Actinobacillus ureae may be a critical pathogen in patients with predispositions: A case report and review of the literature.

RATIONALE: Actinobacillus ureae (A. ureae) is an unusual commensal of human respiratory flora, rarely causing human infection. The predisposing factors, identification, clinical features, and antibiotic therapy of A. ureae are seldomly reported. Herein, we present a case of 64-year-old man affected by A. ureae pneumonia after intracranial surgery. PATIENT CONCERNS AND DIAGNOSES: A 64-year-old male was admitted with vomiting, drowsiness, and a severe disturbance of consciousness and was later diagnosed with cerebral hemorrhage by computed tomography images. After a craniocerebral surgery, the patient suffered from intractable pneumonia, experiencing treatment failure with multiple anti-bacterial agents. Sputum culture yield pure colonies of A. ureae, confirmed by matrix-assisted laser desorption/ionization time of flight and 16S rRNA gene sequencing. INTERVENTIONS: Minocycline (100 mg p.o. per 12 hours) with a course of 15 days was administrated for this patient. OUTCOMES: The respiratory symptoms, presenting as intermittent coughing with purulent and yellowish sputum, were gone. A 3-month follow-up examination showed a complete resolution of radiological findings. LESSONS: Clinically, the actual incidence of A. ureae pneumonia may be higher than that we generally recognized, and clinicians should consider A. ureae as a possible etiologic agent in patients with predispositions. Currently, A. ureae may be susceptible to penicillin, ampicillin, and third-generation cephalosporins. Other antibacterial agents, such as tetracycline, amoxicillin/clavulanic acid, and aminoglycosides also respond well and can be a choice in the treatment of A. ureae infections.

Tea Polyphenols Protects Tracheal Epithelial Tight Junctions in Lung during Actinobacillus pleuropneumoniae Infection via Suppressing TLR-4/MAPK/PKC-MLCK Signaling.

Actinobacillus pleuropneumoniae (APP) is the causative pathogen of porcine pleuropneumonia, a highly contagious respiratory disease in the pig industry. The increasingly severe antimicrobial resistance in APP urgently requires novel antibacterial alternatives for the treatment of APP infection. In this study, we investigated the effect of tea polyphenols (TP) against APP. MIC and MBC of TP showed significant inhibitory effects on bacteria growth and caused cellular damage to APP. Furthermore, TP decreased adherent activity of APP to the newborn pig tracheal epithelial cells (NPTr) and the destruction of the tight adherence junction proteins ß-catenin and occludin. Moreover, TP improved the survival rate of APP infected mice but also attenuated the release of the inflammation-related cytokines IL-6, IL-8, and TNF-α. TP inhibited activation of the TLR/MAPK/PKC-MLCK signaling for down-regulated TLR-2, TLR4, p-JNK, p-p38, p-PKC-α, and MLCK in cells triggered by APP. Collectively, our data suggest that TP represents a promising therapeutic agent in the treatment of APP infection.

Caspase-1 inhibitor reduced the lung injury in a mouse model of pleuropneumonia caused by Actinobacillus pleuropneumoniae.

The pathogenesis of porcine contagious pleuropneumonia is poorly understood. In the present study, a mouse model of intranasal infection by Actinobacillus pleuropneumoniae (App) was used to examine lung inflammation. The pathogical results of lung tissues showed that App-infected mice showed dyspnea and anorexia, with severe damage by acute hemorrhage, and infiltration of eosinophils and lymphocytes, as well as increased expression of caspase-1 p20, interleukin (IL)-1ß, IL-6, IL-8, IL-18 and tumor necrosis factor (TNF)-α. Caspase-1 inhibitors reduced both lung tissue damage and the expression of caspase-1 p20, IL-1ß, IL-6, IL-8, TNF-α and IL-18 in infected mice. These findings suggest that the caspase-1 dependent pyroptosis involved in the pathogenesis of the mouse pleuropneumonia caused by App and the inhibition of caspase-1 reduced the lung injury of this pleuropneumonia.

Experimental arthritis exacerbates Aggregatibacter actinomycetemcomitans-induced periodontitis in mice.

AIM: This study aimed to investigate whether chronic antigen-induced arthritis (AIA) influences infection-induced periodontitis (PD) in mice and whether PD modifies the clinical course of AIA. The contribution of anti-TNF-α therapy was also evaluated. MATERIALS AND METHODS: The PD was induced in C57BL/6 mice by oral infection with Aggregatibacter actinomycetemcomitans. AIA was induced after infection. Anti-TNF-α and chlorhexidine therapies were used to investigate the role of TNF-α and oral infection on PD and AIA interaction. Maxillae, knee joints, lymph nodes and serum samples were used for histomorphometric, immunoenzymatic and/or real time-PCR analyses. RESULTS: Antigen-induced arthritis exacerbated alveolar bone loss triggered by PD infection. In contrast, PD did not influence AIA in the evaluated time-points. PD exacerbation was associated with enhanced production of IFN-γ in maxillae and expression of the Th1 transcription factor tBET in submandibular lymph nodes. Increased serum levels of IL-6 and C-reactive protein were also detected. Anti-TNF-α and antiseptic therapies prevented the development and exacerbation of infectious-PD. Anti-TNF-α therapy also resulted in reduced expression of IFN-γ, TNF-α and IL-17 in maxillae. CONCLUSIONS: Altogether, the current results indicate that the exacerbation of infection-induced PD by arthritis is associated with an alteration in lymphocyte polarization pattern and increased systemic immunoreactivity. This process was ameliorated by anti-TNF-α and antiseptic therapies.

A.actinomycetemcomitans-induced periodontal disease promotes systemic and local responses in rat periodontium.

AIM: To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection. MATERIAL & METHODS: Wistar rats infected with Aa were evaluated for antibody response, oral Aa colonization, loss of attachment, PMN recruitment, TNF-α in the junctional epithelium and connective tissue, osteoclasts and adaptive immune response in local lymph nodes at baseline and 4, 5 or 6 weeks after infection. Some groups were given antibacterial treatment at 4 weeks. RESULTS: An antibody response against Aa occurred within 4 weeks of infection, and 78% of inoculated rats had detectable Aa in the oral cavity (p < 0.05). Aa infection significantly increased loss of attachment that was reversed by antibacterial treatment (p < 0.05). TNF-α expression in the junctional epithelium followed the same pattern. Aa stimulated high osteoclast formation and TNF-α expression in the connective tissue (p < 0.05). PMN recruitment significantly increased after Aa infection (p < 0.05). Aa also increased the number of CD8(+) T cells (p < 0.05), but not CD4(+) T cells or regulatory T cells (Tregs) (p > 0.05). CONCLUSION: Aa infection stimulated a local response that increased numbers of PMNs and TNF-α expression in the junctional epithelium and loss of attachment. Both TNF-α expression in JE and loss of attachment was reversed by antibiotic treatment. Aa infection also increased TNF-α in the connective tissue, osteoclast numbers and CD8(+) T cells in lymph nodes. The results link Aa infection with important characteristics of periodontal destruction.

In vitro efficacy of diallyl sulfides against the periodontopathogen Aggregatibacter actinomycetemcomitans.

The in vitro antibacterial effects of diallyl sulfide (DAS) against the Gram-negative periodontopathogen Aggregatibacter actinomycetemcomitans, the key etiologic agent of the severe form of localized aggressive periodontitis and other nonoral infections, were studied. A. actinomycetemcomitans was treated with garlic extract, allicin, or DAS, and the anti-A. actinomycetemcomitans effects of the treatment were evaluated. Garlic extract, allicin, and DAS significantly inhibited the growth of A. actinomycetemcomitans (greater than 3 log; P < 0.01) compared to control cells. Heat inactivation of the garlic extracts significantly reduced the protein concentration; however, the antimicrobial effect was retained. Purified proteins from garlic extract did not exhibit antimicrobial activity. Allicin lost all its antimicrobial effect when it was subjected to heat treatment, whereas DAS demonstrated an antimicrobial effect similar to that of the garlic extract, suggesting that the antimicrobial activity of garlic extract is mainly due to DAS. An A. actinomycetemcomitans biofilm-killing assay performed with DAS showed a significant reduction in biofilm cell numbers, as evidenced by both confocal microscopy and culture. Scanning electron microscopy (SEM) analysis of DAS-treated A. actinomycetemcomitans biofilms showed alterations of colony architecture indicating severe stress. Flow cytometry analysis of OBA9 cells did not demonstrate apoptosis or cell cycle arrest at therapeutic concentrations of DAS (0.01 and 0.1 µg/ml). DAS-treated A. actinomycetemcomitans cells demonstrated complete inhibition of glutathione (GSH) S-transferase (GST) activity. However, OBA9 cells, when exposed to DAS at similar concentrations, showed no significant differences in GST activity, suggesting that DAS-induced GST inhibition might be involved in A. actinomycetemcomitans cell death. These findings demonstrate that DAS exhibits significant antibacterial activity against A. actinomycetemcomitans and that this property might be utilized for exploring its therapeutic potential in treatment of A. actinomycetemcomitans-associated oral and nonoral infections.

Invasive infections of Aggregatibacter (Actinobacillus) actinomycetemcomitans.

BACKGROUND/PURPOSE: Aggregatibacter (Actinobacillus) actinomycetemcomitans, part of the normal flora of the mouth, is frequently found in human periodontal cultures and is an important pathogen causing various invasive infections, particularly infective endocarditis. In this study, we describe the clinical course and outcome of patients with A. actinomycetemcomitans infection. METHODS: All patients suffering invasive A. actinomycetemcomitans infections at the National Taiwan University Hospital from January 1985 to December 2004 were included in this study. Relevant data regarding clinical presentation, antimicrobial treatment and outcome of these patients were analyzed. RESULTS: During the study period, there were 11 patients with invasive A. actinomycetemcomitans infections, including eight patients with infective endocarditis, one with osteonecrosis and two with pneumonia and chest wall lesions. Among the patients with infective endocarditis, four had prosthetic valve replacement, four suffered from rheumatic heart disease and one had undergone surgical repair of ventricular septal defect. Lesions in the oral cavity were the probable portals of entry of the microorganism, and included carious teeth, periodontitis or radiotherapy of the ear-nose-throat field, and were noted in nine patients. Transthoracic echocardiography and/or transesophageal echocardiography were performed on the patients with probable infective endocarditis but growth was demonstrated in only four of these patients. Blood culture yielded A. actinomycetemcomitans after prolonged incubation. Three isolates were resistant to penicillin and two of these were also resistant to ampicillin. CONCLUSION: The diagnosis of invasive A. actinomycetemcomitans infection was delayed due to the indolent clinical course, non-specific presentation and slow growth of the organism. Antibiotic therapy using amoxicillin/clavulanic acid, ampicillin, ampicillin/sulbactam, ceftriaxone, clindamycin, cefotaxime, or levofloxacin was successful in all patients. None of the patients demonstrated recurrence of infection 2-36 months following treatment.

Actinobacillus (Aggregatibacter) actinomycetemcomitans (HACEK) identified by PCR/16S rRNA sequence analysis from the heart valve in a patient with blood culture negative endocarditis.

We report a case of infective endocarditis caused by Actinobacillus actinomycetemcomitans (Aggregatibacter actinomycetemcomitans) from the HACEK group diagnosed by PCR/16S from the heart valve. Multiple blood cultures and cultures from heart valve were negative and cardiac surgery was performed due to therapeutic and cardiac failures. Molecular biological methods are useful in such a patient, to choose an optimal antibiotic treatment post-surgery.

Interleukin 6, serum amyloid A and haptoglobin as markers of treatment efficacy in pigs experimentally infected with Actinobacillus pleuropneumoniae.

The possibility to use acute phase proteins to monitor the elimination of a bacterial infection in pigs would facilitate an objective assessment of treatment with various antimicrobial substances. To examine this possibility, the acute phase response (IL-6, serum amyloid A (SAA), and haptoglobin) elicited by Actinobacillus pleuropneumoniae and its reduction on treatment with various antibiotics was studied in serum from specific pathogen free (SPF) pigs. Pigs were infected intranasally with A. pleuropneumoniae serotype 2, and either left as non-treated control pigs or treated with different antibiotics intramuscularly at onset of respiratory disease (20h post-infection). Pigs responded to the infection with prominent increases in activity and concentrations of IL-6, SAA, and haptoglobin. These responses were to a certain extent overlapping and covered the time span from a few hours after infection until development of detectable levels of specific antibodies (7-10 days post-infection in untreated pigs). The haptoglobin response lasted until the end of the study on day 17 and thereby partly coincided with the antibody response. Treatment with antimicrobials that effectively reduced establishment of the infection with A. pleuropneumoniae also reduced the duration of all three acute phase responses, and reduced the concentration of serum haptoglobin. In contrast, less efficacious treatments did not reduce these acute phase responses. Thus, acute phase reactants can be applied to monitor therapeutic effects of antimicrobial drugs in the pig and measurements of IL-6, SAA and haptoglobin could add valuable information about the stage of infection during a disease outbreak.

Putative biomarkers for evaluating antibiotic treatment: an experimental model of porcine Actinobacillus pleuropneumoniae infection.

Biomarkers of infection were screened for their possible role as evaluators of antibiotic treatment in an aerosol infection model of porcine pneumonia caused by Actinobacillus pleuropneumoniae (Ap). Following infection of 12 pigs, clinical signs of pneumonia developed within 20 h, whereafter the animals received a single dose of either danofloxacin (2.5mg/kg) or tiamulin (10 mg/kg). To test the discriminative properties of the biomarkers, the dosage regimens were designed with an expected difference in therapeutic efficacy in favour of danofloxacin. Accordingly, the danofloxacin-treated pigs recovered clinically within 24h after treatment, whereas tiamulin-treated animals remained clinically ill until the end of the study, 48 h after treatment. A similar picture was seen for the biomarkers of infection. During the infection period, plasma C-reactive protein (CRP), interleukin-6 and haptoglobin increased, whereas plasma zinc, ascorbic acid and alpha-tocopherol decreased. In the danofloxacin-treated animals, CRP, interleukin-6, zinc, ascorbic acid and alpha-tocopherol reverted significantly towards normalisation within 24h of treatment. In contrast, signs of normalisation were absent (CRP, zinc and ascorbic acid) or less marked (interleukin-6 and alpha-tocopherol) in the tiamulin-treated animals. Plasma haptoglobin remained elevated throughout the study in both groups. This indicates that CRP, zinc, ascorbic acid and to a lesser extent interleukin-6 and alpha-tocopherol might be used to evaluate antibiotic treatment of acute Ap-infection in pigs. The present model provides a valuable tool in the evaluation of antibiotic treatments, offering the advantage of clinical and pathological examinations combined with the use of biochemical infection markers.

Postoperative infection with Actinobacillus spp in horses: 10 cases (1995-2000).

OBJECTIVE: To determine features of postoperative wound infection caused by Actinobacillus spp in horses undergoing clean, elective surgery and to evaluate bacterial susceptibility profiles of bacteria isolated. DESIGN: Retrospective study. ANIMALS: 10 horses. PROCEDURE: Data were retrieved from medical records and the microbiology laboratory database. RESULTS: 1,604 horses underwent clean, elective surgical procedures during the study period. Of these, 23 (1.43%) had postoperative wound infections, and Actinobacillus spp was isolated from 10 of these 23 (43%). Surgical procedures in these 10 horses included laryngoplasty with ventriculocordectomy (n = 3), arthroscopy (3), desmotomy of the accessory ligament of the superficial digital flexor tendon (2), removal of laryngoplasty prostheses (1), and hygroma resection (1). Seven horses survived, and 3 were euthanatized. All 10 Actinobacillus isolates were resistant to penicillin, and 6 were resistant to trimethoprim-sulfamethoxazole. All isolates were susceptible to ceftiofur and gentamicin. During the 5-year period of the study, Actinobacillus organisms were isolated from 35 of 513 (6.8%) samples from the general hospital population submitted for bacterial culture and antimicrobial susceptibility testing. CONCLUSIONS AND CLINICAL RELEVANCE: During the study period, Actinobacillus spp was isolated from a higher than expected percentage of horses that developed postoperative wound infections after clean, elective surgery. Susceptibility profiles for these isolates were different from typical susceptibility profiles for Actinobacillus isolates, suggesting that a pattern of resistance may be emerging.

Effects of pentoxifylline on inflammatory cytokine expression and acute pleuropneumonia in swine.

Pentoxifylline, a methylxanthine derivative and nonspecific type 4 phosphodiesterase inhibitor, has been used to improve survival of animals with sepsis and to attenuate lung injury in acute lung inflammation. The purpose of this study was to examine whether pentoxifylline would inhibit the expression of inflammatory cytokines, particularly tumor necrosis factor alpha (TNF), and thereby decrease the pathophysiology of acute porcine pleuropneumonia. E. coli lipopolysaccharide (LPS) and bacterial extracts of A. pleuropneumoniae--induced elevations in TNF mRNA which were fully abrogated by addition of pentoxifylline in both alveolar macrophage and neutrophil cultures. A 30% reduction in the level of LPS-induced interleukin (IL)-1beta mRNA levels also was achieved in macrophages. Pentoxifylline did not affect either IL-1alpha or IL-8 expression in vitro. Pentoxifylline therapy in vivo significantly reduced the number of band neutrophils in swine but did not reduce the pathology associated with pleuropneumonia, including changes in serum zinc, iron, or haptoglobin. Neither did it alter TNF, IL-1, IL-6, or IL-8 expression. Measurement of pentoxifylline and its metabolites in pig sera suggested that efficacious doses of pentoxifylline were probably not achieved in vivo. However, subcutaneous doses of pentoxifylline higher than 25 mg/kg produced transient diarrhea, vomiting, and tremors. These results suggest that pentoxifylline is an effective pharmacological tool for the dissection of cytokine regulation in vitro, but inhibitory concentrations may not be achievable for in vivo pharmacological use in swine.

Actinomyces and actinobacillus actinomycetemcomitans-Actinomyces-associated lymphadenopathy mimicking lymphoma.

We present 2 unusual cases of long-standing, extensive reactive lymphadenopathy secondary to Actinomyces infection, 1 of which was also accompanied by Actinobacillus actinomycetemcomitans-Actinomyces complex infection. To our knowledge, histologic features of lymph node involvement by these organisms have not been previously reported in the literature. One patient had extensive cervical, posterior mediastinal, and abdominal lymphadenopathy. The second patient presented with a submandibular mass and cervical lymphadenopathy. Clinical features strongly suggested lymphoma. The histologic examination of the lymph nodes from both patients revealed reactive follicular hyperplasia, marked interfollicular and capsular fibrosis, and multiple interfollicular microabscesses. Characteristic Actinomyces colonies were identified at the center of the microabscesses in deep sections. Cultures were obtained from the lymph nodes of 1 patient, and were positive for A actinomycetemcomitans. Both patients had poor dental hygiene. Lymphadenopathy subsided with antibiotic therapy and appropriate dental care.

Fluoroquinolones in the treatment of Actinobacillus actinomycetemcomitans-associated periodontitis.

BACKGROUND: Periodontitis patients harboring Actinobacillus actinmycetemcomitans (Aa) are prime candidates for systemic antibiotic therapy. Besides tetracycline and the combination of metronidazole and amoxicillin the fluoroquinolones are also believed to have antibacterial activity against Aa. The aim of the present study was to evaluate systemic ofloxacin therapy as adjunct to flap surgery. METHODS: Twenty-five adult periodontitis patients with subgingival detection of Aa were treated with 2x200 mg/d ofloxacin for 5 days as adjunct to open flap surgery (test). Another 10 patients received only flap surgery (control). Probing depth (PD) and clinical attachment level (CAL) was recorded and subgingival plaque samples were cultivated on TSBV agar for detection of Aa at baseline as well as 3 and 12 months following therapy. RESULTS: At 3 and 12 months following therapy mean PD at monitored sites in the test group changed from 6.8 mm (+/-1.3) to 3.6 mm (+/-1.0), 3.8 mm (+/-1.1) and CAL from 7.5 mm (+/-1.4) to 5.4 mm (+/-1.4), 5.5 mm (+/-1.3). In the control group PD changed from 6.5 mm (+/-0.7) to 4.0 mm (+/-1.7), 4.1 mm (+/-1.6) and CAL from 7.5 mm (+/-1.0) to 6.3 mm (+/-1.7), 6.4 mm (+/-1.8). P was <0.05 for CAL between groups. Three and 12 months following adjunctive systemic ofloxacin therapy, Aa was suppressed below detectable levels in 22 of 22, test patients, whereas Aa could not be recovered in only 2 of the 10 controls. (P<0.0001). CONCLUSIONS: Systemic ofloxacin as adjunct to open flap surgery is able to suppress A. actinomycetemcomitans below detectable level in patients harboring this organism at baseline.

[Subacute endocarditis caused by Actinobacillus actinomycetemcomitans]. / Endocarditis subaguda por Actinobacillus actinomycetemcomitans.

BACKGROUND: We describe the cases of endocarditis caused by Actinobacillus actinomycetemcomitans (EAA) observed at our hospital. PATIENTS AND METHODS: We revised clinical records and microbiological documents from patients admitted at our hospital, with A. actinomycetemcomitans in blood cultures occurred from 1972-1998. We used Dukes's diagnostic criterion of infectious endocarditis. RESULTS: Four patients were diagnosed of EAA for twelve years, there were males and two females. Two cases have had valvular prosthesis and three patients suffered a previous odontological manipulation. All cases were clinical subacute presentation. Two patients have had at a distance endocarditis clinical manifestation (neurological deficit and Osler nodules). All patients were febrile and elevation of acute reactants, two cases had inflammatory anemia and one had cardiac failure. We observed growing signs after 7 days of culture and it was necessary, on solid medium, adequate atmosphere and nutritional composition to procure A. actinomycetemcomitans growing. All isolates were susceptible to studied penicillins or aminopenicillins (except one isolate with intermediate susceptibility), aminoglycosides and quinolones. Treatment with penicillin G, lone or combined with aminoglycosides, controlled infection in three patients. No case needed cardiac surgery. CONCLUSIONS: In our experience, EAA is a strange entity and there isn't a previous cardiac disease always. Usually, the place of entrance is a buccal focus. Subacute-chronic course and, sometimes, uncommon, can delay diagnostic during months. Our isolates have an uniform sensibility to penicillins and others betalactamic, anyway aminoglycosides and quinolones, therefore an antibiotic combination of two antibiotics from these families at least could be the choice treatment. Except evolutive complications in some patient, prognostic has been excellent with only antibiotic treatment, without valvular surgery.

Evaluation of various cytokines (IL-6, IFN-alpha, IFN-gamma, TNF-alpha) as markers for acute bacterial infection in swine--a possible role for serum interleukin-6.

A total of 64 specific pathogen free pigs were divided into eight experimental groups. Pigs in Group I served as non-infected controls while the other 56 pigs were infected intranasally with approximately 7 x 10(8) CFU of Actinobacillus pleuropneumoniae serotype 2 (strain 700/89) in 1 ml saline. When more than 25% of the infected animals showed clinical signs of disease, i.e. 20 h post infection, 48 of the infected pigs were treated with different antibiotics (8 pigs per group), leaving 8 infected animals untreated. Serum samples collected 0, 10, 20, 28 and 44 h, and 3, 4, 7, 13 and 17 days post infection were analysed for their content of interferon (IFN)-alpha, IFN-gamma, tumor necrosis factor (TNF)-alpha by immunoassays and interleukin-6 (IL-6) by a bioassay. In addition, the development of specific antibodies was determined in sera. Among the cytokines analysed, the experimental infection only induced detectable serum levels of IL-6. The appearance of IL-6 positive animals coincided with the onset of clinical signs of disease and increased body temperatures. Varying levels of IL-6 (range, 1-220 U ml-1) were detected in serum from a majority of the infected pigs (80%). In general, the highest levels of IL-6 were detected in serum collected for 10 or 20 h after infection. Among the animals not treated with antibiotics, the number of pigs displaying IL-6 in serum continued to increase until 28 h post infection and then declined. The duration of the IL-6 response varied between individuals and lasted from eight hours to three days. Treatment with antibiotics that ceased the infection also terminated the IL-6 production in most of the pigs. In a pilot field survey, IL-6 was detected in an approximately 30% of serum samples collected from conventional reared pigs before allocation to finishing units. Thus, serum IL-6 seems to be a potential marker for ongoing bacterial infections in swine.

Avaliaçäo clínica e microbiológica da utilizaçäo da doxiciclina no tratamento de pacientes com periodontite juvenil / Clinical and microbiological evaluation of the utilization of doxycycline in the treatment of patients with juvenile periodontitis

Esta pesquisa se propôs avaliar a resposta clínica e microbiológica frente a um tratamento periodontal sequenciado em dois grupos de pacientes, um submetido à raspagem e outro à raspagem e antibiótico. Observou-se a resposta frente à raspagem (análise 1-0), os resultados da manutençäo com e sem antibiótico (análise 2-1) e a terapia mais efetiva em retardar a recidiva clínica e microbiológica (análise 3-2). Os dados obtidos permitiram concluir que com o estabelecimento de terapias de manutençäo com raspagem näo houve diferenças clínicas significantes entre os grupos com e sem antibiótico. O antibiótico foi incapaz de eliminar totalmente o actinobacillus actinomycetemcomitans, sendo mais eficiente na eliminaçäo dos microrganismos BANA positivos nas bolsas periodontais com o passar do tempo

Bone marrow infection caused by Actinobacillus ureae in a rheumatoid arthritis patient.

A patient with rheumatoid arthritis is described who presented with low-grade fever for 3 months, in whom Actinobacillus ureae was cultured from bone marrow aspirate. Fever responded favourably to penicillin therapy. It is the first reported isolation of A. ureae from bone marrow.

Actinobacillus actinomycetemcomitans pneumonia with chest wall and subphrenic abscess.

A 14-year-old girl had progressive dyspnea and right lower chest pain for about 1 1/2 months and a weight loss of 3 kg in 2 months. Chest X-ray revealed right pleural effusion and a round infiltration over the right lower chest, initially suspected to be malignant. Image study revealed consolidation in the right middle and lower lobes with abscess-like lesions around the right lower pleura and transdiaphrenic involvement to the subphrenic region. The lesion had also invaded the intercostal muscle. The pleural abscess was obtained by fiberoptic thoracoscopy, and culture of the pus grew typical colonies of Actinobacillus actinomycetemcomitans. After the causative microorganism had been identified, cefoxitin was given for 2 weeks followed by oral amoxicillin (250 mg/6 h) for a total period of 3 months. Follow-up chest X-ray revealed resolution of the lung lesions and the patient recovered gradually without any sequelae.

Transdiaphragmatic Actinobacillus actinomycetemcomitans infection: case report.

To our knowledge, we report the first case of transdiaphragmatic Actinobacillus actinomycetemcomitans infection in which the patient presented with an abdominal tumor. The clinical manifestation of this infection was similar to that of Actinomyces israelii infection and was initially misinterpreted as a malignancy. The actual diagnosis was made following prolonged culture of the biopsy specimen of the involved tissue. The pathogen was susceptible to penicillin, ampicillin, tetracycline, cephalosporins, metronidazole, aminoglycosides, and quinolones. The patient was treated with a combination of amoxicillin and norfloxacin, and 3 months later his condition had clinically improved.