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The serum proteins in Sapphire mink from the experimental and control groups in 2 endotoxin experiments and in a group of normal mink of the Standard type, were separated electrophoretically on cellulose acetate membranes. In experiment No. 1, in which the experimental mink were given repeated injections of endotoxin, and the controls were untreated, significantly increased total protein and significantly decreased albumin concentrations in the experimental group compared to the normal group were demonstrated. The concentration of the alpha(1)-globulin was significantly elevated and the alpha(2)-globulin significantly reduced in the experimental and the control groups compared to the normal group. Significant differences between the gamma-globulin concentrations in the various groups were not found. In experiment No. 2, all the animals were inoculated intraperitoneally with a crude tissue suspension containing the plasmacytosis agent 10 days before the experimental animals received the first of a series of injections with endotoxin. Significantly increased concentrations of total protein and gamma-globulin and significantly decreased albumin concentrations were, compared with the normal group, demonstrated in sera collected from the experimental group on the 94th, 201st and 254th day after the first injection of endotoxin. In the control group, compared with the normal group, significantly elevated concentrations of total protein, alpha(2)-, beta- and gamma-globulins and significantly reduced albumin- and alpha(1)-globulin were found but only in the second set of samples, while significantly decreased albumin- and significantly increased gamma-globulin concentrations were found in the third set. The results showed no significant differences between the gammaglobulin concentrations or between the other serum fractions in the experimental and the control groups in the 2 experiments. A possible explanation may be that there is no direct interrelationship between hypergammaglobulinaemia and amyloidosis, and that a common basic mechanism may stimulate related stem cells which thereafter differentiate in different ways.

During recent years nosematosis has been a major problem in the breeding of blue fox in the Scandinavian countries, causing heavy losses among growing pups (Nordstoga 1972, Nordstoga et al. 1974). The lack of reliable methods for diagnosing the infection in live foxes has so far made epizootiologic studies of the disease very difficult. However, reports on the IFAT in rabbits with nosematosis (Cox et al. 1972, Chalupsky et al. 1971, 1973, 1974), encouraged the search for a method of detecting Nosema antibodies in fox sera.

During recent years, nosematosis (syn. encephalitozoonosis) has caused serious losses among young blue foxes (Alopex lagopus) in Norway; the causative organism is considered to be Nosema (syn. Encephalitozoon) cuniculi. Descriptions of clinical symptoms and patho-morphological changes on which the diagnosis is based have been given in previous papers (Nordstoga 1972, Nordstoga et al 1974, Nordstoga & Westbye 1976). The disease, as a rule, is restricted to certain litters, in which several or all pups are affected, a pattern which indicates a congenital infection. In a previous report we presented experimental evidence for transplacental transmission, after oral infection of the dam (Mohn et al. 1974). Although we feel that oral exposure, resulting in subclinical infection, is the most common way in which the dams are infected, field observations indicate that the organisms, in rare cases, may be transmitted from the male during matins.

Two groups of blue fox pups about 1½— 2 and 2½—3 months old, respectively, suffering from experimental encephalitozoonosis, were examined clinically and serologically. Antibodies to Encephalitozoon cuniouli were detected in all pups, the titres varying within the range 10–12,800. In addition to unspecific signs of disease the pups showed various neurological disturbances including ataxia, posterior weakness, lameness and circling behaviour, terminaiting in recumbency, paralysis or convulsions. Reduced sight or blindness was observed occasionally. Some of the pups appeared thirsty. Haematological examinations revealed pronounced leukocytosis without any conspicuous shift within the various groups of leukocytes. Biochemical examinations of serum showed significant elevated values of urea nitrogen, creatinine, and magnesium concentrations, reflecting renal dysfunction. Alanine aminotransferase was found significantly depressed in both groups. Raised levels of total protein were demonstrated due to pronounced hyperglobulinaemia. This finding, together with the common occurrence of generalized polyarteritis nodosa and proliferations of plasma cells in clinically affected pups, is probably a result of autoimmune disturbances initiated directly or indirectly by the protozoan infection.

The infectivity of Toxoplasma gondii cysts in the brains of mice, after storage at -21 degrees C for various periods of time, was studied by intraperitoneally inoculation into mice. Infective parasites were not demonstrated after freezing for 5 hours or longer. Even after 1 1/2 hours exposure to -21 degrees C, many cysts seemed to lose their infectivity. The role of low temperatures as a limiting factor in the epidemiology of cyst-induced toxoplasmosis, is discussed.

The serum proteins in 1 group of healthy breeders, 1 group of healthy pups and 4 groups of foxes suffering from various diseases were separated electrophoretically on cellulose acetate membranes. In most of the sera, the proteins were separated into 1 albumin fraction and 5 globulin fractions designated alpha(1), alpha(2), alpha(3), beta and gamma. The mean concentrations of the total proteins and the various serum fractions in the disease groups were compared statistically with the mean values of the normal groups. A nosematosis group was characterized by a distinct hypergammaglobulinaemia together with an increase in the total protein — and a decrease in the albumin concentrations. However, in 2 cubs recovering from nosematosis the hypergammaglobulinaemia was shown to be reversible. In a feed intoxication group the concentration of albumin was found to be lower and the alpha(3)-globulin higher than the corresponding values in the healthy group. A virus hepatitis group was characterized by a decrease in the concentrations of albumin and beta-globulin and an increase in the alpha(1)- and alpha(3)-globulins. In the toxoplasmosis group the total protein and alpha(1)- and alpha(3)-globulins showed concentrations below the normal values.

Newborn and young pups up to the age of 15 days were exposed to E. cuniculi, either by keeping the pups in cages together with orally inoculated foster-mothers and their offspring, or by oral inoculation with E. cuniculi spores. A majority of pups appeared sero-positive to E. cuniculi with the india-ink immuno-reaction from 35 to 87 days post exposure; spores of E. cuniculi were detected in organs of some of the animals. The non-inoculated pups kept together with the orally inoculated pups became seropositive from 49 to 129 days after the oral inoculations. However, the exposure of newborn and young pups failed to induce clinical encephalitozoo-nosis, and when killed at the time of pelting the body weights and fur quality appeared to be within the normal range in all exposed foxes. No macroscopic lesions were detected in the various organs. Histologically focal interstitial nephritis occurred in the great majority of the seropositive animals. Meningoencephalitis was seen in some of the foxes, whereas slightly thickened walls of some arteries, mainly in the myocardium, were found in a few animals. The lesions of the brain and kidneys seem to be very similar to those seen in chronic cases of rabbit encephalitozoonosis. Polyarteritis nodosa and severe encephalitis and interstitial nephritis with extensive proliferations of plasma cells, which are almost constant findings in cases of clinically diseased foxes, were not detected in any of the subclinically infected animals. Various factors that might be of significance in the pathogenesis of the disease are discussed, and it is concluded that intrauterine infection of the pups via the transplacental route appears to be an essential supposition for the establishment of clinical fox encephalitozoonosis.

Spores of Encephalitozoon cuniculi were recovered from foetal and placental tissues from blue fox females orally inoculated with the parasite. The results provided evidence for transplacental transmission of the causative agent of fox encephalitozoonosis.

Enzymoserological comparison of a selection of leptospira strains tested with sera from rabbits immunized with unpurified DNase of Leptospira interrogans, serotype canicola, indicates the production of DNase of serologically very similar properties by the serotypes canicola, autumnalis, icterohemorrhagiae and pomona. The DNase produced by serotype hyos was serologically different from the others, while the serotypes grippotyphosa and bataviae did not produce DNases at all. The method used made it possible to differentiate between leptospiral DNase and normally occurring DNases in the serum samples. Neither leptospira DNase nor specific leptospira-DNase-antibodies could be detected in dog sera with high agglutinationlysis titres after natural infection.

Sera from 32 foxes sampled at intervals varying from 20 to 70 days after oral inoculation with E. cuniculi spores were tested by the india-ink immunoreaction (IIR) and the indirect fluorescent antibody test (IFAT). Using the IFAT, antibodies were detected at low levels in sera sampled on days 20 and 29 post inoculation, whereas the IIR failed to reveal antibodies in the same sera. In sera sampled from day 35 until day 70 post inoculation, antibodies were detected by both tests, the IIR-titres reaching the magnitude of the IFAT-titres after about 50 days posit inoculation. In 14 sera sampled from foxes of at least 46 days of age and with signs of encephalitozoonosis, the tests gave almost identical results. Comparing IIR- and IFAT-determined antibody titres using E. cuniculi antigens of blue fox and rabbit origin in the test, the antigens seemed to be closely related, supporting the suggestion that the isolates are strains of the same microsporidian species.