Ultrasonographic findings in two sheep with enzootic calcinosis.

INTRODUCTION: This report describes 2 sheep with enzootic calcinosis characterized by abnormal cardiovascular and respiratory findings and ascites causing abdominal distension. Both sheep were anorexic and listless and had increased heart and respiratory rates. Auscultation of the heart revealed a gallop rhythm in sheep 1 and a loud systolic heart murmur in sheep 2. The activities of liver enzymes were severely increased in both sheep. Abdominal ultrasonography showed severe ascites and congestion of the liver and caudal vena cava. Echocardiography in sheep 2 showed hyperechoic and markedly thickened mitral and aortic valves with moderate-severe mitral insufficiency and generalized cardiomegaly. Both sheep were euthanized and examined postmortem. In addition to ascites and pleural effusion, the principal lesions were nodular thickening of the heart valves and calcification of the aorta and other arteries. Nutrition of the sheep did not include hay pellets, but the sheep were kept together with alpacas and lamas and had access to the hay pellets of these animals. In addition visitors were allowed to feed the sheep with hay pellets offered by the zoo in a dispenser. The two types of hay pellets had Vit D concentrations of 9'900 IU VitD3/kg and 7'000 IU Vit D2/kg, respectively. The definitive diagnosis was enzootic calcinosis.

Fyx is associated with two missense point mutations in its gene and can be detected by PCR-SSP.

The Duffy blood group antigens are encoded by the Duffy gene with its three major alleles: Fy*A (Fya+), Fy*B (Fyb+), and a nonexpressed Fy*Fy (Fya-b-), which is most commonly found among black people. Additionally, a fourth allele, Fyx, is found among white people and defined as weak Fyb not detectable by all anti-Fyb. Three polymerase chain reactions (PCRs) using sequence-specific priming (SSP) for detection of the major FY alleles were developed. Eighteen Fy(a-b-) samples of Tanzanian origin were correctly typed and of 300 random donors of Caucasian origin with known Fy phenotype, only four out of 59 Fy(a+b-) donors showed the discrepant DNA-type Fy(a+b+). Serologic reinvestigation by adsorption and elution techniques confirmed weakly expressed Fyb antigen in these cases and DNA sequencing of the entire Duffy gene revealed identical point mutations in all of them. Specific PCR reactions were used to reinvestigate the C265T (Arg89Cys) and G298A (Ala100Thr) substitution in the 300 samples. A298 was found to be present in both FY*X and FY*B alleles, pointing to an allelic variation among FY*B alleles. T265 was encountered exclusively in FY*X and is thought to be FY*X specific. Combining the T265 specific reaction with the three PCR-SSPs described above, we were able to correctly DNA-type all phenotypes investigated in our study.

RHD/CE typing by polymerase chain reaction using sequence-specific primers.

BACKGROUND: Current DNA-based Rh system typing strategies may detect the two RH genes and their prevalent alleles, but they are known to fail sometimes, when rare RH alleles (e.g., D category phenotypes) are encountered. It is almost impossible to find a single DNA-based method that can accommodate the great heterogeneity within the human Rh system. STUDY DESIGN AND METHODS: An easy-to-perform DNA-based method for the detection of the two RH genes and their alleles, including variant RHD alleles, was developed. By the use of one RHD/C-, seven RHD-, and four RHCE-specific polymerase chain reactions, all triggered to work at identical thermocycling conditions, the DNA of 77 blood donors carrying weak D and that of 200 random donors with common D phenotype was investigated. In addition, 77 selected samples of ccDee and rare Rh system phenotypes were examined. RESULTS: Among 77 samples of weak D, one Rh33 and six DVI categories were detected, one of which showed new RHD-specific nucleotide patterns. In DFR and CCee samples, novel variant RHD alleles were found. RHD DNA types of 200 random donors were found to be concordant with their D phenotype. For RHE and RHe genotyping, a full correlation with serologic phenotypes was found. Our method for genotyping RHC and RHc failed in some cases, because of an already published RHc allelic variation, which we have called RHc(cyt48). An estimate of the frequency of this RHc(cyt48) allele in a white population was made. CONCLUSION: The presented exon-scanning RHD/CE polymerase chain reaction using sequence-specific primers complements current DNA-based Rh system typing strategies and is superior in the detection of variant RHD alleles.

Helicobacter pylori infection and blood group antigens: lack of clinical association.

OBJECTIVES: Blood group antigens traditionally have been associated with a risk of developing peptic ulcer and gastric cancer. Helicobacter pylori is a bacterium associated with chronic active gastritis and ulcer disease, and its attachment to gastric mucosa was recently shown in vitro to be mediated by blood group Lewisb and H antigens. This study was designed to test the clinical relevance of this laboratory observation in patients undergoing endoscopy and gastric biopsy. METHODS: Blood group phenotypes and gastric biopsies for H. pylori and histology were determined and correlated in 384 patients undergoing upper endoscopy. Blood from healthy blood donors was tested for the same blood group antigens and used as a control group. RESULTS: The distribution of blood groups ABO, Lewis, Rhesus, and MN was similar among the patients undergoing endoscopy and a control group of 2369 healthy blood donors from the same geographic area. There was no correlation between H. pylori infection or the H. pylori-associated diseases, peptic ulcer or chronic active gastritis, with any blood group phenotype, including Lewisb, blood group O, or both. CONCLUSION: No in vivo correlation between H. pylori infection or disease and Lewisb or H antigen could be demonstrated. Moreover, patients with H. pylori infection and disease have a distribution of blood group antigens similar to a control population.

Cold haemagglutinin disease complicating Mycoplasma pneumoniae infection in a child under cytotoxic cancer treatment.

Acute cold haemagglutinin disease, most commonly associated with underlying mycoplasma infection, is rare in children. A 3-year-old girl who developed this auto-immune disease under intensive cytotoxic treatment for rhabdomyosarcoma is presented. Clinically, a livedo reticularis skin pattern upon exposure to cold which was reversible at room temperature and a spontaneous red cell agglutination of blood samples in vitro led to the diagnosis. Together with bronchopneumonia the girl developed hyper-IgM, high antibody titres against Mycoplasma pneumoniae, as well as high titres of cold agglutinins. Laboratory signs of mild intravascular haemolysis were found. Positive direct antiglobulin test resulted from coating of red cells with C3d and C4. Three different antibodies were identified in serum: nonspecific cold agglutinins without complement activation, anti-I specific cold agglutinins with complement activation, as well as a weak biphasic Donath-Landsteiner haemolysin. Under antibiotic treatment and a short course of predisolone the clinical course was mild.

Apparent 'auto'-anti-DE of the IgA and IgG classes in a 16-year-old girl with a mature cystic ovarian teratoma.

Prior to the removal of a mature cystic teratoma in a girl, aged 16, we had difficulties in Rh typing due to immunoglobulin coating of the red blood cells (RBCs). Further examination revealed the presence of anti-D and anti-E antibodies; the clinical course and the serological characteristics indicated that the Rh antibodies originated from the tumor itself, that is, there was alloantibody formation against the host's RBCs. The specific alloantibody production, as well as the fact that these antibodies belong to the IgA and IgG1 classes provide further evidence for the pluripotency of mature cystic ovarian teratomas.

[Current problems of blood transfusion. Responsibility of the physician in transfusion]. / Aktuelle Probleme der Bluttransfusion. Die Verantwortlichkeit des transfundierenden Arztes.

The physician's responsibility regarding the indication and induction of blood transfusion, the request for fresh whole blood and the decision for the degree of urgency are outlined. The risk of hemolytic transfusion reaction, one of many transfusion hazards, is calculated on the basis of the results obtained from a 7-year antibody screening program in blood recipients. Measures for the prevention of hemolytic transfusion-reactions are discussed.

[Autoimmune hemolysis caused by anti-Pr]. / Autoimmunhämolyse durch Anti-Pr.

Following an infection with mycoplasma pneumoniae, an anti-Pr-antibody developed in a hitherto healthy man, aged 41. Within a period of 5 days the antibody caused a severe autoimmune hemolytic reaction. The patient died on the fifth day after admission due to hemolysis and uremia. The autoantibody showed a reactivity with a broad thermal range from 4 degrees C to 37 degrees C. As an initial warning sign, the patient presented an expressed livedo reticularis. Massive wholeblood exchanges could not stop the fatal process.