Journal articles: 'Animal model of infection'

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Zak, O., and T. O'Reilly. "Animal infection models and ethics--the perfect infection model." Journal of Antimicrobial Chemotherapy 31, suppl D (January 1, 1993): 193–205. http://dx.doi.org/10.1093/jac/31.suppl_d.193.

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Han, Mingyuan, Charu Rajput, Tomoko Ishikawa, Caitlin Jarman, Julie Lee, and Marc Hershenson. "Small Animal Models of Respiratory Viral Infection Related to Asthma." Viruses 10, no. 12 (December 1, 2018): 682. http://dx.doi.org/10.3390/v10120682.

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Respiratory viral infections are strongly associated with asthma exacerbations. Rhinovirus is most frequently-detected pathogen; followed by respiratory syncytial virus; metapneumovirus; parainfluenza virus; enterovirus and coronavirus. In addition; viral infection; in combination with genetics; allergen exposure; microbiome and other pathogens; may play a role in asthma development. In particular; asthma development has been linked to wheezing-associated respiratory viral infections in early life. To understand underlying mechanisms of viral-induced airways disease; investigators have studied respiratory viral infections in small animals. This report reviews animal models of human respiratory viral infection employing mice; rats; guinea pigs; hamsters and ferrets. Investigators have modeled asthma exacerbations by infecting mice with allergic airways disease. Asthma development has been modeled by administration of virus to immature animals. Small animal models of respiratory viral infection will identify cell and molecular targets for the treatment of asthma.

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Glupczynski, Y., and A. Burette. "Animal model of Helicobacter pylori infection." Antimicrobial Agents and Chemotherapy 34, no. 7 (July 1, 1990): 1462. http://dx.doi.org/10.1128/aac.34.7.1462.

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Janitschke, Klaus, A. Julio Martinez, Govinda S. Visvesvara, and Frederick Schuster. "Animal Model Balamuthia Mandrillaris CNS Infection." Journal of Neuropathology and Experimental Neurology 55, no. 7 (July 1996): 815–21. http://dx.doi.org/10.1097/00005072-199607000-00006.

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Haenle, Maximilian, Carmen Zietz, Tobias Lindner, Kathleen Arndt, Anika Vetter, Wolfram Mittelmeier, Andreas Podbielski, and Rainer Bader. "A Model of Implant-Associated Infection in the Tibial Metaphysis of Rats." Scientific World Journal 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/481975.

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Objective. Implant-associated infections remain serious complications in orthopaedic and trauma surgery. A main scientific focus has thus been drawn to the development of anti-infective implant coatings. Animal models of implant-associated infections are considered helpful in thein vivotesting of new anti-infective implant coatings. The aim of the present study was to evaluate a novel animal model for generation of implant-associated infections in the tibial metaphysis of rats.Materials and Methods. A custom-made conical implant made of Ti6Al4V was inserted bilaterally at the medial proximal tibia of 26 female Sprague-Dawley rats.Staphylococcus aureusin amounts spanning four orders of magnitude and each suspended in 15 μl phosphate buffered saline (PBS) was inoculated into the inner cavity of the implant after the implantation into the defined position. Controls were treated accordingly with PBS alone. Animals were then followed for six weeks until sacrifice. Implant-associated infection was evaluated by microbiological investigation using swabs and determination of viable bacteria in the bone around the implant and the biofilm on the implants after sonification.Results. Irrespective of the initial inoculum, all animals in the various groups harbored viable bacteria in the intraoperative swabs as well as the sonication fluid of the implant and the bone samples. No correlation could be established between initially inoculated CFU and population sizes on implant surfaces at sacrifice. However, a significantly higher viable count was observed from peri-implant bone samples for animals inoculated with 106 CFU. Macroscopic signs of animal infection (pus and abscess formation) were only observed for implants inoculated with at least 105 CFUS. aureus.Discussion/Conclusion. The results demonstrate the feasibility of this novel animal model to induce an implant-associated infection in the metaphysis of rats, even with comparatively low bacterial inocula. The specific design of the implant allows an application of bacteria in reproducible numbers at well-defined contact sites to the animal bone.

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Iyer, Rajiv R., Noah Gorelick, Karen Carroll, Ari M. Blitz, Sarah Beck, Caroline M. Garrett, Audrey Monroe, et al. "Evaluation of an in vivo model for ventricular shunt infection: a pilot study using a novel antimicrobial-loaded polymer." Journal of Neurosurgery 131, no. 2 (August 2019): 587–95. http://dx.doi.org/10.3171/2018.1.jns172523.

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OBJECTIVEVentricular shunt infection remains an issue leading to high patient morbidity and cost, warranting further investigation. The authors sought to create an animal model of shunt infection that could be used to evaluate possible catheter modifications and innovations.METHODSThree dogs underwent bilateral ventricular catheter implantation and inoculation with methicillin-sensitive Staphylococcus aureus (S. aureus). In 2 experimental animals, the catheters were modified with a polymer containing chemical “pockets” loaded with vancomycin. In 1 control animal, the catheters were polymer coated but without antibiotics. Animals were monitored for 9 to 11 days, after which the shunts were explanted. MRI was performed after shunt implantation and prior to catheter harvest. The catheters were sonicated prior to microbiological culture and also evaluated by electron microscopy. The animals’ brains were evaluated for histopathology.RESULTSAll animals underwent successful catheter implantation. The animals developed superficial wound infections, but no neurological deficits. Imaging demonstrated ventriculitis and cerebral edema. Harvested catheters from the control animal demonstrated > 104 colony-forming units (CFUs) of S. aureus. In the first experimental animal, one shunt demonstrated > 104 CFUs of S. aureus, but the other demonstrated no growth. In the second experimental animal, one catheter demonstrated no growth, and the other grew trace S. aureus. Brain histopathology revealed acute inflammation and ventriculitis in all animals, which was more severe in the control.CONCLUSIONSThe authors evaluated an animal model of ventricular shunting and reliably induced features of shunt infection that could be microbiologically quantified. With this model, investigation of pathophysiological and imaging correlates of infection and potentially beneficial shunt catheter modifications is possible.

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Kenney, Scott P., and Xiang-Jin Meng. "Hepatitis E Virus: Animal Models and Zoonosis." Annual Review of Animal Biosciences 7, no. 1 (February 15, 2019): 427–48. http://dx.doi.org/10.1146/annurev-animal-020518-115117.

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Hepatitis E virus (HEV) is an important human pathogen that historically has been difficult to study. Limited levels of replication in vitro hindered our understanding of the viral life cycle. Sporadic and low-level virus shedding, lack of standardized detection methods, and subclinical infections made the development of animal models difficult. Better diagnostic techniques and understanding of the virus increased our ability to identify and characterize animal strains and animals that are amenable to model human-relevant infection. These advances are translating into the development of useful HEV animal models so that some of the greatest concerns associated with HEV infection, including host immunology, chronic infection, severe pregnancy mortality, and extrahepatic manifestations, can now be studied. Continued development of these animal models will be instrumental in understanding the many complex questions associated with HEV infection and for assessing therapeutics and prevention strategies to minimize HEV becoming a greater risk to the human population.

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Shimamura, Tsuyoshi, Nobuo Kubota, and Kazutoshi Shibuya. "Animal Model of Dermatophytosis." Journal of Biomedicine and Biotechnology 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/125384.

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Dermatophytosis is superficial fungal infection caused by dermatophytes that invade the keratinized tissue of humans and animals. Lesions from dermatophytosis exhibit an inflammatory reaction induced to eliminate the invading fungi by using the host’s normal immune function. Many scientists have attempted to establish an experimental animal model to elucidate the pathogenesis of human dermatophytosis and evaluate drug efficacy. However, current animal models have several issues. In the present paper, we surveyed reports about the methodology of the dermatophytosis animal model for tinea corporis, tinea pedis, and tinea unguium and discussed future prospects.

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Groseth, Allison, Don Gardner, Kimberly Meade-White, Susanne Amler, and Hideki Ebihara. "Immunocompetent hamsters as a model for orthobunyavirus-induced neuroinvasion and neuropathology." PLOS Neglected Tropical Diseases 17, no. 5 (May 26, 2023): e0011355. http://dx.doi.org/10.1371/journal.pntd.0011355.

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Background Bunyavirus infections, including those caused by Bunyamwera serogroup orthobunyaviruses, represent a significant and yet likely still vastly underappreciated cause of mild to moderate human febrile infections. In severe cases, these infections can also cause neurological disease, particularly meningitis and encephalitis, and infection can even be fatal. However, with a few exceptions, information regarding the mechanisms underlying the neuroinvasion and neuropathogenesis of such infections is limited. This is due in part to a lack of animal models to facilitate such studies. Methodology/Principal findings In an effort to develop an immunocompetent model of infection with Bunyamwera serogroup orthobunyaviruses, we infected 4-6-week-old female hamsters via either the intraperitoneal or subcutaneous route with 106 pfu/animal of Bunyamwera virus (BUNV), Batai virus or Ngari virus. Only BUNV infection resulted in clinical disease, which was characterized by weight loss, lethargy and neurological signs (i.e. tremor of the head or limbs, loss of righting reflex, “waltzing”). While symptoms were of similar severity for both routes, they occurred more frequently following subcutaneous inoculation. Consistent with these clinical signs, both antigen staining and histopathological abnormalities were found extensively throughout the brain. Conclusions/Significance The reported hamster model of BUNV infection provides a new tool for studying orthobunyavirus infection, and particularly neuroinvasion and the development of neuropathology. This model is particularly significant because it makes use of immunologically competent animals and relies on a subcutaneous inoculation route that more closely mimics the natural infection route for arboviruses, thereby providing a more authentic cellular and immunological context at the initial site of infection.

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TSUKIYAMA-KOHARA, Kyoko, and Michinori KOHARA. "Animal model for hepatitis C virus infection." Uirusu 65, no. 2 (2015): 255–62. http://dx.doi.org/10.2222/jsv.65.255.

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Yáñez, Antonio, Azucena Martínez-Ramos, Teresa Calixto, Francisco Javier González-Matus, José Antonio Rivera-Tapia, Silvia Giono, Constantino Gil, and Lilia Cedillo. "Animal model of Mycoplasma fermentans respiratory infection." BMC Research Notes 6, no. 1 (2013): 9. http://dx.doi.org/10.1186/1756-0500-6-9.

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Variyam, Easwaran P., Prema Gogate, and Kathryn Eaton. "Animal Model of Noninvasive Entamoeba histolytica Infection." Archives of Medical Research 31, no. 4 (July 2000): S245—S246. http://dx.doi.org/10.1016/s0188-4409(00)00144-2.

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Gao, L., S. Qian, L. Zeng, R. Wang, G. Wei, J. Fan, and S. Zheng. "An Animal Model of Human Cytomegalovirus Infection." Transplantation Proceedings 39, no. 10 (December 2007): 3438–43. http://dx.doi.org/10.1016/j.transproceed.2007.06.077.

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Rytik, Petr G., Igor I. Kutcherov, Werner E. G. Muller, Nikolay N. Poleschuk, Galina P. Duboiskaya, Mark Kruzo, and Irina A. Podolskaya. "Small animal model of HIV-1 infection." Journal of Clinical Virology 31 (December 2004): 83–87. http://dx.doi.org/10.1016/j.jcv.2004.09.010.

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Bravo, Fernando J., Nigel Bourne, Mark R. Schleiss, and David I. Bernstein. "An animal model of neonatal cytomegalovirus infection." Antiviral Research 60, no. 1 (September 2003): 41–49. http://dx.doi.org/10.1016/s0166-3542(03)00151-7.

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White, Tiffany M., Donald H. Gilden, and Ravi Mahalingam. "An Animal Model of Varicella Virus Infection." Brain Pathology 11, no. 4 (October 2001): 475–79. http://dx.doi.org/10.1111/j.1750-3639.2001.tb00416.x.

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Ordway, D., M. Henao-Tamayo, E. Smith, C. Shanley, M. Harton, J. Troudt, X. Bai, R. J. Basaraba, I. M. Orme, and E. D. Chan. "Animal model of Mycobacterium abscessus lung infection." Journal of Leukocyte Biology 83, no. 6 (March 19, 2008): 1502–11. http://dx.doi.org/10.1189/jlb.1007696.

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Petrušiū, Vladimir, Irena Živkoviū, Lina Muhandes, Rajna Dimitrijeviū, Marijana Stojanoviū, and Ljiljana Dimitrijeviū. "Infection-induced autoantibodies and pregnancy related pathology: an animal model." Reproduction, Fertility and Development 26, no. 4 (2014): 578. http://dx.doi.org/10.1071/rd13057.

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In addition to being the main cause of mortality worldwide, bacterial and viral infections can be the cause of autoimmune and pregnancy disorders as well. The production of autoantibodies during infection can be explained by various mechanisms, including molecular mimicry, bystander cell activation and epitope spreading. Conversely, bacterial and viral infections during pregnancy are especially dangerous for the fetus. It is documented that infection-induced inflammatory processes mediated by Toll-like receptors (TLR) represent the main cause of preterm labour. We used two crucial bacterial components and TLR ligands, namely peptidoglycan and lipopolysaccharide, to stimulate BALB/c mice before immunisation with tetanus toxoid. Tetanus toxoid is an inactive form of the toxin produced by bacterium Clostridium tetani and shares structural similarity with plasma protein β2-glycoprotein I. Treatment with peptidoglycan and lipopolysaccharide in combination with tetanus toxoid induced the production of pathological autoantibodies, different fluctuations in natural autoantibodies and different types of reproductive pathology in treated animals, with peptidoglycan treatment being more deleterious. We propose that the production of pathological autoantibodies, TLR activation and changes in natural autoantibodies play crucial roles in infection-induced reproductive pathology in our animal model.

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Gonçalves, Denise, Rafael de Queiroz Prado, Eric Almeida Xavier, Natália Cristina de Oliveira, Paulo Marcos da Matta Guedes, João Santana da Silva, Luiz Tadeu Moraes Figueiredo, and Victor Hugo Aquino. "Imunocompetent Mice Model for Dengue Virus Infection." Scientific World Journal 2012 (2012): 1–12. http://dx.doi.org/10.1100/2012/525947.

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Dengue fever is a noncontagious infectious disease caused by dengue virus (DENV). DENV belongs to the familyFlaviviridae, genusFlavivirus, and is classified into four antigenically distinct serotypes: DENV-1, DENV-2, DENV-3, and DENV-4. The number of nations and people affected has increased steadily and today is considered the most widely spread arbovirus (arthropod-borne viral disease) in the world. The absence of an appropriate animal model for studying the disease has hindered the understanding of dengue pathogenesis. In our study, we have found that immunocompetent C57BL/6 mice infected intraperitoneally with DENV-1 presented some signs of dengue disease such as thrombocytopenia, spleen hemorrhage, liver damage, and increase in production of IFNγand TNFαcytokines. Moreover, the animals became viremic and the virus was detected in several organs by real-time RT-PCR. Thus, this animal model could be used to study mechanism of dengue virus infection, to test antiviral drugs, as well as to evaluate candidate vaccines.

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Zhang, Hang. "Advances in Animal Models of Hepatitis B Virus Infection." Infection International 4, no. 4 (December 1, 2015): 96–101. http://dx.doi.org/10.1515/ii-2017-0115.

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Abstract Hepatitis B virus (HBV) infection seriously affects human health. Stable and reliable animal models of HBV infection bear significance in studying pathogenesis of this health condition and development of intervention measures. HBV exhibits high specificity for hosts, and chimpanzee is long used as sole animal model of HBV infection. However, use of chimpanzees is strictly constrained because of ethical reasons. Many methods were used to establish small-animal models of HBV infection. Tupaia is the only nonprimate animal that can be infected by HBV. Use of HBV-related duck hepatitis virus and marmot hepatitis virus infection model contributed to evaluation of mechanism of HBV replication and HBV treatment methods. In recent years, development of human–mouse chimeric model provided possibility of using common experimental animals to carry out HBV research. These models feature their own advantages and disadvantages and can be complementary in some ways. This study provides an overview of current and commonly used animal models of HBV infection.

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Silva, Teane M. A., Erica A. Costa, Tatiane A. Paixão, Renée M. Tsolis, and Renato L. Santos. "Laboratory Animal Models for Brucellosis Research." Journal of Biomedicine and Biotechnology 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/518323.

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Brucellosis is a chronic infectious disease caused byBrucellaspp., a Gram-negative facultative intracellular pathogen that affects humans and animals, leading to significant impact on public health and animal industry. Human brucellosis is considered the most prevalent bacterial zoonosis in the world and is characterized by fever, weight loss, depression, hepato/splenomegaly, osteoarticular, and genital infections. Relevant aspects ofBrucellapathogenesis have been intensively investigated in culture cells and animal models. The mouse is the animal model more commonly used to study chronic infection caused byBrucella. This model is most frequently used to investigate specific pathogenic factors ofBrucellaspp., to characterize the host immune response, and to evaluate therapeutics and vaccines. Other animal species have been used as models for brucellosis including rats, guinea pigs, and monkeys. This paper discusses the murine and other laboratory animal models for human and animal brucellosis.

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L. Brinkman, Cassandra, Suzannah M. Schmidt-Malan, Melissa J. Karau, and Robin Patel. "A novel rat model of foreign body osteomyelitis for evaluation of antimicrobial efficacy." Journal of Experimental and Applied Animal Sciences 3, no. 1 (May 14, 2019): 7–14. http://dx.doi.org/10.20454/jeaas.2019.1555.

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The most common organism-type causing orthopedic foreign body infection is the staphylococci, of which Staphylococcus aureus and Staphylococcus epidermidis are especially common. These organisms form biofilms on orthopedic foreign body surfaces, rendering such infections challenging and time consuming to treat. Our group evaluates novel therapeutics for orthopedic foreign body infection in animal models. A current limitation of most animal models is that that they only allow for the removal of one sample per animal, at the time of sacrifice. Herein, we describe a novel rat model of foreign body osteomyelitis that allows removal of foreign bodies at different time points, from the same infected animal. We demonstrate that this model can be used for both S. aureus and S. epidermidis orthopedic foreign body infection, with 3.56, 3.60 and 5.51 log10 cfu/cm2 S. aureus recovered at four, five and six weeks, respectively, after infection, and 2.08, 2.17 and 2.62 log10 cfu/cm2 S. epidermidis recovered at four, five and six weeks, respectively, after infection. We evaluated the model with S. aureus infection treated with rifampin 25 mg/kg twice daily for 21 days. Using quantitative cultures, we were no longer able to detect bacteria as of the 14th day of treatment with bacteria becoming detectable again 7 days following the discontinuation of rifampin a period. This novel model allows monitoring of evolution of infection at the infection site in the same animal.

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Kashino, Suely S., Pamela Ovendale, Angelo Izzo, and Antonio Campos-Neto. "Unique Model of Dormant Infection for Tuberculosis Vaccine Development." Clinical and Vaccine Immunology 13, no. 9 (September 2006): 1014–21. http://dx.doi.org/10.1128/cvi.00120-06.

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ABSTRACT Most individuals exposed to Mycobacterium tuberculosis become infected but hinder the infectious process in dormant foci, known as latent tuberculosis. This limited infection usually stimulates strong T-cell responses, which provide lifelong resistance to tuberculosis. However, latent tuberculosis is still poorly understood, particularly because of the lack of a reliable animal model of dormant infection. Here we show that inoculation of mice with a unique streptomycin-auxotrophic mutant of Mycobacterium tuberculosis recapitulates dormant infection. The mutant grows unimpaired in the presence of streptomycin and no longer grows but remains viable for long periods of time after substrate removal, shifting from the log growth phase to the latent stage, as indicated by augmented production of α-crystallin. Mice challenged with the mutant and inoculated with streptomycin for ∼3 weeks developed a limited infection characterized by a low bacteriological burden and the presence of typical granulomas. After substrate withdrawal, the infection was hindered but few microorganisms remained viable (dormant) in the animals' tissues for at least 6 months. In addition, the animals developed both potent T-cell responses to M. tuberculosis antigens, such as early culture filtrate, Ag85B, and ESAT-6, and resistance to reinfection with virulent M. tuberculosis. Therefore, infection of mice or other animals (e.g., guinea pigs) with M. tuberculosis strain 18b constitutes a simple and attractive animal model for evaluation of antituberculosis vaccines in the context of an M. tuberculosis-presensitized host, a prevailing condition among humans in need of a vaccine.

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Ansari, Shamshul, and Yoshio Yamaoka. "Animal Models and Helicobacter pylori Infection." Journal of Clinical Medicine 11, no. 11 (May 31, 2022): 3141. http://dx.doi.org/10.3390/jcm11113141.

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Helicobacter pylori colonize the gastric mucosa of at least half of the world’s population. Persistent infection is associated with the development of gastritis, peptic ulcer disease, and an increased risk of gastric cancer and gastric-mucosa-associated lymphoid tissue (MALT) lymphoma. In vivo studies using several animal models have provided crucial evidence for understanding the pathophysiology of H. pylori-associated complications. Numerous animal models, such as Mongolian gerbils, transgenic mouse models, guinea pigs, and other animals, including non-human primates, are being widely used due to their persistent association in causing gastric complications. However, finding suitable animal models for in vivo experimentation to understand the pathophysiology of gastric cancer and MALT lymphoma is a complicated task. In this review, we summarized the most appropriate and latest information in the scientific literature to understand the role and importance of H. pylori infection animal models.

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Or Rashid, M. "Characterization of innate immune response to hepatitis B virus genotype F acute infection in tree shrew (Tupaia belangeri) model." American Journal of Clinical Pathology 160, Supplement_1 (November 1, 2023): S83—S84. http://dx.doi.org/10.1093/ajcp/aqad150.185.

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Abstract Introduction/Objective Hepatitis B virus (HBV) infection is a global public health problem. The clinical outcomes of HBV infections are influenced by the host as well as viral factors, including viral genotypes and subgenotypes. The interplay between HBV and host innate immunity remains unclear because of the lack of a suitable small animal model. Tree shrews (Tupaia belangeri) have been utilized as a useful animal model for hepatitis viruses such as hepatitis B and C viruses. Methods/Case Report In this study, we characterized acute infections by HBV genotype F (HBV-F) wild type (Wt) and mutant type (Mt) viruses in adult tree shrews. Serum alanine aminotransferase levels were measured before and post-infection 7 and 14 dpi. Both HBV-F-Wt and Mt were detected in the HBV-F-infected tree shrew serum and liver tissue at 7 and 14 dpi. Results (if a Case Study enter NA) We examined the intrahepatic expression patterns of Toll-like receptors (TLRs) (TLR1–9 mRNAs), cGAS, several transcription factors such as STAT1, STAT2, IRF7, HNF4, PD-L1, and cytokines, including IFN-β, IFN-γ, IL-6, and TNF-α in HBV-F Wt/Mt-infected tree shrews. When compared with an uninfected animal group, significant suppression of TLR8 in HBV-F-Wt infected animals and significant suppression of PD-L1 in both HBV-F-Wt and Mt infected animals were observed. Conclusion Thus, tree shrew can be a useful animal model to characterize HBV-F pathogenesis.

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Egermann, M., J. Goldhahn, R. Holz, E. Schneider, and C. A. Lill. "A sheep model for fracture treatment in osteoporosis: Benefits of the model versus animal welfare." Laboratory Animals 42, no. 4 (October 2008): 453–64. http://dx.doi.org/10.1258/la.2007.007001.

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Summary Animal models are necessary to evaluate new options for the treatment of fractures in osteoporotic bone. They permit both the biological response of a living system and the influence of the pathological processes to be taken into account. A sheep model for osteoporosis was established by combining oestrogen deficiency, calcium and vitamin D-deficient diet with steroid medication. Bone mineral density (BMD) was reduced by >30% after 12 weeks of combined treatment. Osteoporosis similar to the human situation with corresponding changes in the micro-architecture and mechanical properties of bone was observed. This publication focuses on the impressive results obtained with the model and contrasts them with considerations of animal welfare. Considerable side-effects associated with steroid medication became manifest. Animals in the treatment groups showed signs of infection of various degrees due to the immunosuppressive effect of the medication. The infections were mostly caused by Corynebacterium pseudotuberculosis. Antibody testing revealed a 100% prevalence of infection in this breed of sheep. A modification of the steroid treatment, i.e. less-frequent injections, reduced the incidence of side-effects. This sheep model shows a significant and reproducible reduction in cancellous BMD of >30%, including relevant changes in biomechanical properties and increased fracture risk. However, the severity of the side-effects cannot be overlooked. The model must be improved if it is to be used in the future. Options to reduce the side-effects are discussed.

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INNOCENT, G., I. MORRISON, J. BROWNLIE, and G. GETTINBY. "A computer simulation of the transmission dynamics and the effects of duration of immunity and survival of persistently infected animals on the spread of bovine viral diarrhoea virus in dairy cattle." Epidemiology and Infection 119, no. 1 (August 1997): 91–100. http://dx.doi.org/10.1017/s0950268897007723.

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This paper describes a computer model that mimics the spread of bovine viral diarrhoea virus (BVDV) infection through a closed herd. The model is able to simulate the spread of infection when a persistently infected (PI) animal is introduced into an infection-free herd, and it is used to investigate the role of persistently infected animals, seroconverting animals, loss of PI calves and duration of immunity on the level of infection within the herd. Under typical management conditions one persistently infected animal poses a real threat to a herd, and the prospect of the herd becoming infection free in a 10-year period without intervention is remote. Seroconverting animals are found to be an important source of infection in herds with few immune animals. The increased loss of PI calves is likely to restrict the numbers of PI animals in a herd, and loss of immunity is important since it increases the possibility of a PI calf being born.

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Terry, Karianne, Susan M. Williams, Lynn Connolly, and Karen M. Ottemann. "Chemotaxis Plays Multiple Roles during Helicobacter pylori Animal Infection." Infection and Immunity 73, no. 2 (February 2005): 803–11. http://dx.doi.org/10.1128/iai.73.2.803-811.2005.

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ABSTRACT Helicobacter pylori is a human gastric pathogen associated with gastric and duodenal ulcers as well as specific gastric cancers. H. pylori infects approximately 50% of the world's population, and infections can persist throughout the lifetime of the host. Motility and chemotaxis have been shown to be important in the infection process of H. pylori. We sought to address the specific roles of chemotaxis in infection of a mouse model system. We found that mutants lacking cheW, cheA, or cheY are all nonchemotactic and infect FVB/N mice with an attenuated phenotype after 2 weeks of infection. If infections proceeded for 6 months, however, this attenuation disappeared. Histological and culture analysis revealed that nonchemotactic mutants were found only in the corpus of the stomach, while the wild type occupied both the corpus and the antrum. Further analysis showed that nonchemotactic H. pylori isolates had an increased 50% infectious dose and were greatly outcompeted when coinfected with the wild type. If nonchemotactic mutants were allowed to establish an infection, subsequent infection with the wild type partially displaced the nonchemotactic mutants, indicating a role for chemotaxis in maintenance of infection. The data presented here support four roles for chemotaxis in H. pylori mouse infections: (i) establishing infection, (ii) achieving high-level infection, (iii) maintaining an infection when there are competing H. pylori present, and (iv) colonizing all regions of the stomach.

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Hayakawa, Masayuki, Haruhiko Taguchi, Shigeru Kamiya, Yasunori Fujioka, Hidehiro Watanabe, Shin Kawai, and Hiroyuki Kobayashi. "Animal Model of Mycoplasma pneumoniae Infection Using Germfree Mice." Clinical and Vaccine Immunology 9, no. 3 (May 2002): 669–76. http://dx.doi.org/10.1128/cdli.9.3.669-676.2002.

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ABSTRACT We have attempted to establish a gnotobiotic mouse model monoassociated with Mycoplasma pneumoniae following single or repeated infection to examine the mechanism of pathogenesis following M. pneumoniae infection. M. pneumoniae inoculated into germfree mice colonized equally well at 105 CFU/lung in both single infection and repeated infection. In histopathological observation, repeatedly infected mice showed pneumonia with mild infiltration of mononuclear cells and macrophages. Antibody titers against M. pneumoniae rose in the repeatedly infected mice but not in the singly infected mice. The percentage of CD4-positive, CD8-positive, and CD25-positive lymphocytes infiltrated in the lung was increased in the repeatedly infected mice. In contrast, the lymphocyte subset in the spleen was not significantly different among mock-, singly, and repeatedly infected mice. In the study of cytokine productivity of spleen cells, production of interleukin (IL)-4 and IL-10 was significantly increased and that of gamma interferon was remarkably increased in the mice following repeated infection. These results indicate that a gnotobiotic mouse model monoassociated with M. pneumoniae was established and that immune mechanisms might be involved in the pathogenesis in pneumonia following M. pneumoniae infection.

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Kugelberg, Elisabeth, Tobias Norström, Thomas K. Petersen, Tore Duvold, Dan I. Andersson, and Diarmaid Hughes. "Establishment of a Superficial Skin Infection Model in Mice by Using Staphylococcus aureus and Streptococcus pyogenes." Antimicrobial Agents and Chemotherapy 49, no. 8 (August 2005): 3435–41. http://dx.doi.org/10.1128/aac.49.8.3435-3441.2005.

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ABSTRACT A new animal model for the purpose of studying superficial infections is presented. In this model an infection is established by disruption of the skin barrier by partial removal of the epidermal layer by tape stripping and subsequent application of the pathogens Staphylococcus aureus and Streptococcus pyogenes. The infection and the infection route are purely topical, in contrast to those used in previously described animal models in mice, such as the skin suture-wound model, where the infection is introduced into the deeper layers of the skin. Thus, the present model is considered more biologically relevant for the study of superficial skin infections in mice and humans. Established topical antibiotic treatments are shown to be effective. The procedures involved in the model are simple, a feature that increases throughput and reproducibility. This new model should be applicable to the evaluation of novel antimicrobial treatments of superficial infections caused by S. aureus and S. pyogenes.

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Rahayu, Widyaningsih, Esti Handayani Hardi, and Gina Saptiani. "PATHOGENICITY OF BACTERIA ENTEROBACTERIACEAE ON ZEBRAFISH AS ANIMAL MODEL." Jurnal Veteriner 21, no. 4 (December 30, 2020): 512–18. http://dx.doi.org/10.19087/jveteriner.2020.21.4.512.

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Enterobacteriaceae are Gram negative bacteria contain endotoxin and exotoxins which are requirements for pathogenic bacteria and act as opportunistic pathogens. The purpose of this research was to determine the ability of Enterobacteriaceae bacteria to infect zebrafish (Danio rerio) by observing anatomical pathology, mortality, time death and cumulative time of death. The method used in this research is a completely randomized design method (CRD). This research was conducted in three stages, first preparation of zebrasfish as animal model by average size 3-5cm and reach three months old. Second, bacterial cultures from 10 species of Enterobacteriaceae were Escherichia coli 1, E. coli 2, Enterobacter cloacae 1, Acinetobacter calcoaceticus, Enterobacter amnigenus 1, Enterobacter amnigenus 1, Escherichia coli 3, Pantoea spp., E. cloacae 1, E. cloacae 2, E. cloacae 3, cultured in Brain Heart Infused Broth (BHIB) and later media washed with Phospate Buffer Saline (PBS) 0.45%. The third stage was bacterial infection to zebrafish using immersion method with each treatment repeated 3 times and observed for 120 hours. The results showed 10 species that used caused death (mortality), the highest mortality in fish that infected with E. coli 2 and E. cloacae 1 with a percentage of 66.67% infected by E. coli 2 and E. cloacae 1. Anatomical pathology in the external organs and internal organs showed post-infectious symptoms. Infection occurred with mean time to death of 12-86 hours, as long as the cumulative time of fish death caused by E. coli 2, A.cinetobacter calcoaceticus and E. cloacae 1 causing death from 24 hours after infection until the end of observation.

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EVANS, R., A. W. L. JOSS, T. H. PENNINGTON, and D. O. HO-YEN. "Progression of Pneumocystis carinii infection in an animal model." Journal of Medical Microbiology 47, no. 6 (June 1, 1998): 543–46. http://dx.doi.org/10.1099/00222615-47-6-543.

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Bawdon, R. E., A. M. Fiskin, B. B. Little, L. L. Davis, and G. Vergarra. "Fibronectin and Postpartum Infection in Rabbits: An Animal Model." Gynecologic and Obstetric Investigation 28, no. 4 (1989): 185–90. http://dx.doi.org/10.1159/000293574.

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Gordon, Y. J., E. Romanowski, and T. Araullo-Cruz. "Development of an animal model for ocular adenoviral infection." Antiviral Research 15 (April 1991): 119. http://dx.doi.org/10.1016/0166-3542(91)90229-k.

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BRAVO, F., R. CARDIN, and D. BERNSTEIN. "An Animal Model of HCMV Infection in SCID Mice." Antiviral Research 74, no. 3 (June 2007): A69. http://dx.doi.org/10.1016/j.antiviral.2007.01.110.

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Ayash‐Rashkovsky, Mila, Zvi Bentwich, Fabian Arditti, Smadar Friedman, Yair Reisner, and Gadi Borkow. "A novel small animal model for HIV‐1 infection." FASEB Journal 19, no. 9 (April 15, 2005): 1149–51. http://dx.doi.org/10.1096/fj.04-3184fje.

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Derouin, Francis, Claire Lacroix, Monique Brun-Pascaud, Françoise Chau, Martine Sinet, Caroline Maslo, and Pierre-Marie Girard. "Animal models of co-infection." Clinical Microbiology and Infection 4, no. 10 (October 1998): 559–62. http://dx.doi.org/10.1111/j.1469-0691.1998.tb00037.x.

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WILSON, ROBERT, and CHARLOTTE RAYNER. "Animal models of respiratory infection." Journal of Antimicrobial Chemotherapy 33, no. 3 (1994): 381–83. http://dx.doi.org/10.1093/jac/33.3.381.

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Lee, Adrian. "Animal models of Helicobacter infection." Molecular Medicine Today 5, no. 11 (November 1999): 500–501. http://dx.doi.org/10.1016/s1357-4310(99)01591-9.

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Dandri, Maura, and Joerg Petersen. "Animal models of HBV infection." Best Practice & Research Clinical Gastroenterology 31, no. 3 (June 2017): 273–79. http://dx.doi.org/10.1016/j.bpg.2017.04.014.

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Nanni, Cristina, Antonella Marangoni, Carmelo Quarta, Donato Di Pierro, Anna Rizzello, Silvia Trespidi, Daniela D’Ambrosio, et al. "Small animal PET for the evaluation of an animal model of genital infection." Clinical Physiology and Functional Imaging 29, no. 3 (May 2009): 187–92. http://dx.doi.org/10.1111/j.1475-097x.2008.00854.x.

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Bernier, Steve P., Laura Silo-Suh, Donald E. Woods, Dennis E. Ohman, and Pamela A. Sokol. "Comparative Analysis of Plant and Animal Models for Characterization of Burkholderia cepacia Virulence." Infection and Immunity 71, no. 9 (September 2003): 5306–13. http://dx.doi.org/10.1128/iai.71.9.5306-5313.2003.

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ABSTRACT A simple alfalfa model was developed as an alternative infection model for virulence studies of the Burkholderia cepacia complex. Symptoms of disease were observed in wounded alfalfa seedlings within 7 days following inoculation of 101 to 105 CFU of most strains of the B. cepacia complex. Strains from seven genomovars of the B. cepacia complex were tested for virulence in the alfalfa model, and the degree of virulence was generally similar in strains belonging to the same genomovar. Strains of Burkholderia multivorans and some strains of Burkholderia stabilis did not cause symptoms of disease in alfalfa seedlings. Representative strains were also tested for virulence using the rat agar bead model. Most of the strains tested were able to establish chronic lung infections; B. stabilis strains were the exception. Most of the strains that were virulent in the alfalfa infection model were also virulent in the lung infection model. The B. cepacia genomovar III mutants K56pvdA::tp and K56-H15 were significantly less virulent in the alfalfa infection model than their parent strain. Therefore, this alfalfa infection model may be a useful tool for assessing virulence of strains of the B. cepacia complex and identifying new virulence-associated genes.

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Illarionova, Victoria, Anastasia Rogova, Ksenia Tuchynskaya, Viktor Volok, Yulia Rogova, Victoria Baryshnikova, Yuriy Turchenko, et al. "Inapparent Tick-Borne Orthoflavivirus Infection in Macaca fascicularis: A Model for Antiviral Drug and Vaccine Research." Vaccines 11, no. 12 (November 25, 2023): 1754. http://dx.doi.org/10.3390/vaccines11121754.

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Tick-borne encephalitis virus (TBEV) and Powassan virus (POWV) are neurotropic tick-borne orthoflaviviruses. They cause mostly asymptomatic infections in hosts, but severe forms with CNS involvement can occur. Studying the early stages of viral infections in humans is challenging, and appropriate animal models are essential for understanding the factors determining the disease severity and for developing emergency prophylaxis and treatment options. In this work, we assessed the model of the early stages of TBEV and POWV mono- and co-infections in Macaca fascicularis. Serological, biochemical, and virological parameters were investigated to describe the infection, including its impact on animal behavior. Viremia, neutralizing antibody dynamics, and viral load in organs were chosen as the main parameters distinguishing early-stage orthoflavivirus infection. Levels of IFNα, monocyte count, and cognitive test scores were proposed as additional informative indicators. An assessment of a tick-borne encephalitis vaccine using this model showed that it provided partial protection against POWV infection in Macaca fascicularis without signs of antibody-dependent enhancement of infection.

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Kayesh, Mohammad Enamul Hoque, Md Abul Hashem, Bouchra Kitab, and Kyoko Tsukiyama-Kohara. "Pathogenesis and Immune Response Caused by Vector-Borne and Other Viral Infections in a Tupaia Model." Microorganisms 7, no. 12 (December 12, 2019): 686. http://dx.doi.org/10.3390/microorganisms7120686.

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The Tupaia or tree shrew (Tupaia belangeri), a small mammal of the Tupaiidae family, is an increasingly used and promising infection model for virological and immunological research. Recently, sequencing of the Tupaia whole genome revealed that it is more homologous to the genome of humans than of rodents. Viral infections are a global threat to human health, and a complex series of events are involved in the interactions between a virus and the host immune system, which play important roles in the activation of an immune response and the outcome of an infection. Majority of immune response data in viral infections are obtained from studies using animal models that enhance the understanding of host-virus interactions; a proper understanding of these interactions is very important for the development of effective antivirals and prophylactics. Therefore, animal models that are permissive to infection and that recapitulate human disease pathogenesis and immune responses to viral infections are essential. Several studies have shown the permissiveness of Tupaia to a number of important human viral infections in vitro and in vivo without prior adaptation of the viruses; the immune responses and clinical manifestations were comparable to those observed in human infections. Thus, the Tupaia is being utilized and developed as a promising immunocompetent small animal model for viral infection studies. In this review, we focused on the immune responses, mostly innate, during viral infection and pathogenesis in the Tupaia model; we evaluated the interaction between the virus and the components of host resistance, the usefulness of this model for immunopathogenesis studies, and the vaccines and antivirals available.

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Farrell, Helen. "Animal models of human cytomegalovirus congenital infection." Microbiology Australia 36, no. 4 (2015): 196. http://dx.doi.org/10.1071/ma15068.

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Human cytomegalovirus (HCMV) infection is highly species-specific, which means that it is unable to productively infect laboratory animals. Despite this caveat, studies of animal CMV counterparts in their natural hosts have revealed significant correlations with observed neuropathological effects of congenital HCMV infection and have improved our understanding of host responses to vaccination. The biological relatedness between human and animal CMVs has been confirmed by phylogenetic analyses; the conservation of ‘core' genes that are essential for virus replication as well as genes that contribute similar mechanisms for virus persistence in their respective host species. The common animal models of HCMV congenital infection include Rhesus CMV (RhCMV), guinea-pig CMV (GPCMV) and mouse CMV (MCMV). Whilst animal models of CMV do not fully recapitulate HCMV infection, they each offer specific advantages in understanding HCMV congenital/perinatal infection (summarised in Table 1).

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Saver, Ashley E., Stephanie A. Crawford, Jonathan D. Joyce, and Andrea S. Bertke. "Route of Infection Influences Zika Virus Shedding in a Guinea Pig Model." Cells 8, no. 11 (November 14, 2019): 1437. http://dx.doi.org/10.3390/cells8111437.

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Due to the recent epidemic of Zika virus (ZIKV) infection and resulting sequelae, as well as concerns about both the sexual and vertical transmission of the virus, renewed attention has been paid to the pathogenesis of this unique arbovirus. Numerous small animal models have been used in various ZIKV pathogenicity studies, however, they are often performed using immunodeficient or immunosuppressed animals, which may impact disease progression in a manner not relevant to immunocompetent humans. The use of immunocompetent animal models, such as macaques, is constrained by small sample sizes and the need for specialized equipment/staff. Here we report the establishment of ZIKV infection in an immunocompetent small animal model, the guinea pig, using both subcutaneous and vaginal routes of infection to mimic mosquito-borne and sexual transmission. Guinea pigs developed clinical signs consistent with mostly asymptomatic and mild disease observed in humans. We demonstrate that the route of infection does not significantly alter viral tissue tropism but does impact mucosal shedding mechanics. We also demonstrate persistent infection in sensory and autonomic ganglia, identifying a previously unrecognized niche of viral persistence that could contribute to viral shedding in secretions. We conclude that the guinea pig represents a useful and relevant model for ZIKV pathogenesis.

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Onlamoon, Nattawat, Sansanee Noisakran, Hui-Mien Hsiao, Alexander Duncan, Francois Villinger, Aftab A. Ansari, and Guey Chuen Perng. "Dengue virus–induced hemorrhage in a nonhuman primate model." Blood 115, no. 9 (March 4, 2010): 1823–34. http://dx.doi.org/10.1182/blood-2009-09-242990.

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AbstractLack of a dengue hemorrhagic animal model recapitulating human dengue virus infection has been a significant impediment in advancing our understanding of the early events involved in the pathogenesis of dengue disease. In efforts to address this issue, a group of rhesus macaques were intravenously infected with dengue virus serotype 2 (strain 16 681) at 1 × 107 PFU/animal. A classic dengue hemorrhage developed 3 to 5 days after infection in 6 of 6 animals. Blood chemistry appeared to be normal with exception of creatine phosphokinase, which peaked at 7 days after infection. A modest thrombocytopenia and noticeable neutropenia concomitant with slight decrease of hemoglobin and hematocrit were registered. In addition, the concentration of D-dimer was elevated significantly. Viremia peaked at 3 to 5 days after infection followed by an inverse relationship between T and B lymphocytes and a bimodal pattern for platelet-monocytes and platelet-neutrophil aggregates. Dengue virus containing platelets engulfed by monocytes was noted at 8 or 9 days after infection. Thus, rhesus macaques inoculated intravenously with a high dose of dengue virus produced dengue hemorrhage, which may provide a unique platform to define the early events in dengue virus infection and help identify which blood components contribute to the pathogenesis of dengue disease.

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Yanke, S. J., M. E. Olson, H. D. Davies, and D. A. Hart. "A CD-1 mouse model of infection with Staphylococcus aureus: Influence of gender on infection with MRSA and MSSA isolates." Canadian Journal of Microbiology 46, no. 10 (October 1, 2000): 920–26. http://dx.doi.org/10.1139/w00-073.

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Staphylococcus aureus is an important pathogen of humans and other animals, causing bacteremia, abscessation, toxemia, and other infectious diseases. An animal model using CD-1 mice was developed to study the pathogenesis of methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-sensitive Staphylococcus aureus (MSSA). When inoculated into the CD-1 mouse model, it was shown that both MSSA isolates, (HR 78 and CSA-1) and MRSA isolates (MRSA 456 and MRSA 457) led to chronic infection of the kidney. Female CD-1 mice inoculated with MRSA 456 proved to be more susceptible to infection and mortality than their male counterparts. Castrated mice became more susceptible to infection than intact male mice, suggesting a hormonal involvement in the infection process.Key words: Staphylococcus aureus, animal model, gender, MSSA, MRSA.

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Scháňková, Š., I. Langrová, I. Jankovská, J. Vadlejch, Z. Čadková, and D. Křivská. "Screening of Model Animals for Experimental Infection with Equine Cyathostomes." Scientia Agriculturae Bohemica 49, no. 1 (March 1, 2018): 17–20. http://dx.doi.org/10.2478/sab-2018-0003.

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Abstract Various laboratory animals – mice (Mus musculus) of six strains, rabbits (Oryctolagus cuniculus), guinea pigs (Cavia porcellus), rats (Rattus norvegicus), and Mongolian gerbils (Meriones unguiculatus) were experimentally infected with larvae of small strongyles (Cyathostominae), obtained from horse faeces and cultured to the infective larval stage L3. The attempt to transfer cyathostome larvae was aimed at developing a model for the investigation of different aspects of the life cycle and biology of these nematodes in the laboratory. Some animals were immunized (hydrocortisone) for the duration of the study. The laboratory animals were orally infected with 2–10 thousand sheathed or ex-sheathed L3 larvae of mixed cyathostome species. All attempts to inoculate any animal failed; there was no larval development in the experimental rodents and it can be stated that none of the investigated animals may serve as a suitable model host for horse nematodes of the subfamily Cyathostominae.

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Anand, T., S. Rajan, and L. Aravind. "Describing the interactive model design of avian influenza : Animal infection and human infection." International Journal of Infectious Diseases 45 (April 2016): 247. http://dx.doi.org/10.1016/j.ijid.2016.02.552.

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Journal articles on the topic 'Animal model of infection'

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