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Biomedical subjects

W Büngener

Publications and source records attributed to W Büngener.

At least 19 recordsLinked to original sources
PubMed1989

Fatal Streptococcus suis septicemia in an abattoir worker.

A 51-year-old abattoir worker became ill with high fever and was admitted to hospital late in the evening, where he died 4 h later. Smears of peripheral blood taken 7 h after death showed numerous cocci. Cultures of the blood grew beta-hemolytic streptococci exhibiting the biochemical properties of Streptococcus suis II. A complete autopsy with extensive microscopical studies showed numerous bacteria in small vessels of several organs, but no bacterial colonisation of tissues, meningitis, or other relevant lesions were found. The group R antigen of the bacteria could be demonstrated by immunofluorescence in paraffin sections of the kidney and the adrenal gland. Two similar cases of fulminant fatal Streptococcus suis II septicemia have been reported from Denmark. This appears to be the first case observed in the Federal Republic of Germany.

Abattoirs↗
PubMed1987

Reticulocytes in peripheral blood of mice infected with Trypanosoma brucei: dramatic decrease of reticulocytes during primary wave of parasitemia.

Infection of mice with rapidly proliferating trypanosomes that killed the mice in the first or second wave of parasitemia led to a dramatic decrease of immature erythrocytes in the peripheral blood during the primary wave of parasitemia. Trypanosome variants producing lower first waves of parasitemia, and/or less rapid deaths, caused a variable, on the average small, decrease of immature erythrocytes. Trypanosome variants causing rapidly lethal infections killed the mice before a decrease of immature erythrocytes became apparent.

Animals↗
PubMed1985

Virulence of plasmodium yoelii line YM is caused by altered preference for parasitized and unparasitized immature and mature erythrocytes.

In the phase of beginning and continuing nearly complete parasitization of all immature erythrocytes and marked multiple parasitization of immature erythrocytes, less merozoites of the virulent type are lost in the population of parasitized and unparasitized immature erythrocytes, more merozoites invade mature erythrocytes. This behaviour determines the rapidly lethal course of the infection. It appears to be related to altered properties of the merozoite surface. Virulent parasites do not show altered ability to develop in mature erythrocytes.

Animals↗
PubMed1984

Histopathological findings in mini-pigs infected with different strains of Trypanosoma brucei.

Two pigs infected with Trypanosoma brucei gambiense developed low parasitemia which became undetectable after 6 months; on autopsy 13 months after infection they showed no histopathological alterations. --Five of six pigs infected with a Trypanosoma brucei brucei strain from the Ivory Coast developed low parasitemia (up to about antilog 6.5 per ml of blood) which became progressively lower but was detectable up to one year after infection. On autopsy they showed interstitial myocarditis and meningo-encephalitis; during the course of the infection, the first became milder, the second more intense; no trypanosomes were seen in the tissues. One of these pigs developed a parasitemia of up to antilog 8 and died 172 days after infection from bacterial pneumonia, histologically it had severe myocarditis with many trypanosomes in the tissue and mild meningo-encephalitis. --Three pigs infected with a Trypanosoma brucei brucei strain from the Serengeti died 47, 68, 130 days after infection. The first dying pig had a high terminal parasitemia, in the others, the parasitemia was low until the end, being only detectable by the hematocrit centrifugation technique or by mouse passage. At autopsy, all showed massive myocarditis and interstitial nephritis with masses of extravascular trypanosomes, moderate meningo-encephalitis with very few trypanosomes, and widespread colonization of other organs and tissues by trypanosomes, still without marked cellular infiltrations.

Animals↗
PubMed1984

Behaviour of a Trypanosoma brucei brucei stock (STIB 348C) in mice. 4. Different course of primary parasitemia in trypanosome variants of different virulence.

In three types of trypanosomes with low virulence, trypanosome numbers increased by a factor of 18-21 per day on average during prepatency and by a factor of 70-219 on average from the first to second day of patency. By contrast, a very virulent trypanosome variant showed an average increase of trypanosome numbers per day by 32 and 28 during prepatency and early patency, respectively. --In detailed studies, trypanosomes of low virulence exhibited a rapidly rising parasitemia in early patency which lasted for 20-30 hours and was followed by a plateau of slowly rising and falling parasitemia. Trypanosomes of high virulence showed a constant logarithmic increase of their numbers, slowing down at concentrations above antilog 5.5 per microliters of blood. In mild trypanosomes with peak parasitemias of antilog 5-5.7 per microliters of blood, after low dose infections the primary parasitemia was abruptly terminated after 70-100 hours of patency, obviously by the action of antibody. After massive infections, the parasitemia was terminated at 109-122 hours after infection. --In trypanosomes with higher peak parasitemias, primary parasitemias were seen to last longer, in some cases for 7 to 12 days. --Mice infected with low doses of highly virulent trypanosomes died with high parasitemias after some 60-90 hours of patency, before antibodies could normally become effective. After massive infections they died at 40-60 hours after infection. There is clearly no need to invoke non-immunogenicity of these trypanosomes or immunosuppression by these trypanosomes to explain this course of the infection.

Animals↗
PubMed1983

[Behavior of a Trypanosoma brucei strain (STIB 348C) in mice. 3. Histopathological findings in the terminal stage of infection].

Histopathological findings in the terminal stage of the infection of mice and rats with different variants of the Trypanosoma brucei brucei stock are described. Mice infected with mild variants showed after 12-149 days intense trypanosome colonization of the interstitial connective tissue, especially of the heart muscle, pancreas and choroid plexus, with severe tissue destructions, especially in the pancreas. With longer duration of the infection, round cell infiltrations of the leptomeninx and around intracerebral vessels developed. The alterations were the same in animals dying with high and low parasitemias. Some animals died with continuous bleeding from the tip of the tail, with serious effusions and massive edema or with generalized bacterial infection. The lymphatic organs showed intense reactive alterations, trypanosomes were only rarely found in lymph nodes. In the liver large fields of lymphatic and myeloid cells were seen, sometimes necroses developed. The kidneys showed marked deposition of eosinophilic material in the glomeruli and precipitation of proteinaceous material in dilated tubules. - Rats infected with mild trypanosomes exhibited intense colonization of the heart by trypanosomes, in some places many trypanosomes in lymph nodes, few trypanosomes in the pancreas. They died after a long phase of high parasitemia.--After infection with virulent parasites which killed the animals with high parasitemia in a few days, mice and rats had single small foci of trypanosome colonization of the interstitial connective tissue of heart, pancreas and choroid plexus as well as of the loose connective tissue in the hilum of the kidney and around lymph nodes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Behaviour of a Trypanosoma brucei brucei stock (STIB 348C) in mice. 2. Course of infections with the basic type and several variant types.

Parasitemia in mice was followed using daily blood smears. Infections with few trypanosomes of the basic type regularly showed a prepatency, a primary wave of parasitemia, a secondary latency and an uncharacteristically fluctuating secondary parasitemia, leading to death 28-144 days after infection. The characteristics of the infection were not altered by serial transfers of 100 trypanosomes every 5th day in mice for several months. Infections with single trypanosomes out of early secondary parasitemias (that is: with expression of other variant antigenic types) mostly led to lower or higher primary peaks, otherwise to similar courses of the infections. In infections with many trypanosomes out of early secondary parasitemias the parasitemia developed similarly to secondary parasitemias after primary peaks. Secondary parasitemias were little influenced by attempts at active or passive immunization, they must be assumed to contain trypanosomes with expression of many different variant antigenic types.--Similar courses of infections were seen in rats.--Trypanosomes transferred to new mice from mice that had been infected for a long time usually caused markedly shortened infections with a) a continuously low parasitemia, b) an initially low parasitemia, rising very soon to lethally high levels, c) a rapidly rising parasitemia, lethal in the first wave or after one remission. These trypanosomes are regarded as variant metabolic types that have lost the density-dependent inhibition of proliferation in blood and/or tissue, characteristic of the original type.

Animals↗
PubMed1980

[Experimental production of variants with lowered preference for polychromatophilic erythrocytes in Plasmodium yoelii (author's transl)].

After 25 massive passages of a Plasmodium yoelii-population (strain 17X) in the phase of high parasitization of mature erythrocytes, parasites with markedly lowered preference for immature erythrocytes could be isolated. Of 3 isolates in 3 independent experiments, one showed a distinctly lower preference than the other two. With very high infecting doses, the isolates caused in most mice high parasitization of mature erythrocytes and death. The original strain had been kept in mice by passage of a few parasites every 1--2 weeks for several months; on testing it exhibited a somewhat lower preference for immature erythrocytes and less polyparasitization of immature erythrocytes for a given multiplicity. Polyparasitization seemed to be unaltered in the 3 isolates. Antiserum against Plasmodium yoelii inhibited 2 tested isolates more than the modified original strain. These observations suggest that Plasmodium yoelii merozites may exist in several types differing in their relative affinity for mature erythrocytes, antibodies and parasitized immature erythrocytes. Different types should become predominant under different selective pressures. The different types are probably formed by mutations determining alterations in molecules of the merozoite surface.

Animals↗
PubMed1979

[Further observations of the course of Plasmodium berghei infection in the mouse].

Invasion of immature and mature erythrocytes by merozoites of Plasmodium berghei seems to obey the following rules: Merozoites prefer unparasitized immature erythrocytes. Multiple infections of immature erythrocytes occur in conditions of high merozoite production and low concentration of unparasitized immature erythrocytes, when frequently repeated contacts between merozoites and unparasitized or freshly parasitized immature erythrocytes become increasingly probable. Mature erythrocytes are invaded when the relative density of unparasitized immature erythrocytes drops below 0.2--0.5%, in other words, when merozoites do not meet unparasitized immature erythrocytes in 200--500 erythrocytes. Failure to invade mature erythrocytes is obviously not due to inability of the merozoites to penetrate the erythrocyte membranes.--Merozoites of Plasmodium vinckei, on the other hand, show random invasion of parasitized and unparasitized mature erythrocytes, leading to frequencies of unparasitized and singly or multiply parasitized erythrocytes approaching a Poisson distribution.--The Plasmodium berghei infection regularly leads to a lowered density of polychromatophilic erythrocytes in the peripheral blood. This depression of polychromatophilic erythrocytes uses to be of very different duration, form and intensity. The relative density of immature erythrocytes may show pronounced fluctuations in this phase. As has been seen in one animal, even monocytes and polymorphonuclear leucocytes may, alongside with the immature erythrocytes, for some time totally disappear from the peripheral blood. The depression of polychromatophilic erythrocytes evidently goes along with pronounced alterations of the erythropoesis in spleen and bone marrow. Leucocytes in the peripheral blood generally show rather uncharacteristic alterations of their concentration, they may form very high concentration peaks.

Animals↗
PubMed1979

[Malaria plasmodia in the mouse. Parasitization of mature and immature erythrocytes by Plasmodium berghei, Plasmodium yoelii and Plasmodium chabaudi (author's transl)].

Plasmodium berghei parasites (strain K173) in mice with developing immunity changed to a variant type with increased resistance against antibodies and enhanced invasion of mature erythrocytes; on passages in normal mice this variant type retransformed to the normal type (Kretschmar 1964). On detailed study, parasites of the variant type showed a markedly decreased predilection for polychromatophilic erythrocytes, leading to slowed multiplication during prepatency, increased invasion of mature erythrocytes and rapidly fatal course of the infection. Avoidance of parasitized immature erythrocytes remained unaltered in the variant type. In presence of antibodies many parasites invaded mature erythrocytes even in blood with high concentrations of immature erythrocytes. --Plasmodium yoelii (strain 17X) showed very high predilection for polychromatophilic erythrocytes, only slight lowering of immature erythrocyte concentration and low parasitization of mature erythrocytes. Parasites with altered preference for polychromatophilic erythrocytes were not observed in animals with parasitemia relapsing after spontaneous disappearance of the primary parasitemia or after injection of antiserum. It is suggested that in a variant of Plasmodium yoelii with high invasion of mature erythrocytes (Yoeli et al. 1975), the decisive virulence factor might be a lowered predilection for polychromatophilic erythrocytes. Avoidance of parasitized immature erythrocytes is less marked in Plasmodium yoelii than in Plasmodium berghei. In presence of antibodies more parasites invade mature erythrocytes. --Plasmodium chabaudi showed an appreciable preference for invasion of immature erythrocytes. Moreover, significantly more multiply parasitized mature and immature erythrocytes were found than would have been produced by random invasion of erythrocytes.

Animals↗
PubMed1977

[Extravascular localization of Trypanosoma vivax in cattle (author's transl)].

In 2 cattle experimentally infected with Trypanosoma vivax, strain EATRO 1695, trypanosomes were found in the marginal sinus of one of several lymph nodes examined. One animal showed trypanosomes in a small focus in the interstitial tissue of the heart. It is concluded that Trypanosoma vivax can not be regarded as a strict plasma parasite.

Animals↗
PubMed1976

[Experimental Trypanosoma infections in Cameroon dwarf goats: histopathological observations (author's transl)].

14 Cameroon Dwarf goats were experimentally infected with Trypanosoma (Duttonella) vivax, T. (Nannomonas) congolense, and T. (Trypanozoon) brucei. Infection with T. burcei caused death of the animals within 45-201 days. All goats which died following T. brucei-infection showed characteristic mononuclear cell infiltrations in brain and heart, most of them showed infiltrations in skin (eye lids), sceletal muscles, kidneys, fat and connective tissue as well. Infections with T. vivax and T. congolense produced no clinical signs and very little histological alterations. Animals infected with T. congolense or T. brucei for more than 5 months showed amyloid deposits in their livers, spleens and kidneys.

Amyloidosis↗
PubMed1976

[Adherence phenomena in Trypanosoma congolense (author's transl)].

Two adherence phenomena in Trypanosoma congolense as a possible cause of trypanosome aggregation in the capillaries of certain organs are described: 1. Adherence of trypanosomes to blood cells of nonimmune mice, 2. dovetailing of trypanosome membranes into one another and into the vessel wall.

Animals↗
PubMed1975

[Course of Trypanosoma musculi infections in Plasmodium berghi-infected mice (author's transl)].

Trypanosoma musculi brought into Plasmodium berghei-infected mice in the later stages of the malaria infection shows rapid, approximately logarithmic multiplication in the peripheral blood. The trypanosome number increases by a factor of 2-9 per day, multiplication of the parasites kills most mice in a few days. Many multiplicative forms of the trypanosomes and a few trypanosomes without nuclei are seen in blood smears. Histologically and in touch preparations, masses of multiplicative forms of the trypanosomes are seen in the sinusoids of the liver. Aggregates of trypanosomes are found, too, in the kidney medulla and, inconstantly, in venous sinuses of the spleen and postcapillary venules of lymph nodes. Occasionally, trypanosomes may be found extravascularly in the interstitial connective tissue especially of the pancreas, in lymph vessels and lymph node sinuses. - Mice infected in earlier stages of the Plasmodium berghei infection achieve stabilization of trypanosome numbers.

Animals↗