[Immunology and bacteriology of post-traumatic bone infections].
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Biomedical subjects
Publications and source records attributed to M Eibl.
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An unusual case is presented of repeated, life-threatening self mutilation, elicited by the topical application of sodium hydroxide, which necessitated several operations, including amputation of the left lower leg. Histological examination revealed colliquation necrosis and a striking eosinophilia. The latter feature, which was not reproducible in an animal experiment, may be related to a defect of leucocyte locomotion in the present case.
Clinicopathological and immunological findings are reported in a boy with X linked agammaglobulinaemia (XLA), who after multiple episodes of purulent infections in various organs developed encephalitis associated with excemata and non suppurative arthritis. Inspite of gammaglobulin administration he developed progressive spastic tetraparesis, convulsions, mental deterioration and blindness and died in a decerebrate state at the age of 8 years. Necropsy revealed a general diminuition of the lymphoid tissue. The atrophic brain showed multiple cystic destructions and chronic, but still active polioencephalitis with prominent inflammatory involvement of basal ganglia and brain stem. Symmetric Wernicke-like lesions were seen in inferior corpora quadrigemina. The aetiology of this particular type of chronic progressive encephalitis in XLA is unknown but some kind of viral infection is to be considered.
Dialysable transfer factor (TF) was given in 10 paediatric patients with severe atopic dermatitis (AD). Ten patients with AD, matched for age and severity of disease, served as controls. Prior to the therapy with TF and at weekly intervals thereafter, T- and B-cells in the blood, PHA-stimulation, total IgE and specific IgG antibodies to inhalant and food antigens were determined. Therapy with TF was followed by IgE depression in 8/10 patients and was most pronounced in three patients with initially high levels. Some decrease of IgE levels was seen in four controls also, none of them, however, fell to normal levels as was seen in two of the treated patients. Specific IgE levels decreased slightly, but always remained within the pathological range. T-cell counts in the blood increased in 2/10 cases as well as PHA-stimulation, B-cells counts remained within normal limits. Clinical improvement was seen in one patient, five improved slightly and four remained unchanged. Our results indicate, that transfer factor can lower total IgE levels in cases with atopic dermatitis. The effect is most marked in patients with high total IgE levels. Skin involvement, however, does not closely follow in vitro findings.
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The case is reported of a 34-year-old patient with diffuse eosinophilic gastroenteritis in connection with agammaglobulinaemia and B-cell defect. The syndrome was manifested by malabsorption, and gastrointestinal protein loss, complicated by temporary pyloric obstruction and duodenal ulceration. As in the case of sprue-like changes in the small intestinal mucosa, and nodular lymphoid hyperplasia, this diffuse eosinophilic gastroenteritis may be a reaction of the stomach and small intestine to immunological abnormalities.
The function of Con A stimulation was investigated in patients with ALL in remission and in patients with ALL in the acute phase of the disease as compared to healthy controls. Suppression of the Con A response brought about by autologous Con A-activated cells was significantly lower in ALL patients in remission (mean value 29.33%) and in the acute phase (mean value 10%) than in the controls (mean value 64.86%). Suppression of the Con A stimulation of control lymphocytes by Con A-activated homologous cells of ALL patients had a mean value of 51.65%. This was significantly higher than the suppression obtained by the same ALL cells in the autologous system and of the same order of magnitude as the suppression obtained by control Con A-activated cells on control Con A stimulation (57.67%). Suppression of the Con a response of ALL lymphocytes produced by control Con A-activated cells was 23.17% and comparable to healthy controls. These results demonstrate that the function of Con A-induced suppression is significantly lower in ALL patients. They further indicate that at least two cell types are involved in this kind of suppression in humans.
Fewer plaque-forming cells (PFC) were found in the cord blood than in adult blood. B cells of newborns seem to be functionally mature. T cells of newborns provide enough help but exert increased suppressor activity.
In order to study a relationship between leukocyte locomotion and hemophilia, three assays to investigate cell motility were performed: Investigations were carried out, firstly, on the leukocyte locomotion (LL), secondly, on the activability of sera by zymosan, and thirdly, on the influence of sera upon LL. 17 patients with hemophilia and 16 healthy control persons were included in the study. While LL of patients and controls did not differ significantly with either cytotaxin, zymosan activated serum of patients or controls, or casein, sera of patients were significantly less activatable (p< 0.0001) than control sera. Locomotion of control leukocytes was significantly inhibited (p<0.002) by sera of hemophiliacs.
The influence of Cohn fraction II, pepsin- and plasmin-treated gammaglobulin on the opsonization of E. coli 0111 was investigated. Normal serum at different dilutions, as well as serum of patients with different forms of antibody deficiency syndromes were tested. No effect was observed by pre-incubation of the bacteria in these gammaglobulins if concentrated or 1:10 diluted serum was used for opsonization. In diluted serum Cohn fraction II potentiated and pepsin-treated gammaglobulin competitively inhibited opsonization, whilst plasmin-treated gammaglobulin potentiated at the low and competitively inhibited at higher dilutions. In serum from patients with antibody-deficiency syndromes, potentiation of opsonization by Cohn fraction II and competitive inhibition by pepsin- and plasmin-treated gammaglobulins was already seen at low serum dilutions.
30 patients with systemic lupus erythematosus (SLE), 19 patients with rheumatoid arthritis (RA) and 34 controls were investigated with regard to measles antibodies (AB). The titres were compared with clinical and immunological parameters. As previously reported by several authors we found increased measles AB titres more frequently (kappa 2-test, p less than 0.05) in patients with SLE than in those with RA and controls. No significant correlation was found between immunoglobulins, antinuclear antibodies, CH50 or rheumatoid factor, and an elevation of the measles AB titre. A trend was noted, however, towards a positive correlation between measles antibodies and IgM. An elevated measles AB titre in SLE can be explained on the basis of several mechanisms. However, hyperimmunoglobulinaemia with non-specific, secondary AB elevation can be ruled out as a cause of elevated measles AB titre according to our results.
Tetanus antitoxins were measured in serum and cerebro spinal fluid from 58 children--35 boys and 23 girls--with viral meningitis. The concentrations of IgG, IgA and IgM were also determined. The appearance of tetanus antitoxins in cerebral spinal fluid depends on absolute antitoxin levels in serum as well as on the antitoxin/IgG ratio. Antitoxin/IgG ratios in serum and cerebro spinal fluid were in the same order of magnitude. Detection of tetanus antitoxins in the cerebral spinal fluid of children with viral meningitis shows clearly that antibody found in cerebral spinal fluid is not an absolute proof of a certain disease. The results further indicate that local production of IgG antibody cannot be postulated by detecting certain antibodies in the CSF. It is also necessary to prove that antibody/globulin ratios are of significantly different magnitude in serum and CFS.
In 35 children with acute lymphatic or undifferentiated leukemia, immunological properties of normal lymphocytes and lymphoblasts were investigated. In most cases the number of circulating normal lymphocytes with surface or B markers and delayed type hypersensitivity was depressed. On the other hand, the response to mitogenic stimulation with PHA as well as the antibody and immunoglobulin serum concentrations were found to be normal. Lymphoblasts did not exhibit surface receptors in any but four patients, who showed 10--18% of leukemic blasts being positive for E-rosette formation at 0 degree but not at 37 degrees.
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Immunologic examination was done in 26 patients on to 20 years after posttraumatic splenectomy at the age of 3 to 6 years of life. Immunologic parameters used were: concentration of IgG, IgA, IgM, isoagglutinins, heterophila antibodies, agglutinins against staphylococci E. coli and pertussis, serum opsonins for E. coli and pneumococci, serum haemolytic complement activity, C3C4, B- and T- subpopulations of lymphocytes, inhibition migration of mononnuclear cells with E. coli. Pathologic susceptibility to infections was not observed clinically. IgM, E. coli agglutinins and E. coli opsonins were significantly lower in the postsplenectomy group than in controls.
Humoral immunity to bacterial antigens was investigated in 68 tissue typed and glucose tolerance tested first degree blood relatives of insulin dependent diabetics (IDD). The data were compared with those obtained in 60 IDDs and in 55 healthy controls. The prevalence of bacterial antibodies to E. coli, staphylococci, pertussis and diphtheria toxins were just slightly, but not significantly reduced in the blood relations compared with controls. Incidence of antibacterial antibodies was almost identical in blood relations with impaired and in those with normal glucose tolerance. By contrast, antibody formation to E. coli and staphylococci (p less than 0,0005, p less than 0,0005) respectively was significantly impaired in IDD. No correlation between genes of the major histocompatibility complex and humoral antibacterial immunity could be observed in IDD and blood relations. In conclusion, antibacterial antibody formation was found to be severely impaired in IDD patients but to be almost normal in blood relations of insulin dependent diabetics. These findings suggest that the humoral antibacterial immunodeficiency observed in IDD is a disease associated process probably independent of major histocompatibility complex linked genes.
Haemolytic complement activity was measured in a long-term study in patients on haemodialysis. Four of the patients studied developed hepatitis B while under investigation. In all four patients a fall in haemolytic complement activity was observed one to three months before hepatitis B surface antigen was detected in the serum. The fall in complement activity also occurred prior to a rise in transaminase. The maximum fall averaged 27%.
An immunological study in a case of nephrotic syndrome in early infancy with mesangioproliferative glomerulonephritis with focal crescents revealed deficiencies in humoral and cellular immunity. Serum Ig-G antibody levels such as pertussis-agglutinins, tetanus and diophtheria-antitoxing were decreased. A loss of tetanus antibodies in the urine could be observed. The production of tetanus-antibodies after immunogenic stimulation with tetanus-antigen was not diminished. The loss of Ig-A in the urine might have been compensated by a higher synthesis rate, which could also be the cause of the increased serum levels of Ig-M, since a loss of Ig-M in urine was not observed. The diminished serum levels of Ig-G antibodies were considered not only to be the result of loss, but possibly also of higher catabolism, and an insufficient compensation by a higher rate of synthesis. The percentage of T-cells in peripheral blood was found to be low. Stimulation of lymphocytes with PHA was at first normal, but in the last investigations diminished. Special experiments lead to the assumption, that this partial defect of cellular immunity might be the result of lacking or diminution of nutritive plasmafactors.