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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Theileria lawrencei tick-derived stabilate infection of 8 cattle resulted in the development of panleukopenia and hypoproteinemia. In addition to these changes, T. parva infection caused mild normocytic, normochromic, non-responsive anemia at either of two dose rates. Disseminated intravascular coagulation, as indicate by positive protamine paracoagulation tests, prolonged prothrombin and partial thromboplastin times, and thrombocytopenia, developed in cattle infected with either of the Theileria spp., and was probably an important intermediary mechanism leading to death. Infection of calves with a high dose of T. parva stabilate resulted in more rapid onset of clinico-pathologic changes than did the low dose infection. Theileria lawrencei infection produced a severe, acute syndrome, the clinico-pathologic alterations of which varied in time of onset and severity between those of the T. parva high dose and low dose groups.
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PMID:A comparative study of the disease in cattle caused by Theileria parva or T. lawrencei: II. Hematology, clinical chemistry, coagulation studies and complement. 720 9

Maternal mortality was examined in a semi-urban Nigerian community over a 10-year period. Maternal mortality was defined as death occurring as the direct result of childbearing and measured per 1000 births. Abortions at below 20 weeks gestation were excluded. From 1966 to 1975, there were 90 maternal deaths out of 13,182, a rate of 6.8/1000. The hospital records of the Baptist Medical Center, located in the western part of Nigeria, were carefully reviewed and cross-checked with obstetric statistical records. Only 13 of the deaths occurred in hospitalized patients. 78 (80%) were due to direct obstetric causes; 12% were from nonobstetric causes. Anemia due to blood loss was the leading casue of death, accounting for 30, or 33%, of the deaths. Anemia, with or without congestive heart failure accounted for 7 deaths. Infection was responsible for 5 deaths. Ruptured uterus, preeclampsia, and eclampsia occurred in equal percentages, 10-11%. Indirect obstetric deaths, such as sudden death, accounted for 10 deaths. 50% of these were anesthetic deaths; the remainder were due to pulmonary embolism. Sickle cell intrapartum crisis was the cause of 1 death. Associated causes included featured pneumonia, nephritis, hepatitis, meningitis, enteritis, and cerebrovascular accident. Parity ranged from 0-11. 25 babies were salvaged in this series. Prevention continues to be the cornerstone in improving maternal mortality figures in developing countries. The Baptist Medical Center's model for providing maternal care is described briefly and is identified as responsible for the encouraging decline in the maternal mortality rate.
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PMID:Maternal mortality in a semi-urban Nigerian community. 720 76

The clinical chemical changes induced by Anaplasma marginale infection were determined in 16 adult, intact cows infected with either of 2 virulent isolates and in 8 others treated with a live sheep-attenuated A marginale vaccine and were compared with the clinical chemical analyses in 7 noninfected controls. Blood samples from the cows were analyzed for various serum components and during clinical disease. Cows infected with the 2 virulent isolates had maximum erythrocyte parasitemias (0.5% to 66%) between 1 and 11 days of patency (DP); 7 of the 16 infected animals died within 5 to 12 DP. Cows given the sheep-attenuated anaplasma vaccine had maximum parasitemias (0.1% to 4.2%) between 1 and 16 DP and none died. Infection with the virulent isolates produced severe anemia (mean RBC count = about 2 million/mm3) and caused increases in serum total bilirubin (TBILI), direct bilirubin (DBILI), serum urea nitrogen (SUN), alkaline phosphatase (ALP), and serum aspartate aminotransferase (AST) that were significantly higher than comparable changes in control values. These increases were highest after peak parasitemias in surviving animals. Vaccination with the attenuated isolate produced a mild anemia (mean RBC count = about 5 million/mm3) and a significant increase only in ALP. Marked increase in TBILI, DBILI, SUN, ALP, and AST were detected 0 to 1 day before death in 3 cows. However, such increases were not observed 2 to 4 days before death in the other cows that died.
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PMID:Clinical chemistry of anaplasmosis: blood chemical changes in infected mature cows. 725 83

The pathogenesis of peripheral blood cytopenias in AIDS patients is clearly multifactorial. Among the various contributing mechanisms, those involving a direct role of HIV-1 have been actively investigated in the past few years. It has now been convincingly demonstrated that HIV can impair the survival/proliferative capacity of purified haematopoietic progenitor cells. Although a subset of haematopoietic progenitor cells are perhaps susceptible to HIV-1 infection, both in vitro and in vivo, the suppressive effect does not require either active or latent infection and is probably mediated by the interaction of viral or virus-associated proteins with the cell membrane of haematopoietic progenitor cells. Both the viral load and the biological characteristics of the virus play an important role in suppression, since different isolates displayed different inhibitory activity. Haematosuppression is not a specific property of monocytotropic versus lymphocytotropic or low-replicating versus high-replicating isolates, and it will be important to exactly establish which viral component is crucial to suppression of haematopoietic progenitor cells. Since the haematopoietic stem cell is the common progenitor to both the myeloid and lymphoid lineages, the capacity of HIV to impair the growth of early haematopoietic progenitor cells could contribute not only to the frequent occurrence of anaemia, granulocytopenia and thrombocytopenia in AIDS patients, but also to the inability of the bone marrow to reconstitute a functional pool of mature CD4+ T-cells. It is also possible that haematopoietic progenitor cells committed to the T-lymphoid lineage are impaired by HIV in their differential pathway within the thymus (Bonyhadi et al, 1993). Infection of megakaryocytes could result in underproduction of platelets and possibly represents a major pathogenetic mechanism of HIV-related thrombocytopenia. Infection of monocytes and T-lymphocytes leads in vitro and probably also in vivo to deranged cytokine production. In the first stages of the disease, increased cytokine production, consequent to a chronic immune activation, is probably responsible for the myelodysplastic/hyperplastic alterations observed at the bone marrow level. In more advanced stages of the disease, the general decline in immune function, the consequent imbalance in cytokine production, and the increase in viral burden, may contribute to dysregulated haematopoiesis and peripheral blood cytopenias.
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PMID:Effect of human immunodeficiency virus infection on haematopoiesis. 754 35

Twenty-two cases of rickettsiosis imported to Germany (13 men, nine women, average age 42 years) in a 5-year period were analyzed retrospectively regarding the travel histories, symptoms and clinical findings, laboratory features and course of the disease. The two primary rickettsial diseases were boutonneuse fever (18 patients) and scrub typhus (three patients). One patient had murine typhus. The main symptom was fever in 91% followed by headache (64%), myalgia (40%), arthralgia (50%) and diarrhea (36%). The most frequent clinical finding was lymphadenopathy in 65%. Eschar was detectable in 55% of patients with Rickettsia conori infection and in one patient with Rickettsia tsutsugamushi infection. All patients with R. tsutsugamushi infection as well as 33% of the patients with R. conori infection had a macular exanthema. One patient with scrub typhus had pleural and pericardial effusions. Seventy-three percent had an increased ESR. Three patients had leucocytosis, three increased transaminases and two normochromic anemia. The incubation period for R. conori infection was 5 to 28 days (average 14 days), for R. tsutsugamushi infection 7 to 21 days (average 16 days). Twenty-one patients were treated with tetracycline or doxycycline, one with erythromycin. All patients were cured. One patient had a relapse. Due to the fact that the symptoms are often not characteristic and that the routine laboratory findings are of only marginal help, the diagnosis of rickettsial diseases is often not easy. A detailed travel history sometimes gives an important hint for diagnosis.
Infection
PMID:Imported rickettsioses in German travelers. 762 71

Reduction of maternal mortality in developing countries is possible through elimination of unsafe abortion, active management of labor, appropriate management of pregnancy complications, and availability of adequate facilities. Prevention and early recognition are key factors in preventing maternal deaths due to ruptured uteri. A well equipped hospital is the appropriate place for delivery of mothers with a history of previous cesarean sections, a grossly contracted pelvis, previous myomectomies, previous multiple births, and previous abnormal births or complications during delivery. Complicated procedures, use of oxytocins, and administration of anesthesia should be performed with experienced, trained medical personnel. Surveillance of and correction for anemia should occur during the course of the pregnancy. Infections can be controlled with tetanus toxoid immunization and use of chest X-rays. The health care system should be tiered with primary health care services located in suburbs and rural districts. Services should be situated to account for population distribution, extent of maternal mortality in the region, transportation facilities, and the nearest secondary hospital. Birthing homes with sanitary facilities are an option for rural districts. A two-way referral system should be established between the primary, secondary, and tertiary level hospitals. Audits should be conducted as a means of checking for needed improvements in the system. Planning that includes proper roads, transportation, and communication facilities is important. Funding can come in the form of money, materials, and manpower. Safe motherhood requires the commitment of local people and local governments. The first step in a safe motherhood program is creating awareness among the political and economic elite. Governments are encouraged to shift resources from the military to housing, transportation, communications, education, and health during peace-times. Local professional associations, women's groups, and nongovernmental organizations are useful resources. Concerted efforts from many different agencies and all the people is required in order to achieve safe motherhood for all.
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PMID:Maternal mortality: a global overview. 765 32

Infection of 60 to 90% of neutrophils with the protozoa, Hepatozoon canis, was detected in 2 dogs. Clinical signs included lethargy, anorexia, and weight loss. Both dogs had severe anemia, leukocytosis, and thrombocytopenia as well as hypoalbuminemia, hyperglobulinemia, and high activities of serum alkaline phosphatase and creatine kinase. Both dogs were treated with imidocarb dipropionate and doxycycline. One dog recovered clinically, with disappearance of parasites from WBC. The other dog died, despite treatment. Necropsy revealed widespread dispersion of schizonts in the parenchymal tissues, but no involvement of skeletal muscle tissues. The disease syndrome that has been identified in the Texas Gulf region is characterized by gait abnormalities associated with multifocal pyogranulomatous myositis, thus, it is distinct clinicopathologically from the syndrome observed in these 2 dogs.
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PMID:Hepatozoon canis infection in two dogs. 779 Mar 3

The results have been reviewed of 41 patients with end stage polycystic kidney disease on maintenance hemodialysis. The patients ranged in age from 34 to 83 years with an average age of 55 years and 25 patients were male, 16 were female. The duration of maintenance hemodialysis in the patients was from 1 to 200 months with an average time of 69 months. Infection of the cysts and pyelonephitis occurred 22 times in 13 patients (32%) and hemorrhage into the cysts occurred 15 times in 13 patients (32%). To control the infection, bilateral nephrectomy was required in 10 patients and 1 patient was undergone unilateral nephrectomy. Of 13 patients with the hemorrhagic cysts, 5 were undergone bilateral nephrectomy and 2 were undergone unilateral nephrectomy. Six patients died during follow up and the cause of death were 1) cardiac failure, 2) cerebral hemorrhage, 3) cardiac infarction, 4) pneumonia after nephrectomy, 5) massive bleeding after second operation for adhesive ileus due to first nephrectomy, 6) unknown. Fourteen patients but one undergone bilateral nephrectomy were followed for an average time of 70 months after nephrectomy. Such as complication due to bilateral nephrectomy, anemia occurred in 13 patients (93%) and hypotension occurred in 5 patients (33%). Bilateral nephrectomy was effective procedure in safety for end stage polycystic kidney patients with the infection and the hemorrhagic cysts because anemia and hypotension which occurred usually after bilateral nephrectomy now can be controlled goodly.
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PMID:[End stage polycystic kidney disease: the study for upper urinary tract infection & hemorrhage into the cysts]. 780 76

Serum samples were analysed for IgM and IgG antibodies to parvovirus by ELISA and for parvovirus B19 DNA by polymerase chain reaction (PCR) in 69 HIV-1 infected Swedish patients with anemia and in 37 HIV-1 infected subjects without anemia. In 5/69 anemic patients, parvovirus B19 DNA was detected despite the lack of IgM antibody activity to the virus. The detection of parvovirus B19 DNA was significantly correlated to the degree of anemia in the anemic patients. In two patients who had a chronic anemia, a persistent parvovirus infection was detected by PCR, but not by serology, for 1 and 1.5 years, respectively. The results suggest that persistent parvovirus infection is a rare cause of anemia, but important to identify, since the infection is potentially treatable with intravenous immunoglobulin.
Infection
PMID:Parvovirus B19 infection in HIV-1 infected patients with anemia. 784 16

Reticuloendotheliosis virus strain A (REV-A) and chicken syncytial virus (CSV), two replication competent avian retroviruses, differ in the extent to which they induce a runting syndrome that includes anemia, lymphoid organ atrophy, and reduced body size. We have isolated an infectious clone of CSV, the less pathogenic of the two viruses, and compared it to REV-A. Partial DNA sequence analysis suggests that it differs from REV-A by no more than 1 to 2% at the nucleotide level. Analysis of viral interference indicates that these two viruses use the same cell receptor for infection of both fibroblasts and hematopoietic cells, DNA sequence of the CSV and REV-A long terminal repeats (LTRs) reveals that these structures differ principally by two small insertions (5 and 19 bp) present in the U3 region of REV-A. The larger of these may encode enhancer sequences that have been reported to influence transcription rates in vitro. Measurement of steady-state levels of viral RNA in infected cells, however, as well as circulating virus in infected chicks indicates that the different pathogenic responses elicited by these two viruses are not due to large differences in viral transcription or replication. Chimeric viruses were constructed in which the LTRs from one virus were used to express the structural genes of the second virus. Infection of 1-day-old chicks by parental virus as well as the reciprocal chimeric constructs demonstrated that the ability to induce both runting and bursal atrophy segregated with the structural genes of REV-A. Infection of birds with additional chimeric viruses in which the env genes of REV-A and CSV were exchanged indicated that the pathogenic response resulting from REV-A infection was due to at least two regions of the viral genome encoding structural genes.
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PMID:Structural genes, not the LTRs, are the primary determinants of reticuloendotheliosis virus A-induced runting and bursal atrophy. 800 26


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