As compared to phenotypically normal (nu/+)NMRI mice showing the typical course of an experimental listeric infection, that of congenitally hypothymic (nude, nu/nu)NMRI mice was found to be characterized from the outset bya chronic trend. During the early phase of the infection, significantly reduced numbers of Listeria monocytogenes were observed in the spleens of nude mice.
Congenitally dysthymic nude (nu/nu) NMRI mice showed increased resistance to viable Listeria monocytogenes cells during the initial phase of infection as compared with euthymic control mice. The intravenous mean lethal dose (LD50), as determined for euthymic mice after an observation time of 7 and 14 days, amounted consistently to 6 X 10(4) Listeria. The corresponding values determined in nude mice were found to be increased by either 20-fold (1.2 X 10(6) Listeria after an observation time of 7 days) or 4-fold (2.4 X 10(5) Listeria after an observation time of 14 days). The transfer of spleen cells from immune euthymic donor mice into chronically infected nude mice caused almost complete elimination of Listeria within 1 week. The injection of dextran sulfate 24 h before a secondary infection with L. monocytogenes caused loss of antibacterial resistance in both chronically infected nude mice and Listeria-immune euthymic mice, this being expressed by a rapid increase in the numbers of bacteria in the spleens as well as the occurrence of serious signs of illness.
Young adult (6–12 weeks old) and aged (20–24 months old) NMRI mice were infected with various intracellular parasites. The following results were obtained: (1) After a sublethal infection with Listeria monocytogenes, aged mice were found to show a resistance similar to that of young adults. A challenge infection with this pathogen was followed by specific immunity of long duration in both age-groups. (2) On the other hand, young animals were significantly more resistant to Salmonellatyphimurium than aged mice. It was concluded that this was due to the LD50 which was 14 times greater for 2-month-old than for 20-month-old mice. Furthermore, during 7 weeks after infection there were more S. typhimurium in the spleens of senescent mice than in those of young adult controls. (3) Aged mice showed highly increased susceptibility to the weakly virulent DX strain of Toxoplasma gondii. Almost all aged animals died whereas the control mice survived. When death of the aged mice was prevented by treatment with sulfadiazine after infection with the DX strain, the aged mice were found to be as well protected against subsequent infection with the strongly virulent BK strain as the young adult mice. These results suggest that the susceptibility of the aged animal to infectious agents may considerably vary from one pathogen to another.
Whooping cough can be caused by either Bordetella pertussis or Bordetella parapertussis. Although the two species share an almost complete DNA identity, Bordetella parapertussis does not produce pertussis toxin, which is thought to be the main virulence factor of Bordetella pertussis. In order to elucidate the role of pertussis toxin in causing the typical symptoms of whooping cough, clinical information from 33 patients with culture-positive Bordetella parapertussis infection was collected and compared to that from 331 patients with infection caused by Bordetella pertussis. Isolated strains of Bordetella parapertussis lacked pertussis toxin expression, as was demonstrated by negative tests for histamine sensitization. This was further substantiated in vivo by a significantly lower leukocyte count in the parapertussis group as compared to the pertussis group. Frequencies of typical symptoms of whooping cough, such as paroxysmal coughing, whooping and vomiting, were almost identical in the two groups. Nocturnal coughing and contact anamnesis were noted more often in the Bordetella pertussis group. Children in the parapertussis group were significantly more often vaccinated with whole-cell pertussis vaccine than children infected with Bordetella pertussis. The results indicate that pertussis toxin may not play a decisive role in causing the typical symptoms of whooping cough, such as paroxysmal coughing, whooping and vomiting.
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