Expulsion of Hymenolepis nana from mice with congenital deficiencies of IgE production or of mast cell development.

The roles of IgE and mast cells on expulsion of adult Hymenolepis nana from the intestine were examined in mice. IgE-dependency was determined by comparing congenitally IgE-deficient SJA/9 and IgE-producing SJL/J mice infected with 50 H. nana eggs. Anti-H. nana IgE antibody was detected at three weeks post infection (p.i.) in SJL but not in SJA mice. The number of adult worms in the intestines of SJA and of SJL mice were similar at two weeks, but significantly more were found in SJA mice at three weeks p.i. Treatment of mice with anti-epsilon antibody also resulted in an increased worm burden at three weeks, suggesting participation of IgE in expulsion of H. nana. Intestinal mastocytosis was induced by infection regardless of the IgE status of the mice. Mast cell-dependency was tested in mast cell-deficient W/Wv and in normal littermate +/+ mice infected with 100 H. nana eggs. Anti-H. nana antibody was detected in both groups of mice at three weeks p.i. Worm expulsion seemed to be mast cell dependent because expulsion was less complete in W/Wv mice at three weeks p.i. Peripheral blood eosinophilia was comparable at three weeks p.i. in both IgE and mast cell sufficient and deficient mice. These results suggest that IgE and mast cells participate in the expulsion of H. nana adults from intestine in mice.

Inability of oral bovine transfer factor to eradicate cryptosporidial infection in a patient with congenital dysgammaglobulinemia.

A 31-year-old man with dysgammaglobulinemia Type I (deficient IgG, IgA, and elevated IgM) and persistent cryptosporidiosis was treated over a 13-week period with oral bovine transfer factor from calves immunized with cryptosporidia. Spiramycin was added toward the end of the treatment period. This patient failed to show clinical response although there was a decrease in the stool oocyst count from the value just prior to therapy. Bovine transfer factor alone and in combination with spiramycin failed to eradicate the infection in this man with well-documented stable cryptosporidiosis.

Herpetic stromal keratitis in congenital dysgammaglobulinemia. Case report.

The clinical picture and laboratory findings of a case of secondary herpes simplex virus type 2 in a patient with congenital dysgammaglobulinemia who was followed for 26 months is described. Local combined therapy of acyclovir and Decadron (dexamethasone) 0.1% was given for management for 14 months. The clinical and immunopathologic findings of our patient match the results described by other investigators in experimental animals.

[Selective IgA deficiency]. / Selektiver IgA-Mangel.

Selective IgA deficiency may be defined as an inborn state characterized by a decrease of serum IgA levels below 8 IU/1 (approximately 5 mg/dl) which may be associated with clinical symptoms of disease. The frequency of this condition in the general population varies between 1 : 400 and 1 : 3000 in different countries. Patients with defects of chromosome 18, ataxia teleangiectatica and with connatal rubella syndrome have a high incidence of IgA deficiency. Inspite of the decrease in circulating IgA there are B-lymphocytes containing IgA molecules in the peripheral blood. Thus it has been concluded that transformation of B-lymphocytes into IgA bearing plasmacells is stunted by another mechanism. While small amounts of IgA may be released by transformed plasmacells the capacity of B-lymphocytes to mature into fully functioning plasmacells releasing normal amounts of IgA is defective. T-cells acting as suppressor cells for IgA differentiation have been demonstrated in peripheral blood and are a possible explanation for this phenomenon. The majority of individuals with IgA deficiency are healthy. Evaluations of increased susceptibility for infections have to consider the fact that 6 respiratory tract infections per year are the average for any preschool child. However a number of children with IgA deficiency suffer from recurrent bacterial infections such as sinusitis, bronchitis and pneumonia, usually responding well to antibiotic treatment. IgA deficiency has an established correlation with atopic disease. There is an 40 fold increase in incidence of allergies and autoimmune diseases such as rheumatoid arthritis, lupus erythematodes and thyroiditis in individuals with IgA deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Tubulo-interstitial nephritis associated with polyomavirus (BK type) infection.

We studied viral injury to the kidney in a six-year-old boy with hyperimmunoglobulin M immunodeficiency who presented with irreversible acute renal failure and eventually died after five months of dialysis. Renal biopsy at the time of his presentation revealed a predominantly tubulo-interstitial process with numerous viral inclusions that were identified as polyomavirus. Urine cultures showed a massive viruria with BK-type, polyomavirus. The kidney disease was end stage, with persistence of BK virus identified by morphologic techniques and by culture. DNA hybridization analysis showed virus in low concentration in the lymph nodes, spleen, and lungs. The marked viruria, the high concentration of BK virus, and the extensive distribution of viral antigen throughout the kidney all suggest that infection with BK virus was the basis of the severe renal parenchymal injury.

Deficiency of IgG subclasses in mothers of infants with group B streptococcal septicemia.

Serum IgG subclasses were studied in 19 mothers of infants with serious infections caused by group B streptococci (GBS) and compared with a control group of 20 mothers of healthy infants. 13 of 19 mothers showed decreased subclass levels: 10 of 19 low IgG2, 9 of 19 low IgG1 and 4 of 19 low IgG3. The levels of IgG1, IgG2 and IgG3 were significantly lower among mothers of GBS-infected infants than among the controls. Thus, there is indirect evidence that the infants were immunodeficient at birth.

IgG deficiency in association with placental oedema.

Deficiency of the immunoglobulin C (IgG) in the human newborn is rare in the absence of maternal hypogammaglobulinaemia. Low concentrations of IgG in cord blood were found in 3 conditions--the donor twin in the fetofetal transfusion syndrome, hydrops fetalis and congenital hepatic disease. These were all associated with placental oedema. It is suggested that the oedema may be responsible for a disturbance in maternofetal placental transfer.