- Volume 15, Issue 3, 1982

No difference between wild type and RA27/3 strains of rubella virus was revealed by sedimentation or polyacrylamide-gel electrophoresis. Antibodies in post-infection and post-vaccination sera differed in their affinity for wild-type and RA27/3 strains, suggesting an antigenic difference.

Nearly 1000 sera from children were tested by immunoelectro-osmophoresis against BK virus, and age-specific prevalence rates were estimated from birth until the age of 12 years. Declining rates during the first 12 months showed the waning of passive immunity, which at birth reflects the mother's immune status. The changes of prevalence suggested that the peak incidence of primary infections occurred at about 2 years, with an estimated peak annual rate of 24·6%.

Two hundred and twelve randomly selected vaginal or uterine cervical specimens were investigated for the presence of anaerobic and aerobic bacteria and yeasts. Anaerobes of possible clinical significance, including Bacteroidaceae, Peptococcaceae and clostridia were isolated from 34% of the specimens and were identified to specific or generic level. Among the Bacteroidaceae isolated, B. bivius was the most common, followed by other propionate-negative species. Members of the Bacteroides fragilis group were seldom isolated. Of the aerobic or facultatively anaerobic isolates, enterococci and Escherichia coli were most often found. The results show that clinically significant anaerobes, especially Bacteroides species, are not regular members of the vaginal flora and that the species distribution of anaerobes occurring in the genital tract is significantly different from that of the intestinal tract.

The virulence of Escherichia coli strains in ascending urinary-tract infection was studied in mice drinking a 5% glucose solution; factors determining the virulence were examined. Of 33 strains, 8 (group I) infected the bladder and kidney, 10 (group II) infected only the bladder, while the remaining 15 strains (group III) did not cause infection. The adherence of group-I and group-II strains to bladder epithelial cells in vitro was inhibited by D-mannose. In group III, 13 strains barely adhered to the epithelial cells, while two strains showed an adherence unaffected by D-mannose. Most strains in groups I and II agglutinated erythrocytes of guinea-pig, chicken, and horse, and cells of Candida albicans in a mannose-sensitive manner. All strains in groups I and II had fimbriae. Virulence for the urinary tract was not directly related with O-serotype, intraperitoneal virulence, ability to grow in mouse urine, ability to ferment dulcitol, production of haemolysin, susceptibility to serum bactericidal activity, or susceptibility to antibiotics. These results suggest that the adherence of the E. coli to mouse-bladder epithelial cells in a mannose-sensitive manner plays an important role in the development of urinary-tract infection in mice and that the adherence is probably mediated by type-1 or closely related fimbriae.

The main pathological feature of experimental legionellosis produced by the intraperitoneal inoculation of guinea-pigs was a fibrinopurulent peritonitis, especially over the liver and spleen. Foci of necrosis were present in these organs from the second to seventh day after infection. Early biochemical changes in the serum included significant decreases in the concentration of zinc and iron, and increases in copper and triglycerides. Phenylalanine to tyrosine ratios increased strikingly, but free amino acid decreased slightly. The total protein concentration did not change, but acute-phase proteins increased. Serum lysozyme activity increased as leucocytosis developed but fell during the subsequent leucopenia. In the later stages of the disease the activity of alkaline phosphatase. y-glutamyl transpeptidase, and creatine kinase decreased; that of dehydrogenases and transaminase increased.

The lipopolysaccharide (LPS) and heat-modifiable outermembrane protein (P') serotypes of 39 coded strains of group-A Neisseria meningitidis isolated from patients during seven geographically and temporally separate outbreaks of infection were determined blindly. LPS serotype discriminated between strains from different outbreaks and between strains of differing sulphadiazine sensitivity within a single outbreak. Thirty-seven strains were of three separate serotypes and no strain was of multiple serotypes. In contrast, P' serotypes did not discriminate between strains. Multiple serotypes for single strains and among strains from a single outbreak were the rule. LPS serotyping appears to be a useful epidemiological tool for distinguishing group-A strains of N. meningitidis.

Various strains of Leptospira interrogans were compared by bacterial restriction-endonuclease DNA analysis (BRENDA). Field strains of serovar hardjo isolated from domestic animals in New Zealand, Australia and Northern Ireland were indistinguishable from one another but differed strikingly from the hardjo reference strain Hardjoprajitno. Similarly, field isolates of balcanica and tarassovi differed from their serovar reference strains, probably owing to a difference in epidemiological niche. Subdivision of these serovars into distinct subtypes as defined by BRENDA is therefore useful and justified. In contrast, analysis of serovars pomona, ballum and copenhageni shows that field and reference strains were identical, or differed only by a single band.

It is suggested that BRENDA will overcome many of the problems associated with serological methods of identifying serovars and allow more precise definition of epidemiological relationships between strains and their hosts.

An attempt was made to protect rhesus monkeys from dental caries by immunisation with Streptococcus mutans, Lactobacillus acidophilus and lipoteichoic acid (LTA). The vaccine composed of S. mutans gave significant protection against caries, a decrease in the number of S. mutans, an increase in IgG antibodies and a moderate increase in complement-fixing antibodies to LTA. When LTA was used as immunogen, there was only a small reduction in caries, without any detectable antibodies to LTA and a slight increase in IgG antibodies to cells of S. mutans. Vaccines of L. acidophilus or L. fermentum gave no protection. A combined vaccine of S. mutans and L. acidophilus did not reduce the incidence of caries but the antibody titre to cells of S. mutans was raised to a level comparable with that in the S. mutans-immunised monkeys. The results of this investigation in a subhuman primate confirm that immunisation with S. mutans induces protection against caries, unlike the attempt to immunise with two selected strains of lactobacilli. More studies are required to establish the role of specific serotypes of lactobacilli in the development of dental caries.

The ability of human polymorphonuclear leucocytes to phagocytose and kill Proteus mirabilis was impaired in vitro when the human serum, used to opsonise the target bacteria, was pretreated with cultures of various Bacteroides species. Live and dead, either heatkilled or clindamycin-treated, bacteroides cells elicited the same phenomenon. When bacteroides-treated serum was used to opsonise different Proteus species, the subsequent uptake of all strains by polymorphonuclear leucocytes was inhibited, whereas bacteroides-treated serum inhibited the uptake of some but not all of the test strains of Escherichia coli. The opsonic activity of untreated human serum was reduced when the classical complement pathway was inhibited by ethyleneglycolbis-(β-aminoethyl ether)N,N1-tetra-acetic acid (EGTA); subsequent treatment with bacteroides did not further reduce the opsonic activity of the serum for P. mirabilis.

A binding assay was used to study the attachment of type-III group-B streptococci (GBS) to buccal epithelial cells. Results indicate that an adhesin, with the characteristics of a protein, is the molecule at the streptococcal cell surface responsible for attachment to the buccal cells. The bacterial adhesin probably recognises a sugar on the surface of the mucosal cell, because periodate oxidation of the buccal cells caused a significant reduction in subsequent adherence of GBS. A sonicate of type-III GBS blocked the binding of the organism to buccal cells. The effects of physical and chemical modifications of the sonicate on its ability to prevent bacterial attachment are described; these corroborate the evidence gained from heat and periodate treatments of the buccal cells and GBS. Results suggest a lectin type of attachment mechanism for type-III GBS which can be blocked by n-acetyl-d-glucosamine, rather than attachment by means of a lipoteichoic acid as described for group-A streptococci.

In a system in which unphagocytosed bacteria were removed by differential centrifugation after a 30-min phagocytosis period, staphylococci associated with rabbit polymorphonuclear (PMN) leukocytes were completely protected from the effects of benzyl penicillin 1 μg/ml, but not completely protected from the effects of 5 μg/ml. When unphagocytosed bacteria were lysed with lysostaphin, effective protection could be observed over a range of penicillin concentrations from 0·25 to 200 μg/ml. 14C-benzyl penicillin failed to accumulate in rabbit PMN leukocytes, whether or not they had previously phagocytosed staphylococci, in conditions in which mouse peritoneal macrophages readily accumulated penicillin. Mixed granule extracts prepared from the PMN leukocytes interacted synergically with penicillin against staphylococci at physiological pH (7·2) but failed to show synergy at an intraphagolysosomal pH of 5·0 unless the bacteria were first sublethally treated with penicillin. Experiments in which the pH value of culture media was changed either from 7·2 to 5·0 or from 5·0 to 7·2 indicated that the partial nature of the protective effect of the intraphagolysosomal environment could be attributed to the growthlimiting effects of the low phagolysosomal pH, which prevents full expression of the synergic potential of granule contents and penicillin. The concentration-dependent nature of the protection and its incompleteness are explained by supposing that a proportion of the staphylococci not ingested during the 30-min phagocytosis period are modified by penicillin in a way that opsonises them and potentiates the intrinsic bactericidal mechanisms of the PMN leukocytes when the bacteria are subsequently ingested.