Induction Of Abscesses Research Articles

Development of an experimental model for liver abscess induction in Holstein steers using an acidotic diet challenge and bacterial inoculation.

Holstein steers (n = 40; initial BW = 84.9 ± 7.1kg) were used to study the genesis of liver abscesses (LA) using an acidotic diet challenge with or without intraruminal bacterial inoculation. Steers were housed in individual pens inside a barn and randomly assigned to one of three treatments: (1) low-starch control diet comprised primarily of dry-rolled corn and wet corn gluten feed (CON); (2) high-starch acidotic diet with steam-flaked corn (AD); or (3) acidotic diet plus intraruminal inoculation with Fusobacterium necrophorum subsp. necrophorum (9.8 × 108 colony forming units [CFU]/mL), Trueperella pyogenes (3.91 × 109 CFU/mL), and Salmonella enterica serovar Lubbock (3.07 × 108 CFU/mL), previously isolated from LA (ADB). Steers in AD and ADB were fed the acidotic diet for 3 d followed by 2 d of the CON diet, and this cycle was repeated four times. On day 23, ADB steers were intraruminally inoculated with the bacteria. At necropsy, gross pathology of livers, lungs, rumens, and colons was noted. Continuous data were analyzed via mixed models as repeated measures over time with individual steer as the experimental unit. Mixed models were also used to determine the difference in prevalence of necropsy scores among treatments. Ruminal pH decreased in AD and ADB steers during each acidotic diet cycle (P ≤ 0.05). LA prevalence was 42.9% (6 of 14) in ADB vs. 0% in AD or CON treatments (P < 0.01). Ruminal damage was 51.1% greater in ADB than in AD (P ≤ 0.04). Culture of LA determined that 100% of the abscesses contained F. necrophorum subsp. necrophorum, 0% contained T. pyogenes, 50% contained Salmonella, and 50% contained a combination of F. necrophorum subsp. necrophorum and Salmonella. The F. necrophorum subsp. necrophorum was clonally identical to the strain used for the bacterial inoculation based on phylogenetic analysis of the whole genome. This experimental model successfully induced rumenitis and LA in Holstein steers and confirms the central dogma of LA pathogenesis that acidosis and rumenitis lead to the entry of F. necrophorum into the liver to cause abscesses. Our findings suggest that an acidotic diet, in conjunction with intraruminal bacterial inoculation, is a viable model to induce LA. Further research is needed to determine the repeatability of this model, and a major application of the model will be in evaluations of novel interventions to prevent LA.

Intramural esophageal abscess as a complication of an eosinophilic esophagitis

Eosinophilic esophagitis is an important differential diagnosis in the presence of dysphagia or bolus obstruction of the esophagus. Delayed diagnosis of eosinophilic esophagitis can lead to strictures of the esophagus.We report on a young patient who presented with initially unclear retrosternal symptoms to our department. The diagnosis of eosinophilic esophagitis, complicated by an intramural abscess of the esophagus, was established. After spontaneous drainage of the abscess, antibiotic therapy and subsequent remission induction of eosinophilic esophagitis with orodispersible budesonide resulted in a good therapeutic outcome.

Misdiagnosis of peripheral abscess caused by duodenal foreign body: a case report and literature review

BackgroundThe induction of chronic inflammation, perforation, and abscess by foreign bodies (FBs) in adults is uncommon. We present a delayed diagnosis case for a patient who had a fishbone stuck in the duodenal bulb, resulting in chronic abdominal pain for nearly 3 months. We present the diagnosis and treatment procedures for chronic patients, which differ from those for acute and emergency FB ingestion, and also summarize the characteristics of such patients through a systematic literature review.Case presentationA 68-year-old woman was brought to our hospital with repeated right upper abdominal pain lasting for 3 months and aggravation for 9 h. Computed tomography (CT) showed a streaky high-density shadow (approximately 3 cm in length) on the posterior wall of the gastric antrum extending outside the wall. Endoscopic ultrasonography showed hyperechoic space with a cross-section of approximately 0.1 × 0.1 cm in the deep submucosal layer of the local stomach, accompanied by an acoustic shadow in the rear. The possibility of a fishbone as well as perforation was considered and the object was removed using FB forceps. Fasting as well as acid inhibition and anti-infection medication were prescribed for the patient. She eventually recovered and was discharged from the hospital.ConclusionEndoscopic intervention can be recommended as the first option for patients with gastrointestinal FBs.

Rs531564 polymorphism in microRNA-214 regulates interleukin-6R expression in anal fissure patients to affect the risk of anal abscess formation.

Anal abscess is an important complication of anal fissure (AF), whereas interleukin-6R (IL-6R) has been implicated in the development of abscess. In this study, we aimed to explore the possible molecular mechanisms underlying the regulatory effects of miRNAs on IL-6R and other inflammatory factors related to the induction of anal abscess in AF. Bioinformatics analysis, luciferase assay, real-time polymerase chain reaction, and Western blot analysis were performed to identify the possible regulatory relationships between IL-6R and miR-124/miR-125a by comparing the differentiated expression of miR-125a, miR-124, tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), and IL-4 among different groups of AF patients. IL-6R messenger RNA (mRNA) was identified as a target gene of miR-124 because the luciferase activity in cells cotransfected with wild-type IL-6R and miR-124 mimics was significantly reduced. In addition, the expression of IL-6R mRNA and protein was significantly inhibited in the presence of miR-124 or an IL-6R inhibitor, confirming the presence of a negative regulatory relationship between miR-124 and IL-6R. Moreover, miR-124 and inflammatory factors were differentially expressed in AF patients carrying different genotypes of rs531564 polymorphism. miR-124 and inflammatory factors TNF-α, IFN-γ, and IL-4 may be used as indicators of anal abscess development in AF patients. In addition, miR-124 polymorphism rs531564 is involved with the pathogenesis of anal abscess in AF patients, and the presence of rs531564 may increase the incidence of anal abscess via upregulating the expression of IL-6R, TNF-α, IFN-γ, and IL-4.

"CLUPS": A New Culture Medium for the Axenic Growth of Entamoeba histolytica.

Amebiasis remains a major health problem in Mexico. Therefore, the search for better culture media and low-cost diagnostic and therapeutic tools is fundamental. We present a new culture medium for Entamoeba histolytica which allows the microbe to preserve its virulence factors and ability to induce hepatic abscesses in animal models. The novel CLUPS medium is an improved version of the PEHPS medium, previously designed in our laboratory. The main difference is the substitution of raw beef liver in PEHPS by raw beef lung in the CLUPS medium. To compare the performance of three-culture media (traditional TYI-S-33, PEHPS, and CLUPS), E. histolytica trophozoites were cultured in quintuplicate, followed by the evaluation of phospholipase activity and the induction of liver abscesses in golden hamsters. E. histolytica trophozoites grew significantly better in CLUPS medium than in TYI-S-33. Likewise, CLUPS-cultured trophozoites produced significantly more phospholipases than TYI-S-33-cultured trophozoites. Finally, trophozoites grown in any of the three tested media had similar potential to induce liver abscesses.

Induction of Abscess by Non-abscess Producer Staphylococci Using Staphylococcal Fatty Acid Modifying Enzyme (FAME)

Stahpylococcus epidermidis (S. epidermidis), S. warneri and S. aureus subsp. anaerobious were isolated from sheep abscess. Crude FAME was extracted from supernatant fluid of a 24hrs culture of S. aureus subsp. anaerobious grown in Trypticase Soy Broth at 37°C with continuous agitation. Fourteen heads of sheep were used. Three of them were inoculated with S. epidermidis + FAME and other three were inoculated with S. warneri + FAME. Eight animals were divided into four groups, two animals in each, used as control and inoculated with S. epidermidis, S. warneri, S. aureus subsp. anaerobious and FAME. All animals were inoculated subcutaneously at the neck region. After fourteen to eighteen days, sites inoculated with S. epidermidis + FAME, S. warneri + FAME and S. aureus subsp. anaerobious showed abscesses grossly then confirmed bateriologically and histopathologically, while those inoculated with S. epidermidis alone, S. warneri alone and FAME showed no abscess.

Wall teichoic acids mediate increased virulence in Staphylococcus aureus.

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) are the cause of a severe pandemic consisting primarily of skin and soft tissue infections. The underlying pathomechanisms have not been fully understood and we report here a mechanism that plays an important role for the elevated virulence of CA-MRSA. Surprisingly, skin abscess induction in an animal model was correlated with the amount of a major cell wall component of S. aureus, termed wall teichoic acid (WTA). CA-MRSA exhibited increased cell-wall-associated WTA content (WTAhigh) and thus were more active in inducing abscess formation via a WTA-dependent and T-cell-mediated mechanism than S. aureus strains with a WTAlow phenotype. We show here that WTA is directly involved in S. aureus strain-specific virulence and provide insight into the underlying molecular mechanisms that could guide the development of novel anti-infective strategies.

The accessory gene regulator (agr) controls Staphylococcus aureus virulence in a murine intracranial abscesses model

BackgroundIntracranial abscesses are associated with high mortality. Staphylococcus aureus is one of the main pathogens that cause intracranial infection. Until now, there is no report to identify the key effectors of S. aureus during the intracranial infection. MethodsThe murine intracranial abscesses model induced by S. aureus was constructed. The vital sign and survival rate of mice were observed to evaluate the infection. Histological examination was used to diagnose the pathological alterations of mouse tissues. The sensitivity of S. aureus to whole blood was evaluated by whole-blood killing assay. ResultsIn murine intracranial abscesses model, it was shown that the mortality caused by the accessory gene regulator (agr) locus deficient strain was significant decreased compared with its parent strain. Moreover, we found that RNAIII, the effector of agr system, was essential for the intracranial infection caused by S. aureus. In the further investigation, it was shown that restoration the expression of α-toxin in agr deficient strain could partially recover the mortality in the murine intracranial abscesses model. ConclusionOur data suggested that the agr system of S. aureus is an important virulence determinant in the induction and mortality of intracranial abscesses in mice.

Feasibility of magnetic resonance electrical impedance tomography (MREIT) conductivity imaging to evaluate brain abscess lesion:In vivocanine model

To show the feasibility of magnetic resonance electrical impedance tomography (MREIT) conductivity imaging in terms of its capability to provide new contrast information of abscess lesion and characterize time-course variations before and after the induction of brain abscess. Brain abscess was induced in healthy beagles by a direct inoculation method using Staphylococcus pseudintermedius. After the induction, four electrodes were attached on the head and the dog was placed inside the magnetic resonance imaging (MRI) bore. Using a current source, we injected a current of amplitude 5 mA and a pulse width of 81 msec. A multi-echo ICNE pulse sequence was used to obtain the magnetic flux density (Bz ) data. The relative conductivity contrast ratios (rCCR, %) of abscess lesion were significantly changed by the postinduction time (P < 0.01). The rCCRs of central abscess lesions were higher than the surrounding area at 6, 12, and 18 hours (P < 0.01). Over 12 hours, the relationship between the induction time and rCCR showed a positive correlation followed by a negative correlation (P < 0.01). We performed in vivo disease model animal experiments to validate the MREIT technique providing conductivity information of tissues in situ to be utilized in clinical applications.

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Transcutaneous Immunization with the Outer Membrane Protein of P. gingivalis Elicits Long-term Protective Immunity in the Oral Cavity

A previous study showed that transcutaneous immunization with the 40-kDa outer membrane protein of Porphyromonas gingivalis (40k-OMP) elicits humoral immunity that protects from abscess induction by P. gingivalis. In this study, we assessed the potential of 40k-OMP as a transcutaneous vaccine against oral P. gingivalis infection. Transcutaneous immunization of mice with 40k-OMP alone or 40k-OMP plus cholera toxin (CT) elicited 40k-OMP-specific IgG and IgA antibody (Ab) responses in serum and IgG Abs in saliva. These Ab responses were maintained for at least 1 year after immunization, except for serum IgA Abs induced by 40k-OMP alone. Importantly, IgG Abs generated by transcutaneous immunization with 40k-OMP alone, or with 40k-OMP plus CT, inhibited hemagglutinating activity of P. gingivalis. Furthermore, mice transcutaneously immunized with 40k-OMP plus CT, but not 40k-OMP alone, showed significant reduction of alveolar bone loss caused by oral infection with P. gingivalis even 1 year after immunization. These results suggest that 40k-OMP is an effective transcutaneous vaccine against P. gingivalis infection and may be an important tool for the prevention of chronic periodontitis.

Gammagrafía con 99mTc-ceftizoxima en ratas normales y en ratas con absceso inducido

This study aimed to investigate the biodistribution of the 99mTc-ceftizoxime in normal rats and in rats bearing septic and sterile induced abscess. Three groups of rats were studied. a) Six normal rats b) 15 rats with E. coli induced abscess and c) 15 rats with sterile zymosan induced abscess. Septic abscess was induced with 2 x 10(8) colony forming units of E. coli and sterile one with 0.1 mL of 5% sterile Zymosan. 24 h after the abscess induction, 12 MBq of 99mTc-CFT were injected iv. and whole body images were collected at 30 min, 1, 2, 4 and 6 h p.i. Areas of interest were drawn and lesion/background index was calculated. The 6 normal rats were scanned at the same times, killed at 6 h p.i and kidney, liver, spleen, lung, heart and muscle activity were measured. Each organ was weighed, cut and its activity measured. Parallelly, the biological activity of the labeled antibiotic and its binding to the E. coli and S. aureus bacteria were analyzed. High biliary excretion was seen in all rats. Organ measurement showed the maximal uptake in kidney and very low uptake in muscles. Mean +/- s.d abscess/background ratio at 30 min, 1, 2, 4 and 6 h were 2.60 +/- 0.36, 2.67 +/- 0.66, 2.6 0 +/- 0.58, 2.78 +/- 0.84, 3.24 +/- 1.00 for septic abscess and 2.37 +/- 0.39, 2.10 +/- 0.38, 1.97 +/- 0.34, 1.82 +/- 0.25, 1.65 +/- 0.23 for aseptic abscess. The 99mTc-CFT uptake was significantly higher in the septic abscess than in sterile one (p < 0.05). The 99mTc-CFT uptake in the septic abscess remains stable or increases until along the 6 h. The 99mTc-CFT uptake in the aseptic abscess decreases along the time. The scintigraphy with 99mTc-CFT seems able to differentiate sterile inflammation from infection. High biliary excretion limits its application in abdomen. Main application could be diagnosis of osteoarticular infection.

Accumulation of radiolabelled low molecular peptides and proteins in experimental inflammation

This study focuses on evaluating accumulation of the low molecular peptides and proteins labelled with 99mTc in rat inflammatory/infection foci. Peptides (human leukocyte dialysate, HLD; thymosin fraction 5, TF5; aprotinin, APT), and proteins (human IgG, HIG) were labelled with 99mTc using redox polymer. The labelling efficiency was evaluated using paper, TLC and/or column chromatography. Biodistribution of labelled substances was evaluated in rats with Staphylococcus aureus infection or with sterile kaolin suspension inflammation 24 h after abscess induction. Accumulation of 99mTc activity was determinated both by external gamma camera imaging and by counting dissected tissues 4 h after administration. The evaluated peptides and proteins show high labelling efficiency ( 99mTc-HLD > 98%, 99mTc-TF5 > 95%, 99mTc-APT > 98%, 99mTc-HIG > 95%). Usage of redox polymer for labelling increases the stability of 99mTc-labelled substances. The labelling efficiency stays nearly the same (95–98%) after 8 h at least. In experimentally induced inflammation the amount of 99mTc-peptides and 99mTc-HIG activity accumulated is 2.5–6.5 and 5.3–10.6 times higher than in a control tissue. When comparing two types of model inflammations (kaolin- and Staphylococcus-induced ones), the values measured with 99mTc-peptides are more than double than those of kaolin suspension inflammation. The studied low molecular peptides labelled with 99mTc allow rapid localisation of infection foci. 99mTc labelled HIG proved useful for detection of infections and inflammatory lesions.

CD4+ T cells mediate abscess formation in intra-abdominal sepsis by an IL-17-dependent mechanism.

Abscess formation associated with intra-abdominal sepsis causes severe morbidity and can be fatal. Previous studies have implicated T cells in the pathogenesis of abscess formation, and we have recently shown that CD4(+) T cells activated in vitro by zwitterionic capsular polysaccharides from abscess-inducing bacteria such as Staphylococcus aureus and Bacteroides fragilis initiate this host response when transferred to naive rats. In this study, we show that mice deficient in alphabetaTCR-bearing T cells or CD4(+) T cells fail to develop abscesses following challenge with B. fragilis or abscess-inducing zwitterionic polysaccharides, compared with CD8(-/-) or wild-type animals. Transfer of CD4(+) T cells from wild-type mice to alphabetaTCR(-/-) animals reconstituted this ability. The induction of abscesses required T cell costimulation via the CD28-B7 pathway, and T cell transfer experiments with STAT4(-/-) and STAT6(-/-) mice demonstrated that this host response is dependent on STAT4 signaling. Significantly higher levels of IL-17, a proinflammatory cytokine produced almost exclusively by activated CD4(+) T cells, were associated with abscess formation in Th2-impaired (STAT6(-/-)) mice, while STAT4(-/-) mice had significantly lower levels of this cytokine than control animals. The formation of abscesses was preceded by an increase in the number of activated CD4(+) T cells in the peritoneal cavity 24 h following bacterial challenge. Confocal laser-scanning microscopy analysis revealed that CD4(+) T cells comprise the abscess wall in these animals and produce IL-17 at this site. Administration of a neutralizing Ab specific for IL-17 prevented abscess formation following bacterial challenge in mice. These data delineate the specific T cell response necessary for the development of intra-abdominal abscesses and underscore the role of IL-17 in this disease process.

Effects of a Tylosin Tartrate Pellet Added to Cattle Growth Implants on the Incidence of Implant Site Abscesses

The antibacterial effects of tylosin tartrate, added to a cattle growth implant, were evaluated in terms of prevention of implant site abscess formation. An implant site abscess induction model was developed to create implant site abscesses reliably in test animals. This model was then used to test the ability of tylosin tartrate, added as a separate compressed pellet to Component® brand implants (Ivy Animal Health, Overland Park, KS), to reduce implant site abscess incidence in animals expected to develop an ear abscess. Abscesses were induced in all cattle at implanting (d 0). Implant sites were observed on d 6, 10, 16, 21, 28, and 35 post-implantation to determine the presence and severity of an abscess. Three steer implant formulations and two heifer implant formulations, each with and without the tylosin tartrate pellet, were tested. The overall implant site abscess rate was 94.1% in animals that did not receive a tylosin tartrate pellet and 4.2% in animals that received a tylosin tartrate pellet. For each implant at each implant site observation, abscess rate was significantly less (P<0.002) in steers or heifers treated with the tylosin tartrate pellet. Results show that a significantly lesser percentage of ear implant site abscesses are induced if a tylosin tartrate pellet is added to the implant.

A new technique of 99mTc-ciprofloxacin kit preparation

Development of a simple and reproducible method for preparing a ciprofloxacin kit using a redox polymer, which would meet the requirements for an easy and reliable technique of labelling with 99mTc and diagnostic efficiency in scintigraphic imaging of infections. To prepare the kit, an insoluble redox polymer containing an end alpha(beta)-alanine-N,N'-diacetate group anchored to the dextran matrix was used. The redox polymer synthesised by the authors was incubated at room temperature (10 h) with a solution of ciprofloxacin (1%) in a suspension (5%). The mixture was then filtered and dispensed into sterile vials (0.2 ml each). The kit was labelled with 99mTc for 10 min at room temperature. The radiochemical purity of the ciprofloxacin-99mTc complex was determined by ITLC and paper chromatography in relation to the following factors: pH, total content of ciprofloxacin, volume of sodium 99mTc-pertechnetate. Ciprofloxacin biodistribution was evaluated in Wistar rats with Staphylococcus aureus infection in the left inguinal region 24 h after abscess induction. Accumulation of 99mTc activity was determined both using external gamma camera imaging and counting dissected tissues 1 h after administration. Radiochemical purity is > 95% for kit-labelling (pH 3.3-3.7). With pH 3.45, labelled ciprofloxacin shows the highest stability and radiochemical purity. The 99mTc-ciprofloxacin complex is stable for at least 8 h. In experimentally induced inflammation, the amount of accumulated 99mTc-ciprofloxacin activity is five times higher than in controls. The developed method of 99mTc-ciprofloxacin kit preparation employs a redox polymer in a new procedure, which enables the preparation of a stable kit with a high 99mTc-labelling efficiency. The labelled kit is suitable for scintigraphic imaging of infection.

B-Cell deficiency predisposes mice to disseminating anaerobic infections: protection by passive antibody transfer.

We have previously demonstrated that a high proportion of RAG-2 SCID knockout mice, which lack T and B cells, develop orofacial abscesses and disseminated infections following pulpal infection, whereas immunocompetent control mice do not. In the present study, we sought to identify the components of the adaptive immune response which contribute to protection against disseminating anaerobic infections and sepsis. For this purpose, various genetically engineered immunodeficient mice were employed, including RAG-2 SCID, Igh-6 (B-cell deficient), Tcrb Tcrd (T-cell deficient) and Hc(0) (C5 deficient). For abscess induction, the mandibular first molars were subjected to pulp exposure on day 0. Teeth were infected with a mixture of four anaerobic pathogens, including Prevotella intermedia, Streptococcus intermedius, Fusobacterium nucleatum, and Peptostreptococcus micros, and teeth were sealed to prevent communication with the oral cavity. The findings demonstrate that both RAG-2 SCID and B-cell-deficient mice, but not T-cell- or C5-deficient mice, have increased susceptibility to the development of disseminating anaerobic infections. Abscess-susceptible RAG-2 SCID and B-cell-deficient mice also showed a significant loss of body weight, splenomegaly, and absent antibacterial antibody production. Furthermore, dissemination was significantly reduced, from 74 to 25%, in susceptible RAG-2 mice by passively transferred antibody, predominantly immunoglobulin G2b (IgG2b) and IgM, against the infecting bacterial innoculum. Fractionated IgG-enriched preparations were more efficient in transferring protection than IgM preparations. We conclude that an antibody-mediated mechanism(s), most likely bacterial opsonization, is of importance in localizing anaerobic root canal infections and in preventing their systemic spread.

Environmental modulation of oral treponeme virulence in a murine model.

This investigation examined the effects of environmental alteration on the virulence of the oral treponemes Treponema denticola and Treponema pectinovorum. The environmental effects were assessed by using a model of localized inflammatory abscesses in mice. In vitro growth of T. denticola and T. pectinovorum as a function of modification of the cysteine concentration significantly enhanced abscess formation and size. In contrast, growth of T. denticola or T. pectinovorum under iron-limiting conditions (e.g., dipyridyl chelation) had no effect on abscess induction in comparison to that when the strains were grown under normal iron conditions. In vivo modulation of the microenvironment at the focus of infection with Cytodex beads demonstrated that increasing the local inflammation had no effect on lesion induction or size. In vivo studies involved the determination of the effects of increased systemic iron availability (e.g., iron dextran or phenylhydrazine) on the induction, kinetics, and size of lesions. T. denticola induced significantly larger lesions in mice with iron pretreatment and demonstrated systemic manifestations of the infectious challenge and an accompanying spreading lesion with phenylhydrazine pretreatment (e.g., increases in circulating free hemoglobin). In contrast, T. pectinovorum virulence was minimally affected by this in vivo treatment to increase iron availability. T. denticola virulence, as evaluated by lesion size, was increased additively by in vivo iron availability, and cysteine modified growth of the microorganism. Additionally, galactosamine sensitized mice to a lethal outcome following infection with both T. denticola and T. pectinovorum, suggesting an endotoxin-like activity in these treponemes. These findings demonstrated the ability to modify the virulence capacity of T. denticola and T. pectinovorum by environmental conditions which can be evaluated by using in vivo murine models.

Protection Against Abscess Formation in a Model for Intraabdominal Sepsis

Obligate anaerobes are known to play a significant role in the development of intraabdominal abscesses. Much of our knowledge about these organisms is based on observations made using an animal model developed by this laboratory in 1974 [1,2]. The basic model system employs Wistar rats surgically implanted with an inoculum of intestinal contents from other rats. The inoculum is prepared in a manner which simulates the microbiologic parameters of the human colon. This is accomplished by placing rats on a diet of lean ground beef for two weeks and then harvesting, homogenizing and freezing aliquots of prepared intestinal contents for subsequent use. Following implantation of the intestinal contents, animals develop a characteristic bi-phasic infection. The first phase of the disease is peritonitis associated with positive blood and peritoneal cultures, death of approximately 50% of implanted animals, free flowing peritoneal exudates and an increase in peripheral white blood cell counts. Animals that survive the initial stage of disease appear to recover within five days of surgery. However, all surviving recipients of the intestinal content inoculum develop intraabdominal abscesses. This second phase of the disease is more chronic and is characterized by the presence of abscesses, adhesions and negative blood cultures. Abscesses contain a polymicrobic flora consisting of both obligate anaerobes and facultative species. The clinical end points for evaluation in this model are mortality and abscess formation, while microbiologic end points include blood, peritoneal and abscess cultures. The two phases of this disease are associated with distinctly different bacterial populations. During the early, acute peritonitis stage, Escherichia coli and other Gram negative organisms are numerically dominant and are responsible for the early mortality. The second more chronic stage of the disease, abscess formation, requires the presence of obligate anaerobes, such as Bacteroides fragilis. It has also been shown that abscess development in this model is associated with either a synergistic combination of obligate anaerobes and facultative species [3], or can be experimentally reproduced with the capsular polysaccharide of B.fragilis [4]. The unique properties of the capsular polysaccharide of B.fragilis and it’s role in both the induction and prevention of abscesses has been well documented in the literature [5–15]. It is the second phase of this experimental disease process that will be discussed in this chapter.

Virulence characteristics of oral treponemes in a murine model.

This study was designed to investigate the virulence characteristics of Treponema denticola, T. socranskii, T. pectinovorum, and T. vincentii following challenge infection of mice. These microorganisms induced well-demarcated, dose-dependent, raised subcutaneous (s.c.) abscesses which were similar in time of onset, lesion progression, and duration of healing. Only viable cells were capable of inducing these characteristic s.c. abscesses. Histological examination of the skin lesion 3 and 5 days postinfection revealed abscess formation in the s.c. tissues, and abundant spiral organisms were demonstrated to be present in the abscess. Host resistance modulation by dexamethasone (neutrophil alteration) and cyclophosphamide (neutrophil depletion) pretreatment had a minimal effect on the virulence expression by any of these treponemes. The T. denticola isolates demonstrated significant trypsin-like protease (TLPase) activity, while both T. socranskii and T. vincentii were devoid of this activity. Interestingly, T. pectinovorum strains were heterogeneous with respect to TLPase as high producers, low producers, and nonproducers. However, no differences in lesion formation were noted regardless of whether the species expressed this proteolytic activity or whether treatment with N alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) and dithiothreitol was performed. These results showed that (i) a murine model may be used to evaluate virulence expression by oral treponemes; (ii) while TLPase activity varies among the oral treponemes, this protease does not appear to participate in abscess induction in the mouse model; and (iii) T. pectinovorum strains show variation in TLPase activity.