Indian Ocean islands are endemic areas for human and animal leptospirosis. Maintenance host species for Leptospira spp. have still not been completely elucidated, and recently the role of cats (Felis catus) has been questioned. This cross-sectional study aims to determine whether cats are part of the maintenance community of different strains of Leptospira spp. in Reunion Island. The prevalence of Leptospira infection in an opportunistic sample of stray and domestic cats (n = 92) from Reunion Island has been studied using serological (microagglutination test) and molecular detection (polymerase chain reaction (PCR)). The results revealed a seroprevalence of 37.0% (34/92) (cut-off 1:40) without a significant difference in the living conditions of animals. The predominant serogroup was Icterohaemorrhagiae, but Ballum, Cynopteri and Australis were also detected. Using PCR, 28.6% (12/42) of stray cats were tested positive. Leptospiral DNA was detected in renal tissue, urine and blood of respectively 14.3% (6/42), 10.3% (4/39) and 11.9% (5/42) of stray cats, but 0% (0/3), 0% (0/50) and 0% (0/36) of domestic cats (P = non-applicable, P = 0,038, P = 0,058 respectively). Partial rrs gene (16S rRNA) sequencing identified Leptospira interrogans in all PCR-positive samples. Our study confirms that renal carriage and urinary shedding are possible, positioning cats, and especially stray cats as potential actors within the maintenance community of L. interrogans in Reunion Island.

A set of 723 diagnostic sera from human patients, submitted for the microscopic agglutination test (MAT) for antibodies to a group of 6 leptospiral serovars, was also tested by MAT for antibodies to the recently-discovered Leptospira fainei serovar hurstbridge. MAT titres of [ges ]128 to serovar hurstbridge were detected in 13·4% of these sera, and titres of [ges ]512 in 7·2%. In contrast, none of 62 sera obtained from a control population of laboratory staff gave titres of [ges ]128. The difference between the number of titres of [ges ]128 given by the two groups of sera was highly significant (P<0·01). The titres observed may have been due to cross-reactions with other leptospiral serovars, but this could not be demonstrated. An alternative explanation is that serovar hurstbridge is present in the human population.

We investigated how different models of HIV transmission, and assumptions regarding the distribution of unprotected sex and syringe-sharing events (‘risk acts’), affect quantitative understanding of HIV transmission process in people who inject drugs (PWID). The individual-based model simulated HIV transmission in a dynamic sexual and injecting network representing New York City. We constructed four HIV transmission models: model 1, constant probabilities; model 2, random number of sexual and parenteral acts; model 3, viral load individual assigned; and model 4, two groups of partnerships (low and high risk). Overall, models with less heterogeneity were more sensitive to changes in numbers risk acts, producing HIV incidence up to four times higher than that empirically observed. Although all models overestimated HIV incidence, micro-simulations with greater heterogeneity in the HIV transmission modelling process produced more robust results and better reproduced empirical epidemic dynamics.

The phenotypic and genotypic profiles of the V. cholerae strains causing the Mozambican 1997–8 epidemic were characterized to provide a reference for comparison with other epidemic strains. A total of 75 strains of V. cholerae O1 isolated in different provinces, were analysed. Strains were characterized by PCR for detecting toxin genes (ctxA, zot and ace), virulence associated genes (tcpA, nanH, hlyA and toxR) and ERIC sequences. All V. cholerae strains were serotype O1, Ogawa, biotype El Tor. MIC testing showed a high proportion of strains multi-resistant to drugs (100% to cotrimoxazole and 52% to tetracycline) and susceptibility to ciprofloxacin. The isolates contained two intact copies of the CTX genetic element and all other genes tested. PCR of restricted DNA revealed two ERIC types: the first in provincial isolates, also predominant in other African epidemic strains, and the second in Maputo isolates (the national capital).

This paper critically assesses the design implications for the analysis of surveys of infections. It indicates the danger of not accounting for the study design in the statistical investigation of risk factors. A stratified design often implies an increased precision while clustering of infection results in a decreased precision. Through pseudo-likelihood estimation and linearisation of the variance estimator, the design effects can be taken into account in the analysis. The intra-cluster-correlation can be investigated through a logistic random effect model and a generalised estimating equation (GEE), allowing the investigation of the extent of spread of infections in a herd (cluster). The advantage of using adaptive Gaussian quadrature in a logistic random effect model is discussed. Applicable software is briefly reviewed. The methods are illustrated with data from a bovine herpesvirus 1 (BHV-1) serosurvey of Belgian cattle.

Wild Norway rats (Rattus norvegicus) from several habitats were tested for their susceptibility and resistance to warfarin. Animals were fed 0·005% warfarin in ground oatmeal for periods varying from 1 to 12 days. Rats having no prior exposure to anticoagulants were shown to be susceptible, none having survived a 6-day feeding period. Resistant rats were found on two farms where anticoagulant materials had been used intensively for about 20 years.

1. It is possible to concentrate the virus of foot-and-mouth disease on filter candles coated with acetic acid collodion. The degree of concentration of the virus effected was to the limit of expectancy, i.e. the increase in titre after concentration corresponded to the reduction of the volume of the liquid.

2. By a combination of the two methods of purification of the virus, viz. washing once in the closed agar-lined cylinder of the Sharpies-Super Centrifuge and repeatedly on a graded collodion membrane of A.P.D. 25 mμ, very potent purified concentrates of virus can be rapidly obtained, especially if the final concentration is made on filter candles, coated with acetic acid collodion. In this way a concentrate of virus with a titre of 10−8 and a negative sulphosalicylic acid test for protein has been prepared in one day from virulent vesicle lymph (diluted 1 : 2) having a titre of 10−6.

3. The possibilities of the different methods of purification and concentration of the virus are discussed and a scheme suggested for their application.

In the summer of 2001 an outbreak of Escherichia coli O157 gastroenteritis affected staff and residents of a care home for the elderly in the West Midlands, UK. E. coli O157 phage type 2 was isolated from faeces in eight patients and 12 staff members. Thirty-five staff and 40 residents met the case definition for clinical gastrointestinal infection. Serological testing identified a further 14 possible cases of infection amongst asymptomatic staff and residents. The outbreak was atypical, as the disease seemed to be milder than has been observed in past outbreaks in similar settings. The index case, a member of staff, developed bloody diarrhoea and haemolytic–uraemic syndrome (HUS), but only one resident developed bloody diarrhoea and required hospitalization. No deaths occurred, despite the high-risk nature of the affected population. The source of the outbreak could not be identified. The prolonged nature of the outbreak and observed lapses in infection control practices indicated that person-to-person spread was the likely route of transmission. This outbreak illustrates the importance of observing appropriate infection control measures in the institutions providing residential and nursing care to the elderly.

Reducing the burden of Salmonella in broiler flocks presents a challenge for public health. Worldwide, grow-out broilers are routinely vaccinated to prevent or lessen clinical manifestation of other infections. In this exploratory analysis we tested if details of a routine vaccination programme delivered to conventional grow-out broilers were associated with the burden of Salmonella in the flock as it progressed through its production cycle. None of the flocks studied were vaccinated against Salmonella or received a competitive exclusion product. The flocks were reared on conventional grow-out farms in southeastern USA, and sampled in a prospective field observational study. We observed significant associations between the content and design of a grow-out vaccination programme targeting other infections and the probability of detecting Salmonella in the broiler flock at different time points throughout the production cycle. To the best of the authors' knowledge, this is the first field report of such associations.

An infusion of E. coli endotoxin (10 μg) into the mammary gland of the cow 16 h before experimental infection with St. agalactiae prevented the establishment of mastitis. A clinical examination of the affected gland did not reveal signs of inflammation, all organisms were eliminated from the milk by 36 h after infection. Mammary glands not pretreated with endotoxin, and injected with the same number of viable streptococci, showed signs of severe inflammation, the milk yield was reduced and the injected pathogen could be isolated from the gland for up to 14 days when sampling was discontinued. The injection of endotoxin alone produced a rapid increase in the cell count of the milk, there were some signs of inflammation and 80% of the cells in the milk were neutrophils. The cell counts in the milk remained above normal for 7–10 days. Untreated control quarters appeared to be unaffected by the injection of E. coli endotoxin into an adjacent quarter, on the other hand the injection of St. agalactiae into the adjacent quarter on the same side of the udder produced a cell response which reached a peak after 2 days and returned to preinoculation levels by the fourth day. No inflammation was observed in these control quarters and no streptococci were isolated from the milk.

As the COVID-19 pandemic continues to escalate and place pressure on hospital system resources, a proper screening and risk stratification score is essential. We aimed to develop a risk score to identify patients with increased risk of COVID-19, allowing proper identification and allocation of limited resources. A retrospective study was conducted of 338 patients who were admitted to the hospital from the emergency room to regular floors and tested for COVID-19 at an acute care hospital in the Metropolitan Washington D.C. area. The dataset was split into development and validation sets with a ratio of 6:4. Demographics, presenting symptoms, sick contact, triage vital signs, initial laboratory and chest X-ray results were analysed to develop a prediction model for COVID-19 diagnosis. Multivariable logistic regression was performed in a stepwise fashion to develop a prediction model, and a scoring system was created based on the coefficients of the final model. Among 338 patients admitted to the hospital from the emergency room, 136 (40.2%) patients tested positive for COVID-19 and 202 (59.8%) patients tested negative. Sick contact with suspected or confirmed COVID-19 case (3 points), nursing facility residence (3 points), constitutional symptom (1 point), respiratory symptom (1 point), gastrointestinal symptom (1 point), obesity (1 point), hypoxia at triage (1 point) and leucocytosis (−1 point) were included in the prediction score. A risk score for COVID-19 diagnosis achieved area under the receiver operating characteristic curve of 0.87 (95% confidence interval (CI) 0.82–0.92) in the development dataset and 0.85 (95% CI 0.78–0.92) in the validation dataset. A risk prediction score for COVID-19 can be used as a supplemental tool to assist clinical decision to triage, test and quarantine patients admitted to the hospital from the emergency room.

In a survey undertaken in an intensive care unit, coliform bacilli were found to be responsible for most infections, Pseudomonas aeruginosa and Staphylococcus aureus being isolated much less frequently. Tracheostomy or endotracheal intubation predisposed to infection, but in our experience intermittent positive pressure ventilation did not significantly affect its incidence. Little cross-infection has occurred, and it has never been possible to incriminate the ventilators in its transmission.

We gratefully acknowledge the assistance we have received from colleagues in the Intensive Therapy Unit and the Department of Bacteriology during the course of this investigation.

Viraemia is an important aspect of the pathogenesis of infectious diseases, but the mechanisms of entry and removal of virus from the vascular system particularly in natural hosts are poorly understood. The results of this study showed that the clearance of foot and mouth disease virus (FMDV) from the circulation of cattle and goats followed the general rules for the clearance of inert particulate materials and other viruses from the circulation. High doses of infused FMDV were cleared less efficiently than low doses, probably as a result of a depletion of the reticulo-endothelial system by the higher doses. FMDV was cleared from the circulation of cattle at a considerably slower rate than from the circulation of goats, but in both species significant individual variation in clearance was observed. These results could explain individual as well as species variations relative to the onset and duration of viraemia.

From an analysis of the telephone reports in ten FMD Control Centres in the West Midlands, the veterinary officers' reports on each outbreak, the farm patrol reports and the daily number of outbreaks announced on the 17.50 h B.B.C. T.V. News, it would appear that the reporting of suspected outbreaks was indirectly related to the local disease activity. Private veterinary practitioners reported older cases of FMD at the beginning and end of the epidemic than in the middle.

Parainfluenza viruses were isolated 165 times during 14 years surveillance of the illnesses of a general practice population of around 3700. Type 1 isolations numbered 57, type 2 isolations 22 and type 3 isolations 86, representing annual rates of 33, 13 and 50 infections respectively per 10000 of population. Type 4 parainfluenza virus was not isolated. Three major classes of illness gave the following rates: sore throats (Throats) nine, acute febrile respiratory diseases (FRD) 23, acute non-febrile respiratory diseases (non-FRD) 71. The illnesses caused by the three types isolated were similar. Type 1 infections were most abundant in November and type 2 infections in December, and only 11.4 % of these types were isolated in the warm semester April through September. Type 3 infections were seasonally bi-modal, with a winter peak in January and an even greater prevalence (66% of the total) in the warm semester. Type 3 infections in the warmer months and in the later years of the Survey were usually more severe. Type 3 virus may therefore be heterogeneous, one subtype possessing and the other lacking the genetic mechanism of ‘cold-season’ prevalence. Geographical discontinuity between summer and winter isolations strengthens the case for the existence of the two subtypes of type 3 parainfluenza virus.

Type 3 infections caused the majority of the infections in very young infants. Type 2 infections were widely distributed at all ages. Females were attacked more often than males: type 1, 68.4%; type 2,636%; type 3, 53.5%. Type 3 infections in males outnumbered those in females up to 60 years of age, whereas female predominance became apparent in types 1 and 2 before 10 years of age.

All types were widely and sparsely distributed, areas of prevalence changing from year to year. Recurrences occurred only twice, both with type 3 infections. Six persons suffered both a type 1 and a type 3 infection, and one person suffered both a type 2 and a type 3 infection.

Five rubella antigens were evaluated in an antiglobulin enzyme-linked immunosorbent assay for rubella-specific IgG subclass antibody. One monoclonal anti-human IgG subclass antibody was used for each of IgG1, IgG2 and IgG4, but two were compared for IgG3. A total of 101 sera were tested from cases of rubella in the distant past and from cases of primary rubella, reinfection and following immunization. Only one serum gave a discrepant result for specific IgG1, being positive with only one rubella antigen, a commercially prepared antigen coated on to microtitre wells (Enzygnost; Behringwerke). No sera contained detectable specific IgG2. Only four sera contained specific IgG4, and this was detectable only with Enzygnost antigen. For specific IgG3 little difference was observed between the two monoclonal anti-human IgG3 subclass antibodies; only two very weakly positive sera gave discrepant results. However, varying results were obtained for specific IgG3 with the different antigens. Enzygnost gave more positive results for specific IgG3 with most categories of sera.

It is concluded that the differences between various reports of the rubella-specific IgG subclass profile cannot be explained entirely by the use of different rubella antigens.

A mathematical model was used to estimate malaria transmission rates based on serological data. The model is minimally stochastic and assumes an age-dependent force of infection for malaria. The transmission rates estimated were applied to a simple compartmental model in order to mimic the malaria transmission.

The model has shown a good retrieving capacity for serological and parasite prevalence data.

Four series of tests, A, B, C and D, have been considered in detail. In the first two series, to obtain the values of the ImD 50, percentages of survivors were transformed into probits, and the best-fitting straight lines connecting the probits with the logarithms of the doses were obtained by the method of maximum likelihood. This is the most accurate method to use. These results showed that the error of the test was large, but there were no significant differences in the slope of the probitlog dose relation in the results of tests from any one laboratory. The slope (1·46 ± 0·09) obtained from series A was greater than that from series B (0·79 ± 0·06). with a consequent increase in accuracy.

Population seroprevalence can be estimated from serosurveys by classifying quantitative measurements into positives (past infection/vaccinated) or negatives (susceptible) according to a fixed assay cut-off. The choice of assay cut-offs has a direct impact on seroprevalence estimates. A time-resolved fluorescence immunoassay (TRFIA) was used to test exposure to human parvovirus 4 (HP4). Seroprevalence estimates were obtained after applying the diagnostic assay cut-off under different scenarios using simulations. Alternative methods for estimating assay cut-offs were proposed based on mixture modelling with component distributions for the past infection/vaccinated and susceptible populations. Seroprevalence estimates were compared to those obtained directly from the data using mixture models. Simulation results showed that when there was good distinction between the underlying populations all methods gave seroprevalence estimates close to the true one. For high overlap between the underlying components, the diagnostic assay cut-off generally gave the most biased estimates. However, the mixture model methods also gave biased estimates which were a result of poor model fit. In conclusion, fixed cut-offs often produce biased estimates but they also have advantages compared to other methods such as mixture models. The bias can be reduced by using assay cut-offs estimated specifically for seroprevalence studies.

Knowledge of epidemiological mechanisms and parameters underlying scrapie transmission in sheep flocks remains very limited at present. Here we introduce a method for fitting stochastic transmission models to outbreak data to estimate bounds on key transmission parameters. We apply this method to data describing an outbreak of scrapie in a closed flock of Romanov sheep. The main findings are that the relative infectiousness of infected animals in this outbreak becomes appreciable early into disease incubation and that the mean incubation period is less than 1·5 years. We also find that the data are consistent with a broad range of values for the basic reproduction number R0 and describe how the boundaries of this range depend on assumptions about the mean incubation period and the contribution to transmission of a long-lived environmental reservoir of infectivity.