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PubMed2004

[The analysis of protracted inflammation after endoscopic surgery].

OBJECTIVE: To study the causes of late inflammation after endoscopic surgery. METHOD: Sixty-five patients of protracted inflammation after endoscopic surgery were investigated, by observing the pathologic spot and matched control of drug. RESULT: The orbit carton and aperture of frontal sinus and maxillary sinus were main spots of protracted inflammation. The drugs had no effect on protracted inflammation. CONCLUSION: The main cause of late inflammations is related to the high risk regions in endoscopic surgery.

Adult↗
PubMed2005

Granulomatous inflammation in Acanthamoeba keratitis: an immunohistochemical study of five cases and review of literature.

PURPOSE: Acanthamoeba keratitis usually presents as a necrotizing stromal inflammation. We report a rare presentation of granulomatous inflammation in Acanthamoeba keratitis METHODS: Retrospective clinico-pathologic case series. RESULTS: Five corneal tissues (3 corneal buttons, 2-eviscerated contents) from patients suffering from severe Acanthamoeba keratitis not responding to anti-Acanthamoeba treatment, revealed a florid granulomotous inflammation with multinucleated giant cells in the posterior stroma and around Descemet's membrane. Phagocytosed parasites were noted within the giant cells. Vascularization of the corneal stroma was noted in two cases. Immunophenotyping revealed a predominance of T lymphocytes and macrophages. Clinically, four of five cases had shown features of limbal and scleral involvement. CONCLUSION: Granulomatous inflammation in the posterior corneal stroma, is not an uncommon finding in Acanthamoeba keratitis and could possibly be immune-mediated, contributing to persistence and progression of disease. CLINICAL RELEVANCE: Presence of granulomatous inflammation in Acanthamoeba keratitis, in most cases is associated with limbal and scleral involvement and therefore could be considered as one of the poor prognostic markers. Further studies are required to ascertain the specific clinical features and appropriate management strategies in these cases.

Acanthamoeba↗
PubMedDate not supplied

Procalcitonin and conventional markers of inflammation in peritoneal dialysis patients and peritonitis.

OBJECTIVES: To determine the significance of a newly described marker of inflammation procalcitonin (PCT), and to investigate its relationship to conventional markers of inflammation, such as C-reactive protein (CRP), fibrinogen, and erythrocyte sedimentation rate (ESR), in patients on peritoneal dialysis (PD) and with peritonitis. DESIGN: A prospective, observational clinical study. SETTING: The Nephrology Division of a University-affiliated teaching hospital. PATIENTS AND METHODS: 51 consecutive patients on PD were included in the study. Of this number, 16 developed peritonitis during the observational period. Baseline PCT, CRP, and fibrinogen concentrations and ESR of 51 PD patients were determined at a time point (TB) prior to any evidence of infection. These results were compared with laboratory values from 74 hemodialysis patients and 34 nonuremic control subjects. All PD patients then were followed prospectively for evidence of peritonitis. In addition to routine blood tests, including hemoglobin and leukocyte count, and routine biochemical tests, blood samples were taken to measure PCT, CRP, and fibrinogen concentrations and ESR at the time (T0) when patients first were diagnosed with PD peritonitis and also on the 4th (T4) and the 14th (T14) days after treatment for peritonitis was initiated. PCT was assayed by immunoluminometry. RESULTS: No significant difference was observed between baseline median serum PCT concentrations in PD and hemodialysis patients; however, in both groups, baseline median PCT concentrations were significantly higher than those of nonuremic controls (p < 0.05). The 16 patients on PD who developed peritonitis had 21 PD peritonitis episodes during the study period. The increased PCT concentration observed at T0 in PD peritonitis episodes decreased with therapy, and this change was statistically significant (p < 0.05). In a receiver operating characteristic curve analysis for peritonitis, the area under the curve (AUC) for PCT was 0.80, which was significantly lower than the AUC for CRP and greater than the AUCs for fibrinogen and ESR. The sensitivity of PCT for peritonitis was lower than the sensitivity of conventional markers of inflammation; however, the specificity of PCT was higher. CONCLUSIONS: Median serum PCT concentration in PD patients was significantly higher than in nonuremic controls but not hemodialysis patients. Serum PCT concentrations may serve as a useful adjunct to traditional markers of inflammation in detecting and monitoring inflammation and peritonitis in PD patients.

Adult↗
PubMed1991

[Clinical and experimental study on shenghong kangyan su in treating 144 cases of pelvic inflammation with blood stasis syndrome].

Using the method of clearing up heat and resolving stasis, the authors treated 144 cases of pelvic inflammation with blood stasis syndrome (BSS) with Shenghong Kangyan Su. The total effective rate was up to 97.92%, cure rate up to 68.75%, without toxicity and side effects. Clinical and experimental study showed that the crux of pelvic inflammation with BSS had some relations with microcirculation obstruction. Inflammation may cause microcirculation obstruction and blood stasis, and is one forms of BSS. Therefore dull purple-tongue, undertongue vein dilated, abdominal pain in lower-part, pathologic mass can be regarded as the basis of diagnosis of pelvic inflammation with BSS The drug of clearing heat and resolving status has the functions of anti-inflammation, anti-pain, diminishing the obstruction of microcirculation, particularly in speeding up the blood flowing, lowering the aggregation of erythrocyte, P less than 0.001.

Adolescent↗
PubMed1991

Cell adhesion molecules and cutaneous inflammation.

Cutaneous inflammation is characterized by the infiltration of leukocytes such as polymorphonuclear neutrophils (PMNs), lymphocytes, and monocytes into the epidermis, dermis, or subcutaneous tissue in response to infectious or immunologic stimuli, in wound healing, or in response to trauma. In recent years, it has been found that cell-surface proteins on leukocytes, endothelial cells, and keratinocytes are critical elements in the initiation and evolution of cutaneous inflammation. In order for peripheral blood leukocytes to leave the circulatory system and enter tissue parenchyma, they must first bind to endothelial cells, pass between them, and traverse the vascular basement membrane. In this article we will examine both leukocyte-endothelial cell binding and evidence indicating that various cell-surface molecules present on leukocytes and endothelial cells, known as cell adhesion molecules (CAMs), interact with one another in specific fashion. This interaction or binding is a critical occurrence and its inhibition leads to downregulation of inflammation. Furthermore, some CAMs can be either induced or upregulated on leukocytes and endothelial cells by various proinflammatory cytokines. This tends to upregulate inflammation. It has become increasingly clear that the time-course of inflammation and its exquisite anatomic specificity are related to the regulation of expression of CAMs.

Animals↗
PubMed1989

Therapy of asthma in adults: the control of bronchial inflammation.

Inflammatory events involve the airways in asthma. Bronchial inflammation can induce and maintain both variable airflow obstruction and bronchial hyperresponsiveness. The rationale of asthma therapy is, therefore, to use drugs which prevent and reduce the inflammation. The control of asthmatic inflammation needs specific management. Interestingly, if corticosteroids are effective, non-steroidal anti-inflammatory drugs have a negligible effect. On the other hand, sodium cromoglycate and ketotifen can act on bronchial inflammation. Moreover, in well-selected patients, immunotherapy and a strict environmental prophylaxis can play a key role in long-term therapy. In asthmatics, a careful control of inflammation can protect airways from irreversible bronchial obstruction and return bronchial hyperresponsiveness to within the range of clinical well-being.

Adrenal Cortex Hormones↗
PubMed1988

[Enzyme histochemical characteristics of prostaglandin synthetase, adenylate cyclase and cAMP in a focus of inflammation in chronic tonsillitis].

Upon enzyme histochemical evaluation of palatine tonsils removed from 80 patients with chronic tonsillitis it was established that there is a close correlation between activity of prostaglandin synthetase (PG-synthetase), adenylate cyclase (AC), cellular cAMP, pattern of inflammation and the size of streptococcal foci. Enhanced enzymatic activity, elevated content of lymphoid and connective tissue cAMP are associated with minor interstitial streptococcal foci, being a frequent finding in mild inflammation. Low cellular cAMP in high PG-synthetase and AC activity occurs in mild inflammation and large-sized interstitial streptococcal foci. When both enzymatic activity and cellular cAMP are low, torpid inflammation indicates lack of tissue response to microbial invasion resulting in emergence of interstitial streptococcal colonies. In view of the essential role of mediator effects in the inflammation focus, high activity of tonsil PG-synthetase should be considered a major indicator of activated chronic tonsillitis.

Adenylyl Cyclases↗
PubMed1989

Hapten-induced model of chronic inflammation and ulceration in the rat colon.

We have developed a simple and reproducible rat model of chronic colonic inflammation by the intraluminal instillation of a solution containing a "barrier breaker" and a hapten. Administration of the hapten 2,4,6-trinitrobenzenesulfonic acid (5-30 mg) in 0.25 ml of 50% ethanol as the "barrier breaker" produced dose-dependent colonic ulceration and inflammation. At a dose of 30 mg, trinitrobenzenesulfonic acid/ethanol-induced ulceration and marked thickening of the bowel wall persisted for at least 8 wk. Histologically, the inflammatory response included mucosal and submucosal infiltration by polymorphonuclear leukocytes, macrophages, lymphocytes, connective tissue mast cells, and fibroblasts. Granulomas were observed in 57% of the rats killed 3 wk after induction of inflammation. Langhan's-type giant cells were also observed. Segmental ulceration and inflammation were common. The characteristics and relatively long duration of inflammation and ulceration induced in this model afford an opportunity to study the pathophysiology of colonic inflammatory disease in a specifically controlled fashion, and to evaluate new treatments potentially applicable to inflammatory bowel disease in humans.

Animals↗
PubMed1988

Effect of immunologic reactions on rat intestinal epithelium. Correlation of increased permeability to chromium 51-labeled ethylenediaminetetraacetic acid and ovalbumin during acute inflammation and anaphylaxis.

In these studies we compared jejunal permeability to two probes--chromium 51-labeled ethylenediaminetetraacetic acid (51Cr-EDTA) (mol wt, 360) and ovalbumin (mol wt, 45,000)--under control conditions, during acute intestinal inflammation, and in response to systemic anaphylaxis. Acute inflammation was produced after infection with Nippostrongylus brasiliensis and rats were studied at day 0 (control), day 4 (early), day 10 (acute), and day 35 (postinfection). At the latter stage, immune rats were also studied during anaphylaxis induced by i.v. N. brasiliensis antigen. In each study, blood and urine were sampled over 5 h after the probes were simultaneously injected into ligated loops in anesthetized rats. In controls, small quantities (less than 0.04% and 0.002% of the administered dose for 51Cr-EDTA and ovalbumin, respectively) appeared in the circulation and plateaued at 1 h. During acute inflammation, the appearance of both probes continued to increase with time. Compared with controls, 5-h values for 51Cr-EDTA and ovalbumin were (a) significantly elevated at day 4 (p less than 0.005), (b) increased approximately 20-fold at day 10 (p less than 0.005 and less than 0.01, respectively), and (c) normal at day 35. Urinary recovery of 51Cr-EDTA followed the same pattern. During anaphylaxis, appearance of the probes in the circulation increased at 1 h to values approximately 10-fold those in controls (p less than 0.001 and less than 0.01, for 51Cr-EDTA and ovalbumin, respectively), and then declined. Urinary recovery of 51Cr-EDTA over 5 h was also significantly increased. We conclude that epithelial barrier function becomes impaired during both acute inflammation and anaphylaxis. In this rat model, gut permeability changes to 51Cr-EDTA reflect gut permeability changes to macromolecular antigens. If similar conditions exist in humans, urinary recovery of 51Cr-EDTA may be useful in monitoring intestinal abnormalities associated with inflammation.

Acute Disease↗
PubMedDate not supplied

[Mitochondrial respiration and oxygen transport during various stages of lung inflammation].

It is shown in rats with experimental lung inflammation that the phosphorylative and uncoupling mitochondrial respiration intensity rises at acute and reverses to the normal level at subacute inflammation. At chronic inflammation the 2,4-DNP-stimulated mitochondrial respiration enhances and the ADPO coefficient lowers. At all stages of inflammation the pO2 rise in muscles after O2-inhalation is less than in healthy animals. The disturbance of O2 transport in organism may be the reason of the described low energy shift at lung inflammation.

Animals↗
PubMed1986

Repeated Escherichia coli endotoxin-induced pulmonary inflammation causes chronic pulmonary hypertension in sheep. Structural and functional changes.

Chronic pulmonary hypertension occurs in several human diseases in which there is evidence of chronic or repeated bouts of pulmonary inflammation. To determine whether prolonged lung inflammation causes persistent pulmonary hypertension Escherichia coli endotoxin was given to seven chronically instrumented awake sheep three times a week for 10 to 14 weeks. Pulmonary artery, left atrial and systemic arterial pressures, cardiac output, arterial blood gases and pH were monitored before starting endotoxin treatment and twice weekly, immediately before endotoxin infusion. Three sheep receiving saline over a similar time period served as controls. Pulmonary vasoreactivity to breathing 12% oxygen and a bolus infusion of an analog of prostaglandin H2 was also assessed. Peripheral lung biopsy tissue was taken at baseline and at periods throughout the experiment to assess pulmonary inflammation. Repeated endotoxin infusions resulted in a significant increase in mean pulmonary artery pressure from the 8th week of treatment and more than a 50% increase from week 10 (baseline = 18.4 cm H2O +/- 1.0 (mean +/- SE); 10 weeks endotoxin = 27.8 +/- 4.3; p less than 0.05). Pulmonary vasoreactivity to both an analog of prostaglandin H2 and 12% oxygen decreased in the period from 4 to 8 weeks of endotoxin treatment. Light microscopic assessment of lung biopsy tissue showed a persistent four-fold increase above baseline in number of peripheral lung granulocytes. Electron microscopy revealed that granulocytes, lymphocytes, and monocytes sequestered in the lungs of these animals, and that structural damage to the endothelium was minimal. Morphometry of lungs obtained at autopsy in which the pulmonary arteries had been distended with barium-gelatin showed extension of muscle into the walls of smaller intra-acinar arteries (than normal) and a reduction in number of filled peripheral arteries. We conclude that repeated infusions of endotoxin into sheep cause persistent lung inflammation, altered pulmonary vasoreactivity, sustained pulmonary hypertension, and some of the structural changes characteristic of this disease. Chronic inflammation may play a role in the pathogenesis of chronic pulmonary hypertension.

Animals↗
PubMed1978

Experimental pneumococcal meningitis. IV. The effect of methyl prednisolone on meningeal inflammation.

This study was undertaken to determine whether adrenal corticosteroids suppress meningeal inflammation in experimental pneumococcal meningitis in rabbits and, if so, whether the mechanism of suppression involves inhibition of chemotactic activity in CSF or modification of granulocyte responses to inflammation mediators. It was found that methyl prednisolone, administered intramuscularly in doses of 15 or 30 mg/kg 24 hr and 48 hr after induction of meningitis, significantly reduced (p less than 0.01) the mass of granulocytes present in the meninges 72 hr after infection, the time of maximum meningeal inflammation. The larger dose of steroid produced approximately twice the suppressive effect of the smaller dose (p less than 0.05). The regime of methyl prednisolone that produced maximal suppression of meningeal inflammation (30 mg/kg/day) did not alter CSF chemotactic activity or chemotactic responsiveness and phagocytic activities of granulocytes from rabbits with meningitis. However, steroid therapy inhibited an increase in granulocyte adherence that was observed in untreated animals with meningitis (p less than 0.05). Thus methyl prednisolone in doses of 15 and 30 mg/kg given daily to rabbits with pneumococcal meningitis produced a suppressive effect on meningeal inflammation that was dose-dependent and was possibly mediated by inhibition of granulocyte adherence.

Animals↗
PubMed1982

The role of the arachidonic acid cascade in the species-specific X-ray-induced inflammation of the rabbit eye.

To identify the mediator(s) of the apparently species-specific X-ray-induced inflammation of the rabbit eye, inhibitors of the synthesis and/or release of known or putative mediators of ocular inflammation were administered prior to irradiation. The X-ray-induced ocular inflammation, particularly the rise in intraocular pressure, was found to be inhibited by intravenous pretreatment of rabbits with flurbiprofen, indomethacin, or imidazole (1, 10, and 100 mg/kg i.v., respectively), or by combined intravitreal and topical administration of flurbiprofen. Systemic, intravitreal, and/or topical pretreatment with prednisolone or disodium cromoglycate or the retrobulbar injection of ethyl alcohol or capsaicin failed to block the inflammatory response, whereas vitamin E apparently exerted some protective effect. These findings show that the X-ray-induced inflammation of the rabbit eye is mediated, at least in part, by prostaglandins (PGs) and/or related autacoids. In addition, these results suggest that the unique sensitivity of the rabbit eye to X-ray-induced inflammation is due either to the presence in this species of a unique or uniquely effective triggering mechanism for the release of PG precursors or to the greater sensitivity of this species to the ocular inflammatory effects of PGs. Thus the rabbit eye may provide a unique model for studying some aspects of arachidonic acid release or ocular PG effects, but extreme caution must be exercised in generalizing such findings to other species.

Animals↗
PubMed1983

Inflammation of the lacrimal drainage system--assessment by thermography.

Thermography is an investigative tool without side effects. To our knowledge thermography has not been evaluated in the assessment of lacrimal passage inflammation and obstruction. It can give an objective assessment of presence and degree of inflammation. An infrared scanning device was used to detect surface temperatures in 29 patients with known disorders of the lacrimal drainage passage. Thermal images were compared for bilateral symmetry and against the normal thermographic appearance of the face. Acute dacryocystitis and canaliculitis showed gross hyperthermia and asymmetry. Forty-two percent of patients with a picture of chronic dacryocystitis and 40% of patients with only tearing and no clinical evidence of inflammation showed temperature elevation on the side of involvement, whereas 58% and 60% of these respective groups showed symmetrical thermal patterns, suggesting no active inflammation. In a few cases there were discrepancies between clinical assessment and objective thermographic evaluation of the degree of inflammation. The implications of our results and possible applications of thermography are discussed.

Acute Disease↗
PubMed1980

A differential effect of C5a and C5a des Arg in the induction of pulmonary inflammation.

Earlier studies have shown that C5 fragments induce an inflammatory reaction when instilled into the rabbit lung. Because C5a is rapidly converted to C5a des Arg in vivo, experiments were performed to determine which fragment was most effective in producing pulmonary inflammation in this animal model. C5a des Arg consistently produced marked inflammation. This was characterized by neutrophil accumulation, edema, hemorrhage, fibrin formation, and damage to alveolar epithelium. The time course of the inflammatory reaction initiated by C5a des Arg showed pulmonary vascular sequestration of neutrophils with no intra-alveolar migration at 30 minutes after injection. By 2 hours, interstitial and alveolar neutrophils were numerous, with the accumulation of neutrophils in the alveoli increasing to a maximum at 6 hours. At 24 and 48 hours, the predominant cells were mononuclear (macrophages). By 120 hours, the lesions were resolving. In contrast, at all doses examined, a similar instillation of C5a induced either no inflammation or a milder, more focal response than C5a des Arg. This inability of C5a to initiate inflammation was not apparently due to the generation of inhibitors, since mixtures of C5a and C5a des Arg were phlogistic. A prolonged, intrapulmonary infusion of C5a (20 minutes), in contrast to a bolus instillation (1 minute), did initiate an inflammatory response, which may reflect the conversion of the C5a to C5a des Arg in the lung. This study points out the inflammatory potential of products of complement activation, particularly of the C5 fragment C5a des Arg, when applied to the airway side of the lungs. This inflammatory response raises the possibility that cleavage of intrapulmonary C5 may play an important role in the initiation of pulmonary inflammation.

Anaphylatoxins↗
PubMedDate not supplied

From inflammation to lesion.

The gastrointestinal tract is continuously in contact with a multitude of antigens and therefore contains a well developed defense mechanism composed of nonspecific and specific elements. The gastrointestinal mucosa immune system (GALT) is the specific defense. Its cellular components firstly appear during the 11th week of pregnancy. Stimulation of the lymphoid tissue starts early after birth and depends upon bacterial colonization. During life the immune system is continuously bombarded by a multitude of antigens. The normal presence of the GALT is the expression of a controlled physiologic inflammation. Inflammation is a complex series of homeostatic reactions involving cellular and molecular mechanisms orchestrated in such a manner as to protect the organism, only yielding pathologic changes when there is overwhelming acute response or when chronicity leads to loss of function. Several phases can be distinguished in the inflammatory reaction. The initial vascular reaction, controlled by vasoactive mediators is followed by a cellular reaction with recruitment of inflammatory cells (immune competent leucocytes and neutrophils). This process requires cellular adhesion and migration and depends on the expression of "adhesion molecules". Leucocytes already present in the tissue (lymphocytes monocyte/macrophage cells, eosinophils, and mast cells) and newly recruited cells (neutrophils, eosinophils, monocyte/macrophage cells and lymphocytes) will release a variety of inflammatory mediators with both positive and negative (tissue destructive) effects. Epithelial cells, fibroblasts and smooth muscle cells are actively involved in the reaction. Normally inflammation ends by healing. In chronic inflammatory bowel diseases healing does not occur or is incomplete. Early lesions described thus far for the small capillary lesions described in Crohn's disease). Yet similar lesions not leading to chronicity have been described in experimental and human clinical conditions. The major question therefore in Crohn's disease and ulcerative colitis is why the early lesions do not heal but lead to chronic inflammation. Intrinsic defects (alterations of epithelial cells, increased permeability or genetic predisposition) are considered as possible causes. Persistent inflammation may also be due to the nature of an extrinsic agent as in tuberculosis. A specific agent has as yet not been demonstrated in chronic idiopathic inflammatory bowel disease. An inappropriate inflammatory reaction to components normally present in the lumen of the gastrointestinal tract must also be considered. Heat shock proteins (HSP) produced by bacterial agents may for instance induce an autoimmune reaction as there is molecular analogy between HSP from bacterial origin and human HSP.

Colitis, Ulcerative↗
PubMed1995

Gut inflammation in psoriatic arthritis: a prospective ileocolonoscopic study.

OBJECTIVE: Some forms of psoriatic arthritis (PsA) are classified as spondylarthropathy, and subclinical gut inflammation is found in spondylarthropathies. Our study was designed to determine if inflammatory gut lesions were also present in PsA, and if the prevalence of subclinical gut involvement was different in the subgroups of this disease. The relationship with HLA subtypes was also determined. METHODS: Ileocolonoscopy was performed on 64 patients with PsA (37 men, 27 women). RESULTS: Inflammatory gut lesions were found in 10 of the 64 patients (16%): in 3 of the 15 patients (20%) with oligoarthritis and in 7 of the 23 patients (30%) with axial involvement. None of the 26 patients with polyarthritis showed these lesions. The prevalence of HLA-B27, Bw62, and B17 was significantly raised in our total group of patients with PsA. HLA-B27 and Bw62 were significantly more prevalent in patients with gut inflammation, 60 and 50%, respectively. CONCLUSION: Gut inflammation is only present in PsA subgroups that belong to the spondylarthropathy concept. This suggests that the gut plays a role in the pathogenesis of locomotor inflammation in these subgroups. The prevalence of gut inflammation in psoriatic spondylarthropathy is significantly lower than in nonpsoriatic spondylarthropathies. Consequently, not only the gut but also the skin may be a portal of entry for causative antigens in PsA.

Adolescent↗
PubMed1976

[Posttraumatic pyogenic and granulomatous encephalitis. An animal experimental contribution on inflammation (author's transl)].

The present studies were performed to elucidate the factors responsible for the relative resistance of the brain to bacterial infections. As a model, group A streptococci were used to produce an experimental brain infection in mice. Attention was focussed on the activity of brain macrophages, the function of which to date is poorly understood. The primary purpose of the experiments was to compare the types of inflammation elicited in the brain by the injection of either killed or living group A streptococci. As a result, two fundamentally different types of encephalitis were observed histologically. A granulomatous inflammation was induced by killed streptococci; when deposited in the brain by intracerebral injection, these were phagocytosed by invading mononuclear macrophages and polymorphonuclear granulocytes during the first day p.i. There was no necrosis of brain tissue excepting the stab wound at the site of injection. The number of granulocytes in the inflammatory infiltrates decreased during the first week p.i. whereas, during the same period, the number of macrophages forming granuloma-like cell accummulations increased. At the beginning of the third week a fading of the granulomatous encephalitis was observed. In contrast, living streptococci produced a pyogenic inflammation of the meninges as well as of the grey and white matter in the region of the stab wound combined with extended tissue necrosis surrounding deposits of bacteria. This pyogenic infection progressed until the end of the first week, forming a brain abscess. A phlegmonous spreading of the pyogenic inflammation predominantly in the white matter and pyocephalus internus was also observed. In contrast to the increase of mononuclear macrophages in the border zone of the abscesses, the granulocytic inflammation decreased. During the second and third weeks p.i. granulation tissue consisting of proliferating connective tissue cells, macrophages and lymphocytes replaced pyogenic necrosis. A secondary purpose was to determine the fate of living and killed streptococci within the pyogenic and granulomatous encephalitis. In these studies immunohistologic, electron microscopic, bacteriologic and serologic methods were employed in addition to the techniques already mentioned. In the majority of the experimental animals streptococci were killed by granulocytes within the first week after injection of the living bacteria. At this time, most of the streptococci were contained within granulocytes and macrophages located to the periphery of the brain abscesses. Corresponding to the granulomatous encephalitis produced by injection of killed streptococci it was possible to detect persistent cell wall material in macrophages by immunohistology. By electronmicroscopy streptococci and their cell walls were found within the phagocytic vacuoles of macrophages. During the course of degradation the group-specific cell wall carbohydrate was enzymatically converted into the group A-variant specific structure...

Animals↗