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Vesicular exanthema of swine.

Vesicular exanthema of swine (VES) was first recognized in 1932. At the time, eradication measures and, later, quarantine procedures were instituted and extension of the disease to surrounding farms appeared to have been prevented. Between 1932 and 1936, however, seemingly unrelated epizootics continued among swine herds being fed raw garbage. In 1936, VES disappeared only to reappear in 1939. The disease was contained within California until 1952, at which time it spread to all the major swine producing areas of the United States. The disease was eradicated in 1959, through the enforcement of laws prohibiting the feeding of raw garbage to swine. Other than the association with raw garbage, a reservoir for VES virus (VESV) was never found. In 1972, a virus isolated from California sea lions--and thus named the San Miguel sea lion virus (SMSV)--proved to be distinguishable from VESV. When SMSV was injected into swine, clinical signs of vesicular exanthema developed, leading to the conclusion that, for all practical purposes, SMSV and VESV were the same. To date, 5 species of marine mammals and 2 species of terrestrial mammals, including feral swine, have been shown to possess antibodies to 1 or more of the 4 distinct SMSV serotypes. Current evidence suggests that SMSV infections occur among both terrestrial and marine mammals inhabiting the California coastal zones. This and the practice of shipping frozen meats known to contain SMSV to mink ranches in Utah point to the possibility that domestic swine in the United States are occasionally being exposed to SMSV. Although marine mammals are a source of SMSV, the primary virus reservoir is thought to be 1 or more submammalian marine species common to the southern California coastline. Such a primary reservoir presumably is the source of a new SMSV serotypes infecting marine mammals and may have been the original source of the VESV serotypes that infected swine through the intermediary of raw garbage.

Abortion, Veterinary

Vesicular exanthema of swine and San Miguel sea lion virus.

San Miguel sea lion virus (SMSV), recently isolated from marine mammals, and vesicular exanthema of swine virus (VESV), which caused epizootics of vesicular exanthema of swine (VES) over a period of 24 years (1932 to 1956), may be the same virus. This finding is of particular interest because the source of the original VES epizootic was never identified, swine were the only known natural host of VESV, and VESV was thought to have been eradicated. The SMSV has been shown to be enzootic in 2 species of marine mammals found off the coast of California and to cause lesions in swine that are indistinguishable from those caused by VESV. Therefore, we should be alert to recognize situations in which swine might become exposed to SMSV and to consider SMSV in differential diagnoses of vesicular conditions.

Animals

A model for vesicular exanthema virus, the prototype of the calicivirus group.

The structure of vesicular exanthema virus, the prototype member of the calicivirus group, has been studied in more detail. The RNA comprises 18% of mol. wt. of about 2.8 x 10(6), based on polyacrylamide gel electrophoresis experiments in the presence of formaldehyde. The virus contains one major polypeptide, mol. wt. 70 x 10(3) as determined by polyacrylamide gel electrophoresis and by chromatography on Sepharose 6B in the presence of 6 M-guanidine. Further evidence for the presence of a single major polypeptide was obtained by tryptic peptide analysis of 35S-methionine labelled virus. The mol. wt. of a protein oligomer produced by adjusting the pH of virus suspensions to 3.5 was c. 200 x 10(3). On the basis of these data we propose a T = 3 model for the virus capsid incorporating 180 copies of the virus protein.

Animals

Coital exanthema in stallions.

Equine coital exanthema can be produced experimentally in stallions by inoculation with an equine herpesvirus (strain 65/61) and be transmitted during coitus with an infected mare. Serological responses to this infection include the production of complement-fixing and serum-neutralizing antibodies which reach maximum levels 14 to 21 days after infection. Complement-fixing antibodies decline rapidly and are usually not detectable by 60 days after infection, whereas serum-neutralizing antibody activity is maintained for at least 1 year. This disparity provides a useful method for the diagnosis of recent infections and estimation of the temporal incidence of infection in groups of mares. It seems likely that clinically normal carrier mares spread the virus on studs where the disease has previously not occurred.

Animals

[Drug-induced fixed exanthema: immuno-allergologic study of 37 patients].

The Authors performed ona group a patients suffering from drug exanthema a thorough clinico-anamnestic and allergo-immunological investigation (skin reactions, patch-tests, Prausnitz-Küstner passive transport, in vitro lymphocyte blastization, total serum IgE radioimmunoassay). The results obtained do not support an immunoallergical pathogenesis of this syndrome. The possible alternative hypotheses and the future perspectives of study are discussed.

Adolescent

Comparative resistance of San Miguel sea lion virus and vesicular exanthema of swine virus to chemical disinfectants.

Two similar calici agents, San Miguel sea lion virus (SMSV) and vesicular exanthema of swine virus (VESV) are susceptible to the virucidal activity of disinfectants of differing formulation. Ten of 12 compounds were effective against six log10 plaque forming units (PFU) of SMSV in a 2-min exposure at 4, 25 and 37 degrees C. However, only seven of these 10 SMSV-positive compounds inactivated VESV under the same conditions of temperature and time. Two compounds were not effective against SMSV in a 20-min exposure at 4 and 25 degrees C, but were effective at 37 degrees C. Two of the three compounds not effective against VESV in a 20-min exposure at 4 and 25 degrees C were also effective at 37 degrees C. The test iodophor compound inactivated SMSV completely but had only minimal inactivating activity against VESV at the three temperatures tested.

Animals

Prevalence of vesicular exanthema of swine antibodies among feral mammals associated with the southern California coastal zones.

Serum-neutralizing antibodies to both vesicular exanthema of swine virus (VESV) and San Miguel sea lion virus (SMSV) were found in a number of animal species having an association with the southern California coastal zones. California sea lions (Zalophus californianus) had antibodies to 9 VESV types (A48, C52, D53, E54, F54, G55, I55, J56, and K56). Fur seals (Callorhinus ursinus) and elephant seal pups (Mirounga angustirostris) were tested for antibodies to 6 VESV types and all were negative. California gray whales (Eschrichtius robustus) were tested for antibodies to 9 VESV types, and sperm whale (Physeter catodon), finback whale (Balaenoptera physalus), and sei whale (Balaenoptera borealis) were tested for 6 VESV types. Among the last 4 species, antibodies were present for each VESV type except C52, and all species were positive for antibodies to 2 or more VESV types. Feral swine from both Santa Cruz Island and Santa Catalina Island were tested and antibodies were present for 8 of 9 VESV types and all SMSV types except SMSV-4. One donkey from San Miguel Island was positive for VESV I55 and 2 were positive for SMSV-2.

Animals

[Etiology and morbidity of drug exanthemas from a clinical viewpoint].

After a brief discussion of the potential errors and uncertainies of statistics about etiology and epidemiology of drug eruptions the 144 cases, seen from 1968 to 1974 in our dermatological clinic, are analysed and compared with the data from the years 1957 to 1965 respectively the quantities of special drugs, consumed during one year in Dresden city. The results are: significant increase of drugs eruptions (from 0,9% in 1957 to 1965 to 1,9% in 1968 to 1974) among the hospitalised patients; absolute and relative increase of penicillin- (36,7%) and chloramphenicolreactions (21,6%) combined with a decreasing importance of sulfonamides and barbiturates among the causes of drug rashes; increase of urticarial - and decrease of fixed exanthemas: a yearly frequency of 3 to 4 clinically treated ore diagnosticated drug eruptions/100 000 inhabitants respectively 1 to 2 chloramphenicol and 1--5 penicillin-rashes/10 000 treatments. Even if only 10% of the drug eruptions are diagnosticated by us and 90% in other clinics or ambulances the frequency of penicillin-rashes merely amounts to 1 to 5%.

Barbiturates

[The value of the thrombocytopenia test in the specific diagnosis of drug allergy, especially drug-exanthema].

125 thrombocytopenia tests (so-called thrombocytopenic index) from 94 patients with suspected drug allergies and negative skin tests were critically examined to determine the value of this in vivo method in the clarification of drug allergy. A consistent decrease of 20% or more in thrombocytes was rated as significant and therefore indicative of drug sensitization. 78.4% of the tests were in agreement with the expected result. Clinically relevant drug sensitivity was apparent in 30.4% of the tests, while the possibility of allergy could be eliminated in 48%. 16.8% of the results were inconclusive and 4.8% were false negatives. A flare-up occurred after 5.6% of the tests. A leukocyte count was considered unnecessary since it proved to be unrelated to a drop in thrombocytes and the existence of drug allergy. The thrombocyte test is a practical and valuable method for investigation of drug allergies, especially as the available in vitro tests are too complex to be used routinely in a diagnostic test program. However, the results must be considered critically in conjunction with an accurate case history, the clinical symptoms and the course of the disease. In the case of blisters and erythema exsudativum multiforme-like drug exanthema, renewed exposure to the suspected drug must be avoided due to the possible danger of a drug reaction. The latest research results have helped to clarify the underlying mechanism of the thrombocyte decrease.

Aspirin

[Complement pattern in children with allergic-toxic exanthema--a contribution to differential diagnosis (author's transl)].

25 Sera from children with the clinical diagnosis: urticaria, allergic-toxic exanthema were examined for the complement components C3, C4 and C3-Activator. We applied the radial immunodiddusion. As controls served 50 helathy children and 25 children with morbili, rubeolae and scarlet fever. C3 was found to be decreased in 23 cases, C4 in 4 and C3-Activator in 19 cases of urticaria. This indicates the possiblity for the differential diagnosis, but children of the control groups did not show any consumption of one of the described complement components.

Child