Phase Of Epidemic Research Articles

Multi‐gene amplification: simultaneous detection of three virulence genes in diarrhoeal stool

Enterotoxigenic Escherichia coli (ETEC) and Shigella account for a substantial proportion of acute diarrhoeal illnesses among Third-World children. Rapid detection of these infectious agents in faeces followed by the prompt implementation of public health measures could help reduce their spread during the early phase of epidemics. Towards this end, three pairs of synthetic oligonucleotide primers were prepared and shown to hybridize specifically to the genes encoding the heat-stable (ST) and the heat-labile (LT) enterotoxins of ETEC and to invasion-associated loci (ial) of the large Shigella virulence plasmid. When the three primer pairs were used together in the polymerase chain reaction (PCR), the three corresponding genetic loci could be simultaneously amplified using DNA extracted directly from stool; the amplified products were readily detected by ST-, LT- and ial-specific, alkaline phosphatase-labelled oligonucleotide probes (AP probes). The performance of this system was evaluated in a Mayan community in southeastern Mexico, where diarrhoeal illnesses are a common cause of childhood morbidity and mortality. Using only simple and inexpensive laboratory equipment, multigene amplification with these primers and probes led to the identification of ETEC and/or Shigella in the stools of 20 out of 71 children with diarrhoea; the procedure could be completed in seven hours and was more sensitive than conventional diagnostic tests or DNA probes used without amplification.

Prevalence of methicillin-resistant Staphylococcus aureus in a Spanish hospital.

Recent reports of the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) in Europe are infrequent compared with reports in the 1960s. Annual incidence of the isolation of MRSA was studied in a general hospital in Guipúzcoa (Basque country) over a 9-year period. Overall prevalence was 4.5%-12.93% in the first 3 years (coinciding with an epidemic phase) and later 0.29%, underlining the cyclic and epidemic nature of this infection.

Sequential epidemic outbreaks of septicaemias by Serratia and Klebsiella species on a medical intensive care unit.

The high rate of septicaemias (20%, 19% and 14%) observed in our Intensive Care Unit (ICU) during the first 3 years was due to an epidemic incidence of Serratia sp. (S) (26% during the first year) and Klebsiella sp. (K) (25% during the third) and decreased significantly in the following 6 years (mean incidence of 11%) (p less than 0.01). During this epidemic phase these organisms were isolated quite frequently (between a 14% and a 6%) from all patients admitted. The K was more regularly present, for the mean time intervals free of its bacteriological presence were shorter (11 days) than those of S (27 days) (p less than 0.01). The K was isolated in more patients (160) than S (79) (p less than 0.01) and in more samples (360) than S (235) (p less than 0.01), but caused less secondary septicaemias per colonized patient (7% versus 29%) (p less than 0.01). In 59% of all S septicaemias the organism was previously isolated in other culture, while this was observed in only 34% of K septicaemias (x2 = 3.78, p = 0.052). The large variations in the incidence of septicaemias within our ICU, the appearance of sequential epidemic outbreaks, with a different behaviour of S and K and the individual risk of septicaemia of patients colonized by these organisms are noted.

Ocorrência da doença meningocócica em japoneses e descendentes no município de Londrina, Paraná, Brasil (1965-1975)

Foi feito estudo visando a determinação das taxas de medida da doença meningocócica em japoneses e seus descendentes, do município de Londrina, Paraná, Brasil. A morbidade por doença meningocócica (DM) foi cerca de 7 meses mais baixa que no restante da população, tendo sido nula entre os mesmos a ocorrência de óbitos, tanto em fase endêmica, como epidêmica, A revisão dos prontuários médicos hospitalares correspondentes aos casos notificados exclui o diagnóstico de DM em 75% dos pacientes de origem japonesa e em 20% da amostra de pacientes não japoneses. É discutida a eventual relação de fatores sócio-econômicos e cultural (alimentar) às observações.

Tuberculosis: susceptibility and resistance.

Introduction l h e ability of an animal host to limit multiplication of tubercle bacilli within its tissues and the degree to which its natural defenses are able to eradicate extracellular and intracellular organisms can be used as a measure of resistance to tuberculosis. This phenomenon was observed first by Koch (1), who showed that it is much more difficult to establish a progressive mycobacterial infection in animals that have been infected previously. The cellular and subcellular mechanisms responsible for this acquired ability to limit spread and replication of the tubercle bacillus have been partially explained in recent years, although many important questions remain. This report will review what has been learned by presenting a historical perspective of the tuberculosis epidemic that began in England in the 16th century and still continues, by reviewing individual risk factors, by examining the cellular and subcellular mechanisms that contain and kill tubercle bacilli within the infected host, and by evaluating data obtained from laboratory and clinical trials designed to induce immunity to tuberculosis. Tuberculosis can be shown to spread in an epidemic wave similar to that seen when other infectious diseases, such as whooping cough or hepatitis, are first introduced into a population of highly susceptible persons. Morbidity and mortality rates rise in a steep ascent, peak, and then show a longer and more gradual decline. In acute communicable diseases, the time course for these phases of the epidemic is measured in weeks, but for tuberculosis it is measured in decades. The present worldwide tuberculosis epidemic began in England in the 16th century, peaked there in 1750, spread to western Europe, and peaked there in the early 1800s. It then peaked in eastern Europe and North and South America by about 1890. At present the epidemic continues —its last peak occurred in Asia and Africa where high morbidity rates persist in many areas. Thus as the wave declined in one geographic area it was ascending and peaking in another. To what extent was the decline of new cases a result of resistance? The wave form of the epidemic is explained by natural selection. As the more susceptible persons are eliminated, the survivors become relatively resistant over a period of several generations, and the epidemic wanes as the disease resumes an endemic pattern (2). The peak tuberculosis mortality along the eastern coast of North America reached 1,000 per 100,000 cases per year in about 1800, and the disease had peaked throughout the continent by 1850, so that tuberculosis has been showing a progressive decline throughout the United States for the past 100 years. All efforts to examine racial and geographic variations in tuberculosis mortality and apparent resistance or susceptibilty must take into account the wave form of the epidemic and its time frame in the particular population under study. The variables of sex and age are especially influenced by the timing of the epidemic wave. In its early stage, occurring now in Asia and Africa, the infant mortality is much greater for males than females followed by a period of increased resistance in early childhood for both sexes. The major peak for females in early adulthood is surpassed at middle age by males, who show an increased susceptibility thereafter. During the late phase of the wave the increasing mortality in the aging population is the most significant feature, as can be seen presently in developed western countries. The proper understanding of the peak in the aged was first reported by Frost in 1939 (3). There is no clear evidence of any racial susceptibility to tuberculosis apart from that best explained as phase differences in the epidemic wave. The effect of poor nutrition is also minimal, because in experimental animals nutritional deficiences must be extreme to reduce resistance to infection. Individual Risk Factors

Forecasting the Progress of Epidemics by Means of a Bayesian-Entropy Framework

In a recent paper a new approach to forecasting based on the Bayesian principles of information theory was proposed and called the Poisson-gamma single-state model. In this paper a two-state version of the Poisson-gamma model is formulated by considering the uncertainty not only in the parameters but also in the model itself. This model is particularly useful for modelling epidemic data such as measles by considering two different situations (states) of the generating process at each time point: viz, state 1—no epidemic phase; state 2—epidemic phase.

Potato blight control in east and south‐east Scotland 1959–68

SUMMARYRoutine protective spray application to commercial Majestic potato crops on two farms in south‐east Scotland for 9 and 10 years respectively gave highly significant average increases in total yield of 1.2 and 2.1 tons per acre (3.0 and 5.3 tonnes per ha) respectively in rows not affected by tractor wheels. In 6 and 7 years respectively the increases were more than 1 ton per acre. These increases were composed almost entirely of ware tubers. There was no average difference in yield whether the first spray application was made when the haulm closed in the rows or after the first general forecast based on the Beaumont period was announced.The average total yield reduction in the four rows affected by tractor wheels tended to offset the benefit given by spray application, and, where an eight‐row spray boom was employed, halved the potential overall yield increase. Reduction was again confined to the ware fraction.Similar experiments with cv. King Edward over a shorter period in eastern Scotland generally showed little consistent effect on yield, possibly partly because of the late appearance of blight in some of these crops.Considerable yield gains were obtained in Majestic crops even when the disease first appeared in mid‐August in some seasons which could not be classified as ‘blight years’. Over the 10 years of the investigation, there were 5 blight years as defined by Large (1959) compared with the 1 in 10 which Large mentioned for the north of England.Spread of blight from local sources, such as discard heaps outside the crop and before the occurrence of the field epidemic phase, was found to interfere with adequate timing of spray applications and with the effectiveness of the general forecast based on the Beaumont period.Infection of Majestic tubers was generally low but at one Majestic site and in the King Edward series the overall average tuber infection was significantly decreased by spraying. Tuber blight was shown to vary inversely with the size of tubers of Majestic as well as of King Edward.

An experimental epidemiological study of Talfan virus infection in pigs

Talfan virus was introduced experimentally into a small herd of MD pigs by the oral dosing of one litter of piglets with virus cultivated in PK cells. Serum samples from all pigs in the herd were examined for Talfan neutralizing antibodies at monthly intervals for 8 months, and virus isolation from rectal swabs was attempted at weekly or monthly intervals for the same period. Samples from the colon were collected for virus isolation from pigs at slaughter. The infection produced diarrhoea in suckling piglets and in one gilt, and nervous signs in suckling piglets, one gilt and one boar during the first 5 weeks of the experiment. Thereafter, clinical disease attributed to Talfan virus was not apparent. In the early (epidemic) phase of the infection, pigs of all ages excreted virus for a period up to 8 weeks and developed circulating antibodies which persisted at fairly high levels throughout the experiment. Piglets born one month or more after the introduction of Talfan virus excreted virus only after weaning and developed a circulating antibody response to Talfan in the post-weaning period.

Panelists' Introductory Statements: Discussion by Walter W. Heller

Within the general topic of this session, my remarks will be more specifically directed to the battle against inflation and an appraisal thereof. Inflation must be a dirtier word than I had thought, for it's nowhere to be found in our AEA program this year (though perhaps our sister organizations have recognized its existence in their sessions and papers). Yet, in economies that orbit in the narrow band around full employment, the toughest economic policy nut to crack, bar none, is inflation. No free economy has yet cracked it. And ever since escalation in Vietnam so rudely interrupted our balanced advance toward full employment, the inflationary fat has been in the fire in the U.S. economy too. Neither tight money, nor restrictive fiscal policy, nor both finally working in tandem since late 1968, has thus far been able to quench the flames. Even when we get past the epidemic phase of inflation-as I believe we will in the next year or so-inflation will still be endemic in our economy. Let's face it: We now live in an inflationprone economy. Given a bipartisan commitment to high-employment, high-growth economics; given unrelenting pressures for capital spending on private and public infrastructure, on housing, on pollution control and the like; and given the stubborn centers of market power in both business and labor, it's not hard to understand why the job of reconciling full employment and reasonable price stability-or should I say, tolerable rates of inflation?-will still confront us even when Vietnam is behind us. It is to this limitless subject that I devote my limited time today. In doing so, I'll have to lay aside the rather remote but not unthinkable possibility that U.S. political economy may force us to choose some day between 4 to 5 percent inflation (and the inequities and inefficiencies that go with it) and 5 percent plus unemployment (and the individual pain and social unrest that go with it). Instead, I'll assume that the American people and those who hold the policy reins are not prepared to put up with more than 2.5 percent to 3 percent inflation a year and address myself to the issues that thus confront us in an economy still afflicted with double that rate of inflation:

CONTRIBUIÇÃO PARA O ESTUDO DA TUBERCULOSE NO MUNICÍPIO DE SÃO PAULO. ASPECTOS EPIDEMIOLÓGICOS DO PROBLEMA

The annual tuberculosis death rate in the Minicipality of São Paulo from 1900 to 1948 is of 128.63 per 100,000 population. Tuberculosis in this Municipality is in its epidemic phase and in the stage of stabilization. The continuous increase of the coefficients verified since 1920 could be explained among other facts, by the rural exodus. The non-resident mortality during the years from 1946 to 1948 increased by 10% the tuberculosis death rate in those years. The tuberculosis mortality rate in the Municipality of São Paulo from 1900 to 1948 is 8,01% of the general mortality. In opposition to what is generally observed, in the Municipality of São Paulo the mortality from tuberculosis observed in the Municipality of São Paulo of mortality from tuberculosis does not follow the decreasing of the general mortality. The tuberculosis death rate related to the general mortality is higher in the last two decades of the studied period. The tuberculosis mortality reaches the higher rates between the ages of 15 and 39 years; the highed rate is located around 25 years of age. Between 15 and 21 years of age the death is higher for women; in the other groups of age the opposite is observed.

Control of Dengue in Hawaii

DENGUE fever appeared in the Territory of Hawaii in July, 1943, for the first time since 1912, and soon after its appearance reached epidemic proportions. Usually when dengue is introduced into a non-immunized community, particularly a community where mosquitoes live and breed all the year around, a majority of the population contracts the disease within a short time. However, only 1,498 cases of dengue occurred during this epidemic in the Territory, out of a population of approximately 500,000 persons. There is, consequently, good cause to believe that the preventive measures taken during this outbreak of dengue may have been responsible for controlling its incidence. All but two of these cases occurred in the city of Honolulu, the population of which is approximately 250,000. After the epidemic phase, dengue continued to occur sporadically in the Territory. This paper deals with the epidemiological aspects of dengue control in the Territory both during the epidemic period and during the endemic period to date. Most of the dengue control measures have had to do with efforts directed at the elimination of Aedes mosquito, the vector of the disease, which breeds in the Territory throughout the year, although it is believed that efforts to obtain early diagnosis and proper segregation of persons so that mosquitoes could not bite them played a part in the successful control of the disease. At the onset of the epidemic, the Honolulu Chamber of Commerce and the U. S. Public Health Service contributed funds toward dengue control, and the Army was soon aiding in the control program by assigning considerable personnel and equipment to control wort. At the request of the Territorial health department, the Public Health Service immediately flew to Hawaii an entomologist (Dr. Robert L. Usinger) and a sanitary engineer (Wesley E. Gilbertson) from the Atlanta office of its Malaria Control in War Areas unit. In March of 1944, Dr. Usinger reported on the entomological phases of the dengue epidemic in Honolulu' and in March of 1945 there was printed in the American Journal of Public Health Mr. Gilbertson's report on the sanitary aspects of the control of this epidemic.2

Entomological Phases of the Recent Dengue Epidemic in Honolulu

Entomological Phases of the Recent Dengue Epidemic in Honolulu

RABBIT POX

The epidemiological significance of age, race, sex, genetic constitution and physiological status were studied by means of a differential analysis of the mortality data derived from a devastating epidemic of rabbit pox and, with the exception of sex, were found to be factors of the utmost importance in the determination of susceptibility. Young animals were more susceptible than adults and although the most susceptible age varied with the epidemic phase, it corresponded in general with the period of weaning. The influence of physiological status was further indicated by the increased susceptibility incident to lactation. Racial variations in susceptibility were obscured by age factors in young animals, but were of profound importance in the adult population and formed the most significant feature of the analysis. A high degree of conformity was found in the susceptibility of racially related breeds, and this similarity in behavior increased with the proximity of relationship. Moreover, a study of the hybrids obtained from the crossing of pure breeds showed that two separable groups of hereditary factors were concerned in the determination of breed susceptibility, one group consisting of essential racial characters, the other of constitutional factors incorporated in the stock by chance association, and that the final expression of susceptibility or resistance was the result of their combined interaction.

THE RÔLE OF MICROBIC VIRULENCE, DOSAGE, AND HOST RESISTANCE IN DETERMINING THE SPREAD OF BACTERIAL INFECTIONS AMONG MICE

1. In September, 1925, explosive and highly fatal epidemics of a Friedländer-like bacillus infection arose in three of four experimentally controlled mouse populations. In the populations to which daily additions were made, characteristic secondary waves ensued. These waves appeared at definite population levels, lasted a definite number of days, and reduced the population to a definite low census. Subsequently, endemic periods intervened, followed by the disappearance of the disease during March, 1926. 2. In August, 1926, renewed epidemics of the infection arose in all four populations. These outbreaks resembled one another but were more enduring than the preceding ones. Moreover, fewer secondary waves followed, and the disease disappeared in February, 1927. 3. The virulence or disease-producing power of the Friedländer-like organisms, as determined by the ability to spread and induce typical epidemics among populations of previously unexposed mice, and by direct inoculation titrations remained constant during pre-epidemic, epidemic, post-, and inter-epidemic phases of the infection. 4. The Friedländer-like organisms were not recovered in cultures from bedding, food, or feces, but they were obtained from the nasal passages. Mice harboring the organisms usually died within a few days of the test; a few, however, survived and ceased to be carriers. The carrier rate in a given community was found to increase prior to epidemic outbreaks and to decrease shortly before the time of peak mortality. 5. The substitution of relatively susceptible for "standard" immigrants in a population was followed by an increase in severity and spread of the disease, whereas a substitution of "standard" for resistant immigrants was followed by a fall in severity and extent of disease.

THE RÔLE OF MICROBIC VIRULENCE, DOSAGE, AND HOST RESISTANCE IN DETERMINING THE SPREAD OF BACTERIAL INFECTIONS AMONG MICE

1. Several mouse populations under experimental observation were infected with B. enteritidis typhoid. The infection took the form of periods of low grade mortality interspersed with epidemiform outbreaks. During the periods of low grade mortality, the number of daily deaths was either relatively constant or rhythmic in 9 day intervals. The epidemiform outbreaks were associated invariably with some definite environmental disturbance. 2. The spread of this infection was not influenced by the presence of bacteriophage or the bacterial-dissociation phenomena. 3. The virulence or disease-producing power of B. enteritidis was found to be constant during all pre-epidemic, epidemic, and endemic phases of the infection. 4. The dosage of B. enteritidis available to a population at a given time was found to vary directly with mortality at a time difference approximating that of the incubation period of the disease. 5. The amount and severity of B. enteritidis infection in the populations were controlled experimentally by varying the diet from adequate to optimum constituents and by varying the daily immigrants from a relatively resistant to a susceptible race of mice.