Relevant bibliographies by topics / Pneumonic Tularemia

Academic literature on the topic 'Pneumonic Tularemia'

Author: Grafiati
Published: 25 July 2024
Last updated: 31 July 2024

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Journal articles on the topic "Pneumonic Tularemia"

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Ellis, Jill, Petra C. F. Oyston, Michael Green, and Richard W. Titball. "Tularemia." Clinical Microbiology Reviews 15, no. 4 (October 2002): 631–46. http://dx.doi.org/10.1128/cmr.15.4.631-646.2002.

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SUMMARY Francisella tularensis is the etiological agent of tularemia, a serious and occasionally fatal disease of humans and animals. In humans, ulceroglandular tularemia is the most common form of the disease and is usually a consequence of a bite from an arthropod vector which has previously fed on an infected animal. The pneumonic form of the disease occurs rarely but is the likely form of the disease should this bacterium be used as a bioterrorism agent. The diagnosis of disease is not straightforward. F. tularensis is difficult to culture, and the handling of this bacterium poses a significant risk of infection to laboratory personnel. Enzyme-linked immunosorbent assay- and PCR-based methods have been used to detect bacteria in clinical samples, but these methods have not been adequately evaluated for the diagnosis of pneumonic tularemia. Little is known about the virulence mechanisms of F. tularensis, though there is a large body of evidence indicating that it is an intracellular pathogen, surviving mainly in macrophages. An unlicensed live attenuated vaccine is available, which does appear to offer protection against ulceroglandular and pneumonic tularemia. Although an improved vaccine against tularemia is highly desirable, attempts to devise such a vaccine have been limited by the inability to construct defined allelic replacement mutants and by the lack of information on the mechanisms of virulence of F. tularensis. In the absence of a licensed vaccine, aminoglycoside antibiotics play a key role in the prevention and treatment of tularemia.
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HORN, M., and L. ZICKUHR. "PNEUMONIC TULAREMIA: A CASE PRESENTATION." Chest 161, no. 6 (June 2022): A142. http://dx.doi.org/10.1016/j.chest.2021.12.174.

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Gregory, Stephen H., Stephanie Mott, Jennifer Phung, Jinhee Lee, Leonard Moise, Julie A. McMurry, William Martin, and Anne S. De Groot. "Epitope-based vaccination against pneumonic tularemia." Vaccine 27, no. 39 (August 2009): 5299–306. http://dx.doi.org/10.1016/j.vaccine.2009.06.101.

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Bonnier, Alyssa, Santu Saha, Adam Austin, and Biplab K. Saha. "An Unusual Etiology of Fluorodeoxyglucose Avid Intrathoracic Lymph Nodes." Prague Medical Report 125, no. 1 (2024): 79–86. http://dx.doi.org/10.14712/23362936.2024.8.

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A middle-aged man in his 50s, active smoker, presented to the pulmonary office for lung cancer evaluation. On a low-dose computed tomography for lung cancer screening, he was found to have an 8 mm endobronchial lesion in the right main stem bronchus. A PET-CT revealed no endobronchial lesion, but incidentally, fluorodeoxyglucose (FDG) avidity was present in the right hilar (SUV 13.2) and paratracheal lymph nodes (LNs). He underwent bronchoscopy and EBUS-TBNA of station 7 and 10 R LNs. The fine needle aspiration (FNA) revealed necrotizing epithelioid granuloma. The acid-fast bacilli (AFB) and Grocott methenamine silver (GMS) stains were negative. He had suffered from pneumonic tularemia 13 months ago and immunohistochemical staining for Francisella tularensis on FNA samples at Center for Disease Control and Prevention was negative. The intense positron emission tomography (PET) avidity was attributed to prior tularemic intrathoracic lymphadenitis without active tularemia, a rare occurrence. To the best of our knowledge, PET-positive intrathoracic lymph node beyond one year without evidence of active tularemia has not been previously reported.
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Nicol, McKayla J., David R. Williamson, David E. Place, and Girish S. Kirimanjeswara. "Differential Immune Response Following Intranasal and Intradermal Infection with Francisella tularensis: Implications for Vaccine Development." Microorganisms 9, no. 5 (April 30, 2021): 973. http://dx.doi.org/10.3390/microorganisms9050973.

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Francisella tularensis (Ft) is a Gram-negative, facultative intracellular coccobacillus that is the etiological agent of tularemia. Interestingly, the disease tularemia has variable clinical presentations that are dependent upon the route of infection with Ft. Two of the most likely routes of Ft infection include intranasal and intradermal, which result in pneumonic and ulceroglandular tularemia, respectively. While there are several differences between these two forms of tularemia, the most notable disparity is between mortality rates: the mortality rate following pneumonic tularemia is over ten times that of the ulceroglandular disease. Understanding the differences between intradermal and intranasal Ft infections is important not only for clinical diagnoses and treatment but also for the development of a safe and effective vaccine. However, the immune correlates of protection against Ft, especially within the context of infection by disparate routes, are not yet fully understood. Recent advances in different animal models have revealed new insights in the complex interplay of innate and adaptive immune responses, indicating dissimilar patterns in both responses following infection with Ft via different routes. Further investigation of these differences will be crucial to predicting disease outcomes and inducing protective immunity via vaccination or natural infection.
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Nelson, Christina A., Jessica Winberg, Taylor D. Bostic, K. Meryl Davis, and Shannon Fleck-Derderian. "Systematic Review: Clinical Features, Antimicrobial Treatment, and Outcomes of Human Tularemia, 1993–2023." Clinical Infectious Diseases 78, Supplement_1 (January 31, 2024): S15—S28. http://dx.doi.org/10.1093/cid/ciad736.

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Abstract Background Francisella tularensis, the causative agent of tularemia, is endemic throughout the Northern Hemisphere and requires as few as 10 organisms to cause disease, making this potential bioterrorism agent one of the most infectious bacterial pathogens known. Aminoglycosides, tetracyclines, and, more recently, fluoroquinolones are used for treatment of tularemia; however, data on the relative effectiveness of these and other antimicrobial classes are limited. Methods Nine databases, including Medline, Global Health, and Embase, were systematically searched for articles containing terms related to tularemia. Articles with case-level data on tularemia diagnosis, antimicrobial treatment, and patient outcome were included. Patient demographics, clinical findings, antimicrobial administration, and outcome (eg, intubation, fatality) were abstracted using a standardized form. Results Of the 8878 publications identified and screened, 410 articles describing 870 cases from 1993 to 2023 met inclusion criteria. Cases were reported from 35 countries; more than half were from the United States, Turkey, or Spain. The most common clinical forms were ulceroglandular, oropharyngeal, glandular, and pneumonic disease. Among patients treated with aminoglycosides (n = 452 [52%]), fluoroquinolones (n = 339 [39%]), or tetracyclines (n = 419 [48%]), the fatality rate was 0.7%, 0.9%, and 1.2%, respectively. Patients with pneumonic disease who received ciprofloxacin had no fatalities and the lowest rates of thoracentesis/pleural effusion drainage and intubation compared to those who received aminoglycosides and tetracyclines. Conclusions Aminoglycosides, fluoroquinolones, and tetracyclines are effective antimicrobials for treatment of tularemia, regardless of clinical manifestation. For pneumonic disease specifically, ciprofloxacin may have slight advantages compared to other antimicrobials.
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Jacobs, Richard F., Yoland M. Condrey, and Terry Yamauchi. "Tularemia in Adults and Children: A Changing Presentation." Pediatrics 76, no. 5 (November 1, 1985): 818–22. http://dx.doi.org/10.1542/peds.76.5.818.

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Tularemia, a febrile zoonosis with six clinical types, recently has been shown to occur at an increased incidence in children compared with previous reports. Ulceroglandular and glandular tularemia are still the most common types, but pneumonic tularemia has increased in incidence. However, with these changes, an overall decline in mortality has been observed. Children exhibit fever, pharyngitis, hepatosplenomegaly, and constitutional symptoms more often than affected adults. The complication of late lymph node suppuration is found in half of the tularemia patients with lymphadenopathy. A high index of clinical suspicion and a good medical history and physical examination confirmed by specific serologic studies are the critical factors in the successful diagnosis of tularemia in children.
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Lovchik, Julie A., Douglas S. Reed, Julie A. Hutt, Fangfang Xia, Rick L. Stevens, Thero Modise, Eileen M. Barry, and Terry H. Wu. "Identification of an Attenuated Substrain of Francisella tularensis SCHU S4 by Phenotypic and Genotypic Analyses." Pathogens 10, no. 6 (May 22, 2021): 638. http://dx.doi.org/10.3390/pathogens10060638.

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Pneumonic tularemia is a highly debilitating and potentially fatal disease caused by inhalation of Francisella tularensis. Most of our current understanding of its pathogenesis is based on the highly virulent F. tularensis subsp. tularensis strain SCHU S4. However, multiple sources of SCHU S4 have been maintained and propagated independently over the years, potentially generating genetic variants with altered virulence. In this study, the virulence of four SCHU S4 stocks (NR-10492, NR-28534, NR-643 from BEI Resources and FTS-635 from Battelle Memorial Institute) along with another virulent subsp. tularensis strain, MA00-2987, were assessed in parallel. In the Fischer 344 rat model of pneumonic tularemia, NR-643 and FTS-635 were found to be highly attenuated compared to NR-10492, NR-28534, and MA00-2987. In the NZW rabbit model of pneumonic tularemia, NR-643 caused morbidity but not mortality even at a dose equivalent to 500x the LD50 for NR-10492. Genetic analyses revealed that NR-10492 and NR-28534 were identical to each other, and nearly identical to the reference SCHU S4 sequence. NR-643 and FTS-635 were identical to each other but were found to have nine regions of difference in the genomic sequence when compared to the published reference SCHU S4 sequence. Given the genetic differences and decreased virulence, NR-643/FTS-635 should be clearly designated as a separate SCHU S4 substrain and no longer utilized in efficacy studies to evaluate potential vaccines and therapeutics against tularemia.
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Williams, Mark S. "Efficacy of Doxycycline and Ciprofloxacin for Treatment of Pneumonic Tularemia in Cynomolgus Macaques." Clinical Infectious Diseases 78, Supplement_1 (January 31, 2024): S7—S14. http://dx.doi.org/10.1093/cid/ciad668.

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Abstract Background The incidence of pneumonic tularemia is very low; therefore, it is not feasible to conduct clinical efficacy testing of tularemia medical countermeasures (MCMs) in humans. The US Food and Drug Administration’s Animal Model Qualification Program under the Drug Development Tools Program is a regulatory pathway for animal models used in MCM efficacy testing and approval under the Animal Rule. The National Institute of Allergy and Infectious Diseases and Biomedical Advanced Research and Development Authority worked together to qualify the cynomolgus macaque model of pneumonic tularemia. Methods Using the model parameters and end points defined in the qualified model, efficacy of the antibiotics doxycycline and ciprofloxacin was evaluated in separate studies. Antibiotic administration, aimed to model approved human dosing, was initiated at time points of 24 hours or 48 hours after onset of fever as an indicator of disease. Results Upon aerosol exposure (target dose of 1000 colony-forming units) to Francisella tularensis SchuS4, 80% of vehicle-treated macaques succumbed or were euthanized. Ciprofloxacin treatment led to 10 of 10 animals surviving irrespective of treatment time. Doxycycline administered at 48 hours post-fever led to 10 of 10 animals surviving, while 9/10 animals survived in the group treated with doxycycline 24 hours after fever. Selected surviving animals in both the placebo and doxycycline 48-hour group showed residual live bacteria in peripheral tissues, while there were no bacteria in tissues from ciprofloxacin-treated macaques. Conclusions Both doxycycline and ciprofloxacin were efficacious in treatment of pneumonic tularemia, although clearance of bacteria may be different between the 2 drugs.
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Hahn, Mark M., Cheryl A. Triplett, Michael S. Anderson, Jennifer I. Smart, Karine Litherland, Stephen Keech, Franziska von Siebenthal, Mark Jones, Andrew J. Phipps, and Lisa N. Henning. "Ceftobiprole Medocaril Is an Effective Post-Exposure Treatment in the Fischer 344 Rat Model of Pneumonic Tularemia." Antibiotics 12, no. 8 (August 19, 2023): 1337. http://dx.doi.org/10.3390/antibiotics12081337.

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Francisella tularensis subspecies tularensis is a category-A biothreat agent that can cause lethal tularemia. Ceftobiprole medocaril is being explored as a medical countermeasure for the treatment of pneumonic tularemia. The efficacy of ceftobiprole medocaril against inhalational tularemia was evaluated in the Fischer 344 rat model of infection. The dose was expected to be effective against F. tularensis isolates with ceftobiprole minimum inhibitory concentrations ≤0.5 µg/mL. Animals treated with ceftobiprole medocaril exhibited a 92% survival rate 31 days post-challenge, identical to the survival of levofloxacin-treated rats. By comparison, rats receiving placebo experienced 100% mortality. Terminally collected blood, liver, lung, and spleen samples confirmed disseminated F. tularensis infections in most animals that died prior to completing treatments (placebo animals and a rat treated with ceftobiprole medocaril), although levels of bacteria detected in the placebo samples were significantly elevated compared to the ceftobiprole-medocaril-treated group geometric mean. Furthermore, no evidence of infection was detected in any rat that completed ceftobiprole medocaril or levofloxacin treatment and survived to the end of the post-treatment observation period. Overall, survival rates, body weights, and bacterial burdens consistently demonstrated that treatment with ceftobiprole medocaril is efficacious against otherwise fatal cases of pneumonic tularemia in the rat model.
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Dissertations / Theses on the topic "Pneumonic Tularemia"

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Gaggar, Amit. "Protease dysregulation role in neutrophilic inflammation in cystic fibrosis /." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2008r/gaggar.pdf.

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Books on the topic "Pneumonic Tularemia"

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Gertz, Alida. Tularemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0067.

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Tularemia, caused by the gram-negative coccobacillus Francisella tularensis, is an extremely infectious bacterial zoonosis. Symptoms depend on site of exposure; they can be nonspecific and may include fever, lymphadenopathy, ulcer or papule, and nausea/vomiting. Natural transmission occurs via small mammals, such as rabbits, or arthropod bites. IV or IM antibiotics are preferred over oral forms. Supportive care is also critical; some patients may require respiratory support. If used as a biological weapon, aerosolized F. tularensis would be the most likely route of transmission. Clinical symptoms would include those of pneumonic tularemia. In the event of a bioterrorist attack, oral administration antibiotics can be used, as the health care system may not be able to accommodate intravenous or intramuscular treatment. Antibiotic resistance should also be considered if patients deteriorate despite use of recommended antibiotics.
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Commission, Boston Public Health. Report of pneumonic tularemia in three Boston university researchers, November 2004 - March 2005. 2005.

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Book chapters on the topic "Pneumonic Tularemia"

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Lefebvre, Cedric W., Jay P. Babich, James H. Grendell, James H. Grendell, John E. Heffner, Ronan Thibault, Claude Pichard, et al. "Pneumonic Tularemia." In Encyclopedia of Intensive Care Medicine, 1782. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_3250.

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Ramanan, Poornima. "The Initial Diagnosis Was Cholecystitis." In Mayo Clinic Infectious Disease Case Review, edited by Larry M. Baddour, John C. O’Horo, Mark J. Enzler, and Rahul Kashyap, 97–100. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190052973.003.0028.

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Tularemia is a rare but potentially fatal zoonotic infection that is most often caused by Francisella tularensis, a fastidious, aerobic, gram-negative coccobacillus. This facultative intracellular pathogen evades the host immune response by surviving in host macrophages. The major reservoirs of F tularensis are various terrestrial and aquatic small mammals such as rabbits, hares, ground squirrels, muskrats, and water rats. In humans, F tularensis causes 6 distinct clinical syndromes that are dictated by its mode of transmission: ulceroglandular, glandular, oculoglandular, typhoidal, oropharyngeal, and pneumonic tularemia. Aminoglycosides are bactericidal to F tularensis and are the first-line treatments for tularemia in humans.
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Conference papers on the topic "Pneumonic Tularemia"

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Horn, M., and L. Zickuhr. "Pneumonic Tularemia: A Case Presentation." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4506.

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Jabra, E., A. Salman, A. Meyer, N. Amilineni, and S. Malik. "Under the Radar: A Case Report of Nearly Overlooked Pneumonic Tularemia." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a2420.

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