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At least 19 recordsLinked to original sources
PubMed1991

Lack of neurological abnormalities in Lewis rats with experimental chronic serum sickness.

Serum sickness in man may occur after treatment with foreign proteins such as tetanus or diphtheria antisera, and in some patients leads to neurological complications such as neuropathy or encephalomyelitis. Many of the effects of serum sickness are associated with the deposition of antigen-antibody complexes in the tissues. Chronic serum sickness in the rabbit has previously been shown to cause perivascular inflammation and demyelination in the nervous system. We induced chronic serum sickness in the Lewis rat by daily intraperitoneal injections of bovine serum albumin (BSA) in male rats that had previously received footpad inoculations of BSA. Two animals died of anaphylaxis and 15 were observed for periods of 39 to 142 days. Three animals injected with 3 mg or 4 mg/day of BSA, and 6 animals injected with up to 16 mg/day of BSA had no clinical abnormalities when sacrificed. Six animals were injected with 36 to 40 mg BSA/day and, at the time of sacrifice, were lethargic and had ruffled fur, but no neurological signs. In these animals, the production of chronic serum sickness was confirmed by the presence of immune complex deposits in the kidneys. In the nervous system, there was no evidence of inflammatory cell infiltration either in the parenchyma or the vessel walls. Immunofluorescence studies identified deposits of immunoglobulin in the choroid plexus of chronic serum sickness rats but not in controls. Staining with antibodies to immunoglobulin, complement and BSA showed marked staining of blood vessels of the nerve roots of the animals with chronic serum sickness.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Serum sickness.

Serum sickness can be induced experimentally in the rabbit by injecting a foreign protein. The pathophysiology has been well described. A similar illness is seen in man after injection of heterologous serum, and well as many other drugs. Included is a discussion of immunopathologic studies of human serum sickness and serum sickness-like diseases, diagnosis, prevention, and treatment.

Animals↗
PubMed1987

Relationship of the quality and quantity of circulating anti-BSA antibodies to the severity of glomerulonephritis in rats with chronic serum sickness.

Chronic serum sickness glomerulonephritis, induced in hyperimmunized rats by daily intravenous administration of bovine serum albumin, occurs in three stages, mild, moderate and severe, with abrupt onsets and distinctive features of kidney pathophysiology and immunopathology. We have studied the relationship between circulating anti-BSA antibodies and the severity of glomerulonephritis at each stage. The total amount of antibodies declined gradually during the course of disease, to low concentrations in the most severe stage of kidney inflammation. High levels of immune complexes were present in the circulation while precipitating antibodies were maintained, and rats remained in the mill stage of disease, exhibiting no abnormalities of kidney function and only mesangial immunopathology. The start of the moderate stage of chronic serum sickness, identified by proteinuria and the accumulation of immune deposits along the glomerular basement membrane, was associated with the disappearance of precipitating antibodies from circulation. With the onset of the severe stage of disease, marked by depressed glomerular filtration and sodium excretion, circulating antibodies of high affinity were no longer detected and circulating immune complex levels were only marginally elevated above normal. The experiments reported here demonstrate that, in chronic serum sickness glomerulonephritis of rats, transitions from one stage of kidney disease to another can be inferred from changes in the population of circulating antibodies. Kidney histopathology, therefore, can be predicted reliably from serological data alone.

Animals↗
PubMed1986

A transition from proliferative to membranous glomerulonephritis in chronic serum sickness.

Chronic serum sickness glomerulonephritis was induced in rats by daily i.v. administration of bovine serum albumin (BSA). Previous studies have shown that the disease progresses through three discrete stages: mild, moderate and severe. The diffuse, proliferative necrotizing glomerulonephritis of severe chronic serum sickness, which is accompanied by a decreased glomerular filtration rate and increased glomerular permeability to macromolecules, has an inevitable fatal outcome. In the experiments reported here, BSA injections were discontinued at the transition from moderate to severe glomerulonephritis, a point which was identified by decreased sodium excretion. Retrospectively, rats could be divided into two categories. Some, called non-survivors, continued to exhibit sodium retention. Those animals progressed rapidly to end-stage renal disease and died within two weeks of the cessation of antigen injections. Others, called survivors, returned to sodium balance and remained alive for many months. The development of progressive membranous glomerulonephritis, with prominent spike formation and disappearance of glomerular hypercellularity, was noted in all survivors. That change in histopathology occurred in the absence of both circulating BSA and precipitating antibodies to BSA. The transition of proliferative to membranous glomerulonephritis was accompanied by partial recovery of glomerular function, although proteinuria persisted. Maintenance of severe proteinuria did not appear to depend on an active immunological process.

Animals↗
PubMed1979

Rat CNS in experimental chronic serum sickness: integrity of the zonulae occludentes of the choroid plexus epithelium and brain endothelium in experimental chronic serum sickness.

The present study is an extensive systematic immunofluorescence and labelled electron microscopic investigation of chronic rat serum sickness brains. It is specifically directed at discerning effects of chronic serum sickness upon the zonulae occludentes of both the choroid plexus epithelium and the intra-cerebral endothelium. Although the choroid plexus is a known site of complex entrapment in systemic immune complex disorders, comprehensive immune studies of the CNS parenchymal vasculature have not yet been reported in either experimental or spontaneous immune complex disease. We examined by direct immunofluorescence techniques over 70 blocks of experimental chronic serum sickness brains taken from 16 animals with severe glomerular disease and found them to be uniformly negative for the presence of immune deposits. No horseradish peroxidase was seen beyond the restricting zonulae occludentes of either the choroid plexus or the cerebral endothelium in tissue from three serious affected animals. These structural barriers retained their integrity despite the extensive circulation and deposition of complexes and complement induced in the experimental model and the associated release of vasoactive substances.

Animals↗
PubMed1993

Antigen size influences the type of glomerular pathology in chronic serum sickness.

Chronic serum sickness was induced in four groups of Wistar rats by immunization with BSA, cationized BSA (cBSA), human IgG (HuIgG), or human IgM (HuIgM), followed by repeated intraperitoneal (i.p.) injection of the antigen used, to study the effect of the characteristics of an antigen on renal immunopathology. Renal tissue sampled 2, 4, 7, and 9 weeks after the start of the i.p. injections was examined by light-, immunofluorescence-, and electron-microscopy. Proteinuria was measured in urine collected over 24 h. All animals given BSA, cBSA, or HuIgG developed progressive renal disease characterized by initial deposition of antigen and rat Ig in the mesangium of rats given BSA or HuIgG, and minimal amounts in those given cBSA, followed by the appearance in the first instance of subendothelial deposits in the animals receiving BSA or HuIgG, and later subepithelial deposits in those given BSA, cBSA, or HuIgG. The appearance of immunoglobulin deposits along the glomerular capillary wall was associated with the onset of massive proteinuria reaching average levels of 450 mg/24 h for rats given BSA or cBSA, and 500 mg/24 h for those given HuIgG. Animals injected with HuIgM showed only mesangial deposits of human IgM and rat Ig without the development of proteinuria. Under light-microscopy, rats given BSA, cBSA, or HuIgM showed minimal abnormalities, whereas those receiving HuIgG showed transient but severe influx of granulocytes in glomeruli with the development of diffuse proliferative glomerulonephritis in association with a long-lasting phase characterized by subendothelially localized immune aggregates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Serum sickness and uveitis.

Serum sickness is immune response to a foreign antigen, usually a heterologous protein. Incidence rate is less than 0.5%. Antigens and responding antibodies form circulating immunocomplex that is characteristic for serum sickness. The condition occurs 7-15 days after exposure to the antigen, usually with clinical picture of glomerulonephritis. The immunocomplex circulates to other tissues where it sediments and causes inflammation, such as arteritis, neuritis, synovitis. The aim of this research is to present the break out of serum sickness in form of anterior uveitis due to azithromycin therapy administered by mouth. Identifying of anterior uveitis may help in early diagnostics and treatment of serum sickness.

Anti-Bacterial Agents↗
PubMedDate not supplied

Serum sickness due to bovine serum albumin sensitization during in vitro fertilization.

Of 32 women included in the in vitro fertilization (IVF) program in our hospital in 1987, in whom a medium containing bovine serum albumin (BSA) (Menezo's medium) was employed for rinsing follicles, 5 (15%) developed a symptom complex compatible with serum sickness within 8-12 days after oocyte retrieval by echographic puncture. All the patients had specific IgG antibodies against BSA, and intradermal skin testing with BSA and Menezo's medium were positive. We could not demonstrate the presence of specific IgE against BSA in serum by RAST, probably due to the presence of high levels of specific IgG antibodies, which can interfere in the RAST procedure. Statistical analysis showed that the volume of Menezo's medium was significantly greater (p < 0.05) in patients developing the disease. The risk of disease development is directly related to the amount of heterologous protein administrated.

Enzyme-Linked Immunosorbent Assay↗
PubMed1984

The macrophage-phagocyte system in rabbits with experimentally induced serum sickness: functional studies.

The objective of this study was to measure the phagocytic functions of the spleen and the liver and, if possible, to correlate them with the morphology and the immunohistology of these organs in rabbits with serum sickness. Serum sickness was induced by repeated intravenous injections of bovine serum albumin (BSA). Rabbits with acute serum sickness (stage A of serum sickness), with chronic serum sickness (stage C), rabbits in a stage of immunization between stage A and stage C (stage B), and rabbits that did not respond to the antigenic challenge [nonresponders (NR)], as well as nonimmunized (NI) rabbits were used. The function of the spleen and of the liver was measured by the clearances of 51Cr-labeled heat damaged (HE), periodate-treated (PE), or immunoglobulin G (IgG)-coated (IgGE) autologous erythrocytes. In NR rabbits the functions of the spleen and liver were normal. In rabbits in stage A of serum sickness the clearance of HE, the only one measured in this stage, was decreased. In rabbits in stage B the clearances of HE and IgGE were determined; both clearances were decreased. In rabbits in stage C, the clearances of HE and IgGE were decreased, while the time of clearance of 50% (T 1/2) of PE was not significantly prolonged. In addition, in rabbits in stages A, B, and C the ratio of whole spleen vs liver radioactivity was increased. In rabbits in stage B the clearance of HE returned to normal 3 days after discontinuation of BSA injections. While all animals with detectable morphologic and immunohistologic changes of the spleen and the liver had prolonged clearances of treated erythrocytes, some animals with similarly prolonged clearances lacked evidence of pathology of these organs. The results obtained indicate that: (1) In NI and in NR rabbits, treated erythrocytes are rapidly removed by the macrophage-phagocyte system (MPS) and preferentially by the liver. (2) In rabbits in stages A, B, and C of serum sickness the clearances of treated erythrocytes are significantly prolonged. Moreover, treated erythrocytes appear to be preferentially removed by the spleen, indicating that the ability of the spleen to clear treated erythrocytes is less impaired than that of the liver. (3) In stages A, B, and C of serum sickness the nonimmunologic clearance of autologous erythrocytes is as altered as the clearance that occurs via Fc receptors. (4) In rabbits in stage B of serum sickness recovery of MPS function occurs after the interruption of BSA injections, suggesting reversible damage.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1976

Participation of monocytes in glomerulonephritis in acute serum sickness of rabbit.

Acute serum sickness in the rabbit was studied with special reference to the role of monocytes in the inflammatory process in the glomerulus. It was revealed that macrophages were the major factor in producing glomerular hypercellularity in acute serum sickness. Proliferation of intrinsic glomerular cells or accumulation of polymorphonuclear leukocytes (PMNs) was minimal. Ultrastructural characteristics of these phagocytic cells were described. Macrophages engulfed various inflammatory products such as fibrin and cell debri in the glomerular capillary. Colloidal carbon administered at the active inflammatory stage was found to be mostly engulfed by macrophages, little by mesangial cells, and was not seen in endothelial or epithelial cells and PMNs. The selective ingestion of the carbon particles by these macrophages made it possible to differentiate them from glomerular cells. This in turn indicated that the macrophages were derived from neither endothelial nor menangial cells and that they were of blood monocytic origin. It was suggested that monocytic cells participated in glomerular inflammation but they, on the other hand, contributed to the repair of glomerular injuries through their active role for phagocytosis.

Animals↗
PubMed1984

Severe systemic vascular necrosis in cyclosporin-treated rabbits with acute serum sickness.

Rabbits given acute serum sickness (ASS) and treated with cyclosporin A (CyA) developed a severe, systemic vascular injury, which was not similar to that normally seen in ASS. Thirty-three NZW rabbits received a single intravenous injection of 250 mg/kg bovine serum albumen (BSA) with or without endotoxin (5 micrograms/kg), on day 0. Groups of rabbits were given intramuscular CyA as follows: 15 mg/kg/day from day -2 to +8, or 25 mg/kg/day from day -2 to +3 or day 0 to 5. Muscular arteries of the heart and splanchnic organs developed an arterial injury in which there was extensive fibrinoid necrosis of the vessel wall but little or none of the mononuclear cell reaction that is normally associated with the arteritis of ASS. A microvascular injury also occurred which led to interstitial haemorrhage in the gastric mucosa and multi-focal necrosis in the heart and liver. These lesions were seen with equal frequency in all groups of rabbits with serum sickness who received CyA, irrespective of whether they also received endotoxin. We suggest that CyA altered the host inflammatory response to the injury initiated by the BSA-anti-BSA immune complexes and this led to enhanced vascular injury. The inhibition by CyA of the perivascular cellular reaction suggests that this reaction may be mediated by T lymphocytes. This model should provide further insight into the pathogenesis of arteritis, as well as the mechanisms of cyclosporin toxicity.

Animals↗
PubMed2006

Severe serum sickness reaction to oral and intramuscular penicillin.

Serum sickness is a type III hypersensitivity reaction mediated by immune complex deposition with subsequent complement activation, small-vessel vasculitis, and tissue inflammation. Although the overall incidence of serum sickness is declining because of decreased use of heterologous sera and improved vaccinations, rare sporadic cases of serum sickness from nonprotein drugs such as penicillins continue to occur. Drug-induced serum sickness is usually self-limited, with symptoms lasting only 1-2 weeks before resolving. We report an unusual case of a severe and prolonged serum sickness reaction that occurred after exposure to an intramuscular penicillin depot injection (probable relationship by Naranjo score) and discuss how pharmacokinetics may have played a role. Clinicians should be familiar with serum sickness reactions particularly as they relate to long-acting penicillin preparations. Accurate diagnosis in conjunction with cessation of drug exposure and prompt initiation of antiinflammatory treatment with corticosteroids can produce complete recovery

Administration, Oral↗
PubMed2001

Childhood serum sickness: a case report.

Childhood serum sickness is a rare allergic disease that follows the administration of a foreign antigenic material, most commonly caused by injecting a protein or haptenic drug. The disease is a type III hypersensitivity reaction mediated by deposits of circulating immune complexes in small vessels, which leads to complement activation and subsequent inflammation. The clinical features are fever, cutaneous eruptions, lymphadenopathy, arthralgias, albuminuria, and nephritis. Serum sickness is an acute self-limited disease. We report a 3-year-old child who presented with fever and a rash; an invasive bacterial infection was strongly suspected. He was therefore given penicillin and gentamicin and responded well. At day 4 after admission, he developed a serum sickness reaction and showed symptoms of arthralgias, generalized edema, purpura, and gross hematuria. The white blood cell count was 12 190/mm3 with 7% eosinophils. Urinalysis revealed red blood cell above 100 per high power field, white blood cell 10 to 15 per high power field, and proteinuria. The antibiotics were discontinued and hydrocortisone (20 mg/kg/d), diphenhydramine HCl (4 mg/kg/d), aspirin (66 mg/kg/d) was administered, plus 1 dose of epinephrine (0.01 mL/kg) administered intramuscularly. On day 7, the 3rd day after withholding antibiotics, his condition dramatically improved. The clinical symptoms resolved progressively and his urinalysis returned to normal.

Child, Preschool↗