Search

Aspergillosis is a life-threatening fungal infection in immunocompromised people, including people infected with human immunodeficiency virus (HIV). We determined the incidence of aspergillosis among HIV-infected people and survival after aspergillosis diagnosis by use of a national HIV surveillance database. Among 35,252 HIV-infected patients, the incidence of aspergillosis was 3.5 cases per 1000 person-years (p-y; 95% confidence interval [CI], 3.0-4.0 per 1000 p-y). Incidence was higher among people agedor =35 years (4.1 per 1000 p-y, 95% CI, 3. 5-4.8), among people with CD4 counts of 50-99 cells/mm(3) (5.1 per 1000 p-y, 95% CI, 2.8-7.3), or CD4 counts of50 cells/mm(3) (10.2 per 1000 p-y, 95% CI, 8.0-12.2), versus people with CD4 counts of200 cells/mm(3), people withor =1 acquired immune deficiency syndrome-defining opportunistic illness (8.6 per 1000 p-y, 95% CI, 7.4-9.9), and people who were prescribed at least one medication associated with neutropenia (27.7 per 1000 p-y, 95% CI, 21.0-34.3). Median survival time after diagnosis of aspergillosis was 3 months, and 26% survived foror =1 year. These findings suggest that aspergillosis is uncommon, occurs especially among severely immunosuppressed or leukopenic HIV-infected people, and is associated with poor survival.

To describe persons with HIV infection and AIDS but with persistently negative HIV antibody enzyme immunoassay (EIA) results.Surveillance for persons meeting a case definition for HIV-1-seronegative AIDS.United States and Canada.A total of eight patients with seronegative AIDS identified from July 1995 through September 1997.Clinical history of HIV disease, history of HIV test results, and CD4 cell counts from medical record review; results of testing with a panel of EIA for antibodies to HIV-1, and HIV-1 p24 antigen; and viral subtype.Negative HIV EIA results occurred at CD4 cell counts of 0-230 x 10(6)/l, and at HIV RNA concentrations of 105,000-7,943,000 copies/ml. Using a panel of HIV EIA on sera from three patients, none of the HIV EIA detected infection with HIV-1, and signal-to-cut-off ratios wereor = 0.8 or all test kits evaluated. Sera from five patients showed weak reactivity in some HIV EIA, but were non-reactive in other HIV EIA. All patients were infected with HIV-1 subtype B.Rarely, results of EIA tests for antibodies to HIV-1 may be persistently negative in some HIV-1 subtype B-infected persons with AIDS. Physicians treating patients with illnesses or CD4 cell counts suggestive of HIV infection, but for whom results of HIV EIA are negative, should consider p24 antigen, nucleic acid amplification, or viral culture testing to document the presence of HIV.

To study the prevalence of and factors associated with the use of alcohol and nonprescription drugs by HIV-seropositive men who have sex with men (MSM) and to describe variations in alcohol and nonprescription drug use by geographic region, we analyzed data from a multistate, population- and facility-based interview study conducted in 12 U.S. states and metropolitan areas. Among 9735 MSM with HIV infection or AIDS who completed a 45-minute interview, nearly one third reported possible alcohol abuse. Large proportions of MSM also reported the use of marijuana (51%), noninjected cocaine (31%), and crack cocaine (16%) in the 5 years before the interview. Smaller proportions of MSM reported ever having injected cocaine (13%), stimulants (8%), and heroin (8%). Results of logistic regression indicated that in the 5 years before interview, white MSM were significantly (p.01) more likely than referent (mostly Hispanic) MSM to report use of hallucinogens, marijuana, nitrites, noninjected amphetamines, and diazepam; black MSM were significantly more likely than referent MSM to report use of noninjected crack cocaine. Use of injected stimulants was significantly associated with white race versus referent MSM, and residing in the West versus East. The prevalence of alcohol and drug use among HIV-seropositive MSM is high, and prevalences and types of substance use differ by region and racial/ethnic group. To prevent HIV transmission in this population, health departments and community-based organizations must understand the unique local patterns of substance use to develop effective substance abuse prevention and treatment programs.

To study the incidence of, the factors associated with, and the effect on survival of anemia in human immunodeficiency virus (HIV)-infected persons, we analyzed data from the longitudinal medical record reviews of 32,867 HIV-infected persons who received medical care from January 1990 through August 1996 in clinics, hospitals, and private medical practices in nine United States cities. We calculated the 1-year incidence of anemia (a hemoglobin level of10 g/dL or a physician diagnosis of anemia); the adjusted odds ratios showing excess risk of anemia associated with demographic factors, prescribed therapies, and concurrent diseases; the risk of death for patients who developed anemia compared with risk for patients who did not develop anemia; and, of patients who did develop anemia, the risk of death for those who did not recover from anemia compared with the risk for those who did recover. The 1-year incidence of anemia was 36.9% for persons with one or more acquired immunodeficiency syndrome (AIDS)-defining opportunistic illnesses (clinical AIDS), 12.1% for patients with a CD4 count of less than 200 cells/micron or CD4 percentage of14 but not clinical AIDS (immunologic AIDS), and 3.2% for persons without clinical or immunologic AIDS. Of anemia diagnoses, 22% were identified by physicians as drug related. Incidence of anemia was associated with clinical AIDS, immunologic AIDS, neutropenia, thrombocytopenia, bacterial septicemia, black race, female sex, prescription of zidovudine, fluconazole, and ganciclovir, and lack of prescription of trimethoprim-sulfamethoxazole. The increased risk of death associated with anemia differed by first CD4 count: for patients with a CD4 count of/=200 cells/microL at the beginning of the survival analysis, the risk of death was 148% (99% confidence interval [CI], 114 to 188) greater for those who developed anemia; for patients whose first CD4 count was200 cells/microL, the risk of death was 56% (99% CI, 43 to 71) greater for those in whom anemia developed. For persons in whom anemia developed, the risk of death was 170% (99% CI, 132 to 203) greater for persons who did not recover from anemia compared with those who did recover. Anemia is a frequent complication of HIV infection, and its incidence is associated with progression of HIV disease, prescription of certain chemotherapeutics, black race, and female sex. Anemia, particularly anemia that does not resolve, is associated with shorter survival of HIV-infected patients.

Mice are frequently used as test animals in blood platelet research studies, but safe and convenient methods are not available to easily assess lifespan. Therefore we have improved an existing method for measuring platelet lifespan by determining the disappearance of biotin-labeled platelets from the circulation of mice with immunofluorescence and flow cytometry. In vivo labeling of platelets with Sulfo-NHS-Biotin, a water-soluble moiety, was used as a direct method for labeling the entire platelet population by direct infusion into mice. Platelet samples were collected daily, washed, labeled with a fluorescent detection agent, and analyzed by flow cytometry to measure the percentage of biotinylated cells. This method allowed a rapid determination of murine platelet lifespan without requiring radioactive labels. Using this method, we have estimated that the platelet lifespan in C3H male mice is approximately 4.8 days.

To determine the RBC lifespan of Greyhounds, using an in vitro labeling technique.RBC from dogs were labeled with NHS-biotin and their disappearance measured over time to determine RBC lifespan.5 Greyhounds that had been vaccinated against distemper, adenovirus 1 and 2 infections, parainfluenza, leptospirosis, parvovirus, and coronavirus infections, Bordetella bronchiseptica infection, and rabies the previous year; 3 sexually intact 14-month-old Beagles served as controls.After venipuncture for CBC, catheters were inserted in the cephalic vein of each dog. Butorphanol was then administered to achieve mild sedation and analgesia, and glycopyrrolate was administered to ensure maintenance of adequate heart rate during phlebotomy. Dogs were positioned in lateral recumbency; blood was removed via jugular venipuncture, using a standard laboratory donor blood bag containing citrate-phosphate-dextrose solution. Blood was transferred aseptically into sterile polystyrene containers and NHS-biotin was added. After incubation, the labeled RBC were reinfused into the dogs and the blood was allowed to recirculate for 1 hour before the first postinfusion sample was taken. At frequent intervals, blood to be analyzed was taken by jugular venipuncture, and the percentage of labeled cells was determined by flow cytometry.The mean RBC lifespan of non-Greyhounds was significantly longer than that of Greyhounds (104.3 +/- 2.2 days vs 53.6 +/- 6.5 days; P = 0.001). A negative linear correlation was also found between age of the Greyhounds and their RBC lifespan (P = 0.01, R2 = 0.91).The shorter RBC lifespan of the Greyhounds may explain the finding of macrocytosis reported in earlier work. The reason for the shorter RBC lifespan in Greyhounds may be caused by differences in Greyhound RBC membrane structure or accelerated RBC removal from the circulation.

BALB/c male mice have higher platelet counts than female mice of the same strain. To test the hypothesis that testosterone influences platelet production, we evaluated indices of both red blood cell and platelet production in intact male BALB/c mice, in male mice 4 weeks after castration, and in castrated mice administered maintenance doses of testosterone as testosterone propionate. As predicted, castration resulted in decreased hematocrit and body weight in BALB/c mice. Body weights and hematocrits returned to noncastrated levels after 2 and 7 days, respectively, of administration of testosterone. Total circulating red blood cell mass and total circulating red blood cell count were both decreased by castration and were returned to control (noncastrated) levels after 2 days of testosterone therapy. Reticulocyte counts were not changed by castration, but they increased above counts of uncastrated and castrated control mice after 3 days of testosterone administration. White blood cell (WBC) numbers were unaffected by castration or testosterone administration. Additionally, platelet count (956 vs 834 x 10(3)/microliters), platelet size (3.87 vs 3.75 microns3), sulfur 35 incorporation into platelets (6.36 vs 4.87 x 10(-3)%), mean megakaryocyte ploidy (17.43N vs 16.89N), total circulating platelet mass (TCPM) (490 vs 379 x 10(8) microns3), and total circulating platelet count (TCPC) (131 vs 103 x 10(7)) were significantly (p0.05) decreased in castrated mice as compared with intact control mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Medical records of 60 thrombocytopenic dogs in which platelet volume analysis was performed between 1984 and 1993 were reviewed. Information collected from the records included signalment, mean platelet volume, the clinical pathologist's assessment of the adequacy of the megakaryocyte population in the bone marrow, and the causes of thrombocytopenia. In all dogs, the bone marrow aspirate had been collected within 48 hours of platelet volume analysis. Sensitivity and specificity of using platelet volume analysis (mean volumeor = 12.00 microns 3 vs mean volume12.00 microns 3) as a test for bone marrow megakaryocyte response (adequate vs inadequate) in thrombocytopenic dogs was determined. Sensitivity was 88%, specificity was 80%, predictive value of a positive test was 96%, and predictive value of a negative test was 57%. Results suggested that megathrombocytosis in a thrombocytopenic dog was a good predictor of adequate bone marrow response (normal or hyperplastic bone marrow megakaryocyte population); however, a mean platelet volumeor = 12.00 microns 3 in thrombocytopenic dogs was not strongly predictive of inadequate bone marrow response.

A 10-month-old Simmental heifer was examined because of a 10-day history of epistaxis and aural hematomas. Examination of the calf also revealed hemarthrosis. Initial laboratory data indicated that platelet count, platelet size, prothrombin time, and partial thromboplastin time were not different from a clinically normal (control) cow. Mucosal bleeding time was prolonged, and platelet adhesion to glass beads was less than expected. The clinical signs, prolonged bleeding time, and platelet adhesion defect were corrected by infusion of bovine plasma. Subsequent laboratory testing revealed that the affected calf had a truncated multimeric structure of von Willebrand factor (vWF), low vWF activity, and impaired platelet aggregation in response to adenosine diphosphate, but concentration of vWF was not different from that in clinically normal control animals. These data were consistent with a diagnosis of variant von Willebrand disease. The relationship of this disease to the thrombopathy of Simmental cattle is unclear.

Hematologic characteristics of 36 Greyhounds were studied and compared with characteristics of 22 non-Greyhound controls. Fourteen of the Greyhounds were tested and found to be seronegative for Ehrlichia canis and Babesia canis. Compared with the non-Greyhounds, Greyhounds had higher mean hemoglobin concentration, PCV, mean corpuscular volume, and mean cellular hemoglobin, and lower mean RBC count, hemoglobin P50 value, Hill coefficient, platelet count, and total plasma protein concentration. The lower mean hemoglobin P50 value in Greyhounds suggested that the higher mean hemoglobin concentration and PCV were not solely a result of selective breeding for superior racing abilities, but that Greyhound hemoglobin may have a greater affinity for oxygen than does the hemoglobin of non-Greyhounds.

Several recent studies show that production of platelets and red blood cells (RBC) are inversely related. For example, it is well established that hypoxia, a stimulator of erythropoiesis, causes thrombocytopenia in laboratory animals. The thrombocytopenia is most likely the result of a reduction in the production of platelets caused by a decrease in the number of colony-forming units-megakaryocyte (CFU-Meg), early precursor megakaryocytes (small acetylcholinesterase-positive cells, SAChE+), and recognizable megakaryocytes in the bone marrow. In all cases, active erythropoiesis was required for the thrombocytopenia. The hypoxia-induced thrombocytopenia was not caused by sequestration of platelets in an enlarged spleen or by expanding blood volumes. We speculate that this thrombocytopenia is caused by competition of a precursor cell of the erythrocytic and megakaryocytic cell lines; that is, marked stimulation of the erythroid cells by erythropoietin (Epo) causes a decrease in the number of immature megakaryocytes, leading to decreased thrombocytopoiesis. In support of this hypothesis, other recent work shows that thyroxine (a stimulator of erythropoiesis) and Epo (when given in large, chronic doses) elevate erythropoiesis and cause thrombocytopenia. Conversely, both endogenous and exogenous sources of thrombopoietin lead to elevated thrombocytopoiesis and anemia in mice. It should also be mentioned that megakaryocytes and erythrocytes have several biochemical similarities, and several clinical conditions point to an inverse relationship between RBC and platelet production. These in vivo, biochemical, and clinical data support the hypothesis that megakaryocytes and erythrocytes share a common precursor cell.

This report describes field and laboratory studies on arboviruses in the metropolitan area of Houston, Texas. Mosquitoes were collected from a large number of sites in the metropolitan Houston area by the following methods: CDC light traps, resting from diurnal shelters, and biting man. Most effort was devoted to Culex quinquefasciatus , the urban vector SLE virus. Over 120,000 females of this species were processed for virus isolation in suckling Swiss mice and 92 strains of Flanders virus were isolated. No SLE virus was detected. Eleven strains of Flanders virus were isolated from 3 other mosquito species. Eighty-five strains belonging to the California encephalitis virus group were isolated from Aedes atlanticustarmentor complex females. Two strains of Cache Valley-like virus were isolated from Culiseta inornate and 1 strain of apparently identical agent from Anopheles quadrimaculatus .