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Serological evidence of rotavirus infection in guinea pig colony
Castro, L. de;Araújo, H. P. de;Fialho, A. M.;Gouvea, V. S.;Pereira, H. G.;
Memórias do Instituto Oswaldo Cruz , 1988, DOI: 10.1590/S0074-02761988000400003
Abstract: antibodies reacting with simian rotavirus saii were detected by enzyme immunoassay (eia) and western blot assay (wba) in sera from guinea pigs bred for experimental use at the funda??o oswaldo cruz, rio de janeiro, brazil. the proportion of antibody-positive animals and the antibody titres rose sharply in 1985, were maintained at a high levels in 1986 and declined in 1987. there were no obvious signs of disease coinciding with serological evidence of infection. results of wba suggest that the virus involved belongs to subgroup 1 of group a rotaviruses.
A Neutralizing Anti-gH/gL Monoclonal Antibody Is Protective in the Guinea Pig Model of Congenital CMV Infection  [PDF]
Marcy R. Auerbach,Donghong Yan,Rajesh Vij,Jo-Anne Hongo,Gerald Nakamura,Jean-Michel Vernes,Y. Gloria Meng,Samantha Lein,Pamela Chan,Jed Ross,Richard Carano,Rong Deng,Nicholas Lewin-Koh,Min Xu,Becket Feierbach
PLOS Pathogens , 2014, DOI: doi/10.1371/journal.ppat.1004060
Abstract: Human cytomegalovirus (HCMV) is the most common cause of congenital virus infection. Congenital HCMV infection occurs in 0.2–1% of all births, and causes birth defects and developmental abnormalities, including sensorineural hearing loss and developmental delay. Several key studies have established the guinea pig as a tractable model for the study of congenital HCMV infection and have shown that polyclonal antibodies can be protective [1]–[3]. In this study, we demonstrate that an anti-guinea pig CMV (GPCMV) glycoprotein H/glycoprotein L neutralizing monoclonal antibody protects against fetal infection and loss in the guinea pig. Furthermore, we have delineated the kinetics of GPCMV congenital infection, from maternal infection (salivary glands, seroconversion, placenta) to fetal infection (fetus and amniotic fluid). Our studies support the hypothesis that a neutralizing monoclonal antibody targeting an envelope GPCMV glycoprotein can protect the fetus from infection and may shed light on the therapeutic intervention of HCMV congenital infection in humans.
Cyclic cidofovir (cHPMPC) prevents congenital cytomegalovirus infection in a guinea pig model
Mark R Schleiss, Jodi L Anderson, Alistair McGregor
Virology Journal , 2006, DOI: 10.1186/1743-422x-3-9
Abstract: Pregnant outbred Hartley guinea pigs were challenged in the early-third trimester with guinea pig CMV (GPCMV) and treated with placebo, or the antiviral agent, cyclic cidofovir. To optimize detection of vertical infection, an enhanced green fluorescent protein (eGFP)-tagged virus was employed. Compared to placebo, cyclic cidofovir-treated dams and pups had reduced mortality following GPCMV challenge. The magnitude of GPCMV-induced maternal and fetal mortality in this study was reduced from 5/25 animals in the placebo group to 0/21 animals in the treatment group (p = 0.05, Fisher's exact test). By viral culture assay, antiviral therapy was found to completely prevent GPCMV transmission to the fetus. In control pups, 5/19 (26%) were culture-positive for GPCMV, compared to 0/16 of pups in the cyclic cidofovir treatment group (p < 0.05, Fisher's exact test).Antiviral therapy with cyclic cidofovir improves pregnancy outcomes in guinea pigs, and eliminates congenital CMV infection, following viral challenge in the third trimester. This study also demonstrated that an eGFP-tagged recombinant virus, with the reporter gene inserted into a dispensable region of the viral genome, retained virulence, including the potential for congenital transmission, facilitating tissue culture-based detection of congenital infection. These observations provide support for clinical trials of antivirals for reduction of congenital CMV infection.Congenital cytomegalovirus (CMV) infection is a major public health problem. Transmission of CMV in utero results in substantial long-term morbidity in newborns, including mental retardation and sensorineural hearing loss (SNHL; reviewed in [1]). Treatment of the affected newborn with the anti-CMV nucleoside analogue, ganciclovir, improves the outcome of SNHL, but the response is incomplete, and significant sequelae may persist even following completion of antiviral therapy [2]. These observations provide support for studying the approach of administeri
Mycobacterium ulcerans Fails to Infect through Skin Abrasions in a Guinea Pig Infection Model: Implications for Transmission  [PDF]
Heather R. Williamson,Lydia Mosi,Robert Donnell,Maha Aqqad,Richard W. Merritt,Pamela L. C. Small
PLOS Neglected Tropical Diseases , 2014, DOI: 10.1371/journal.pntd.0002770
Abstract: Transmission of M. ulcerans, the etiological agent of Buruli ulcer, from the environment to humans remains an enigma despite decades of research. Major transmission hypotheses propose 1) that M. ulcerans is acquired through an insect bite or 2) that bacteria enter an existing wound through exposure to a contaminated environment. In studies reported here, a guinea pig infection model was developed to determine whether Buruli ulcer could be produced through passive inoculation of M. ulcerans onto a superficial abrasion. The choice of an abrasion model was based on the fact that most bacterial pathogens infecting the skin are able to infect an open lesion, and that abrasions are extremely common in children. Our studies show that after a 90d infection period, an ulcer was present at intra-dermal injection sites of all seven animals infected, whereas topical application of M. ulcerans failed to establish an infection. Mycobacterium ulcerans was cultured from all injection sites whereas infected abrasion sites healed and were culture negative. A 14d experiment was conducted to determine how long organisms persisted after inoculation. Mycobacterium ulcerans was isolated from abrasions at one hour and 24 hours post infection, but cultures from later time points were negative. Abrasion sites were qPCR positive up to seven days post infection, but negative at later timepoints. In contrast, M. ulcerans DNA was detected at intra-dermal injection sites throughout the study. M. ulcerans was cultured from injection sites at each time point. These results suggest that injection of M. ulcerans into the skin greatly facilitates infection and lends support for the role of an invertebrate vector or other route of entry such as a puncture wound or deep laceration where bacteria would be contained within the lesion. Infection through passive inoculation into an existing abrasion appears a less likely route of entry.
Intranasal Mucosal Boosting with an Adenovirus-Vectored Vaccine Markedly Enhances the Protection of BCG-Primed Guinea Pigs against Pulmonary Tuberculosis  [PDF]
Zhou Xing, Christine T. McFarland, Jean-Michel Sallenave, Angelo Izzo, Jun Wang, David N. McMurray
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005856
Abstract: Background Recombinant adenovirus-vectored (Ad) tuberculosis (TB) vaccine platform has demonstrated great potential to be used either as a stand-alone or a boost vaccine in murine models. However, Ad TB vaccine remains to be evaluated in a more relevant and sensitive guinea pig model of pulmonary TB. Many vaccine candidates shown to be effective in murine models have subsequently failed to pass the test in guinea pig models. Methods and Findings Specific pathogen-free guinea pigs were immunized with BCG, AdAg85A intranasally (i.n), AdAg85A intramuscularly (i.m), BCG boosted with AdAg85A i.n, BCG boosted with AdAg85A i.m, or treated only with saline. The animals were then infected by a low-dose aerosol of M. tuberculosis (M.tb). At the specified times, the animals were sacrificed and the levels of infection in the lung and spleen were assessed. In separate studies, the long-term disease outcome of infected animals was monitored until the termination of this study. Immunization with Ad vaccine alone had minimal beneficial effects. Immunization with BCG alone and BCG prime-Ad vaccine boost regimens significantly reduced the level of M.tb infection in the tissues to a similar extent. However, while BCG alone prolonged the survival of infected guinea pigs, the majority of BCG-immunized animals succumbed by 53 weeks post-M.tb challenge. In contrast, intranasal or intramuscular Ad vaccine boosting of BCG-primed animals markedly improved the survival rate with 60% of BCG/Ad i.n- and 40% of BCG/Ad i.m-immunized guinea pigs still surviving by 74 weeks post-aerosol challenge. Conclusions Boosting, particularly via the intranasal mucosal route, with AdAg85A vaccine is able to significantly enhance the long-term survival of BCG-primed guinea pigs following pulmonary M.tb challenge. Our results thus support further evaluation of this viral-vectored TB vaccine in clinical trials.
Favipiravir (T-705) Inhibits Junín Virus Infection and Reduces Mortality in a Guinea Pig Model of Argentine Hemorrhagic Fever  [PDF]
Brian B. Gowen ,Terry L. Juelich,Eric J. Sefing,Trevor Brasel,Jennifer K. Smith,Lihong Zhang,Bersabeh Tigabu,Terence E. Hill,Tatyana Yun,Colette Pietzsch,Yousuke Furuta,Alexander N. Freiberg
PLOS Neglected Tropical Diseases , 2013, DOI: 10.1371/journal.pntd.0002614
Abstract: Background Junín virus (JUNV), the etiologic agent of Argentine hemorrhagic fever (AHF), is classified by the NIAID and CDC as a Category A priority pathogen. Presently, antiviral therapy for AHF is limited to immune plasma, which is readily available only in the endemic regions of Argentina. T-705 (favipiravir) is a broadly active small molecule RNA-dependent RNA polymerase inhibitor presently in clinical evaluation for the treatment of influenza. We have previously reported on the in vitro activity of favipiravir against several strains of JUNV and other pathogenic New World arenaviruses. Methodology/Principal Findings To evaluate the efficacy of favipiravir in vivo, guinea pigs were challenged with the pathogenic Romero strain of JUNV, and then treated twice daily for two weeks with oral or intraperitoneal (i.p.) favipiravir (300 mg/kg/day) starting 1–2 days post-infection. Although only 20% of animals treated orally with favipiravir survived the lethal challenge dose, those that succumbed survived considerably longer than guinea pigs treated with placebo. Consistent with pharmacokinetic analysis that showed greater plasma levels of favipiravir in animals dosed by i.p. injection, i.p. treatment resulted in a substantially higher level of protection (78% survival). Survival in guinea pigs treated with ribavirin was in the range of 33–40%. Favipiravir treatment resulted in undetectable levels of serum and tissue viral titers and prevented the prominent thrombocytopenia and leucopenia observed in placebo-treated animals during the acute phase of infection. Conclusions/Significance The remarkable protection afforded by i.p. favipiravir intervention beginning 2 days after challenge is the highest ever reported for a small molecule antiviral in the difficult to treat guinea pig JUNV challenge model. These findings support the continued development of favipiravir as a promising antiviral against JUNV and other related arenaviruses.
Fever, Haematuria, and Acute Graft Dysfunction in Renal Transplant Recipients Secondary to Adenovirus Infection: Two Case Reports  [PDF]
J. Ramírez,I. C. Bostock,A. Martin-Onra?t,S. Calleja,A. Sánchez-Cedillo,L. A. Navarro-Vargas,A. L. Noriega-Salas,O. Martínez-Mijangos,N. O. Uribe-Uribe,M. Vilatoba,B. Gabilondo,L. E. Morales-Buenrostro,J. Alberú
Case Reports in Nephrology , 2013, DOI: 10.1155/2013/195753
Abstract: We report two cases of adenoviral infection in kidney transplant recipients that presented with different clinical characteristics under similar demographic and posttransplant conditions. The first case presented with fever, gross haematuria, and acute graft dysfunction 15 days following renal transplantation. A graft biopsy, analyzed with immunohistochemistry, yielded negative results. However, the diagnosis was confirmed with blood and urine real-time PCR for adenovirus 3 days after the initial clinical manifestations. The immunosuppression dose was reduced, and ribavirin treatment was started, for which the patient quickly developed toxicity. Antiviral treatment allowed for transient response; however, a relapse occurred. The viral real-time PCR became negative upon immunosuppression reduction and administration of IVIG; graft function normalized. In the second case, the patient presented with fever and dysuria 1 month after transplantation. The initial imaging studies revealed graft enlargement and areas of hypoperfusion. In this case, the diagnosis was also confirmed with blood and urine real-time PCR for adenovirus 3 days after the initial clinical manifestations. Adenoviral nephritis was confirmed through a graft biopsy analyzed with light microscopy, immunohistochemistry, and PCR in frozen tissue. The immunosuppression dose was reduced, and IVIG was administered obtaining excellent clinical results along with a negative real-time PCR. 1. Introduction In the scenario of transplantation, infection with adenovirus is more common after bone marrow transplantation and affects children more commonly than adults (31–47% versus 13.6%) with an estimated mortality of 26% in symptomatic patients [1, 2]. Adenovirus infection, particularly with serotypes B 7, 11, 34, and 35, presents more frequently as hemorrhagic cystitis and is usually a rare and limited infection in renal transplant recipients [3]. A disseminated disease with more serious systemic complications or death is uncommon (58% of cases are self-limited). Throughout the literature there have only been a small number of case reports of adenoviral-related nephritis in kidney transplant recipients [2–10]. In this report, we describe two unusual cases of early onset infection with adenovirus, as well as a review of previous cases reported in the literature. 2. Case 1 A 26-year-old man with end-stage renal disease of undetermined etiology received a living donor renal transplantation on February 2012. The adult donor was his sister sharing 1-haplotype; the AHG-CDC cross match was negative, the PRA
Inactivated and adjuvanted vaccine for the control of the African horse sickness virus serotype 9 infection: evaluation of efficacy in horses and guinea-pig model
Rossella Lelli,Umberto Molini,Gaetano Federico Ronchi,Emanuela Rossi
Veterinaria Italiana , 2013,
Abstract: African horse sickness (AHS) is a non-contagious viral disease of solipeds transmitted by Culicoides. The disease is endemic in most African countries. Past experience has shown that Italy is a country exposed to emerging infectious diseases endemic to Africa; an incursion of AHS virus together with the widespread presence of Culicoides vectors could be the cause of a serious epidemic emergency. A live attenuated vaccine containing seven of the nine viral serotypes, serotype 5 and 9 are excluded, is commercially available from Onderstepoort Biological Products. However, the use of live vaccines is a matter of endless disputes, and therefore inactivated or recombinant alternative products have been investigated over the years. Since research on AHS is hampered by the use of horses to evaluate vaccine potency, in a previous experiment serological response to serotypes 5 and 9 was assayed in guinea-pigs and horses. A durable and comparable serological response was observed in the two animal species. In the present study antibody response in horses and guinea-pigs, immunised with the inactivated-adjuvanted vaccine formulated with serotype 9, was tested over a period of 12 months. When immunity was challenged, horses were protected from infection and disease. Antibody response in horses and guinea-pigs compared favourably.
Plasmid-Cured Chlamydia caviae Activates TLR2-Dependent Signaling and Retains Virulence in the Guinea Pig Model of Genital Tract Infection  [PDF]
Lauren C. Frazer, Toni Darville, Kumar Chandra-Kuntal, Charles W. Andrews, Matthew Zurenski, Margaret Mintus, Yasser M. AbdelRahman, Robert J. Belland, Robin R. Ingalls, Catherine M. O'Connell
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0030747
Abstract: Loss of the conserved “cryptic” plasmid from C. trachomatis and C. muridarum is pleiotropic, resulting in reduced innate inflammatory activation via TLR2, glycogen accumulation and infectivity. The more genetically distant C. caviae GPIC is a natural pathogen of guinea pigs and induces upper genital tract pathology when inoculated intravaginally, modeling human disease. To examine the contribution of pCpGP1 to C. caviae pathogenesis, a cured derivative of GPIC, strain CC13, was derived and evaluated in vitro and in vivo. Transcriptional profiling of CC13 revealed only partial conservation of previously identified plasmid-responsive chromosomal loci (PRCL) in C. caviae. However, 2-deoxyglucose (2DG) treatment of GPIC and CC13 resulted in reduced transcription of all identified PRCL, including glgA, indicating the presence of a plasmid-independent glucose response in this species. In contrast to plasmid-cured C. muridarum and C. trachomatis, plasmid-cured C. caviae strain CC13 signaled via TLR2 in vitro and elicited cytokine production in vivo similar to wild-type C. caviae. Furthermore, inflammatory pathology induced by infection of guinea pigs with CC13 was similar to that induced by GPIC, although we observed more rapid resolution of CC13 infection in estrogen-treated guinea pigs. These data indicate that either the plasmid is not involved in expression or regulation of virulence in C. caviae or that redundant effectors prevent these phenotypic changes from being observed in C. caviae plasmid-cured strains.
Severe allergic reactions to guinea pig
Michael C Zacharisen, Michael B Levy, Jeffrey L Shaw, Viswanath P Kurup
Clinical and Molecular Allergy , 2005, DOI: 10.1186/1476-7961-3-14
Abstract: We report two patients with severe allergic reactions following non-occupational exposure to guinea pigs. The first patient, an 11-year-old female, developed ocular, nasal, skin and laryngeal edema symptoms immediately after handling a guinea pig. The second patient, a 24-year-old female, developed symptoms of isolated laryngeal edema after cleaning a guinea pig cage. Percutaneous skin testing, RAST, ELISA and ELISA inhibition testing with guinea pig extract were performed.Both patients had IgE-mediated allergy to guinea pig confirmed by ELISA and either RAST or skin testing. ELISA inhibition studies confirmed the specificity of the IgE reactivity to guinea pig.Severe IgE-mediated reactions can occur following non-occupational guinea pig exposure. Physicians should be aware of this possibility.Guinea pigs are popular household pets and also used in laboratory research. Allergic symptoms including rhinitis, conjunctivitis, and asthma have been documented in laboratory animal workers exposed to guinea pigs [1-5]. An extensive review of the literature revealed no reports of severe allergic reactions resulting from guinea pig exposure. We report two patients with severe allergic reactions following direct exposure to guinea pigs in domestic settings.An 11-year-old female with a history of migraine headaches and exercise-induced asthma (EIA) was evaluated in the Allergy clinic two months after experiencing symptoms while holding a guinea pig at her hairdresser's home. This was the only episode of symptoms associated with guinea pig exposure; she had handled the pet previously without exhibiting symptoms. Within minutes of holding the guinea pig, she developed ocular itching, lacrimation, and periorbital angioedema. Symptoms rapidly progressed to facial urticaria and angioedema, rhinorrhea, throat tightness, and dyspnea. She had difficulty speaking, repeatedly attempted to clear her throat, and expressed feelings of impending doom. There was no coughing or audible wheezin
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