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Biomedical subjects

A D Heggie

Publications and source records attributed to A D Heggie.

At least 19 recordsLinked to original sources
PubMed1992

Prevalence and characteristics of pharyngeal group A beta-hemolytic streptococci in US Navy recruits receiving benzathine penicillin prophylaxis.

US military recruits receive benzathine penicillin prophylaxis because of endemicity of group A beta-hemolytic streptococcal (GABHS) infections. GABHS prevalence in Navy recruits receiving single-dose benzathine penicillin prophylaxis was assessed during spring and fall 1989 by culturing throat specimens from randomly selected groups of approximately 230 men before and 2, 4, and 7 weeks after prophylaxis and from men with pharyngitis diagnosed at sick call. Of 60 GABHS isolates, 75% were serotype M-3. The pharyngitis rate increased from 0.18% in the spring to 1.55% in the fall with a concurrent increase in serotype M-3 prevalence from 35% to 91%. The GABHS prevalence rate was three- to fourfold lower after prophylaxis. There were no cases of acute rheumatic fever (ARF) despite predominance of M-3, a rheumatogenic serotype. It was concluded that penicillin prophylaxis continues to be effective for control of GABHS infections and prevention of ARF in Navy recruits.

Drug Hypersensitivity↗
PubMed1990

Induction of cervical neoplasia in the mouse by an extract of cells infected by varicella-zoster virus.

Since several human herpesviruses, including varicella-zoster virus (VZV), have been demonstrated to transform mammalian cells in vitro, VZV was tested in a mouse model of virus-induced cervical neoplasia to determine whether it is oncogenic in vivo. Herpes simplex viruses types 1 and 2 and cytomegalovirus have been previously shown to induce cervical neoplasia in this mouse model. VZV was propagated in WI-38 cell cultures and inactivated by ultraviolet irradiation. Control material was prepared in an identical manner from uninfected cell cultures. Cotton tampons, saturated with inactivated virus or control material, were inserted into the vaginas of C57BL mice three times a week for 60 weeks. Cervical dysplasia was detected in 40% and invasive carcinoma in 34% of virus-exposed mice by histological examination. No lesions were detected in control animals. These observations indicate that VZV, or some product of virus-infected cells, is oncogenic in vivo for the mouse cervix.

Animals↗
PubMed1990

Incidence and etiology of conjunctivitis in Navy recruits.

Recruit sick call at the Naval Training Center, Great Lakes, Illinois was monitored for cases of conjunctivitis during two 2-week periods in March in 1981 and 1982. Twenty-three cases were detected. The incidence of conjunctivitis was 1.1 cases per 1000 recruits per week. Peak incidence occurred during the third and fourth weeks of training and two recruit companies had multiple cases. Conjunctival cultures for viruses and Chlamydia trachomatis were negative in all cases. Concurrent cultures of conjunctival exudate were obtained from 12 cases. Haemophilus influenzae was isolated from three of these cases and Streptococcus pneumoniae from one. Despite the high percentage of negative cultures, the clinical characteristics and pattern of occurrence of conjunctivitis in Navy recruits suggest that it is caused by an infectious agent or agents.

Adolescent↗
PubMed1989

Induction of cervical neoplasia in the mouse by herpes simplex virus type 2 DNA.

Induction of cervical neoplasia in the mouse cervix by herpes simplex virus types 1 (HSV-1) and 2 (HSV-2) has been reported. The present study was done to determine if transfection with DNA of HSV-2 can induce carcinogenesis in this animal model. Genomic HSV-2 DNA was isolated from infected HEp-2 cells and separated from host cell DNA by cesium chloride density gradient centrifugation. The DNA was applied to mouse cervix for periods of 80-100 weeks. Experimental controls were treated with uninfected genomic HEp-2 cell DNA or with calf thymus DNA. Vaginal cytological preparations from all animals were examined monthly to detect epithelial abnormalities. Animals were sacrificed and histopathology studies were done when cellular changes indicative of premalignant or malignant lesions were seen on vaginal smears. Cytologic and histologic materials were coded and evaluated without knowledge of whether they were from animals treated with virus or control DNA. Premalignant and malignant cervical lesions similar to those that occur in women were detected in 61% of the histologic specimens obtained from animals exposed to HSV-2 DNA. The yield of invasive cancers was 21% in animals treated with HSV-2 DNA. No cancers were detected in mice treated with either HEp-2 or calf thymus DNA. Dysplasia was detected in only one of these control animals.

Animals↗
PubMed1988

Resistance of mouse nasopharynx to induction of neoplasia by herpes simplex virus.

In previous studies, carcinoma of the uterine cervix of the mouse was induced by repeated vaginal exposure to inactivated herpes simplex viruses, type 1 or 2. To determine if the mouse nasopharynx is also susceptible to the carcinogenic effects of these viruses, animals were inoculated intranasally with suspensions of formaldehyde-inactivated herpes simplex viruses, type 1 or 2, or control material, four to five times a week. After exposure periods of 12, 20, and 32 weeks, groups of animals were killed randomly and the nasopharynx, along with the larynx, trachea, bronchi, and lungs, were examined histologically. No preinvasive or invasive lesions were detected. These data suggest that the nasopharynx and cervix of the mouse differ in susceptibility to induction of carcinogenesis by inactivated herpes simplex viruses.

Animals↗
PubMed1986

Cell-mediated immune responses to Chlamydia trachomatis in mothers and infants.

Cell-mediated immunity to Chlamydia trachomatis was studied in pregnant women with chlamydial infection of the cervix, in infants born vaginally to these women, and in infants presenting with chlamydial conjunctivitis. Uninfected pregnant women and their infants were studied as controls. McCoy cell cultures were used to isolate C. trachomatis from clinical specimens. Cell-mediated immunity was measured by lymphocyte proliferative responses in vitro to stimulation by chlamydial antigens. Chlamydial IgG antibody in serum specimens was detected by a microenzyme-linked immunosorbent assay technique. The mean lymphocyte proliferative responses to chlamydial antigens were greater in infected women than in uninfected women both during pregnancy and in the postpartum period. Lymphocyte responsiveness in infected pregnant women, however, was less than in postpartum women. Despite failure to detect chlamydial infection in exposed infants, lymphocyte proliferative responses were greater in umbilical cord blood and later in peripheral blood samples from neonates born to infected mothers than in infants born to uninfected mothers. These responses were also greater in infants with chlamydial conjunctivitis than in infants of uninfected mothers. These data suggest that cellular immune responses to chlamydial antigens are increased in infected mothers and infants and that infants may acquire chlamydial cell-mediated immunity transplacentally.

Antibodies, Viral↗
PubMed1986

Roles of cytomegalovirus and Chlamydia trachomatis in the induction of cervical neoplasia in the mouse.

Cytomegalovirus and Chlamydia trachomatis are prevalent sexually transmissible pathogens. They produce persistent infections of the cervix and have been associated with cervical neoplasia. Cytomegalovirus has also been shown to induce transformation of cells in culture. Because of the high prevalence of genital infections with these pathogens and evidence that they may have oncogenic effects on the cervix, cytomegalovirus (strain AD-169) and C. trachomatis (serovar LGV-2) were tested for oncogenicity in a mouse model in which induction of cervical neoplasia by repeated exposure to inactivated herpes simplex viruses has been demonstrated previously. Cotton tampons, saturated with UV-inactivated cytomegalovirus, C. trachomatis, or corresponding control fluids, were inserted into the vaginas of virgin C57 mice 3 times a week. Smears of vaginal aspirates for cytological examination were obtained every 5 weeks. After 75-90 weeks of exposure, the mice were sacrificed and serial sections of their reproductive tracts were examined. Cervical dysplasia was detected by histological examination in 51% and cervical carcinoma in 10% of mice exposed to cytomegalovirus. In control mice, in contrast, dysplasia developed in 3% and carcinoma in none. The progression from normal cervical epithelium to dysplasia to carcinoma observed with cytomegalovirus exposure was similar to that observed previously in this model after exposure of mice to herpes simplex virus types 1 and 2. The frequencies of cervical abnormalities in mice exposed to C. trachomatis or corresponding control fluid were low, and differences between the two groups were not statistically significant. These data indicate that strain AD-169 of cytomegalovirus is oncogenic for the mouse cervix and suggest that the LGV-2 serovar of C. trachomatis is not.

Animals↗
PubMed1985

Topical sulfacetamide vs oral erythromycin for neonatal chlamydial conjunctivitis.

Conjunctival and nasopharyngeal cultures for Chlamydia trachomatis were obtained from infants 30 days of age or younger with purulent conjunctivitis. Conjunctival specimens were also tested for other bacterial pathogens and for viruses. Most of the infants studied were black and came from a low-income, urban population. By random assignment infants received either topical treatment with 10% sulfacetamide sodium ophthalmic solution or systemic treatment with oral erythromycin estolate (50 mg/kg/day). Treatment was continued for 14 days if C trachomatis was isolated from the conjunctivae. Treatment was considered to be effective if conjunctivitis resolved and if follow-up chlamydial cultures of the conjunctivae and nasopharynx were negative at completion of therapy and two to four weeks later. Chlamydia trachomatis was isolated in the absence of other pathogens from the eyes of 37 (73%) of 51 infants with conjunctivitis. Other bacterial pathogens were isolated from four infants (8%) and viruses from none. Chlamydial infection was eradicated from 14 (93%) of 15 infants treated orally. In contrast, persistent conjunctival infection was detected in eight infants (57%) and nasopharyngeal colonization in three (21%) of 14 infants after topical treatment. It was concluded that C trachomatis is the most frequent cause of neonatal conjunctivitis in the low-income, urban population studied; that erythromycin estolate administered orally for 14 days eradicates chlamydial conjunctival and nasopharyngeal infection; and that topical sulfacetamide therapy may result in persistent conjunctival infection and nasopharyngeal colonization.

Administration, Oral↗
PubMed1983

Effect of prior immunization on induction of cervial cancer in mice by herpes simplex virus type 2.

Previous studies at this laboratory showed that repeated application of inactivated herpes simplex virus type 2 to the mouse cevix produced premalignant and malignant lesions. In the present study mice were inoculated with inactivated herpes simplex virus type 2 or control solution and Freund's adjuvant by intraperitoneal and subcuaneous routes before exposure of the cervix to inactivated virus. It appears that immunization with inactivated virus conferred a protection against the induction of cervical carcinoma.

Animals↗
PubMed1981

Induction of uterine cancer with inactivated herpes simplex virus, types 1 and 2.

A series of studies were performed to evaluate the oncogenic potential of inactivated herpes simplex viruses types 1 (HSV-1) and 2 (HSV-2) in the mouse cervix. HSV-1 or HSV-2 prepared in HEp-2 cell cultures and inactivated by exposure to formalin or ultraviolet light was applied to the mouse cervix for periods ranging from 20 to 90 weeks. Control mice were exposed for the same period to control fluids. Vaginal cytologic preparations from all animals were examined weekly to detect epithelial abnormalities. Animals were sacrificed and histopathological studies were carried out when cellular changes seen on vaginal smears resembled those indicative of premalignant or malignant changes as previously established in a similar model system using coal tar hydrocarbons. Other animals were exposed for periods up to 90 weeks, or until there was cellular evidence of invasive cancer. Cytologic and histologic materials were coded and evaluated without knowledge of whether they were from virus-exposed or control animals. Premalignant and malignant cervical lesions similar to those that occur in women were encountered in 78 to 90% of the virus-exposed animals. All controls were normal. Invasive cancer was detected in 24 to 60% of the animals and dysplasia was found in 18 to 66%. The yield of invasive cancer was twice as great after exposure to ultraviolet-inactivated HSV-2 as compared with formalin-inactivated virus. Various histologic grades of carcinoma of the cervix and endometrium were found. No primary lesions were found in the vagina or ovaries.

Adenocarcinoma↗
PubMed1979

Effects of viral exposure of the two-cell mouse embryo on cleavage and blastocyst formation in vitro.

The effect of viral exposure of two-cell mouse embryos on their capacity to undergo subsequent cleavage and blastocyst formation in vitro was determined. Exposure to Coxsackie viruses B-4 and B-6, reovirus type 2, influenza virus type A, mouse cytomegalovirus, adenovirus type 5, and mouse adenovirus resulted in statistically significant inhibition of blastocyst formation. Development in vitro was unaffected by exposure to ECHO virus type 11, attenuated poliomyelitis virus type 2, parainfluenza virus type 1, mumps, rubella, and herpes simplex viruses types 1 and 2. Blastocyst formation was also unaffected by exposure of embryos to mouse interferon in a concentration 24 units/ml of culture fluid. Coxsackie virus B-4 was recovered from exposed embryos.

Animals↗
PubMed1978

Pathogenesis of the rubella exanthem: distribution of rubella virus in the skin during rubella with and without rash.

In a previous assessment of the role of rubella virus in the pathogenesis of the rubella exanthem, virus was consistently isolated from cell cultures of skin biopsy specimens of the rash, and it was concluded that presence of virus in the skin was essential to evolution of the rash. For determination of whether virus is present in the skin only in association with rash, punch biopsies were performed concurrently on areas of skin with and without rash. Among paired skin specimens of 16 patients, virus was isolated from sites of rash in 12 and from the uninvolved skin in 10. In another patient, shown by serologic response and recovery of virus from the pharynx to have rubella without a rash, virus was also isolated from the skin. It is concluded that rubella virus is widely disseminated in the skin of patients with rubella irrespective of the presence or distribution of the rash, and that the presence of virus in the skin, although a constant feature of the disease, is only one of the factors involved in the pathogenesis of the exanthem.

Biopsy↗
PubMed1977

Growth inhibition of human embryonic and fetal rat bones in organ culture by rubella virus.

Paired organ cultures of metacarpal, metatarsal, and long bones of previable human embryos of 7 to 12 weeks' gestation and tibias of 17-day rat fetuses with inoculated with live or ultraviolet-inactivated rubella virus or control fluids and the growth of the bones was measured by increase in wet weight. In several cultures the ability of the human bones to incorporate 35S, a measure of rate of mucopolysaccharide synthesis, was tested. Growth of human and rat bones was retarded in cultures inoculated with live virus but not in cultures inoculated with inactivated virus or control fluids. Mean 35S uptake was increased by approximately 25% in virus-inoculated cultures of bones of 9- to 12-week human embryos. No histological abnormalities were seen. These findings suggest that (1) defective bone growth in congenital rubella is a direct effect of viral infection of bone, (2) a disorder of mucopolysaccharide syntheses may contribute to the osseous lesions that occur in this disease, and (3) organ cultures of human embryonic and fetal rat bones may serve as convenient models for studying the pathogenesis of this virus-induced congenital osteopathy.

Animals↗
PubMed1975

Cervical carcinogenesis with herpes simplex virus, type 2.

In the past few years there have been a number of reports correlating a high frequency of herpes simplex virus type 2(HSV-2) infection with lesions of the uterine cervix. These studies have used a clinical history of herpetic infection or the demonstration of herpetic antibodies in the cancer patients. The present study was performed to evaluate any possible carcinogenic activity of the formalin-inoculated herpes simplex virus type 2 in the reproductive tract of the female mouse. This approach to the study was selected because of previous experience with a model system of carcinogenesis of the cervix uteri using coal tar hydrocarbons. Cytologic and histologic preparations from experimental animals and controls are presented to demonstrate the mucosal alterations and tumors observed in the animals. Noninvasive lesions of the cervix were identified in 76.8% and invasive adenocarcinoma detected in 30.2% of the mice.

Adenocarcinoma↗