33 research outputs found

    The role of iron in the pathogenesis of Escherichia coli septicemia of turkeys (Meleagris gallopavo)

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    The effect of inoculation with Escherichia coli on serum iron concentrations of turkeys and the effect of exogenous iron as ferric ammonium citrate, on E. coli septicemia in turkeys were determined. Inoculation of air sacs with E. coli produced hypoferremia in 18-day-old turkeys. Administration of iron with E. coli significantly increased mortality, frequency and degree of bacteremia, and severity of lesions in inoculated turkeys, compared with those turkeys given E. coli but not given iron. Similar results were seen whether iron was inoculated at the same location as E. coli or at a different location;Rabbit antiserum was prepared against iron-regulated outer membrane proteins of E. coli. Eighteen-day-old turkeys were passively immunized with rabbit antiserum and challenged by air sac inoculation of 1 to 2 x 10(\u276) colony-forming units of E. coli (078:K80:H9). Turkeys injected with normal rabbit serum or saline solution prior to challenge served as controls. Fatalities (8 of 51 inoculated) occurred only in groups given saline solution or normal rabbit serum. Remaining turkeys were necropsied 96 hours after challenge. Passive immunization with antiserum significantly reduced the frequency of bacteremia at 96 hours after challenge, the frequency of recovery of E. coli from air sacs, and the severity of gross lesions in inoculated birds as compared to birds given normal rabbit serum or saline solution before challenge

    Experimental Canine Leptospirosis Caused by Leptospira Interrogans Servars Pomona and Bratislava

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    Objective—To evaluate gross, histopathologic, and serum biochemical findings caused by Leptospira interrogans serovars pomona and bratislava inoculated in dogs. Animals—Twenty-seven 8-week-old female Beagles. Procedure—Dogs were randomly assigned to challenge or control groups. Challenge groups were conjunctivally inoculated on 3 successive days with 5 X 107 L interrogans serovar pomona (n = 12) or serovar bratislava (11). Clinical signs were recorded throughout the experiment, and clinical pathology assays, bacteriologic culture, and necropsies (6 or 7 dogs necropsied at each time point) were done on postinoculation day (PID) 7, 10, 14, and 20. Results—Infection could not be confirmed in any serovar bratislava–inoculated dog, and control dogs remained healthy throughout the experiment. Positive culture and fluorescent antibody test results were confirmed in 11 of 12 serovar pomona–inoculated dogs. Fever and lethargy starting at PID 7 were the most common clinical signs in serovar pomona–infected dogs. On day 10, gross lesions included multifocal renal and pulmonary hemorrhage and perirenal edema. Serovar pomona–inoculated dogs had histopathologic lesions including hepatitis, interstitial nephritis, and pneumonia at PID 7, 10, 14, and 20. Increases in BUN, anion gap, and bilirubin concentration occurred on PID 10, 14, and 20. Platelet counts in dogs with positive results of bacteriologic culture were decreased from baseline values on PID 10, 12, and 14. Conclusions and Clinical Relevance— Conjunctival inoculation with L interrogans serovar pomona resulted in a high rate of infection with concomitant hemorrhagic and inflammatory lesions of the kidneys, liver, and lungs

    Clinical and Pathologic Comparison of Acute Leptospirosis in Dogs Caused by Two Strains of Leptospirosis Kirschneri Serovar Grippotyphosa

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    Objective—To develop a method for inducing acute leptospirosis in dogs. Animals—31 nine-week-old female Beagles. Procedure—Beagles were randomly assigned to 2 inoculation groups or a control group. Dogs were inoculated on 3 successive days by conjunctival instillation of 5 X 107 cells of Leptospira kirschneri serovar grippotyphosa strain 82 (12 dogs) or strain RM 52 (14 dogs). Control dogs (n = 5) were similarly inoculated with sterile leptospiral culture media. Clinical signs, clinicopathologic variables, anti-leptospiral antibody titers, and evidence of leptospires in tissues and body fluids were evaluated. Dogs were euthanatized and necropsied on days 7, 14, 22, or 28 after inoculation or as required because of severe illness. Results—Clinical signs in infected dogs included conjunctivitis, lethargy, diarrhea, dehydration, vomiting, and icterus. Consistent clinicopathologic alterations included azotemia, hyperphosphatemia, increased anion gap, hyperbilirubinemia, and an increase in alkaline phosphatase activity. Leptospires were cultured from the kidneys (11/12), urine (6/9), aqueous humor (9/12), blood (12/12), and liver (12/12) of dogs inoculated with strain 82. Only 3 of 14 dogs became infected after inoculation with strain RM 52. Histopathologic lesions in infected dogs included interstitial nephritis, renal tubular degeneration and necrosis, pulmonary hemorrhage, and hepatic edema and perivasculitis. Conclusions and Clinical Relevance—Conjunctival exposure to L kirschneri serovar grippotyphosa strain 82 resulted in acute leptospirosis in all inoculated dogs, but only 3 of 14 dogs inoculated with strain RM 52 became infected. This method of infection by serovar grippotyphosa can be used to study the pathogenesis and prevention of leptospirosis in dogs

    A Study of the Persistence of Mycobacterium bovis in the Environment under Natural Weather Conditions in Michigan, USA

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    Reisolation of Mycobacterium bovis from inoculated substrates was used to follow the persistence of viable M. bovis bacteria exposed to natural weather conditions over a 12-month period. Environmental factors were recorded continuously, and factors affecting M. bovis persistence (i.e., temperature, season, and substrate) were studied using survival analysis and Cox's proportional hazards regression. Persistence of M. bovis in the environment was significantly shorter in the spring/summer season, characterized by the highest average daily temperatures over the 12-month period. M. bovis persisted up to 88 days in soil, 58 days in water and hay, and 43 days on corn. These studies demonstrate that M. bovis bacteria persist long enough to represent a risk of exposure for cattle and/or wildlife and strengthen evidence that suggests cattle farm biosecurity and efforts to eliminate supplemental feeding of white-tailed deer will decrease the risk of bovine TB transmission among and between cattle and deer populations

    Epidemic Leptospirosis Associated with Pulmonary Hemorrhage—Nicaragua, 1995

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    In October 1995, epidemic “hemorrhagic fever,” without jaundice or renal manifestations, was reported in rural Nicaragua following heavy flooding; 2259 residents were evaluated for nonmalarial febrile illnesses (cumulative incidence, 6.1%) and 15 (0.7%) died with pulmonary hemorrhage. A case-control study found that case-patients were more likely than controls to have ever walked in creeks (matched odds ratio [MOR], 15.0; 95% confidence interval [CI], 1.7–132.3), have household rodents (MOR, 10.4; 95% CI, 1.1–97.1), or own dogs with titers ≥ 400 to Leptospira species (MOR, 23.4; 95% CI, 3.6–`). Twenty-six of 51 case-patients had serologic or postmortem evidence of acute leptospirosis. Leptospira species were isolated from case-patients and potential animal reservoirs. This leptospirosis epidemic likely resulted from exposure to flood waters contaminated by urine from infected animals, particularly dogs. Leptospirosis should be included in the differential diagnosis for nonmalarial febrile illness, particularly during periods of flooding or when pulmonary hemorrhage occurs

    The role of iron in the pathogenesis of Escherichia coli septicemia of turkeys (Meleagris gallopavo)

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    The effect of inoculation with Escherichia coli on serum iron concentrations of turkeys and the effect of exogenous iron as ferric ammonium citrate, on E. coli septicemia in turkeys were determined. Inoculation of air sacs with E. coli produced hypoferremia in 18-day-old turkeys. Administration of iron with E. coli significantly increased mortality, frequency and degree of bacteremia, and severity of lesions in inoculated turkeys, compared with those turkeys given E. coli but not given iron. Similar results were seen whether iron was inoculated at the same location as E. coli or at a different location;Rabbit antiserum was prepared against iron-regulated outer membrane proteins of E. coli. Eighteen-day-old turkeys were passively immunized with rabbit antiserum and challenged by air sac inoculation of 1 to 2 x 10('6) colony-forming units of E. coli (078:K80:H9). Turkeys injected with normal rabbit serum or saline solution prior to challenge served as controls. Fatalities (8 of 51 inoculated) occurred only in groups given saline solution or normal rabbit serum. Remaining turkeys were necropsied 96 hours after challenge. Passive immunization with antiserum significantly reduced the frequency of bacteremia at 96 hours after challenge, the frequency of recovery of E. coli from air sacs, and the severity of gross lesions in inoculated birds as compared to birds given normal rabbit serum or saline solution before challenge.</p

    Genetic Resistance to Fowl Cholera Is Linked to the Major Histocompatibility Complex

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    Chickens of the Iowa State S1 line have been selected for ability to regress Rous sarcoma virus-induced (RSV) tumors, humoral immune response to GAT (Ir-GAT), and erythrocyte antigen B. Sublines homozygous at the major histocompatibility complex (MHC), as well as F1 heterozygotes and F2 segregants, were tested for resistance to fowl cholera by challenge with Pasteurella multocida strain X73. Control of the response at high doses was associated in a preliminary study with Ir-GAT and response to RSV tumors. Genetic control of resistance to low doses of P. multocida was demonstrated via sublines and F2 segregants to be linked with genes of the B-Gregion. Thus, genetic control of resistance to fowl cholera in chickens after exposure to Pasteurella multocida was shown to be linked to the major histocompatibility B complex, in this first demonstration of MHC-linked resistance to bacterial disease challenge.This article is from Immunogenetics 25 (1987): 284, doi:10.1007/BF00404420.</p
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