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Biomedical subjects

C J Peters

Publications and source records attributed to C J Peters.

At least 127 records · Page 7Linked to original sources
PubMed1997

Hantavirus pulmonary syndrome.

The objective of this report is to summarize the medical literature relevant to the epidemiology, diagnosis, treatment, and control of hantavirus pulmonary syndrome (HPS). The English language literature was searched from January 1993 through March 1995, manually and using Medline, including conference proceedings and reference lists. We selected relevant articles on clinical aspects of HPS. HPS is a newly described illness that progresses through three phases: prodromal, cardiopulmonary, and convalescent. Its hallmark is the rapid progression from nonspecific prodromal symptoms to respiratory insufficiency caused by noncardiogenic pulmonary edema. Unlike other hantavirus infections, renal involvement and hemorrhagic manifestations are not dominant features in HPS. Treatment is based on close intensive care monitoring, oxygen, and cardiovascular support with inotropic and vasopressor drugs. Preventive measures include avoiding contact with rodents and their excrement. Peromyscus maniculatus is the primary rodent vector for the Sin Nombre virus, which caused the epidemic of HPS in the southwest United States in May 1993. HPS has a unique set of clinical findings and is caused by a genetically distinct hantavirus. Physicians and other health professionals should consider this disease when evaluating patients with unexplained respiratory insufficiency after a febrile prodrome, especially when history suggests possible rodent contact. Sporadic cases and possibly epidemics of HPS are likely in the future, particularly when ecological changes increase the population of infected rodent vectors in an area.

Animals↗
PubMed1997

Immunohistochemical and in situ localization of Crimean-Congo hemorrhagic fever (CCHF) virus in human tissues and implications for CCHF pathogenesis.

BACKGROUND: Crimean-Congo hemorrhagic fever (CCHF) is a potentially fatal disease that occurs in parts of Africa, Asia, and eastern Europe, and that is caused by a recently emerged bunyavirus. Rapid laboratory diagnosis of CCHF infection is essential and is currently performed by virus isolation and serology. Histopathologic studies have been limited to a small number of cases, and little is known about the cellular tropism of CCHF virus and the pathogenesis of this disease. DESIGN: We conducted a retrospective case analysis of 12 patients with a diagnosis of CCHF infection, confirmed by virus isolation, who were evaluated at the Special Pathogens Unit, National Institute for Virology, South Africa. The clinicopathologic features of CCHF and the diagnostic role of virus isolation as compared with serology, immunohistochemistry, and in situ hybridization were evaluated. Additionally, the distribution of CCHF virus in human tissues was examined. RESULTS: The clinical and histopathologic features of CCHF resemble those of other viral hemorrhagic fevers. Of the 12 patients with virus isolation-confirmed CCHF infection, 5 were positive by serology, 10 by immunohistochemistry, and 5 by in situ hybridization. Immunohistochemistry and in situ hybridization analyses showed that the mononuclear phagocytes, endothelial cells, and hepatocytes are main targets of infection. Association of parenchymal necrosis in liver with viral infection suggests that cell damage may be mediated by a direct viral cytopathic effect. CONCLUSIONS: The diagnosis of CCHF, suspected by history and clinical features, can be supported histopathologically. However, since the pathologic features resemble those of other viral hemorrhagic fevers, an unequivocal diagnosis can be made only by laboratory tests. The utility of immunohistochemistry as a sensitive and rapid diagnostic modality was established by the high degree of concordance with virus isolation. Infection of mononuclear phagocytes, endothelial cells, and hepatocytes may play a critical role in the pathogenesis of CCHF.

Adolescent↗
PubMed1997

Safety and efficacy of a mutagen-attenuated Rift Valley fever virus vaccine in cattle.

OBJECTIVE: To examine safety and efficacy of a mutagen attenuated Rift Valley fever virus (RVFV) vaccine (RVF MP-12) in cattle. ANIMALS: 38 pregnant cows, 14 steers, and 10 lactating dairy cows. PROCEDURE: Pregnant cows in their third, fifth, or eighth month of gestation were vaccinated (1 ml of RVF MP-12 containing 5 log10 plaque-forming units [PFU] of virus) and were monitored daily through parturition for signs of disease, viremia, and immunologic response. Additionally, 10 vaccinated pregnant cows were challenge inoculated with virulent RVFV at post-vaccination day (PVD) 30 and were monitored daily for untoward effects. Ten unvaccinated pregnant cows also were challenge inoculated with virulent RVFV and served as challenge controls. Vaccinated lactating dairy cows were monitored for viremia and virus shedding in the milk through PVD 14. Yearling steers were vaccinated to assess their immunologic response to various doses of vaccine and were challenge inoculated with virulent RVFV at PVD 28 to assess protection. RESULTS: 10 of 38 (26.3%) cows vaccinated during pregnancy developed transient postvaccination viremia titer > or = 2.5 log10 PFU/ml of serum. All vaccinated cows delivered live, healthy calves that were RVFV seronegative at birth, but which quickly acquired colostral antibodies. Vaccinated cows and their fetuses were protected when challenge exposed with virulent RVFV at PVD 30, whereas unvaccinated pregnant cows inoculated with RVFV became febrile and viremic, and aborted. Vaccine virus was unsuccessfully sought from milk of lactating dairy cows after vaccination, suggesting that shedding of vaccine virus through milk should not be a concern. Steers, inoculated with tenfold escalating vaccine doses, beginning with 1.0 log10 PFU, were protected against virulent RVFV challenge exposure. CONCLUSIONS: RVF MP-12 may be safe and efficacious for use in pregnant or lactating bovids, and a minimal dose of vaccine may provide suitable protection against viremia.

Animals↗
PubMed1997

Safety of a mutagen-attenuated Rift Valley fever virus vaccine in fetal and neonatal bovids.

OBJECTIVE: To examine effects of in utero inoculation with a mutagen-attenuated Rift Valley fever virus (RVFV) vaccine (RVF MP-12) on fetal bovids and to assess the safety and efficacy of calfhood vaccination with RVF MP-12. ANIMALS: 18 pregnant Hereford and Hereford-type cows in the third or fifth month of gestation, their progeny, and 25 calves from cows immunized with RVF MP-12 during pregnancy. PROCEDURE: Bovine fetuses were inoculated, via laparotomy, with 1 ml of RVF MP-12 containing 5 log10 plaque-forming units (PFU) of virus. Blood was obtained from newborn calves prior to their ingestion of colostrum. Immune-naive calves and calves born to RVF MP-12-vaccinated dams, ranging in age from 2 to 45 days, were vaccinated with RVF MP-12, and some were later challenge exposed with 1 ml of 5.7 log10 PFU of virulent RVFV strain ZH-501. Cows were monitored for viremia and antibody responses and for hematologic and serum biochemical alterations through parturition or abortion. RESULTS: Surviving in utero-vaccinated calves were healthy, with no noticeable defects. Except for 1 vaccine-inoculated fetus that died on postinoculation day 21, all in utero-vaccinated fetuses had serum neutralizing antibody titer > or = 1:20 at the time of delivery. All dams of in utero-vaccinated fetuses also developed neutralizing antibody titer. Calves born to cows vaccinated during gestation did not have antibody at birth, and all but 1 quickly acquired colostral antibody. Postparturient inoculation of immune-naive calves and calves with colostral antibodies resulted in no untoward effects, and all calves with detectable neutralizing antibodies were protected against virulent virus challenge exposure. CONCLUSIONS: Fetal death and abortion would be rare even if fetuses were exposed to RVF MP-12. The trauma and complications associated with in utero inoculation do not make this a practical method of immunization. RVF MP-12 was safe, immunogenic, and protective in calves as young as 2 days of age.

Abortion, Veterinary↗
PubMed1996

Isolation and characterization of Whitewater Arroyo virus, a novel North American arenavirus.

Rodents are principal hosts for each of the well-characterized arenaviruses. Prior to the present study, Tamiami (TAM) virus was the sole arenavirus known to be indigenous to North America; it has been isolated only from southern Florida where its primary host is the cotton rat Sigmodon hispidus. Recently, arenavirus antibody was found in Neotoma albigula woodrats collected from the southwestern United States. The purpose of the present study was to isolate and characterize the arenavirus associated with N. albigula. Three isolates of a novel arenavirus (proposed name "Whitewater Arroyo," WWA) were recovered from two arenavirus antibody-positive N. albigula collected from Whitewater Arroyo in McKinley County, New Mexico. Two-way serologic tests indicated that WWA virus is antigenically distinct from other arenaviruses but most closely related to TAM virus. Phylogenetic analysis of nucleocapsid protein gene sequence data showed that WWA virus is a novel arenavirus that is genetically most closely related to TAM virus. The recovery of WWA virus from antibody-positive N. albigula suggests that WWA virus infection in this species can be chronic and thus that N. albigula is a reservoir host of the virus.

Animals↗
PubMed1996

Sin Nombre virus mRNA synthesis.

Sin Nombre (SN) virus is the major etiologic agent of hantavirus pulmonary syndrome, a severe respiratory disease with high mortality. Like other hantaviruses, SN virus causes an inapparent chronic infection of the natural rodent reservoir and tends to grow slowly and produce little cytopathic effect even in highly susceptible Vero E6 tissue culture cells. An electrochemiluminescent quantitative PCR approach was developed to allow examination of SN virus RNA transcription in synchronously infected cells. Although virion particles contain equimolar ratios of the three negative-strand genome RNA segments (S, M, and L), rates and levels of accumulation of the corresponding N, GPC, and L viral mRNAs varied. The smallest mRNA (N) was detectable earliest and plateaued at the highest level, where as the largest mRNA (L) appeared latest and at the lowest plateau level. In addition, all three mRNAs were found to share a common 5' capped primer initiation mechanism, but appeared to have different mRNA termination mechanisms. The N mRNA 3' terminus mapped to position 1435 on the S segment, in close proximity to a CCC-rich suspected transcription termination motif. The GPC mRNA 3' terminus contained a poly(A) tall and mapped to a U8 transcription termination-polyadenylation motif reminiscent of those seen in other negative-strand RNA viruses. Finally, the L mRNA 3' terminus appeared identical to the L segment antigenome 3' terminus.

Animals↗
PubMed1996

The phylogeny of New World (Tacaribe complex) arenaviruses.

Several New World (Tacaribe complex) arenaviruses (Arenaviridae) are known to cause severe hemorrhagic disease in humans. Phylogenetic reconstruction of the Tacaribe complex arenaviruses previously has been limited by the relative scarcity of sequence data for arenavirus genomes. In the present study, oligonucleotide primers were designed based on conserved regions of the nucleocapsid (N) protein gene and then used to amplify, by reverse transcription--polymerase chain reaction, a 613-to 649-nucleotide region of the N gene of all known Tacaribe complex arenaviruses. This has allowed completion of the first detailed genetic characterization and phylogenetic analysis of all known members of the Tacaribe complex. These viruses formed three lineages. Lineage A contained Flexal, Parana, Pichinde, and Tamiami viruses; lineage B contained Amapari, Guanarito (GUA), Junin (JUN), Machupo (MAC), Sabia (SAB), and Tacaribe viruses. Latino and Oliveros viruses occupied lineage C. The highly pathogenic Tacaribe complex arenaviruses (GUA, JUN, MAC, SAB) were all members of lineage B, suggesting the possibility that the highly pathogenic phenotype is the result of evolutionary radiation from a common ancestor. The approach described here provides a rapid method for characterization of novel Tacaribe complex arenaviruses and may provide clues as to their potential public health importance.

Arenaviruses, New World↗
PubMed1996

The virion glycoproteins of Ebola viruses are encoded in two reading frames and are expressed through transcriptional editing.

In late 1994 and early 1995, Ebola (EBO) virus dramatically reemerged in Africa, causing human disease in the Ivory Coast and Zaire. Analysis of the entire glycoprotein genes of these viruses and those of other EBO virus subtypes has shown that the virion glycoprotein (130 kDa) is encoded in two reading frames, which are linked by transcriptional editing. This editing results in the addition of an extra nontemplated adenosine within a run of seven adenosines near the middle of the coding region. The primary gene product is a smaller (50-70 kDa), nonstructural, secreted glycoprotein, which is produced in large amounts and has an unknown function. Phylogenetic analysis indicates that EBO virus subtypes are genetically diverse and that the recent Ivory Coast isolate represents a new (fourth) subtype of EBO virus. In contrast, the EBO virus isolate from the 1995 outbreak in Kikwit, Zaire, is virtually identical to the virus that caused a similar epidemic in Yambuku, Zaire, almost 20 years earlier. This genetic stability may indicate that EBO viruses have coevolved with their natural reservoirs and do not change appreciably in the wild.

Animals↗
PubMed1996

Oliveros virus: a novel arenavirus from Argentina.

During the past few decades several newly recognized rodent-borne arenaviruses have been shown to be associated with severe hemorrhagic fever cases in South America. Changes in ecology and farming practices throughout the region have increased the concern over the potential public health threat posed by such emerging virus diseases. Oliveros (OLV) virus is a recently discovered arenavirus of the rodent Bolomys obscurus in Argentina. Genetic analysis of the small genomic RNA segment, which encodes the nucleocapsid protein and the envelope glycoproteins, shows that Oliveros is a novel, phylogenetically distinct member of the Arenaviridae family which differs in nucleotide sequence from the previously characterized members by approximately 35% or more. Despite this level of diversity, OLV virus possesses the same ambisense genome structure and many overall RNA and protein features in common with other arenaviruses. These data represent an important first step in the development of specific immunological and PCR diagnostic reagents to allow assessment of the prevalence and disease potential of this virus.

Animals↗
PubMed1996

Experimental infection of cynomolgus macaques with Ebola-Reston filoviruses from the 1989-1990 U.S. epizootic.

This study describes the pathogenesis of the Ebola-Reston (EBO-R) subtype of Ebola virus for experimentally infected cynomolgus monkeys. The disease course of EBO-R in macaques was very similar to human disease and to experimental diseases in macaques following EBO-Zaire and EBO-Sudan infections. Cynomolgus monkeys infected with EBO-R in this experiment developed anorexia, occasional nasal discharge, and splenomegaly, petechial facial hemorrhages and severe subcutaneous hemorrhages in venipuncture sites, similar to human Ebola fever. Five of the six EBO-R infected monkeys died, 8 to 14 days after inoculation. One survived and developed high titered neutralizing antibodies specific for EBO-R. The five acutely ill monkeys shed infectious virus in various bodily secretions. Further, abundant virus was visualized in alveolar interstitial cells and free in the alveoli suggesting the potential for generating infectious aerosols. Thus, taking precautions against aerosol exposures to filovirus infected primates, including humans, seems prudent. This experiment demonstrated that EBO-R was lethal for macaques and was capable of initiating and sustaining the monkey epizootic. Further investigation of this animal model should facilitate development of effective immunization, treatment, and control strategies for Ebola hemorrhagic fever.

Animals↗
PubMed1996

Passive immunization of Ebola virus-infected cynomolgus monkeys with immunoglobulin from hyperimmune horses.

A commercially available immunoglobulin G (IgG) from horses, hyperimmunized to Ebola virus, was evaluated for its ability to protect cynomolgus monkeys against disease following i.m. inoculation with 1 000 PFU Ebola virus (Zaire '95 strain). Six monkeys were treated immediately after infection by i.m. infection of 6.0 ml IgG; these animals developed passive ELISA titers of 1:160 to 1:320 to Ebola, two days afer inoculation. However, the beneficial effects of IgG treatment were limited to a delay in onset of viremia and clinical signs, in comparison with untreated controls. The six IgG recipients had no detectable viremia day 5, in contrast with three virus infected controls whose viremias exceeded 7.0 log10 PFU/ml that day. The controls died on days 6, 6, and 7, while two IgG recipients died day 7 and the remaining 4 died day 8, all with high viremias. These results document that passively acquired antibody can have a beneficial effect in reducing the viral burden in Ebola-infected primates; however, effective treatment of human patients may require antibodies with higher specific activities and more favorable pharmacokinetic properties than the presently available equine IgG.

Animals↗
PubMed1996

Patients infected with high-hazard viruses: scientific basis for infection control.

Most of the viral hemorrhagic fevers (VHFs) are caused by viruses that are handled in high containment laboratories in Europe and the United States because of their high pathogenicity and their aerosol infectivity. Special precautions should be taken when caring for patients infected with these viruses, but most hospitals can safely provide high-quality care. The major danger is parenteral inoculation of a staff member. Fomites and droplets must be considered as well. The role of small particle aerosols in inter-human transmission continues to be controversial. We believe that the aerosol infectivity observed for these viruses in the laboratory and the rare clinical situations that suggest aerosol spread dictate caution, but the many instances in which no transmission occurs provide a framework in which a measured approach is possible. The major challenge is in early recognition by an educated medical staff and rapid specific etiological diagnosis.

Aerosols↗
PubMed1996

Long-term duration of detectable neutralizing antibodies after administration of live-attenuated VEE vaccine and following booster vaccination with inactivated VEE vaccine.

The US Army successfully developed a live-attenuated Venezuelan Equine Encephalitis (VEE) vaccine, TC-83, in 1961, and subsequently developed a formalin-inactivated vaccine, C-84, in 1974. Initial evaluation of both vaccines was promising, but no long-term safety and immunogenicity data have been reported. This study is the first analysis of the long-term safety and immunogenicity of TC-83 and C-84. From January 1976 to December 1990, 821 laboratory workers at the USAMRIID were vaccinated with a single 0.5 ml subcutaneous (s.c.) dose of TC-83; 128 were boosted with a single 0.5 ml s.c. dose of C-84. Eighty-two per cent of vaccinees responded to TC-83 with an 80% plaque reduction neutralization titer (PRNT80) of > or = 1:20. Minor side-effects were noted in 23% of vaccinees. No long-term sequelae were recorded. Kaplan-Meier analysis showed a 60% probability of vaccinees maintaining a PRNT80 of > or = 1:20 for 5.5-8 years. C-84 was given to two groups: 76 initial nonresponders to TC-83, Group A, and 52 initial responders to TC-83 whose PRNT80 became < 1:20 over time, Group B. C-84 successfully boosted 76% of Group A and 100% of Group B to a PRNT80 > or = 1:20 Kaplan-Meier analysis showed 100% probability of Group B members maintaining a titer of > or = 1:20 for the duration of follow-up, which, in some cases, exceeded 10 years; while Group A had only a 60% probability of maintaining a titer for 1-2 years. Only minor local reactions to C-84 were noted in 6.3% of vaccinees. We conclude that, although TC-83 is reactogenic, when administered as the primary vaccine and C-84 is administered as a boost, these vaccines provide good long-term immunity and are safe in humans. However, a single dose vaccine that is more immunogenic and less reactogenic is needed.

Adolescent↗
PubMed1996

Hantavirus pulmonary syndrome in Florida: association with the newly identified Black Creek Canal virus.

Hantavirus pulmonary syndrome (HPS) is a recently recognized viral zoonosis. The first recognized cases were caused by a newly described hantavirus. Sin Nombre virus (previously known as Muerto Canyon virus), isolated from Peromyscus maniculatus (deer mouse). We describe a 33-year-old Floridian man who resided outside the ecologic range of P maniculatus but was found to have serologic evidence of a hantavirus infection during evaluation of azotemia associated with adult respiratory distress syndrome. Small mammal trapping conducted around this patient's residence demonstrated the presence of antihantaviral antibodies in 13% of Sigmodon hispidus [cotton rat). Serologic testing using antigen derived from the Black Creek Canal hantavirus subsequently isolated from this rodent established that this patient was acutely infected with this new pathogenic American hantavirus. HPS is not confined to the geographical distribution of P maniculatus and should be suspected in individuals with febrile respiratory syndromes, perhaps associated with azotemia, throughout the continental United States.

Acute Kidney Injury↗