Journal of Hygiene最新文献

Forty-six gnotobiotic calves aged less than 16 days or 42-116 days were infected with three strains of bovine rotavirus designated C3-160, CP-1 and PP-1. Each virus was passaged and cloned in cell culture (cloned viruses) but CP-1 and PP-1 were also used before culture (faecal viruses). Infection of calves aged less than 16 days with faecal or cloned CP-1 caused disease whereas cloned C3-160 and faecal or cloned PP-1 caused subclinical infections. The clinical signs of disease were change in faecal colour to pale yellow or cream, increase of 2- to 7-fold in the volume of faecal output and, usually, anorexia. With the virulent CP-1 virus and the avirulent C3-160, similar amounts of virus were excreted in the faeces for 4-6 days. Infection of calves aged 56-116 days with faecal CP-1 produced disease of similar severity to that seen in calves aged 7-10 days infected with the same virus. No differences in clinical signs, virus excretion or levels of convalescent antibody were seen between the two groups. With cloned CP-1, 5 of 8 older calves developed disease but 3 showed only mild signs of infection. It was concluded that two strains of rotavirus caused sub-clinical infections in young calves while a third was virulent in calves up to at least 116 days of age.

The role of broiler eggs in the transmission of Campylobacter jejuni to broiler grow-out flocks was investigated. Six breeder flocks supplying broiler eggs to hatcheries were examined for cloacal carriage of C. jejuni. Of 240 birds tested, 178 (74%) were C. jejuni-positive. Eggs from these birds examined for C. jejuni penetration of the egg shell indicated that 185 of 187 were campylobacter-free. Eggs from breeder flocks of unknown C. jejuni status were also examined for C. jejuni shell penetration. C. jejuni was not isolated from 142 eggs examined. A further 193 hatchery eggs incubated and hatched in the laboratory were campylobacter-free. Six farms containing the progeny of C. jejuni-positive breeder flocks were monitored. Eight hundred and forty birds from 14 flocks in these grow-out farms were campylobacter-free during their 6-week grow-out period. Experimental egg-penetration studies indicated that C. jejuni transmission via the egg is not easily effected. Of 257 eggs surface-challenged with C. jejuni, 162 hatched; all were campylobacter-free. Of 167 eggs injected with C. jejuni, 12 hatched; 2 of these were colonized with C. jejuni. Our data do not support a role for vertical transmission of C. jejuni in commercial broiler production.

Susceptibility studies were undertaken to determine the response of some South African wild rodent species to experimental plague (Yersinia pestis) infection. A degree of plague resistance was found in three gerbil species captured in the plague enzootic region of the northern Cape Province, these being the Namaqua gerbil, Desmodillus auricularis, (LD50 1 X 10(6) organisms), the bushveld gerbil, Tatera leucogaster, (LD50 9.1 X 10(5)) and the highveld gerbil, T. brantsii (LD50 4 X 10(2)). Animals from a population of the four-striped mouse, Rhabdomys pumilio, captured in the plague area of Port Elizabeth, proved moderately resistant to experimental plague infection (LD50 1.3 X 10(4)) while those from another population of the same species captured in a plague-free area of the Orange Free State were extremely susceptible (LD50, 5 organisms). The response of both populations however was a heterogeneous one. Marked differences in susceptibility were also found between two populations of multimammate mice, Mastomys natalensis (2n = 32) although both originated from areas outwith the known distribution of plague in southern Africa. The 50% infectious dose was relatively high in T. leucogaster (3.2 X 10(2)) and D. auricularis (1.7 X 10(3)), but was low (2-16 organisms) in the other rodent species tested. The plague antibody response, determined by enzyme-linked immunosorbent assay (ELISA), was extremely short-lived in T. leucogaster, only 10% of inoculated animals remaining seropositive at low titres after 11 weeks. Antibodies persisted for only slightly longer in the sera of T. brantsii which were reinoculated with 2 X 10(3) plague organisms 6 weeks after initial challenge. The demonstration of the existence of both susceptible and resistant populations of R. pumilio and M. natalensis indicates that these species must be considered as potential plague reservoir hosts in parts of South Africa. The results suggest that resistance to plague infection in previously epizootic hosts in the northern Cape Province such as Tatera sp. and D. auricularis has arisen through continual selective pressure of the organism. If the findings are applicable to gerbil populations in other plague enzootic regions of South Africa it is probable that acquired plague resistance has been responsible for the absence of gerbil epizootics and consequently for the dramatic decline in human plague outbreaks in South Africa since 1950.

In developing countries tuberculous meningitis is a difficult infection to differentiate from other central nervous system (CNS) infections. This paper presents the history, physical findings, laboratory data, and clinical course of 100 patients who were admitted to a special ward and had CSF cultures positive for Mycobacterium tuberculosis. Fifty-four patients were comatose when admitted and 76 had meningeal signs. Mean admission CSF values were WBC 531, glucose 23 mg/dl, and protein 166 mg/dl. Only two CSF AFB smears were positive. Sixty-one percent of the chest X-rays taken were consistent with pulmonary tuberculous and 39% were normal. Twenty-four patients died within the first week after admission, before the clinical diagnosis was made and anti-tuberculous therapy could be started. Fifty-three of 76 patients given antituberculous therapy died. Neurologic sequelae developed in 48% of the survivors. The high mortality and morbidity rates in this patient-group were due to the severity of illness on admission and the predominance of children (54%).

Eight monoclonal antibodies have been derived from Balb/c mice hyperimmunized with the purified flagella from Campylobacter jejuni strain 81116. These monoclonal antibodies are directed against flagella as demonstrated by reaction in ELISA against flagellate and aflagellate antigens, radio-immunoprecipitation and electro-immunoblotting techniques. Some of the antibodies react with a 60K minor protein as well as the 62K flagella protein. This protein may be related to an antigen expressed on the surface of the organism and detectable by immunogold labelling with one of the monoclonal antibodies. None of the antibodies causes the aggregation of bacteria or inhibits bacterial motility, unlike polyclonal anti-flagella antiserum. Moreover, none of the antibodies tested protected infant mice from colonization with C. jejuni strain 81116 even though partial protection (28%) was observed with syngeneic anti-flagella anti-serum. Absence of protection is probably due to the cryptic nature of the flagella epitopes investigated or lack of antibody activity in the gastrointestinal tract.

Evidence for influenza-associated excess mortality in the three centuries before the 20th has been sought from parish burial registers in Cumbria, Devon, Dyfed, East Anglia, Gloucestershire and Northumbria, compared with inter-epidemic years. Most of the registers showed excess of burials concordant with eight historic influenza epidemics. Comparison of the dates of these epidemics, deduced from the burials data in different areas, showed a rate of spread difficult to reconcile with direct person-to-person spread of influenza from the sick. An alternative explanation based on development of latency of the virus in the sick person and subsequent seasonal reactivation is discussed.

The cellular fatty acid composition of 41 strains of suspected Campylobacter jejuni, 23 from human cases of gastroenteritis and 18 from animals, was examined by gas-liquid chromatography. Three of the 23 human isolates and 2 of 18 animal isolates did not contain 19:0 cyclopropane fatty acid and were identified as C. laridis. The remaining 36 strains had cellular fatty acid profiles consistent with C. jejuni but could be divided into three groups on the ratio of the concentration of 18:1 and 19:0 cycloproprane. Most human isolates (85%) were in groups II or III whereas most animal isolates (56%) were in group I. It is proposed that gas-liquid chromatographic analysis of cellular fatty acids is a relatively easy method for epidemiological typing of C. jejuni isolates.

The paper examines predictions of the impact of various one-, two- and three-stage vaccination policies on the incidence of congenital rubella syndrome (CRS) in the United Kingdom with the aid of a mathematical model of the transmission dynamics of rubella virus. Parameter estimates for the model are derived from either serological data or case notifications, and special attention is given to the significance of age-related changes in the rate of exposure to rubella infection and heterogeneous mixing between age groups. Where possible, model predictions are compared with observed epidemiological trends. The principal conclusion of the analyses is that benefit is to be gained in the UK, both in the short and long term, by the introduction of a multiple-stage vaccination policy involving high levels of vaccination coverage of young male and female children (at around two years of age) and teenage girls (between the ages of 10-15 years), plus continued surveillance and vaccination of adult women in the child-bearing age classes. Model predictions suggest that to reduce the incidence of CRS in future years, below the level generated by a continuation of the current UK policy (the vaccination of teenage girls), would require high rates of vaccination (greater than 60%) of both boys and girls at around two years of age. Numerical studies also suggest that uniform vaccination coverage levels of greater than 80-85% of young male and female children could, in the long term (40 years or more), eradicate rubella virus from the population. The robustness of these conclusions with respect to the accuracy of parameter estimates and various assumptions concerning the pattern of age-related change in exposure to infections and 'who acquires infection from whom' is discussed.

Following its reintroduction in 1978 influenza A H1N1 spread widely in the child population. By the autumn of 1979, 75% of 11-year olds entering a boys' boarding school had detectable antibody. The protective effect of previous experience could be assessed during two outbreaks in the school. In the first outbreak in 1979, 90% of those known to have been infected in the previous year were protected against reinfection. In 1983 after strains of the H1N1 subtype had undergone antigenic drift a large outbreak occurred. It was estimated that past infection conferred protection against clinical influenza in 55%. Where past infection resulted in the presence of antibody which reacted with the outbreak strain the attack rate was further reduced. A large number of sub-clinical infections was detected in all groups.