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PubMed1997

In vitro and in vivo antichlamydial activities of HSR-903, a new fluoroquinolone antibiotic.

The in vitro and in vivo antichlamydial activities of HSR-903 were investigated. The MICs of HSR-903 for different species of chlamydia were 0.016 to 0.063 microg/ml, which were superior to those of conventional fluoroquinolones. The therapeutic effect of HSR-903 in experimental mouse Chlamydia psittaci pneumonia was also excellent and almost equal to that of minocycline and superior to that of ofloxacin. These results indicate that HSR-903 may be useful in the treatment of respiratory infections caused by chlamydiae.

Animals↗
PubMed1978

Loss of inorganic ions from host cells infected with Chlamydia psittaci.

Mouse fibroblasts (L cells) infected with the 6BC strain of Chlamydia psittaci released potassium ion (K(+)) into the extracellular milieu in a way that depended on size of inoculum and time after infection. When the multiplicity of infection was 500 to 1,000 50% infectious units (ID(50)) per L cell, loss of intracellular K(+) was first apparent 4 to 10 h after infection and was nearly complete at 6 to 20 h. Magnesium ion and inorganic phosphate (P(i)) were also released. Similar multiplicities of ultraviolet-inactivated C. psittaci also caused release of K(+). Leakage of inorganic ions probably resulted from immediate damage to the host-cell plasma membrane during ingestion of large numbers of chlamydiae. With multiplicities of 1 to 50 ID(50) per L cell, ingestion of C. psittaci was not by itself enough to cause release of K(+) and P(i) from infected L cells. There was a delay of 36 to 72 h between infection and massive leakage of intracellular ions during which time the chlamydiae multiplied extensively. Fifty ID(50) of ultraviolet-inactivated C. psittaci per L cell did not bring about significant leakage of K(+), even after 72 h. The mechanism whereby these multiplicities of infection destroy the ability of host cells to retain intracellular molecules is not known. HeLa 229 cells also released K(+) and P(i) after infection, but these losses occurred more slowly than in comparably infected L cells, possibly because C. psittaci did not multiply as extensively in HeLa cells as it did in L cells. The significance of the inability of chlamydiae-infected cells to regulate the flow of molecules through their plasma membranes is discussed.

Cell Membrane Permeability↗
PubMed1979

Stimulation of peroxidase by chlamydial infection: cytochemistry of guinea pig conjunctival epithelium.

Guinea pig inclusion conjunctivitis, a naturally occurring chlamydial disease of guinea pigs, resolves spontaneously after 3 to 4 weeks. The factors responsible for curbing the infection have not yet been specifically defined. Since Iwata (Invest. Ophthalmol. 15:297-301, 1976) reported cytochemical activity for peroxidase in the conjunctival epithelium of the normal rat, we undertook these studies to determine whether a similar activity exists in the guinea pig, and if so, whether it functions in the elimination of this Chlamydia psittaci infection. Tarsal conjunctivas of 14 normal guinea pigs, 34 infected ones, and 7 control guinea pigs (inoculated with yolk sac only) were excised and tested for peroxidase by the Graham and Karnovsky method (J. Histochem. Cytochem. 14:291-302, 1966). We found that peroxidase activity, virtually absent in normal animals, was intensely stimulated by the infection. This enzymatic activity appeared 2 days after inoculation of the conjunctiva with chlamydia and persisted for 6 to 7 weeks. The enzyme was localized in the rough endoplasmic reticulum and perinuclear cisternae of all layers of the conjunctival epithelium from the external surface to the basal lamina, including cells with no apparent inclusions as well as those heavily parasitized. Reaction in the Golgi complex was variable. No reaction, however, was ever evident in the chlamydial vacuoles or lysosomes, and the organisms continued to grow and multiply during peak enzymatic activity. We therefore concluded that the stimulated enzyme is apparently not directly responsible for the waning of the infection, but instead reflects an alteration of host metabolism that occurs as a consequence of the infection.

Animals↗
PubMed1979

Humoral immunity in the resolution of genital infection in female guinea pigs infected with the agent of guinea pig inclusion conjunctivitis.

Female guinea pigs infected in the genital tract with the chlamydial agent of guinea pig inclusion conjunctivitis were selectively immunosuppressed by varying regimens of cyclophosphamide (Cy) treatment. Temporary suppression of both humoral and cell-mediated immunity by daily treatment of Cy (25 mg/kg) for 13 days resulted in a prolonged infection, whereas daily treatment for the duration of the experiment totally prevented the development of humoral and cell-mediated responses and produced an intense and prolonged infection which did not resolve. When humoral immunity alone was suppressed by treatment with Cy (250 and 150 mg/kg) at 9-day intervals, the infection again did not resolve. Treatment with 100 mg of Cy per kg at 9-day intervals resulted in an extended infection which resolved concomitantly with the development of antibody to guinea pig inclusion conjunctivitis. These data indicate that humoral immunity is essential for the recovery of female guinea pigs from guinea pig inclusion conjunctivitis genital infection. A market weight loss was observed which could not be attributed to Cy treatment alone. Edematous and ulcerative changes of the external genitalia were also noted.

Animals↗
PubMed1979

Experimental chlamydial salpingitis in immunosuppressed guinea pigs infected in the genital tract with the agent of guinea pig inclusion conjunctivitis.

At necropsy indication of spread of infection to fallopian tubes was found in 25 of 41 (60%) female guinea pigs infected in the genital tract with the chlamydial agent of guinea pig inclusion conjunctivitis and immunosuppressed with cyclophosphamide. Eighteen were examined histologically, and the diagnosis of acute salpingitis was confirmed in 10, based on inflammatory reaction, detection of guinea pig inclusion conjunctivitis in tissue, and formation of cysts (pyosalpinx and hydrosalpinx). Infection of fallopian tube tissue was confirmed by indirect immunofluorescence and electron microscopy. Infection of endometrial tissue and peritoneum was also recognized. Data suggested that the immunosuppression mediated by cyclophosphamide resulted in a prolonged genital tract infection and concomitant ascending infection leading to salpingitis.

Animals↗
PubMed1980

Persistent infection of mouse fibroblasts (L cells) with Chlamydia psittaci: evidence for a cryptic chlamydial form.

When monolayers of mouse fibroblasts (L cells) were infected with enough Chlamydia psittaci (strain 6BC) to destroy most of the host cells, 1 in every 10(5) to 10(6) originally infected cells gave rise to a colony of L cells persistently infected with strain 6BC. In these populations, the density of L cells and 6BC fluctuated periodically and reciprocally as periods of host cell increase were followed by periods of parasite multiplication. Successive cycles of L-cell and 6BC reproduction were sustained indefinitely by periodic transfer to fresh medium. Isolation of L cells and 6BC from persistent infections provided no evidence that there had been any selection of variants better suited for coexistence. Persistently infected populations consisting mainly of inclusion-free L cells yielded only persistently infected clones, grew more slowly, and cloned less efficiently. They were also almost completely resistant to superinfection with high multiplicities of either 6BC or the lymphogranuloma venereum strain 440L of Chlamydia trachomatis. These properties of persistently infected L cells may be accounted for by assuming that all of the individuals in these populations are cryptically infected with 6BC and that cryptic infection slows the growth of the host cell and makes it immune to infection with exogenous chlamydiae. According to this hypothesis, the fluctuations in host and parasite density occur because some factor periodically sets off the conversion of cryptic chlamydial forms into reticulate bodies that multiply and differentiate into infectious elementary bodies in a conventional chlamydial developmental cycle.

Animals↗
PubMed1982

Modulation of the host immune response as a result of Chlamydia psittaci infection.

After intraperitoneal injection of mice with infectious, inactivated, or envelope preparations of the elementary body of Chlamydia psittaci, lymphocyte transformation of spleen cells to the mitogens concanavalin A, phytohemagglutinin, and lipopolysaccharide was significantly reduced 1 and 2 weeks postinjection. Lymphocyte response returned to the control values by 4 weeks. Similarly, transformation of cells by chlamydial antigen was not detected until 4 weeks postinjection. Injection of the noninfectious intracellular reticulate body, in contrast, had little effect on transformation of cells to concanavalin A. When control spleen cells were incubated with infectious or inactivated elementary bodies in vitro, response to all three mitogens was also reduced. The sooner the organisms were added after the addition of mitogen, the greater the reduction in transformation. Incubation with elementary body envelopes and reticulate bodies had no effect on lymphocyte transformation of the spleen cells to concanavalin A. The relationship between the observed ability to reduce the response in the in vitro assay of lymphocyte transformation and the actual in vivo establishment of infection is discussed.

Animals↗
PubMed1982

Cytotoxic cells induced after Chlamydia psittaci infection in mice.

The ability of spleen cells from Chlamydia psittaci-infected mice to lyse C. psittaci-infected and uninfected target cell monolayers was studied. The cytotoxicity assay used was a terminal label method in which the number of adherent target cells surviving the interaction with effector cells was determined by measuring the uptake of [3H]uridine by such cells. It was observed that in the first few days postinfection (3 to 5), spleens contained cells that lysed infected and uninfected targets with equal efficiency. Subsequently, infected targets were killed primarily. The activity of effector spleen cells for infected targets continued, although at a reduced level, beyond 21 days postinfection. Intact effector cells were required since a disruption by sonication resulted in a loss of cytotoxicity. The enhanced killing observed with infected targets was also observed when target cells were sensitized with heat- or UV-inactivated C. psittaci. This study suggests that the induction of cytotoxic cells after C. psittaci infection may contribute to the ability of the host to control multiplication of the microorganism.

Animals↗
PubMed1983

Isolation of Chlamydia psittaci from naturally infected African clawed frogs (Xenopus laevis).

An inclusion-forming agent was isolated from the livers of commercially raised African clawed frogs (Xenopus laevis) involved in an epizootic of high morbidity and mortality. Original isolation was made in McCoy cells. This agent was identified as Chlamydia psittaci based on the formation of typical intracytoplasmic inclusions which developed within 48 h, were not stained by iodine, and were resistant to sulfadiazine. The isolate from one particular frog (designated as strain 178) was further studied and found to be lethal for 7-day-old embryonated chicken eggs after intra-yolk sac inoculation. This strain was demonstrated not to be pathogenic for mice when inoculated intraperitoneally. The cell culture isolate of C. psittaci was transmitted to uninfected X. laevis, causing disease and death.

Animals↗
PubMed1983

In vitro and in vivo properties of chemically induced temperature-sensitive mutants of Chlamydia psittaci var. ovis: screening in a murine model.

Two temperature-sensitive (ts) strains, 1B and 1H, were obtained after nitrosoguanidine treatment of the wild-type virulent abortive ovine strain Chlamydia psittaci AB7. Optimum growth temperature on McCoy cells was 38 degrees C for the three strains, but at the restrictive temperature, 39.5 degrees C, ts strains differed from the parental strain in their total infective yield of chlamydiae, their efficiency of plating, and the morphology of the plaques and cytoplasmic inclusions. Their survival at 51 degrees C was also reduced compared with that of the wild field strains. The virulence of the two ts strains was attenuated for pregnant mice, but these two ts strains were able to multiply in mice and to induce a strong immunity to virulent challenge with either the parental AB7 strain or the caprine or bovine abortive field strains.

Animals↗
PubMed1985

Persistent infection of L cells with an ovine abortion strain of Chlamydia psittaci.

L cells inoculated at multiplicities of infection greater than or equal to 1 inclusion-forming unit of the abortigenic chlamydial strain B577 were destroyed within 10 to 15 days. Upon continued incubation in fresh medium, a few surviving cells repopulated the flasks, and the reemerging cultures remained persistently infected. The persistent state was characterized by cycles of repopulation with a low ratio of infected cells and cycles of extensive cytopathic changes in which greater than 90% of the cells had chlamydial inclusions and which could be delayed or even terminated by penicillin treatment. Immunofluorescence and superinfection during the period of repopulation revealed that the persistently infected cells could adsorb chlamydiae but their multiplication was arrested. This nonpermissive state could be terminated by the specific action of cycloheximide. L cells spontaneously cured from a persistent infection exhibited no change in susceptibility to chlamydiae when compared with normal L cells. However, chlamydiae derived from L cells after 7.5 months of persistence destroyed L-cell monolayers more rapidly and at lower multiplicities of infection than the wild type. This state of chlamydia-host cell interaction could not be established with the arthropathogenic strain LW613 because chlamydial infectivity was lost after the first cytolytic burst of infection in the cell cultures. The persistence described for the strain B577-L-cell system appears to differ from previously described models involving other chlamydial strains.

Abortion, Septic↗
PubMed1987

Effect of vaccination on feline Chlamydia psittaci infection.

Experimental ocular infection of specific-pathogen-free cats with the feline pneumonitis strain of Chlamydia psittaci produced an acute, severe conjunctivitis characterized by blepharospasm, conjunctival hyperemia, chemosis, and ocular discharge. Organisms were recovered from the conjunctiva for several weeks, and persistent genital and gastrointestinal infection also resulted from the ocular infection in some cats. Subcutaneous vaccination with live feline pneumonitis C. psittaci 4 weeks before ocular challenge significantly reduced the severity of the conjunctivitis. However, there was no effect on shedding of organisms from the eye or on the transmission of infection to the gastrointestinal and genital tracts. It is suggested that the acute stage of this ocular disease is caused largely by release of pathogenic antigen(s) from chlamydia-infected conjunctival cells, rather than by a direct cytopathic effect of chlamydial replication. Thus, vaccination with whole live organisms reduced the acute disease in experimentally infected cats but did not prevent shedding of the organism. The implications of these findings are discussed.

Animals↗
PubMed1988

In vivo-activated mononuclear phagocytes and protective immunity to chlamydiae in mice.

Peritoneal macrophages (M phi s) collected from Chlamydia psittaci 6BC-immune mice after intraperitoneal challenge with 10(6) 6BC (immune-boosted [IB] M phi s) were compared by various functional criteria with other in vivo- and in vitro-activated M phi populations. While casein-, protease peptone-, and thioglycolate (Thio)-elicited M phi s were equally susceptible to in vitro infection with 6BC, IB M phi s did not support chlamydial growth and M phi s from Mycobacterium tuberculosis BCG- or Listeria monocytogenes-sensitized mice exhibited intermediate susceptibility to infection. The resistance of IB M phi s was not due to the ingestion of fewer 6BC organisms, nor were these cells persistently infected, since chlamydiae could not be recovered from infected IB M phi s after in vitro infection, even after extended incubation times. In contrast, Thio M phi s stimulated in vitro with gamma interferon (IFN-gamma), with or without lipopolysaccharide, resulted in cells that exhibited chlamydiastatic activity which was lost shortly after IFN-gamma was removed from the culture medium. Conversely, the antichlamydial activity of IB M phi s was stable over time but not through the production of autostimulatory cytokines, as evidenced by the lack of stimulation of Thio M phi s to restrict 6BC replication in coculture experiments. IB M phi s exhibited enhanced oxidative activity, but anti-IFN-gamma antibody did not abrogate this response. IB M phi s were recovered only from immunized mice that survived an otherwise lethal 6BC intraperitoneal challenge. These cells appear to be important for development of protective immunity to chlamydiae, and evidence suggests that stimulation by cytokines other than IFN-gamma (with or without lipopolysaccharide) is required for the observed heightened in vivo activation.

Animals↗
PubMed1990

Protection of sheep against Chlamydia psittaci infection with a subcellular vaccine containing the major outer membrane protein.

An outer membrane (OM) preparation from elementary bodies (EBs) of Chlamydia psittaci (ovine abortion strain) was used to vaccinate pregnant ewes in a single subcutaneous dose and was found to achieve protection after subcutaneous challenge with infectious organisms. Inactivated purified EBs used as a single-dose vaccine also gave protection. The ratio of live to dead lambs was significantly higher in the vaccinated groups (16:1 and 15:1, respectively) than in the placebo group (8:9). Polyacrylamide gel electrophoresis and immunoblotting showed that a 40-kilodalton protein was the main protein constituent of the OM preparation, and this was positively identified as the major outer membrane protein by protein microsequencing. Electron microscopy revealed that fine particulate structures on the outermost surface of the EB were also present in the OM preparation. The findings suggest that the major outer membrane protein is an important immunoprotective determinant in ovine abortion vaccines.

Amino Acid Sequence↗
PubMed1994

Protein antigens of Chlamydia psittaci present in infected cells but not detected in the infectious elementary body.

Ocular infection of guinea pigs with the guinea pig inclusion conjunctivitis (GPIC) strain of Chlamydia psittaci produces a clinical condition representative of acute chlamydial conjunctivitis in humans. Guinea pigs which had recovered from two challenges with GPIC were used as a source of sera for the identification of antigens present in GPIC-infected tissue culture cells but absent in the infectious elementary body (EB). Immunoblots of lysates of infected HeLa cells probed with the convalescent-phase sera identified protein antigens of 22, 34, and 52 kDa (p22, p34, and p52, respectively) that were not detected in lysates of purified EB or in uninfected HeLa cells. Protein p22 was also not detected in lysates of purified reticulate bodies. Immunoblotting of lysates of HeLa cells infected with other chlamydiae demonstrated that the antigenicity of p22 and p34 was subspecies specific. Immunoblotting was also used to detect p22 and p34 in lysates of the conjunctivae of infected guinea pigs. Adsorption of convalescent-phase sera with GPIC EB produced a reagent with dominant reactivity toward p22, p34, and a 28-kDa EB protein. Immunofluorescent staining of GPIC-infected HeLa cells demonstrated that these adsorbed sera labeled the inclusion and inclusion membrane, with no apparent reactivity toward EB or reticulate bodies. Collectively, these data identify non-EB chlamydial components which may be released into the inclusion during intracellular growth.

Animals↗
PubMed1995

Deviation of immune response to Chlamydia psittaci outer membrane protein in lipopolysaccharide-hyporesponsive mice.

The outcome of infection is determined by both the quantity and the quality of an induced immune response. In particular, it has been demonstrated for selected pathogens that induction of TH1 or TH2 type helper T-cell subsets determines whether an immune response gives rise to protective immunity or disease-associated immunopathology. The nature of the antigen and the type of antigen-presenting cells recruited in the induction of a response are critical factors that influence the quality of the immune response. Of particular interest in this respect is the immune response to bacterial particles and the impact of cell wall-associated lipopolysaccharide (LPS) on that response. Nonspecific activation of macrophages and B lymphocytes by LPS could skew the phenotype of activated antigen-presenting cells and selectively alter the immunoglobulin isotypes and helper T-cell subsets that are induced following infection. In an initial attempt to detect immune deviation associated with LPS stimulation, we have compared the immunoglobulin isotypes of antibodies specific for the cysteine-rich outer membrane protein Omp2 induced in normal and LPS-hyporesponsive mice following immunization with Chlamydia psittaci strain guinea pig inclusion conjunctivitis whole elementary bodies. We report that there is a dramatic shift of Omp2-specific antibody from predominantly immunoglobulin G2a (IgG2a) isotype in LPS-hyporesponsive mice to high levels of IgG1 isotype in LPS-responder strains. The dependence of the IgG1 isotype shift on the LPS responder status is linked to the structure of the antigen and its natural processing pathway since LPS-hyporesponsive mice are not, in general, deficient in IgG1 antibody production. In particular, the antibody response to purified recombinant Omp2 is predominantly of the IgG1 isotype even in LPS-hyporesponsive mice.

Animals↗
PubMed1996

Pregnancy failure following vaginal infection of sheep with Chlamydia psittaci prior to breeding.

Enzootic abortion in sheep, caused by Chlamydia psittaci, has been associated with pregnancy failure in most sheep-producing countries. Late-term abortions or the birth of weak low-birth-weight lambs occurred following primary C. psittaci infection in pregnant ewes. However, the mode by which C. psittaci can be transmitted among sheep has not been established. The present study was designed to determine whether the vaginal tracts of nonpregnant ewes were susceptible to C. psittaci infection and whether such infections had an impact during the next pregnancy. At day 0 of the estrus cycle, the vaginal tracts of 10 nonpregnant ewes were inoculated with C. psittaci and 10 ewes were exposed by subcutaneous injection. The ewes were bred 6 weeks postinfection. Five ewes from the vaginally infected group and four from the subcutaneously infected group were reinfected by subcutaneous injection at day 60 of gestation. Pregnancy outcomes and antibody responses to infection were compared with that of ewes that were infected with C. psittaci, either subcutaneously or intravaginally, for the first time during pregnancy and with that of noninfected control ewes. Subcutaneous infection of nonpregnant ewes did not cause subsequent pregnancy failure; rather, this provided protection against abortion following reinfection during pregnancy. As expected, abortions or the birth of weak lambs was observed in those ewes that received primary C. psittaci infection by either route during pregnancy. Similarly, abortion or the birth of weak lambs was a consequence of vaginal inoculation prior to breeding, thereby confirming the susceptibility of the vaginal mucosa to infection and demonstrating the potential for venereal transmission.

Abortion, Veterinary↗
PubMed1996

Murine granulated metrial gland cells are susceptible to Chlamydia psittaci infection in vivo.

Granulated metrial gland (GMG) cells are the most numerous lymphoid cells in the uteroplacental unit in rodent pregnancy. In an experimental murine model of abortion-causing infection, we have studied the responses of GMG cells to Chlamydia psittaci. Chlamydial inclusions have been found within GMG cells, both in apparently healthy cells and in cells with degenerative changes. Establishing the existence of GMG cells infected by C. psittaci opens a new and interesting chapter in the study of these cells.

Animals↗