adjuvant failed to increase the resistance of wallabies to subcutaneous challenge with a moderate dose of the homologous strain. The control of necrobacillosis in captive wallabies must therefore depend on managemental measures aimed at minimising faecal contamination of the environment and damage to the buccal mucous membrane and skin.
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.
Our objective was to study the immune response to 2 anaerobic bacteria in patients with chronic maxillary sinusitis. Immunoglobulin G class antibody titers to Fusobacterium nucleatum and Prevotella intermedia were measured by enzyme-linked immunosorbent assay. Serum levels in the patients were determined on the day sinus aspiration for culture was done, and 75 to 90 days later, after completion of antimicrobial therapy, Prevotella intermedia was isolated from 16 aspirates, and F. nucleatum from 12. Median antibody levels at day 1 for F. nucleatum and P. intermedia were significantly higher in patients whose serum aspirates harbored these organisms than at days 75 to 90 in those who were cured (p < .05). However, the levels stayed elevated in the 5 patients who did not improve. The elevated antibody levels to F. nucleatum and P. intermedia, known oral pathogens, suggest a potential pathogenic role for these organisms in chronic maxillary sinusitis.
The foot-pad test was performed to reveal the induction of delayed-type hypersensitivity (DTH) to Fusobacterium necrophorum in mice experimentally infected with F. necrophorum. For the foot-pad test, heat-killed cells of F. necrophorum were found to be better than viable bacteria as eliciting antigens. The thickness of foot-pad could be measured properly at 48 hr after administration to the foot-pad of heat-killed bacteria. An intraperitoneal dose of the order of 10(5) or 10(6) of viable bacteria evoked a similar foot-pad response. Peak responses were found on days 4 and 14 after the sensitization. The response was found to be specific. This response could be transferred by spleen cells to genetically homogeneous mice, but not to genetically heterogeneous mice. Serum could not transfer the response to either heterogeneous or homogeneous mice. Thus, these results indicate that DTH could be induced by F. necrophorum.
A 37-day-old male Japanese black calf showing marked salivation and leucocytosis died and was examined the tissues histologically. Histological lesions were characterized by severe focal necrotic glossitis on the ventral side of the root of the tongue. Immunohistochemically, Fusobacterium necrophorum subsp. necrophorum antigen was detected in the necrotic tissues and its distribution corresponded to that of the gram-negative, nonsporeforming, long filamentous organisms. Ultrastructural similarities between the organism and F. necrophorum subsp. necrophorum, but not subsp. funduliforme were observed. These findings clearly demonstrated that the fatal necrotic glossitis was caused by F. necrophorum subsp. necrophorum. This is the first report of bovine fatal necrotizing glossitis with leucocytosis caused by F. necrophorum subsp. necrophorum infection, and this organism may be an important fatal pathogen in calves with glossal lesions.
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.
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.
The genetic diversity of 23 oral Fusobacterium nucleatum isolated from 15 periodontal patients, eight from seven healthy subjects, nine from nine AIDS patients and two from two Cebus apella monkeys were analyzed. EcoRI restricted the bacterial DNA and 28 ribotypes grouped from A to J groups were obtained. Isolates formed 24 ribotypes which were contained into A, B, C, D, E and F groups, and three reference strains and two clinical isolates of A. actinomycetemcomitans, and E. coli CDC formed four different ribotypes into the G, H, I and J groups. Moreover, from nine F. nucleatum from AIDS patients, six were ribotyped as group C and three as group D. By using ribotyping we distinguished F. nucleatum recovered from different sources. It is possible that isolates from AIDS patients may contain some phenotypic or genotypic factor did not observed in this study.
The relationship between serum-neutralizing antibody against Fusobacterium necrophorum leukotoxin and hepatic abscesses was investigated in cattle fed diets supplemented with or without tylosin. Sixteen cattle (eight each in tylosin and in control groups) were inoculated intraportally with F. necrophorum. Ultrasonographic scanning showed that all control animals developed hepatic abscesses after inoculation. In the tylosin group, two animals were free of abscess by d 7 and one was free by d 14. Leukotoxin-neutralizing antibody titers were low on d 0, but increased (P < .05) markedly after intraportal inoculation in both groups. In a second study, blood was collected at the time of slaughter from 141 feedlot cattle (36 fed diets with tylosin and 105 fed diets without tylosin), and livers were examined for presence or severity of hepatic abscesses at slaughter. The incidences of hepatic abscesses were 32% in the control group and 6% in the tylosin group. Antibody was detected in all animals; however, antibody titers were greater (P < .05) in cattle with abscessed liver than those without, and greater (P < .01) in the nontylosin than in the tylosin group. Abscess score and antibody titer were correlated (r = .34; P < .0001). We conclude that F. necrophorum leukotoxin is highly antigenic and that anti-leukotoxin antibody titer is related to the severity of hepatic abscesses.
A previously healthy 42-year-old man developed, after a neglected tonsillitis, a severe Fusobacterium necrophorum septicemia with disseminated intravascular coagulation. Peripheral, painful, cyanotic and gangrenous lesions appeared on toes, external ears and nose tip. The patient survived. Consumption coagulopathy associated with tonsillitis should suggest F. necrophorum infection. Growth of these bacteria in blood cultures is slow and confirmation of the infection may thus be delayed.
Three chemotherapy-induced neutropenic hematologic patients with severe systemic infection caused by Fusobacterium nucleatum, a Gram-negative anaerobic rod, are described. Anaerobic infections are not very common in this patient category, but in a short period of time, several such patients were seen. The infection was considered to be caused by a combination of chemotherapy-induced mucositis, which served as a portal of entry for the systemic infection, and the antibiotic regime used in these patients. This is a serious infection with a high mortality. In hematological neutropenic patients suffering from severe mucositis and fever, antibiotic therapy should cover anaerobic bacteria.
We describe a case in which recurrent vertebral osteomyelitis and psoas abscess due to Streptococcus constellatus and Fusobacterium nucleatum developed in a patient with a previously unrecognized atrial septal defect with bidirectional shunts. Disease recurrence was ascribed to the presence of dental disease, which served as the source of infection. To the best of our knowledge, this is the first case in which vertebral osteomyelitis and psoas abscess have been associated with atrial septal defect.