[The isolation hospital on Katten in Bergen]. / Isolasjonslasarettet på Katten i Bergen.

In 1864 the Board of Health in Bergen, Norway, feared that an epidemic of smallpox might break out in the city. A house on the bastion Katten (Norwegian for "the cat") on the Fredriksberg fortress was adapted and made a provisional smallpox hospital. Later on it also served as a cholera hospital during a minor cholera epidemic in 1873, and as an isolation hospital for patients suffering from scarlet fever. The hospital housed only five to seven patients and two nurses. The doctor and hospital orderlies were isolated in an adjacent house. The Board of Health presented several plans for enlarging the hospital. Only in 1891 was the hospital on Katten replaced by a new and larger isolation hospital in another part of the city (Sandviken). At first, the Board of Health introduced rigid isolation regulations which were difficult to satisfy. When the pathogenic bacteria were discovered and the spread of infection was better understood, the view on isolation and other measures became more rational.

[Cholera hospitals in Bergen]. / Koleralasaretter i Bergen.

As early as 1831 premises for a cholera hospital were discussed in Bergen, but no decision was taken. On the same day that Bergen was declared to be cholera-infected, i.e. December 18th, 1848, a Board of Health was appointed. The Board immediately established the city's first cholera hospital, the Christi Krybbe hospital. Two additional hospitals were later established in other parts of Bergen. The hospitals had a total of 200 beds for a population of 24,000. Bergen was therefore relatively well equipped with hospital beds for cholera patients. A number of other plans for cholera hospitals were discussed. The Board wanted the county to establish a cholera hospital outside Bergen, to avoid new infection being introduced into the city. However, no hospital other than the three mentioned above was taken into use.

[Hospital records from the cholera epidemic in Bergen 1848-1849]. / Lasarettjournalene fra koleraepidemien i Bergen 1848-49.

During the great cholera epidemic in Bergen in 1848-49, three cholera hospitals were established. Records from the three hospitals have been found and studied. Of the 1,024 cholera patients in the city, 707 were hospitalized, and of these 430 (60.8 per cent) died. Overall, slightly more women than men were admitted to hospital. The women were older than the men but the mortality was the same. The Christi Krybbe hospital had the oldest patients but the lowest mortality. The staff probably acquired more experience at Christi Krybbe, which was in action during the whole epidemic, and the nursing may have been better there. The mortality in the hospitals reached a peak during the first weeks of the epidemic and later decreased considerably.

[The Board of Health and its activities during the cholera epidemic in Bergen in 1848-49]. / Sunnhetskommisjonen og dens virksomhet ved koleraepidemien i Bergen 1848-49.

In Norway temporary regulations were issued for control of cholera. An important provision was that Municipal Boards of Health should be appointed. The author describes the duties of the Board of Health, and how it functioned during the cholera epidemic in Bergen in 1848-49. The cholera broke out on 10 December 1848, and a Board of Health was appointed exactly one week later. The Board held frequent meetings and the minutes provide good information on the development of the epidemic and the activities of the Board. The fact that the Chief Medical Officer was not a member of the Board was in violation of the regulations. However, he usually attended the meetings and strongly influenced the decisions. It may have been considered an advantage that the Chief Medical Officer acted relatively freely, even if the overall responsibility lay with the Board. This led, however, to some doubt about responsibility, and concerning what were the official channels.

[Cholera in Bergen in 1848-1849--what caused the epidemic?]. / Koleraen i Bergen 1848-49--hvordan oppstod epidemien?

In December 1848, a big cholera epidemic broke out in Bergen. It lasted until April 1849, by which time 605 victims had died. The cholera spread by contact from person to person. How it came to Bergen, and how it was introduced into the population however, been open to doubt. This question is subject of this article. Primary sources have been studied and compared with contemporary medical reports. There is no doubt that a schooner from the Dutch city of Vlaardingen brought the cholera to Bergen. A passenger died of cholera on the day before the ship arrived, and was buried in Bergen. How the infection was transmitted to the first victim in the city, a watchman's wife who lived on the outskirts, is more difficult to explain. Later information, telling that she had washed the passenger's clothing, has not been confirmed in the primary sources. Most probably, healthy carriers among the crew transmitted the cholera to the population after the quarantine had been suspended. The watchman's wife need not have been the first one to catch the infection.

[Some cholera graveyards in western Norway]. / Noen vestnorske kolerakirkegårder.

The Norwegian provisional regulations from 1832 for the control of cholera included detailed directions for the burial of cholera victims. How these directions for graveyards were followed up has been studied in the context of the cholera epidemic in Western Norway in 1848-49. In Bergen an ordinary graveyard was used for burying cholera victims at the beginning of the epidemic, while all later burials took place in a graveyard for cholera victims only. 549 victims were buried here. On the island of Sotra the majority of the cholera victims were buried in three cholera graveyards, and further south in the county several small graveyards were planned or laid out. In general, the directions for cholera graveyards were followed. The cholera graveyard in Bergen was levelled over one hundred years ago, while several other cholera graveyards in Western Norway still exist as reminders of the epidemic.

Regulation of vasopressin expression in cultured diencephalic neurons by glucocorticoids.

Glucocorticoids have long been recognized as playing a major role in the regulation of vasopressin synthesis. However, the factors determining cellular specificity and molecular mechanisms of glucocorticoid action on the vasopressin gene are not understood. In the present investigation, we used primary cell cultures derived from 14-day-old fetal rat diencephalon to investigate the regulation of vasopressin expression under controlled conditions. The experimental paradigm used ensured that only magnocellular, but not parvocellular neurons grew in the cultures. The following criteria were used to establish this phenotype. (1) Cultures were derived from fetal brain well before the time parvocellular neurons are generated, and neuronal precursors did not proliferate in vitro. (2) Vasopressinergic neurons measured some 18 x 25 microns, being conspicuously larger than the average neuronal population in vitro, and clearly larger than parvocellular neurons in vivo. (3) Neurons did not express corticotropin releasing factor in vitro. Selective neutralization of glucocorticoids contained in the serum-supplemented culture medium by the drug RU 38 486 resulted in an about 2-fold increase of numbers of vasopressinergic cells and about 4-fold increase in vasopressin mRNA, but did not affect numbers of oxytocinergic neurons or expression of general neuronal marker proteins. The effects of RU 38,486 were not dependent on synaptic communication between cultured cells, as the drug was still effective when cells were synaptically isolated by growth is in 14 mM Mg2+. RU was not mitogenic for vasopressinergic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

[Cholera in Drammen 1832--the first time in Norway]. / Kolera i Drammen 1832--første gang i Norge.

Cholera came to Norway for the first time in autumn 1832. The outbreak was limited to the city of Drammen and some densely populated areas on the Drammen fjord. Mortality was low compared with later Norwegian epidemics. 80 persons died of cholera, 59 of them in Drammen. The morbidity is difficult to estimate, because cholera could not be distinguished from the frequent summer diarrhoeas. This article tries to present a picture of how the doctors interpreted the disease and what was done to prevent it from spreading. In the light of the available information the author discusses how cholera was imported to Drammen and how it spread in the city.

[The black death in Norway]. / Svartedauden i Norge.

The old Icelandic annals tell that the Black Death came to Bergen, Norway, in 1349 with a ship from England. This was probably at the beginning of September. From Bergen the plague spread rapidly northwards and southwards along the coast and over land to Eastern Norway. The Black Death remained in Norway for approximately six months. The epidemic must have been started by infected black rats and rat fleas in the grain cargo of the ship. The account in the annals, and experiences from other countries, indicate that pneumonic plague was dominant in Bergen at the start of the epidemic. After that the Black Death must have spread partly as pneumonic plague but mainly probably as bubonic plague, transmitted via human fleas from person to person. The rats cannot have played a part except in the initial phase. The annals say that 2/3 of Norway's population died. This is probably a big exaggeration. The mortality in Norway can hardly have been more than 40-50%. Even this is high compared with an estimated mortality of approximately 33% in England and on the continent.

[Plague epidemics in Bergen and population crises]. / Pestepidemier i Bergen og befolkningskriser.

Ten epidemics of plague are known to have occurred in Bergen, Norway, from the Black Death in 1349 to the last epidemic in 1637. Seven of them took place after 1530, and the primary sources of only three are known from the first 180 years of the plague period. Therefore, additional epidemics have probably occurred of which we have no knowledge. After the Black Death, bubonic plague probably hit Bergen, and the infection seems to have always been imported by ships, especially ships from Baltic cities. During the last five epidemics in Bergen 12,900-14,500 people died on plague in the course of 70 years, i.e. twice the population of the city. Extended immigration following each epidemic kept the size of the population up to 6,000-7,000. The death rate was clearly lower among the Germans at the Hanseatic Office than in the Norwegian city population. This was probably because an increasing percentage of Germans had become immune to plague after each epidemic, since the losses at the Office were not compensated for by immigration. It is concluded that the plague epidemics are the main reason for the population crises in Bergen in this period.

[Absalon Pederssøn's report on the plague in Bergen during 1565-1567]. / Absalon Pederssøns beretning om pesten i Bergen 1565-67.

The plague in Bergen 1565-67 was reported by Absalon Pederssøn, a citizen of Bergen, in his diary. The diary describes the onset of the epidemic and reports the deaths from day to day. The plague was brought to Bergen on about 10th August 1565 by a ship from Danzig. Altogether 1,500 people died of bubonic plague in Bergen, i.e. 21-25% of its population. The peaks of the epidemic occurred during the autumn months of 1565 and 1566. In both years the city was almost free from plague from February to July. During the first phase the infection must have been transmitted by rat fleas, but human fleas were the carrier during the cold autumn months. The recurrence in August 1566 and 1567 must have been due to the establishment of a plague reservoir among the rats in the grain stores.

[The medical situation in Bergen during the late medieval period described in the diary of Absalon Pederssøn in 1552-1572]. / Medisinske forhold i Bergen i senmiddelalderen omtalt i Absalon Pederssøns dagbok 1552-72.

First-hand information on Norwegian medical matters in the late Middle Ages is very scarce. Occasional brief information of medical interest may be found in private letters and in more systematic general records. However, a unique and particularly interesting document from this period is Master Absalon Pederssøn's diary. The diary covers a twenty-year period of the history of Bergen from the middle of the 16th century, and is characterized by its detailed information, also on matters of medical interest. Absalon was a well-educated man who without doubt had considerable medical insight. The events he describes have been personally experienced and analysed. He has seen the sick and describes the symptoms, and today, the information he provides allows us to draw conclusions about the nature of the diseases. Absalon's diary therefore provides interesting insight into medical matters in Bergen at that time and knowledge on diseases and what was known about them, causes of death, barber surgeons and hospitals.

Antibodies to staphylococcal peptidoglycan and its peptide epitopes, teichoic acid, and lipoteichoic acid in sera from blood donors and patients with staphylococcal infections.

Antibodies to the staphylococcal antigens peptidoglycan, beta-ribitol teichoic acid, and lipoteichoic acid, as well as to the peptidoglycan epitopes L-Lys-D-Ala-D-Ala, L-Lys-D-Ala, and pentaglycine, were found over a wide range of concentrations in sera from both blood donors and patients with verified or suspected staphylococcal infections. The patient group was heterogeneous with regard to both age and type of staphylococcal infections, being representative for sera sent to our laboratory. In single-antigen assays antibodies to pentaglycine had the highest predictive positive value (67%), although only 32% of the patients had elevated levels of such antibodies. Combinations of test antigens could yield positive predictive values as high as 100%, but then the fraction of positive sera was low. Indeed, the fraction of patient sera which was positive in multiple-antigen tests never exceeded 61%. The clinical usefulness of these seroassays for identifying Staphylococcus aureus as a causative agent was limited, owing to the considerable overlap in the range of antibody concentrations between patient and blood donor sera.

Antibodies to Yersinia enterocolitica in a healthy population in Tanzania.

A micro-agglutination technique was used for the detection of antibodies to Yersinia enterocolitica serogroups 03, 08 and 09 in sera from healthy individuals in Dar es Salaam, including 38 school children and 81 adults. Antibody titres greater than or equal to 128 to serogroup 03 were found in 2.6% of the children and 0.8% of the adults, and to serogroup 09 in 5.3% of the children and 2.5% of the adults. Antibody titres greater than or equal to 128 serogroup 08 were not detected.

Antibodies to Staphylococcus aureus peptidoglycan and lipoteichoic acid in sera from blood donors and patients with staphylococcal infections.

An enzyme-linked immunoassay (ELISA) was used to detect antibodies in human sera to Staphylococcus aureus peptidoglycan (PG) and lipoteichoic acid (LTA). All the sera from the blood donors contained IgG antibodies to both substances. Among the sera from 34 patients with bacteriologically verified, serious S. aureus infections, 71 per cent contained significantly elevated levels of anti-PG antibodies and 76 per cent of anti-LTA antibodies. Among the sera from 38 patients with suspected but not bacteriologically verified staphylococcal infections, 58 per cent contained significantly elevated levels of anti-PG antibodies and 74 per cent of anti-LTA antibodies. The levels of antibodies to PG correlated well with the levels of antibodies to LTA, but the latter occurred over a broader range in the patient sera. Elevated antibody values were, however, also found in some patients with serious, non-staphylococcal infections. The diagnostic value of PG and LTA antibodies has to be further investigated.

Comparison of four methods for differentiation of Staphylococcus aureus from other Micrococcaceae in the routine laboratory.

Four methods for the identification of Staphylococcus aureus (tube coagulase test, thermostable nuclease test, indirect agglutination of fibrinogen coated erythrocytes and a commercial latex kit: SeroSTAT Staphylococcus Test) have been compared. Clinical isolates (698) and 40 reference strains of Micrococcaceae were included in the study together with control organisms. The coagulase test gave no false positive results but 39/406 clinical isolates of S. aureus were negative at 2h and one half were only weakly positive. At 18 h, all but 2 of 406 isolates gave a positive reaction. The thermostable nuclease test was very specific; no clinical isolates of S. aureus gave negative results and no "coagulase-negative" clinical isolates gave a definite positive reaction. The indirect haemagglutination method was sometimes difficult to interpret and frequently gave negative or doubtful results for S. aureus. The SeroSTAT test was easy to use and interpret and was specific; the method is suitable for routine laboratory use, particularly when a rapid result is desirable.