Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Laboratory Infection”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Accidental laboratory infection with Treponema pallidum, Nichols strain.

This case report describes a laboratory-acquired infection with Treponema pallidum, Nichols strain. The specific details of the accidental exposure are presented, along with a description of the clinical observations. This infection indicates that the rabbit adapted Nichols strain of T pallidum retains its capability to infect humans. In addition, aerosols of concentrated preparations of these organisms, generated within the laboratory, represent a definite biohazard.

Aerosols↗

Population dynamics of Plasmodium falciparum sporogony in laboratory-infected Anopheles gambiae.

The population dynamics of cultured Plasmodium falciparum parasites was examined during their sporogonic development in Anopheles gambiae mosquitoes. Estimates of absolute densities were determined for each life stage, and life tables were constructed for each of 38 experimental infections. Macrogametocyte and ookinete mortalities contributed equally to the overall mortality. On average, there was a 40-fold decrease in parasite numbers in the transition from the macrogametocyte to the ookinete stage, a 69-fold decrease in the transition from ookinete to oocyst stages, and a total net decrease in parasite numbers from macrogametocyte to oocyst stage of 2,754-fold (i.e., multiplicative). There was no relationship between macrogametocyte and ookinete densities due to the inherent variability in fertility among different gametocyte cultures. There was a curvilinear relationship (r2 = 0.66) between ookinete and oocyst densities. Above a threshold of about 30 ookinetes/mosquito, the oocyst yield per ookinete became increasingly greater with increasing ookinete density. There was a linear relationship (r2 = 0.73) between oocyst and sporozoite densities, with an average of 663 salivary gland sporozoites produced per oocyst. Sporozoite production per oocyst was not affected by oocyst density and virtually all oocyst infections resulted in sporozoite infections of the salivery glands. This quantitative study indicates that the sporogony of cultured P. falciparum in laboratory-infected A. gambiae is an inefficient process and that the ookinete is the key transitional stage affecting the probability of vector infectivity.

Animals↗

Rubella and cytomegalovirus (CMV) infections: laboratory aspects of investigation of antenatal, congenital, persistent, and subclinical infections.

Rubella specific IgM tests carried out on pregnant women with history of rubella contact or rubella-like rash indicated the presence of rubella-IgM by the second week after contact, persistence to 3-4 weeks followed by a decline and non-detectability around 8-9 weeks and at delivery. Laboratory investigation of cases of rubella infection in infants and children, including clinically proven and suspected congenital rubella revealed distinct patterns of combinations of positivity and negativity of IgM and IgG antibodies. Three cases of persistence of rubella specific IgM antibodies with one even up to 3 years in congenital rubella and a case of CMV-IgM persistence in congenital CMV are described. Rubella-IgM and CMV-IgM were detected in the serum of two patients aged 12 years and 24 years with CMV mononucleosis. Utilization of rubella-IgM/CMV-IgM tests enabled the identification of four cases of subclinical rubella and one of subclinical CMV in a pediatric population.

Adolescent↗

Increased sensitivity to CD4 binding site-directed neutralization following in vitro propagation on primary lymphocytes of a neutralization-resistant human immunodeficiency virus IIIB strain isolated from an accidentally infected laboratory worker.

We previously described the adaptation of the neutralization-sensitive human immunodeficiency virus type 1 (HIV-1) strain IIIB to a neutralization-resistant phenotype in an accidentally infected laboratory worker. During long-term propagation of this resistant isolate, designated FF3346, on primary peripheral blood leukocytes in vitro, an HIV-1 variant appeared that had regained sensitivity to neutralization by soluble CD4 (sCD4) and the broadly neutralizing monoclonal antibody b12. When an early passage of FF3346 was subjected to limiting-dilution culture in peripheral blood mononuclear cells, eight virus variants with various degrees of neutralization resistance were isolated. Two of them, the sCD4 neutralization-resistant variant LW_H8(res) and the sCD4 neutralization-sensitive variant LW_G9(sens), were selected for further study. Interestingly, these two viruses were equally resistant to neutralization by agents that recognize domains other than the CD4 binding site. Site-directed mutagenesis revealed that the increased neutralization sensitivity of variant LW_G9(sens) resulted from only two changes, an Asn-to-Ser substitution at position 164 in the V2 loop and an Ala-to-Glu substitution at position 370 in the C3 domain of gp120. In agreement with this notion, the affinity of b12 for monomeric gp120 containing the N164S and A370E substitutions in the background of the molecular clone LW_H8(res) was higher than its affinity for the parental gp120. Surprisingly, no correlation was observed between CD4 binding affinity for monomeric gp120 and the level of neutralization resistance, suggesting that differences in sCD4 neutralization sensitivity between these viruses are only manifested in the context of the tertiary or quaternary structure of gp120 on the viral surface. The results obtained here indicate that the neutralization-sensitive strain IIIB can become neutralization resistant in vivo under selective pressure by neutralizing antibodies but that this resistance may be easily reversed in the absence of immunological pressure.

Acquired Immunodeficiency Syndrome↗

Modeling survival of experimentally virus-infected laboratory animals--exploration of the survival diagram.

In a recent paper (Sühnel & Veckenstedt, 1989, J. theor. Biol. 137, 27) we have proposed a new method of plotting survival data from experimentally virus-infected laboratory animals; the survival diagram. In this diagram two experiments, for which the mean number of virions inoculated is kept fixed but other parameters may vary, are compared. The variations in two basic quantities of survival analysis are simultaneously displayed: the standard mean survival time and the relative mean challenge virus dose, which is via a dose-response relation interrelated with the fraction of animals dying. It is analyzed in which manner variations in the kinetic parameters and the critical virus level necessary to produce a particular effect influence the location of the points of comparison in the survival diagram. The analysis presented is a prerequisite for further applications of this diagram and of the underlying mathematical model.

Animals↗

Immunoglobulins on the surfaces of tetrathyridia of Mesocestoides corti Hoeppli 1925 (Cestoda), from laboratory infections of ICR mice.

7Sgamma2b antibody was detected, by fluorescein labeled antibodies, on the body surfaces and wall of excretory bladder of tetrathyridia of M. corti removed from the peritoneums of 5--24-week laboratory infections of ICR/TIMCO mice. 7Sgamma1, 7Sgamma2a, 7Sgamma3, IgM, IgA, and C3 were not found by use of the same techniques. Tetrathyridia maintained in culture medium to which pooled normal mouse, infected mouse, and horse (control) serums containing all known classes and subclasses of immunoglobulins had been added showed only mouse 7Sgamma2b on their surfaces and wall of the excretory bladder, and then only when incubated in pooled serum from infected mice. No other mouse immunoglobulin classes or subclasses were found attached to the worms, nor was any reaction obtained from tetrathyridia incubated in culture medium alone, normal mouse serum, or horse serum. This suggests a highly selective nonspecific absorption of 7Sgamma2b, or more likely demonstrates the specificity of the antibody for the parasite surfaces and wall of the excretory bladder. The possibility that 7Sgamma2b may be acting in an enhanceing mode is discussed.

Animals↗

Temporal analysis of the antibody response to HIV envelope protein in HIV-infected laboratory workers.

Three laboratory workers have been infected with the IIIB strain of HIV; their antibody response to HIV has been studied in serial serum specimens. Because the infecting virus is known, the fine specificity of the antibody response was studied on the homologous strain of HIV. Anti-p17, anti-p24, anti-gp160, CD4/gp120 blocking and neutralizing antibodies developed in parallel. Epitope mapping of the anti-gp160 response indicated several regions that consistently induced an antibody response. Serum contained antibody which reacted with V3-specific peptides corresponding to the very tip of the loop and crossreactivity was seen with V3 loop peptides from other sequence divergent strains of HIV. Antibody to the V1 loop was produced at levels comparable with that seen for the V3-loop. Anti-V1 neutralized HIV with a titration curve equivalent to an anti-V3 monoclonal antibody. Because the infecting virus is known and serial reisolates have been obtained, we explored the relationship between production of antibody to a given epitope and mutation in the virus. The data suggest that an association exists, but do not clearly indicate that antibody drives the selection for mutant viruses. The findings presented here provide a fine specificity analysis of the evolution of the antibody response to HIV in greater detail than has previously been performed.

Amino Acid Sequence↗

Treatment with Ivermectin in drinking water against Myobia musculi and Myocoptes musculinus mange in naturally infected laboratory mice.

Ivomec in drinking water at dilutions of 1 ml/l (10 micrograms of Ivermectin/ml), 2.5 ml/l (25 micrograms of Ivermectin/ml) and 5 ml/l (50 micrograms of Ivermectin/ml) was successful against Myobia musculi and Myocoptes musculinus mange in naturally infected laboratory mice after 4 consecutive treatment days. One day before treatment drinking water was withheld. Ivermectin solutions were administered ad libitum.

Animals↗

Observations on natural and laboratory infection of rodents with the etiologic agent of Korean hemorrhagic fever.

Studies were conducted to define the natural host range of the Korean hemorrhagic fever (KHF) agent in South Korea, and to identify colonized rodents susceptible to this infection. Eight species of field rodents were captured in areas of Korea endemic for KHF and their tissues were examined by immunofluorescence for the presence of KHF antigen. One hundred and fourteen of 817 Apodemus agrarius coreae captured between 1974 and 1978 had one or more positive organs. No positive organ was found in 239 rodents of the other seven species examined. Two hundred and thirty-eight specimens of Apodemus agrarius jejuensis captured on Jeju Island, an area thought to be free of disease, were also negative. Attempted laboratory infection of nine species of rodents captured in the field but maintained in the laboratory was successful only in the two subspecies of Apodemus. The 46 specimens of A. a. jejunesis tested in this manner were all uniformly susceptible to infection as determined by immunofluorescence. Serial sacrifice of experimentally infected A. a. jejuensis revealed viremia of short duration terminating on day 10 postinfection. In contrast, other tissues of this animal, including lung, kidney, liver and parotid gland were positive on day 10 and remained so through the 100-day observation period. When 12 species of colonized laboratory rodents were inoculated with KHF agent five were found to develop KHF antibody by indirect immunofluorescence and two, Calomys callosus and Apodemus agrarious ningpoensis, developed detectable KHF antigen in their tissues.

Animals↗

Loss of a neutralizing epitope by a spontaneous point mutation in the V3 loop of HIV-1 isolated from an infected laboratory worker.

The third hypervariable region, or V3 loop, represents the principal neutralizing domain of the gp120 envelope glycoprotein of human immunodeficiency virus type 1 (HIV-1). Sequential viral isolates from a laboratory worker (LW) accidentally infected with HIV-1IIIB in 1985 were analyzed using type-specific neutralizing monoclonal antibodies directed to the V3 loop. A single amino acid substitution, Ala-->Thr at position 21 in the V3 loop of HIV-1LW isolated in 1987, was shown to determine the loss of the neutralizing epitope recognized by one of the monoclonal antibodies (M77). However, this antibody efficiently recognized linear V3 loop peptides containing either the Ala or Thr residue at position 21, indicating that a local change in conformation was responsible for the epitope loss in the native gp120. Molecular modeling studies, experimentally supported by different amino acid replacements at position 21, indicated that the Ala-->Thr substitution leads to a drastic change in the domain of the V3 loop, which contains the complementary surface for antibody binding. These results provide evidence for the first time that a conformation-dependent epitope within the V3 loop of HIV-1 is involved in the generation of neutralization escape mutants in vivo.

Acquired Immunodeficiency Syndrome↗