PubMed · 11357846
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M J Sagarin, J Roberts. 2001-05-10. Acute pharyngitis.. https://pubmed.ncbi.nlm.nih.gov/11357846/
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Hematological and coagulation profiles were studied in crossbred dogs experimentally infected with Angiostrongylus vasorum. Two groups of five dogs were experimentally inoculated with 50 and 100 third stage infective larvae (L(3)) of A. vasorum per kilogram of body weight. A third group of five uninfected animals was used as control. One sample of 10 ml of blood was collected from each animal on the 10, 20, 30, and 45 days after inoculation (dai) and at 30-day intervals thereafter for the remainder of the 210-day experimental period. The blood sample was used for the complete hemogram and platelet count, as well as measurements of prothrombin time, partial thromboplastin time and factors V and VIII. Anemia was observed in infected dogs, 6 weeks after the infection. The eosinophils presented peaks in four periods after infection. Thrombocytopenia became accentuated on the 72 dai. Decreased prothrombin time activity and increased partial thromboplastin time were observed at the 6 and 9 weeks after infection and decreased of factors VIII and V activities occurred from 4 to 6 weeks after infection. It may be conclude that infection by A. vasorum in dogs may cause a discrete anemia during the acute phase which is probably regenerative. In addition, important hemostatic alterations due to the infection suggest a chronic intravascular consumption coagulopathy.
A1 is an anti-apoptotic member of the Bcl-2 family that is up-regulated in inflammatory myeloid cells. In the present study, we investigated the role of A1 in the maintenance of acute inflammation in mice. Mice possess three genes encoding highly related isoforms of A1. A1-a isoform mRNA was minimally expressed in resident peritoneal macrophages, but was present at a 300-fold higher level in inflammatory macrophages elicited by i.p. infection with Toxoplasma gondii. In comparison, A1-b and A1-d levels were 3- and 10-fold higher, respectively. Peritoneal leukocytosis was decreased in infected A1-a-deficient mice compared with wild-type, and this reduction was associated with a small but reproducible enhancement of survival. These effects could not be explained by an alteration in peritoneal parasite load, nor by increased apoptosis of infected inflammatory cells, which were protected from cell death by an A1-a-independent mechanism. Increased apoptosis in inflammatory neutrophils was observed sporadically in A1-a-deficient mice. Regulation of apoptosis by A1-a may be an important proinflammatory event in acute host responses.
BACKGROUND: An anesthesiologist was diagnosed as having acute hepatitis C 3 days after providing anesthesia during the thoracotomy of a 64-year-old man (patient A). Eight weeks later, patient A was diagnosed as having acute hepatitis C. METHODS: We performed tests for antibody to hepatitis C virus (HCV) on serum samples from the thoracotomy surgical team and from surgical patients at the 2 hospitals where the anesthesiologist worked before and after his illness. We determined the genetic relatedness of the HCV isolates by sequencing the quasispecies from hypervariable region 1. RESULTS: Of the surgical team members, only the anesthesiologist was positive for antibody to HCV. Of the 348 surgical patients treated by him and tested, 6 were positive for antibody to HCV. Of these 6 patients, isolates from 2 (patients A and B) were the same genotype (1a) as that of the anesthesiologist. The quasispecies sequences of these 3 isolates clustered with nucleotide identity of 97.8% to 100.0%. Patient B was positive for antibody to HCV before her surgery 9 weeks before the anesthesiologist's illness onset. The anesthesiologist did not perform any exposure-prone invasive procedures, and no breaks in technique or incidents were reported. He denied risk factors for HCV. CONCLUSIONS: Our investigation suggests that the anesthesiologist acquired HCV infection from patient B and transmitted HCV to patient A. No further transmission was identified. Although we did not establish how transmission occurred in this instance, the one previous report of bloodborne pathogen transmission to patients from an anesthesiologist involved reuse of needles for self-injection.