Chasing the elusive animal model of late-phase bronchoconstriction: Studies in dogs, guinea pigs and rats

1992 ◽  
Vol 37 (3-4) ◽  
pp. 178-180 ◽  
Author(s):  
I. M. Richards ◽  
R. L. Griffin ◽  
S. K. Shields ◽  
M. S. Reid ◽  
S. F. Fidler
Keyword(s):  
Animal Model ◽  
Guinea Pigs ◽  
Late Phase

scholarly journals Pathology and Pathophysiology of Inhalational Anthrax in a Guinea Pig Model

2013 ◽  
Vol 81 (4) ◽  
pp. 1152-1163 ◽  
Author(s):  
Vladimir Savransky ◽  
Daniel C. Sanford ◽  
Emily Syar ◽  
Jamie L. Austin ◽  
Kevin P. Tordoff ◽  
...  
Keyword(s):  
Animal Model ◽  
Guinea Pig ◽  
Lymph Nodes ◽  
Guinea Pigs ◽  
Alternative Model ◽  
Lethal Dose ◽  
Clinical Signs ◽  
Regional Lymph Nodes ◽  
Content Type ◽  
Ames Strain

ABSTRACTNonhuman primates (NHPs) and rabbits are the animal models most commonly used to evaluate the efficacy of medical countermeasures against anthrax in support of licensure under the FDA's “Animal Rule.” However, a need for an alternative animal model may arise in certain cases. The development of such an alternative model requires a thorough understanding of the course and manifestation of experimental anthrax disease induced under controlled conditions in the proposed animal species. The guinea pig, which has been used extensively for anthrax pathogenesis studies and anthrax vaccine potency testing, is a good candidate for such an alternative model. This study was aimed at determining the median lethal dose (LD50) of theBacillus anthracisAmes strain in guinea pigs and investigating the natural history, pathophysiology, and pathology of inhalational anthrax in this animal model following nose-only aerosol exposure. The inhaled LD50of aerosolized Ames strain spores in guinea pigs was determined to be 5.0 × 104spores. Aerosol challenge of guinea pigs resulted in inhalational anthrax with death occurring between 46 and 71 h postchallenge. The first clinical signs appeared as early as 36 h postchallenge. Cardiovascular function declined starting at 20 h postexposure. Hematogenous dissemination of bacteria was observed microscopically in multiple organs and tissues as early as 24 h postchallenge. Other histopathologic findings typical of disseminated anthrax included suppurative (heterophilic) inflammation, edema, fibrin, necrosis, and/or hemorrhage in the spleen, lungs, and regional lymph nodes and lymphocyte depletion and/or lymphocytolysis in the spleen and lymph nodes. This study demonstrated that the course of inhalational anthrax disease and the resulting pathology in guinea pigs are similar to those seen in rabbits and NHPs, as well as in humans.

scholarly journals Effects of an antiplatelet glycoprotein Ib antibody on hemostatic function in the guinea pig

Blood ◽  
1989 ◽  
Vol 74 (2) ◽  
pp. 690-694 ◽  
Author(s):  
BH Becker ◽  
JL Miller
Keyword(s):  
Animal Model ◽  
Platelet Count ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Bleeding Time ◽  
Model System ◽  
Platelet Counts ◽  
Equal Dose ◽  
Guinea Pig Model

Abstract Previous studies in the guinea pig model system have established a close structural homology between human and guinea pig glycoproteins Ib (GPIb) and IIb/IIIa (GPIIb/IIIa). Moreover, the murine monoclonal antibody (MoAb) PG-1, which recognizes GPIb in guinea pig platelets and megakaryocytes, exerted full inhibition on von Willebrand factor (vWF)- dependent platelet agglutination without inhibiting aggregation induced by ADP, collagen, or thrombin. The present research extends this animal model system to study of the effects on hemostatic function following the in vivo injection of MoAb PG-1 or its F(ab')2 fragments. A hind limb template bleeding time methodology was developed for use in guinea pigs. Normal bleeding time was determined to be 2.7 +/- 0.5 minutes (mean +/- SD), with an observed range of two to four minutes. Platelet counts in these same animals were 501 +/- 82 x 10(3)/microL. After intraperitoneal (IP) injection of busulfan, guinea pigs became increasingly thrombocytopenic. As long as the platelet count remained above approximately 150 x 10(3)/microL, the bleeding time was not more than five minutes; however, further decrease in the platelet count was accompanied by more marked prolongations of the bleeding time. For 14 to 72 hours after IP injection of 1.3 mg/kg intact PG-1 MoAb, a hemorrhagic state was produced with a bleeding time greater than 20 minutes. The platelet count concurrently decreased to approximately 50% of its baseline value but could not be further decreased either by raising the initial PG-1 dosage tenfold or by administering a second, equal dose 24 hours after the initial injection. This finding may reflect a heterogeneity of circulating platelets with respect to GPIb, to Fc receptors, or to an interaction between them. After IP injection of 0.63 to 2.5 mg/kg PG-1 F(ab')2 fragment, platelet counts did not decrease more than 21% below baseline levels in a 72-hour period, and bleeding times never increased by more than one minute over baseline values. Nevertheless, platelets obtained from animals 24 hours after injection of 2.5 mg/kg PG-1 F(ab')2 showed full inhibition of agglutination induced by ristocetin. The response of these platelets to aggregation by asialo-vWF was also severely inhibited as compared with control platelets. PG-1 F(ab')2 produced no effect on aggregation induced by ADP. These studies show that virtually complete functional block of the vWF receptor by F(ab')2 fragments of the anti-GPIb MoAb PG- 1 is not sufficient to produce a hemorrhagic state in the guinea pig animal model system.

scholarly journals Pichinde Virus Infection of Outbred Hartley Guinea Pigs as a Surrogate Animal Model for Human Lassa Fever: Histopathological and Immunohistochemical Analyses

Pathogens ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 579 ◽  
Author(s):  
Wun-Ju Shieh ◽  
Shuiyun Lan ◽  
Sherif R. Zaki ◽  
Hinh Ly ◽  
Yuying Liang
Keyword(s):  
Animal Model ◽  
Surrogate Model ◽  
Guinea Pigs ◽  
Virulent Strain ◽  
Small Animal ◽  
Immunohistochemical Analysis ◽  
Lassa Fever ◽  
Lassa Virus ◽  
Pichinde Virus ◽  
Guinea Pig Model

Lassa virus (LASV) is a mammarenavirus (arenavirus) that causes zoonotic infection in humans that can lead to fatal hemorrhagic Lassa fever (LF) disease. Currently, there are no FDA-approved vaccines or therapeutics against LASV. Development of treatments against LF and other related arenavirus-induced hemorrhagic fevers (AHFs) requires relevant animal models that can recapitulate clinical and pathological features of AHF diseases in humans. Laboratory mice are generally resistant to LASV infection, and non-human primates, while being a good animal model for LF, are limited by their high cost. Here, we describe a small, affordable, and convenient animal model that is based on outbred Hartley guinea pigs infected with Pichinde virus (PICV), a mammarenavirus that is non-pathogenic in humans, for use as a surrogate model of human LF. We conducted a detailed analysis of tissue histopathology and immunohistochemical analysis of different organs of outbred Hartley guinea pigs infected with different PICV strains that show differential disease phenotypes and pathologies. Comparing to infection with the avirulent PICV strain (P2 or rP2), animals infected with the virulent strain (P18 or rP18) show extensive pathological changes in different organs that sustain high levels of virus replication. The similarity of tissue pathology and viral antigen distribution between the virulent PICV–guinea pig model and lethal human LASV infection supports a role of this small animal model as a surrogate model of studying human LF in order to understand its pathogenesis and for evaluating potential preventative and therapeutic options against AHFs.

scholarly journals Effects of Theophylline Compared with Prednisolone on Late Phase Airway Leukocyte Infiltration in Guinea Pigs

1991 ◽  
Vol 94 (1-4) ◽  
pp. 293-294 ◽  
Author(s):  
R.W. Gristwood ◽  
J. Llupiá ◽  
A.G. Fernández ◽  
P. Berga
Keyword(s):  
Guinea Pigs ◽  
Late Phase ◽  
Leukocyte Infiltration

Maternal Nutrient Restriction in Guinea Pigs as an Animal Model for Inducing Fetal Growth Restriction

2015 ◽  
Vol 23 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Alexander A. Elias ◽  
Andrew Ghaly ◽  
Brad Matushewski ◽  
Timothy R. H. Regnault ◽  
Bryan S. Richardson
Keyword(s):  
Animal Model ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Guinea Pigs ◽  
Growth Restriction ◽  
Nutrient Restriction

The susceptibility of mammals to Fasciolopsis buski

1985 ◽  
Vol 59 (1) ◽  
pp. 19-22 ◽  
Author(s):  
H. C. Malviya
Keyword(s):  
Animal Model ◽  
Experimental Work ◽  
Guinea Pigs ◽  
Fasciolopsis Buski

AbstractThe susceptibility of various mammals to infection with Fasciolopsis buski has been studied. Mice, rats, monkeys and dogs were completely refractory. Guinea-pigs were only partially susceptible. However, young rabbits (6 to 8 weeks old) were found to be susceptible and can be used as an animal model for experimental work on this parasite.

Cyclooxygenase-2 participates in the late phase of airway hyperresponsiveness after ozone exposure in guinea pigs

2000 ◽  
Vol 403 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Hiroyuki Nakano ◽  
Hisamichi Aizawa ◽  
Koichiro Matsumoto ◽  
Satoru Fukuyama ◽  
Hiromasa Inoue ◽  
...  
Keyword(s):  
Guinea Pigs ◽  
Airway Hyperresponsiveness ◽  
Late Phase ◽  
Cyclooxygenase 2 ◽  
Ozone Exposure

Experimental meningococcal infection in neonatal animals: models for mucosal invasiveness

1984 ◽  
Vol 30 (8) ◽  
pp. 1022-1029 ◽  
Author(s):  
Irving E. Salit ◽  
Elaine Van Melle ◽  
Lewis Tomalty
Keyword(s):  
Animal Model ◽  
Meningococcal Disease ◽  
Guinea Pigs ◽  
Blood Cultures ◽  
Meningococcal Infection ◽  
Iron Dextran ◽  
Complete Understanding ◽  
Nasopharyngeal Colonization ◽  
Rats And Mice ◽  
Intranasal Instillation

A more complete understanding of meningococcal disease has been hampered by lack of an appropriate animal model. We subjected 5-day-old guinea pigs, rats, and mice to intranasal challenge with meningococci and we measured rates of bacteremia as a marker of mucosal invasion. After a single intranasal instillation of 107 serotype 2 meningococci, positive blood cultures were found in 0% of guinea pigs, 16% of rats, and 39% of mice, and so mice were used for further studies. Death occurred in 4% of mice and was associated with a purulent leptomeningitis and ventriculitis. Forty percent of mice had nasopharyngeal colonization which increased to 65% with repeated injections. Carrier strains were avirulent, a nonserotype 2 disease strain had low invasiveness, and serotype 2 strains were most virulent. Iron dextran increased rates of bacteremia after challenge with serotype 2 strains. Adult animals were not susceptible to bacteremia after intranasal challenge. The neonatal mouse model fulfills most of the criteria for an appropriate experimental model of meningococcal disease.

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