Agammaglobulinemia in a horse with evidence of functional T lymphocytes.

Agammaglobulinemia was diagnosed in a 1-year-old Thoroughbred horse on the basis of the following observations: (1) absence of serum immunoglobulins M, A, and G(T); (2) small amounts of serum immunoglobulin G (16 mg/100 ml); (3) absence of specific antibody in the serum of the horse following immunization and challenge exposure to 2 antigens; (4) absence of plasma cells, primary follicles, and germinal centers in a lymph node removed after antigenic stimulation; (5) absence of "natural" serum antibodies to rabbit-erythrocytes which were easily detectable in age-matched control horse serums; and (6) increased susceptibility to infections. There was evidence of functional cell-mediated immunity which included a skin response to injected phytolectins, skin response to antigen challenge following sensitization, and in vitro proliferative response of lymph node cells to phytohemagglutinin. An intact cell-mediated immune response was also supported by the observation that the horse lived to 17 months of age without antibody production, whereas horses with an absence of both antibody production and cell-mediated immunity (combined immunodeficiency) die by 4 months of age without immunologic intervention. The known features of agammaglobulinemia in this horse are similar to those in sex-linked agammaglobulinemia in persons and are unique among the immunodeficiences described in other animals.     

The effect of the administration of Solanum malacoxylon on the chick.

Replacement of the drinking water of chicks maintained on a normal mixed protein diet with an aqueous extract containing the equivalent of 5 g of the dried leaves of Solanum malacoxylon (DLSM) per 100 ml for one month produces a hypercalcaemia (23-49 per cent), hypomagnesamia (28-37 per cent), hypophosphataemia (26-34 per cent), hypouricaemia (29-34 per cent) and a decrease in plasma alkaline phosphatase activity (54-98 per cent). The ash content of the defatted, dried tibiae and the body weight of the DLSM treated chicks were also significantly lower (37-7 per cent and 17-79 per cent respectively) than the corresponding values for the untreated birds. The results obtained are similar to those reported for hypervitaminosis D3 in the chick.     

Changes in the ultrastructure of cardiac muscle in steers deprived of copper.

Young Friesian steers were fed for nine months on copper supplemented or depleted diets. Immediately after they had been killed, tissues were taken from the myocardium for examination by electron microscopy. Copper deficiency was associated with extensive changes in myofibrillar and mitochondrial morphology and distribution. It is suggested that the ultra-structural changes in the myocardium were specifically attributable to copper deficiency, the most likely underlying biochemical defect being lost of cytochrome oxidase activity.     

Comparison of the specificty of human and bovine tuberculin PPD for testing cattle. 1--Republic of Ireland.

A tuberculin testing trial in cattle was carried out in the Republic of Ireland to compare the specificity for bovine tuberculosis of a human purified protein derivative (PPD) tuberculin (Weybridge) with that of a bovine PPD (Rotterdam), and to determine whether discrimination between specific and non-specific reactions to mammalian tuberculin is better with doses of tuberculins smaller than those traditonally used for testing cattle. Tests were carried out in 510 cattle, 395 of which were shown by post mortem examination to be tuberculous and 115 non-tuberculous. Three dilutions at five-fold intervals of both mammalian tuberculins were used together with two dose levels of avian tuberculin PPD (Weybridge), and all reactions were measured both by increase in skin fold thickness and by diameter of induration. In the environment of this trial, the bovine PPD was shown to be more specific for bovine tuberculosis than the human PPD, and particularly in differentiating from "skin tuberculosis". There was no indication of greater specificity at lower doses of tuberculin. Measurement of induration diameter proved a satisfactory alternative method of reading tuberculin reactions in cattle under field conditions.     

Pathology of Mycoplasma agalactiae induced granular vulvovaginitis (GVV) in goats.

Granular vulvovaginitis (GVV) was experimentally produced in female kids by topical application of M. agalactiae on the scarified vulvar mucosa. Grossly visible GVV lesions were seen in 25 out of 30 infected kids, yet all were positive for microscopic lesions. Microscope lesions that appeared by 7 days post infection (DPI) were comprised of stromal oedema, lymphocytic infiltration into the lamina propria and perivascular accumulation of a few lymphocytes. The lesions observed between 28 and 49 DPI were comparable to those of spontaneous cases (severe). The changes seen in kids euthanized between 56 to 70 DPI were suggestive of the chronic stage of the disease. M. agalactiae was reisolated from all the infected kids from 7 to 70 days after inoculation. The pathology and pathogenesis of this condition have been described and discussed.     

THE USE OF FLUFF COUNTS IN A STUDY OF HYGIENE IN QUEENSLAND HATCHERIES

During 1972, 333 fluff samples were tested from 13 Queensland hatcheries and assessed according to the English standards for total count, coliforms and fungi. They were also assessed as being "standard" or "substandard", using a combination of the criteria of the English system. All hatcheries had at least 2 substandard samples and all the samples from 2 hatcheries were substandard.     

Q fever (Coxiella burnetii) investigations in dairy cattle: persistence of antibodies after vaccination.

The immune response and persistence of antibodies were investigated in dairy cattle vaccinated with formalin-inactivated phase (ph) I Coxiella burnetii vaccine agglutinating antibody geometric mean titer (GMT) of 193.2 at 1 month after vaccination compared to a GMT of 2.0 for nonvaccinated calves. The agglutinating antibodies gradually decreased in vaccinated cattle, but the GMT remained approximately 4 times higher than that for the nonvaccinated group for at least 20 months. Results of serotests at 2 months after revaccination indicated a rapid increase in the GMT to 177.0 with agglutinating titers between 1:64 and 1:512.     

Endotoxin from Fusobacterium necrophorum of bovine hepatic abscess origin.

The endotoxic activity of Fusobacterium necrophorum bov 5 was investigated. The supernatant (S) fluid and cell wall (CW) preparation, obtained after differential centrifugation of the ruptured cell mass, were lethal for mice. The toxicity of the S fluid was stable during prolonged storage, treatment with formalin, and heating for 15 minutes at 80, 100, and 121 C, but was destroyed by alkaline hydrolysis with 0.25 N NaOH. The toxic factor was found in a high molecular weight (MW) fraction after gel filtration. The properties exhibited by the toxic S fluid resembled those of endotoxic lipopolysaccharide (LPS). Extracted and partially purified LPS (endotoxin) from F necrophorum bov 5 demonstrated a mouse median lethal dose (mouse LD50) of 16.8 mg/kg of body weight. The toxic LPS material, a high molecular weight moiety as estimated by gel filtration, was resistant to ribonuclease (RNase), deoxyribonuclease (DNase), and pronase treatment. A positive Shwartzman reaction (median skin lesion dose (SLD50) equal to 3.32 mug/kg of body weight) and biphasic fever response (minimal dose required to produce a fever index of 40 sq cm which falls on the linear portion of dose-response curve (FL40) equal to 0.41 mug/kg of body weight) further indicated the toxin was endotoxin in nature. The LPS from F necrophorum bov 5 was less toxic than Salmonella typhimurium LPS; but had considerable toxicity for experimental animals. The toxic activity of the partially purified F necrophorum bov 5 endotoxin was separated into 2 fraction regions by diethylaminoethyl (DEAE)-cellulose chromatography. The data provide evidence for the production of a potent endotoxin, possibly composed of more than one toxic component, which may be released upon cell disruption.