Trends in different contraception methods among women attending the Melbourne Sexual Health Centre from 2011 to 2020.

OBJECTIVES: The efficacy and availability of contraception have changed in the last several decades; however, unintended pregnancies continue to be an issue in Australia. This study aimed to describe trends in contraception in women attending a sexual health service over 9 years. STUDY DESIGN: Repeated cross-sectional study. METHODS: Women aged 16-49 years attending Melbourne Sexual Health Centre between 2011 and 2020 were included. Women were asked what methods of contraception they currently use. Contraception were categorised into long-acting reversible contraception (LARC; e.g. intrauterine devices and implants classified as highly effective), moderately effective contraception (e.g. oral contraception pill), less effective contraception (e.g. condom and withdrawal) and no contraception, as defined by US Centers for Disease Control and Prevention guidelines. Multivariable logistic regression was used to examine the factors associated with the use of moderate-high-efficacy contraception. RESULTS: A total of 38,288 women were included with a median age of 25 (interquartile range: 22-29). Between 2011 and 2020, there was a decreasing trend in condom (63.3%-56.1%; Ptrend <0.001) and oral contraception (27.2%-20.5%; Ptrend <0.001) use, whilst there was an increasing trend in the use of LARCs: implant (4.6%-6.0%; Ptrend = 0.002) and intrauterine device (2.8%-11.8%; Ptrend <0.001). Increasing age was associated with decreased odds of using moderate-high-efficacy contraception (Ptrend <0.001). Compared with Oceanian-born women, Asian (adjusted odds ratios [aOR] = 0.63, 95% confidence interval [CI]: 0.56-0.72) and Middle Eastern-born women (aOR = 0.60, 95% CI: 0.48-0.74) had lower odds of using moderate-high-efficacy contraception, whilst European (aOR = 1.23, 95% CI:1.07-1.41) and North American-born women (aOR = 1.51, 95% CI: 1.22-1.87) had higher odds of using moderate-high-efficacy contraception. CONCLUSIONS: Between 2011 and 2020, LARC use has increased, whilst less effective contraceptives, such as condom and oral contraception, have decreased among women at Melbourne Sexual Health Centre. Further research is required to understand age and ethnic disparities in contraception methods for future family planning programmes.

Feline immunodeficiency virus as a model for study of lentivirus infection of the central nervous system.

Feline immunodeficiency virus infects the CNS and results in predictable pathophysiology strikingly similar to that seen with HIV-1 infection of humans. The observed pathophysiology is mimicked in several physiologically assessed modalities, further supporting the validity of the feline model. Peripheral and control evoked potential findings and the occurrence of the sleep architecture changes in both cat and human disease provide an intriguing focus for further investigation. Although structurally diverse in an absolute sense, FIV and HIV-1 share basic structural features and commonalities of their life cycle. It is likely that by understanding the common mechanisms by which these lentiviruses influence CNS function, a more complete understanding of the neurological deficits seen in HIV-1 infected patients will be obtained. The cat model is particularly valuable for study of CNS disease, since it allows detailed analyses of events during the acute phase of infection, under circumstances in which the nature and timing of the infection are carefully controlled. The availability of molecular clones for mutational analysis will facilitate mapping of genomic regions critical to the perturbation of CNS function. It is suggested that development of intervention strategies in the cat model will yield treatment modalities directly applicable to HIV-1 infection of humans.

Methamphetamine and AIDS: 1HMRS studies in a feline model of human disease.

Potential interactions between psychostimulant drugs and infection with feline immunodeficiency virus (FIV) on brain metabolism were evaluated. Four groups of cats were studied: control, FIV positive, methamphetamine (MA) exposed, and FIV positive plus MA exposed. Frontal gray matter, frontal white matter, and caudate brain extracts were studied with proton magnetic resonance spectroscopy (1HMRS). In the frontal white matter, FIV-infected cats showed decreases in creatine and choline, while MA-treated cats had elevated gamma-aminobutyric acid (GABA). The decreased glutamate in FIV cats normalized with MA exposure. FIV and MA both affect brain metabolites individually and combined. 1HMRS is useful for evaluating the effects of FIV and drug abuse in the brain.

Failure of vaccine or virulent strains of canine parvovirus to induce immunosuppressive effects on the immune system of the dog.

It is generally believed that canine parvovirus (CPV) is immunosuppressive and that immunosuppression plays an important role in the pathogenesis of canine parvovirus disease. However, there is little experimental evidence to support this assertion. The effects of virulent and vaccine strains of CPV on natural effector (NE) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), chemiluminescence (CL) of neutrophils, lymphocyte response to mitogen, specific antibody response to CPV, and dermal reaction to phytohemagglutinin (PHA) were examined. Neither a virulent nor a vaccine strain of CPV significantly suppressed the immune system. The only potential effect noted was that dogs infected with the virulent strain of CPV developed a transient peripheral blood leukopenia. It was concluded that CPV does not cause immunosuppression and that immunosuppression does not play a significant role in the pathogenesis of canine parvovirus disease.

Intraventricular administration of a FIV-envelope protein induces sleep architecture changes in rats.

Fifteen adult male Sprague-Dawley rats were implanted with a set of electrodes for standard sleep recordings. A stainless steel cannula was also implanted into the lateral ventricle of these rats. Fifteen additional rats were implanted with a cannula alone. Rats with electrodes were habituated for 3 days or more to the recording environment, then placed into 3 groups (n = 5). One group received saline (i.c.v.), while the other two groups received either the feline immunodeficiency virus envelope glycoprotein (FIV SU-Env) or a fragment of the Epstein-Barr virus envelope glycoprotein (EB gp105). Rats were then recorded for electrographic sleep-wake cycle evaluation for the following 4 h. Core temperature was assessed through a thermistor probe inserted into the rectum, immediately before and 1, 2, 3 and 4 h after the i.c.v. treatment condition. Results demonstrated that compared to saline, FIV SU-Env increased wakefulness and decreased REM sleep throughout the 4 h of recording. Likewise, FIV SU-Env decreased SWS2 for 2 h. In addition, EB gp105 administration elicited minor modifications of the sleep-wake cycle, causing only a transient reduction of REM sleep in the first hour of recording. None of the treatments altered body temperature. These findings strongly support and extend studies in FIV-infected cats in which we have found similar sleep abnormalities. In addition, these results are consistent with the hypothesis that the FIV SU-Env proteins are responsible for these neurological disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)

Feline immunodeficiency virus envelope protein (FIVgp120) causes electrophysiological alterations in rats.

Close to 20% of the patients infected with the AIDS virus develops neurological deficit; eventhough HIV does not invade neurons. Consistently with the neurological deficit, HIV(+) subjects show abnormalities in brainstem auditory and visual evoked potentials (BSAEP and VEP) and in sleep patterns. The HIV-derived glycoprotein 120 has been postulated as a neurotoxic; therefore, it may be playing a crucial role in the generation of BSAEP and VEP, as well as in sleep disturbances. To study the role of the virus-derived proteins on the development of these electrophysiological signals' alterations, we have used the feline immunodeficiency virus (FIV)-derived gp120 and evaluated the changes in these electrophysiological signals. We employed 15 adult male Sprague-Dawley rats (250-350 g), chronically implanted for evoked potential and sleep recordings. Results showed that the i.c.v. administration of FIVgp120 (5 ng/10 microliter) produces changes in the latency of both cortical auditory evoked potentials (CAEPs) and VEPs and a decrease in both REM sleep and SWS. These data support the notion that FIVgp120 is neurotoxic to the central nervous system of cats and rats and that this protein suffices to cause electrophysiological alterations. In addition, it suggests that a similar effect may be occurring in humans as a result of HIVgp120's neurotoxic effects.

Partial characterization and tissue distribution of the feline mu opiate receptor.

Heroin abuse is a common route of acquiring HIV-1 infection. However, the effects of opiates on lentivirus disease progression are not well understood. Feline immunodeficiency virus is recognized as a good animal model for HIV-1, but characterization of the opiate receptor system in cats is lacking. Here we report the partial sequencing of the feline mu opiate receptor (MOR) and demonstrate a homology of 92 and 93% to the published human MOR sequences. Additionally, MOR transcripts were detected in the feline brain and tonsil but not in the spleen. Also, specific receptor ligand interactions were observed using microphysiometry.

Methamphetamine and HIV-1: potential interactions and the use of the FIV/cat model.

The interaction of methamphetamine with human immunodeficiency virus (HIV), the aetiologic agent of Acquired Immune Deficiency Syndrome (AIDS), has not been thoroughly investigated. However, increasingly, a larger proportion of HIV infected individuals acquire the virus through methamphetamine use or are exposed to this drug during their disease course. In certain populations, there is a convergence of methamphetamine use and HIV-1 infection; yet our understanding of the potential effects that simultaneous exposure to these two agents have on disease progression is extremely limited. Studying the interactions between methamphetamine and lentivirus in people is difficult. To thoroughly understand methamphetamine's effects on lentivirus disease progression, an animal model that is both clinically relevant and easily manipulated is essential. In this report, we identified potential problems with methamphetamine abuse in individuals with a concurrent HIV-1 infection, described the Feline Immunodeficiency Virus (FIV)/cat model for HIV-1, and reported our early findings using this modelling system to study the interaction of methamphetamine and lentivirus infections.

The effects of glucocorticosteroids on the chemiluminescence response of bovine phagocytic cells.

The effects of corticosteroids on the chemiluminescence response of bovine phagocytic cells were determined both in vitro and in vivo. The in vitro addition of hydrocortisone or dexamethasone had no significant effect on the chemiluminescence response of leukocytes in a whole blood or purified polymorphonuclear leukocyte (PMN) population. Cattle that received a single 20 mg dose of dexamethasone or three 20 mg doses of dexamethasone (given 24 hours apart) demonstrated the expected effects on the bovine leukogram (leukocytosis, neutrophilia, lymphopenia, eosinopenia, and monocytosis) and also demonstrated the expected suppressive effect on lymphocyte response to phytohemagglutinin (PHA). However, neither a single nor multiple dexamethasone treatment(s) had an effect on the chemiluminescence response of phagocytes in whole blood, but significantly enhanced the chemiluminescence response of the purified PMN leukocyte population. There was no significant difference between the two dexamethasone treatment groups in either the degree or duration of the effects observed in the chemiluminescence or lymphocyte response assays.

In vitro effects of prostaglandin E1, prostaglandin E2, indomethacin, histamine, and tuftsin on chemiluminescence response of bovine polymorphonuclear leukocytes.

The in vitro effects of prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), indomethacin, histamine, and tuftsin on the chemiluminescence response of bovine polymorphonuclear cells (PMN) were determined. Addition of PGE1, PGE2, indomethacin, and histamine in vitro significantly suppressed the chemiluminescence response of bovine PMN's, whereas tuftsin had no effect. Suppression was dependent upon the continued presence of PGE1, PGE2, and histamine in the culture media. However, indomethacin's suppressive effect remained even after it was removed from the culture media. Hydrogen peroxide generated chemiluminescence was suppressed by high concentrations of indomethacin and histamine. Results of this study suggest possible pharmacologic or regulatory mechanisms for certain of these immune modulators in the control of the oxidative burst reaction of bovine PMN's.

Effects of vaccines on the canine immune system.

The effects of several commercially available polyvalent canine vaccines on the immune system of the dog were examined. The results demonstrated that the polyvalent vaccines used in this study significantly suppressed the absolute lymphocyte count and that most of the polyvalent vaccines significantly suppressed lymphocyte response to mitogen, but had no effect on natural effector cell activity, neutrophil chemiluminescence, nor antibody response to canine distemper virus. The individual vaccine components from the polyvalent vaccines when inoculated alone did not significantly suppress the lymphocyte response to mitogen. However, when canine distemper virus was combined with canine adenovirus type 1 or canine adenovirus type 2, significant suppression in lymphocyte responsiveness to mitogen occurred. The results indicate that interactions between canine distemper virus and canine adenovirus type 1 or canine adenovirus type 2 are responsible for the polyvalent vaccine induced suppression of lymphocyte responsiveness.

Effects of feline immunodeficiency virus on astrocyte glutamate uptake: implications for lentivirus-induced central nervous system diseases.

Feline immunodeficiency virus (FIV) is a lentivirus of domestic cats that causes a spectrum of diseases remarkably similar to AIDS in HIV-infected humans. As part of this spectrum, both HIV-1 and FIV induce neurologic disorders. Because astrocytes are essential in maintaining the homeostasis of the central nervous system, we analyzed FIV for the ability to infect feline astrocytes. Through immunocytochemistry and reverse transcriptase activity, it was demonstrated that two molecular clones of FIV (FIV-34TF10 and FIV-PPR) produce a chronic low level productive infection of feline astrocyte cultures. To investigate the consequences of this infection, selected astrocyte functions were examined. Infection with FIV-34TF10 significantly decreased the ability of astrocytes to scavenge extracellular glutamate (with a peak inhibition of 74%). The effects of the infection did not appear to be a result of toxicity but rather were more selective in nature because the glucose uptake function of the infected astrocyte cultures was not altered. Our data demonstrate that FIV productively infected, at a low level, feline astrocyte cultures, and as a consequence of this infection, an important astroglial function was altered. These findings suggest that a chronic low grade infection of astrocytes may impair the ability of these cells to maintain homeostasis of the central nervous system that, in turn, may contribute to a neurodegenerative disease process that is often associated with lentivirus infections.

Conversion of poorly immunogenic malaria repeat sequences into a highly immunogenic vaccine candidate.

The recent success of a Plasmodium falciparum malaria vaccine consisting of circumsporozoite protein (CSP) T and B cell epitopes has rekindled interest in the development of a pre-erythrocytic vaccine. In order to optimize immunogenicity, well-characterized CSP-specific neutralizing B cell epitopes and a universal T cell epitope were combined with an efficient and flexible particulate carrier platform, the hepatitis B core antigen (HBcAg), to produce a novel pre-erythrocytic vaccine candidate. The vaccine candidate, V12.PF3.1, is a potent immunogen in mice eliciting unprecedented levels (greater than 10(6) titers) of sporozoite-binding antibodies after only two doses. The anti-sporozoite antibodies are long lasting, represent all IgG isotypes, and antibody production is not genetically restricted. CSP-specific CD4+ T cells are also primed by V12.PF3.1 immunization in a majority of murine strains. Furthermore, the hybrid HBcAg-CS particles can be produced inexpensively in bacterial expression systems. These and other characteristics suggest that V12.PF3.1 represents an efficient and economical P. falciparum vaccine candidate for use separately or in combination with other formulations.

Borna disease virus persistence causes inhibition of glutamate uptake by feline primary cortical astrocytes.

Borna disease virus (BDV), a nonsegmented, negative-stranded (NNS) RNA virus, causes central nervous system (CNS) disease in a broad range of vertebrate species, including felines. Both viral and host factors contribute to very diverse clinical and pathological manifestations associated with BDV infection. BDV persistence in the CNS can cause neurobehavioral and neurodevelopmental abnormalities in the absence of encephalitis. These BDV-induced CNS disturbances are associated with altered cytokine and neurotrophin expression, as well as cell damage that is very restricted to specific brain regions and neuronal subpopulations. BDV also targets astrocytes, resulting in the development of prominent astrocytosis. Astrocytes play essential roles in maintaining CNS homeostasis, and disruption of their normal activities can contribute to altered brain function. Therefore, we have examined the effect of BDV infection on the astrocyte's physiology. We present here evidence that BDV can establish a nonlytic chronic infection in primary cortical feline astrocytes that is associated with a severe impairment in the astrocytes' ability to uptake glutamate. In contrast, the astrocytes' ability to uptake glucose, as well as their protein synthesis, viability, and rate of proliferation, was not affected by BDV infection. These findings suggest that, in vivo, BDV could also affect an important astrocyte function required to prevent neuronal excitotoxicity. This, in turn, might contribute to the neuropathogenesis of BDV.

Rapid phenotypic reversion of zidovudine-resistant feline immunodeficiency virus without loss of drug-resistant reverse transcriptase.

We have selected and plaque purified zidovudine (3'-azido-3'-deoxythymidine [AZT])-resistant mutants from an infectious molecular clone of feline immunodeficiency virus (FIV). The patterns of cross-resistance and drug susceptibilities of these mutants were similar to those of the AZT-resistant FIV that we previously selected in vitro from a wild-type FIV population and to those of the most common AZT-resistant clinical isolates of human immunodeficiency virus type 1. Two AZT-resistant mutants of FIV, one selected from a normal population and one selected from the molecular clone, each reverted rapidly to an AZT-sensitive phenotype when passaged in the absence of drug. Sequence analysis of the reverse transcriptase (RT)-encoding region from the plaque-purified AZT-resistant FIV revealed a single base change at position 2939, resulting in a Glu-to-Lys substitution at amino acid 202 of the RT. Similar analyses of plaque-purified revertants showed that the phenotypic reversion was not the result of a genotypic reversion at this position and that no additional mutations existed within the RT-encoding region of the revertants. Moreover, RTs purified from the mutant and revertant were both resistant to the 5'-triphosphate of AZT. These results indicate the complexity of AZT resistance and suggest the presence of additional factors, outside the RT-encoding region, which may contribute to AZT resistance.

Replication rate of feline immunodeficiency virus in astrocytes is envelope dependent: implications for glutamate uptake.

Feline immunodeficiency virus (FIV) induces neurological abnormalities in domestic cats. Previously, we demonstrated that two disparate strains of FIV (FIV-34TF10 and FIV-PPR) varied greatly in the ability to replicate in feline cortical astrocytes. To investigate the impact of the env region on the replication efficiency of these strains, we constructed two env chimera viruses, FIV-34TF10-PPRenv and FIV-PPR-34TF10env, to infect feline cortical astrocytes in vitro. Although all of these viruses infected cortical astrocytes, the efficiency of replication depended on strain, and the env region played an essential role. The viruses containing the env of 34TF10, FIV-34TF10, and FIV-PPR-34TF10env had the greatest replication rate, whereas the viruses containing the env of PPR replicated at a lower level. Other viral regions had modulatory effects on the replication rate, with the FIV-PPR genome providing a slight replication advantage over the FIV-34TF10 genome. We also monitored the effects of these viruses on an important astrocyte function, glutamate uptake; all viruses significantly decreased this activity, but only the viruses containing the env of PPR significantly impaired glutamate uptake without altering the culture viability. These results may be particularly relevant in the context of lentivirus-induced central nervous system disease in which a selective breakdown of astroglial function may contribute to neurodegeneration.

Epidemiologic and immunologic evaluation of an outbreak of canine blastomycosis.

Five confirmed cases of canine blastomycosis occurred over the 10-month period of December 1983 to September 1984 in a south-eastern Wisconsin colony of 30 dogs maintained for sled competition. Contrary to other published reports of canine blastomycosis, the sex-specific attack rates were higher among females than males. Four of the five confirmed cases and all four deaths occurred among young female dogs. Differences in the age distribution and/or the micro-environment of the females may have contributed at least in part to the difference in sex-specific attack rates. The serologic response and leukocyte function of the clinically affected and apparently healthy dogs from this colony were assessed during the outbreak. A survey of the adult dogs in the colony suggested that the mitogen-induced lymphocyte blastogenesis of dogs with clinical signs of blastomycosis was suppressed compared with that of dogs that remained free of clinical signs. In contrast to previous reports that autologous sera from dogs and humans with clinical blastomycosis inhibited mitogen-induced lymphocyte blastogenesis, lymphocyte responsiveness was similar to, or greater in the presence of autologous canine serum than it was in the presence of fetal bovine serum.