
Gut samples from 50 nonselected slaughtered chickens were obtained in two poultry processing plants and cultured for Campylobacter jejuni and Salmonella. Positive results were obtained in 84% and 4%, respectively. Viable C. jejuni and Salmonella were detected in every phase of processing, even during packaging for commercial purposes. Of surface samples taken from 118 slaughtered chickens prepared for delivery to consumers, 88 were contaminated by C. jejuni and 17 by Salmonella.
Based on the literature and the authors' studies, the genetic markers of Shigella and the chromosome regions connected with pathogenicity are listed. A provisional map of Shigella chromosome and another provisional map indicating the chromosomal regions related to Shigella virulence have been constructed. Both maps could be useful for further genetic investigations of Shigella.
Mycobacterium xenopi was isolated from the sputum of 21 patients with clinical signs of pulmonary disease and of 52 asymptomatic subjects living in the environment of a sludge pool. M. xenopi was cultured in high numbers from sludge samples. The infections were assumed to occur partly via dry sludge particles scattered by the wind in summer, and partly by sludge used as fertilizer.
Lipopolysaccharide of the Salmonella minnesota Re mutant R595 was irradiated with 60Co gamma doses of 50, 100, 150 and 200 kGy. The irradiated preparations were less toxic, less active in the Shwartzman reaction and as activators of the complement system, but they had retained the protection activity against the lethal action of endotoxin. The irradiation resulted in a dose-dependent decrease in the amounts of constituents (glucosamine, KDO, fatty acids) of the original lipopolysaccharide. With increasing irradiation doses increasing amounts of the irradiated material became dialysable (up to 21% in the 200 kGy sample). Only 50% of total fatty acids were present in the 200 kGy preparation compared to the parent lipopolysaccharide. The degradation products formed during irradiation have not been identified.
The sensitizing activity to egg protein of an A1PO4-adjuvant purified and concentrated influenza-A vaccine was examined in animal experiments and in man. Intravenous injection of ovalbumin caused anaphylactic symptoms and/or fatal anaphylactic shock in prevaccinated guinea-pigs. Ovalbumin-specific antibodies detectable by the passive haemagglutination reaction (PHA) appeared in the blood serum of the vaccinated animals. Model experiments with purified ovalbumin suggested that 1 human dose of the vaccine contained egg protein in the range from 0.1 to 1 ng, and that the antigenic effect of the vaccine grew to more than 10(3)-fold by its adsorption to A1PO4 gel. Adults who in previous years had been immunized with similarly prepared influenza vaccine several times responded with mild reactions; symptoms suggestive of hyperergy did not occur, irrespective of the vaccination history. In the prevaccination serum sample of some vaccines, ovalbumin-specific PHA antibodies were found up to titres independent of the number of the previous immunizations. The concentration of the ovalbumin-specific antibodies of the IgE class was by several orders of magnitude lower in the postvaccination samples than in the serum of some patients hypersensitive to egg protein.
Cytotoxic substance(s) of about 4 X 10(3) molecular weight, containing 9.5% peptide and 73% carbohydrate was released from Staphylococcus epidermidis in phosphate buffered saline. The material was soluble in ethanol and was heat-resistant. It blocked amino acid uptake and E-rosette formation of human tonsillar and blood lymphocytes. In isolated mouse hepatocytes the toxin inhibited protein synthesis, but only in the presence of calcium ions. The results suggest that eukaryotic cell membranes are damaged by the coccal agent.
One of the HEp-2 sublines maintained in the authors' laboratory was found to carry LCM virus. The virus proved to be identical with the prototype strain LCM-Am except that its multiplication rate in cell cultures and its mouse pathogenicity were limited. Forty-six cell cultures maintained in 10 Hungarian laboratories were examined for LCM carriership. Sixteen cultures including 11 HEp-2 sublines, all originating from a culture brought into Hungary in 1959, proved to carry the virus. Three FL sublines maintained in two laboratories and two sublines, viz. an RK-13 and a HeLa, maintained in a third one, were also contaminated by LCM virus. In these cases, the carrier HEp-2 subline was the probable source of infection and virus transmission is thought to have occurred in the course of manipulation with cell cultures. The necessity of introducing strict preventive measures in tissue culture laboratories is emphasized in the interest of the laboratory workers and for obtaining reliable laboratory results.
The diagnostic value of the leukocyte migration inhibition test was examined by comparing it to other specific laboratory methods i.e. complement fixation, indirect haemagglutination and skin test in 10 patients with acquired lymphoglandular toxoplasmosis. In the acute phase the serological tests gave more reliable results than did the LMI test. In subacute and chronic cases, however, there was a good correlation between dermal reactivity and LMI test. LMI is believed to represent a specific test for the detection of cellular hypersensitivity in human toxoplasmosis and so it can be used as a non-invasive method instead of dermal tests.
Methylated bases of the DNA of two mycobacteria (Mycobacterium phlei and Mycobacterium smegmatis var. butyricum) and two mycobacteriophages (Phage phlei and Phage butyricum) have been studied. In both the bacterial and the phage DNAs 5-methyl-cytosine and 6-methyl-aminopurine could be detected. Using L-(methyl-H3)-methionine as methyl donor not only the methylated bases of bacterium and phage DNA proved to be radioactive, but also the non-methylated purine residues and thymine. Possible pathways of this phenomenon are discussed.
Herbicide 2,4-D at a dosage of 500 mg l-1 stimulated the proliferation of the heterotrophic bacterial community present in the water of three fish ponds over a period of one year. 2,4-D due to its toxic action might kill the planktonic algal population occurring in the pond water, which on degradation generated more nutrients conductive to bacterial proliferation. The microbial density in different hours were closely correlated (p less than 0.01 less than 0.05) with the variations of each of NH4-N, NO2-N and specific conductivity of water, while the relationship between the former and PO4-P was reciprocal (P less than 0.001).
Death occurred earlier and its rate was higher in suckling mice treated with parent or radio-detoxified endotoxin and subsequently inoculated intracerebrally with lymphocytic choriomeningitis (LCM) virus than in their virus infected but untreated control littermates. Thus, in suckling mice both the parent and the radio-detoxified endotoxin pretreatment contributed to the outcome of LCM virus infection in the form of lethal meningitis indicating its increasing effect on the cellular immunological reaction to the virus infection.
Incorporation of [3H]thymidine ([3H]TdR) into tonsil lymphocytes was inhibited by native Staphylococcus epidermidis while Staphylococcus aureus Cowan I caused stimulation. The inhibitory effect of S. epidermidis was abolished by formalin treatment but not by heat killing. A toxic agent was released from S. epidermidis on gentle water extraction without lysing the bacteria. The extract contained protein and other UV-absorbing material, but did not exhibit haemolytic, lysozyme, catalase or protease activity. The heat-resistant, formalin-sensitive inhibitor present in the aqueous extract of S. epidermidis inhibited [3H]TdR incorporation of lymphocytes in a dose-dependent manner and decreased the viability of lymphocytes.