Diarrhea associated with Enterococcus durans in calves.
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Biomedical subjects
Publications and source records attributed to D G Rogers.
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A midwestern producer reported high incidence of conjunctivitis and keratoconjunctivitis in a herd of crossbred finishing swine. Complete necropsy was performed on 3 pigs with bilateral mucopurulent conjunctivitis and chemosis; other gross lesions were not seen. Mycoplasma sp was isolated from conjunctival swab specimens obtained from 1 pig; small numbers of streptococci and coagulase-negative staphylococci were isolated from conjunctival swab specimens from all 3 pigs. Neither swine influenza virus nor pseudorabies virus was isolated from conjunctival swab specimens. Histologically, the 3 pigs had chronic lymphoplasmacytic conjunctivitis with lymphofollicular hyperplasia and foci of epithelial and goblet cell hyperplasia. Ultrastructural examination of conjunctival specimens from the 3 pigs revealed large numbers of Mycoplasma-like organisms adhered to superficial conjunctival cells. Mycoplasma-like organisms also were seen in membrane-bound vacuoles in superficial conjunctival cells. Bacteria (including chlamydiae) or viruses were not seen ultrastructurally. The lymphoproliferative nature of the conjunctival lesion and the evidence of adhered and intracellular organisms suggested an etiologic role for a Mycoplasma-like organism in the disease in these pigs.
A total of 18 Australian isolates of Bordetella avium and seven reference B. avium strains from Europe and the USA were tested for the presence of a mouse-lethal toxin. Five of the seven reference strains of B. avium, but none of the 18 Australian isolates, produced the toxin.
We recently found circulating corticosterone (CS) levels to be significantly lower in diabetic female rats as compared with proestrous control animals. This reduction in CS was correlated with the hypoestrogenic state of the diabetic female. It was the purpose of this study to evaluate basal and corticotropin releasing hormone (CRH)-stimulated CS secretion in ovariectomized (OVX) control (C) and streptozotocin-induced diabetic (D) rats given blank, 5 mcg and 20 mcg estradiol (E2) implants to determine if adrenal CS secretion in the diabetic is normalized by E2 treatment. After 3 weeks of diabetes, pituitary-adrenal function was assessed in rats from each group with a CRH stimulation test. The remaining rats were sacrificed for determination of CS, E2, testosterone and fructosamine in serum. Suppressed CS secretion in OVX female diabetic rats was partially restored with E2 therapy. Basal CS levels were significantly higher in 20 mcg E2 treated C and D rats compared with OVX rats. However, C rats had significantly higher basal CS compared with D rats in similarly E2 treated groups. The CS response to CRH stimulation was not different between OVX female diabetic and control rats. Estrogen enhanced the CS response to CRH stimulation in control animals but not in diabetic animals suggesting altered estrogen action at the pituitary level in diabetic animals.
Studies in diabetic rats have found abnormalities at the hypothalamic, pituitary, and/or ovarian level but have not controlled for changes in estrogen levels induced by diabetes. The purpose of this investigation was to study the effect of diabetes on the hypothalamic-pituitary axis in ovariectomized rats treated with estradiol (E2). Ovariectomized 60 day old female rats were assigned to control (C, n = 42), diabetic (D, n = 47) or insulin-treated diabetic (DI, n = 16) groups. Diabetes was induced with an injection of streptozotocin in the D and DI groups. In the C, D, and DI groups, estrogen was replaced by implanting blank, 5 micrograms or 20 micrograms E2 pellets sc. Pituitary LH responsiveness to GnRH was assessed in C and D animals. Anterior hypothalamic and midhypothalamic concentrations of proGnRH and GnRH, pituitary LH and FSH and serum levels of LH, and E2 were measured by RIA. Anterior hypothalamic proGnRH concentrations were decreased in diabetic rats treated with 5 micrograms E2 compared to 5 micrograms E2 control animals (P less than 0.05). Midhypothalamic GnRH concentrations were also reduced in D vs. C animals despite comparable estrogen therapy (P less than 0.004). GnRH-stimulated LH levels were greater in E2-treated diabetic females than in similarly treated control rats (P less than 0.001). D and DI animals were more sensitive than controls to the inhibitory effect of estrogen on basal LH levels. Pituitary LH and FSH content was lower in 20 micrograms E2-replaced animals but was not influenced by the diabetic state. These data demonstrate a diabetes-induced decrease in hypothalamic proGnRH and GnRH concentration which is not corrected with E2 replacement. The hyper-responsiveness of the diabetic rat pituitary to GnRH also suggests a chronic lack of GnRH stimulation from the hypothalamus but a continued ability of the pituitary to respond to GnRH.
OBJECTIVE: To assess the effect of puberty on the relationship between glycemic control and insulinlike growth factor I (IGF-I) levels in children with insulin-dependent (type I) diabetes mellitus. RESEARCH DESIGN AND METHODS: Simultaneous HbA1 and plasma IGF-I levels were determined in 71 prepubertal (Tanner stage I) and 112 pubertal (Tanner stages II-V) subjects aged 2.7-17.8 yr. RESULTS: Overall, IGF-I levels were positively correlated with both age (r = 0.31, P less than 0.001) and Tanner stage (r = 0.32, P less than 0.001) but only weakly associated with HbA1 values (r = -0.16, P = 0.025). A strong negative association existed between IGF-I and HbA1 levels (r = -0.45, P less than 0.001) in the pubertal subjects, but no such association was apparent in the prepubertal subjects. Multiple regression analyses disclosed a significant independent negative association between IGF-I and HbA1 levels in the pubertal group (P less than 0.001) but not in the prepubertal group. CONCLUSIONS: Glycemic control appears to strongly influence IGF-I levels only after the onset of puberty.
When insulin was administered to streptozotocin-induced diabetic female rats, the percentage of glycohemoglobin, growth rate, ovulatory cycle, uterus to body weight ratio, and insulin-like growth factor (IGF-I) level returned to near normal. In untreated diabetic rats there were no normal estrous cycles, and hepatic IGF-I mRNA (7.94 +/- 1.02 O.D. units per micrograms total RNA) levels were significantly lower than the control or insulin-treated groups in proestrus (16.47 +/- 0.91 and 17.15 +/- 1.84, respectively). Insulin therapy restored the hypothalamic-pituitary-ovarian axis with the reinstitution of normal estrous cycles. Plasma IGF-I levels were highest in non-diabetic proestrous animals (277 +/- 36.9 ng/ml), significantly higher than IGF-I levels in insulin-treated diabetic rats in diestrus (174 +/- 23.1 ng/ml), non-diabetic diestrus rats (165 +/- 18.4 ng/ml) and untreated diabetic rats (135 +/- 19.7 ng/ml). Plasma IGF-I levels were elevated in insulin-treated diabetic rats in proestrus (221 +/- 78.3 ng/ml), however this was not significantly different from any other group. The increases observed in plasma IGF-I and hepatic IGF-I mRNA after insulin therapy correlate with the normalization of sex hormone secretion. Though this study does not prove a causal relationship between restoration of ovarian function and normalization of circulating IGF-I levels, a relationship has been established, as evidenced by higher levels of IGF-I in both the control and insulin-treated diabetic proestrous groups when compared to the diestrus groups.
By using the Kume hemagglutinin serotyping scheme, 13 Australian isolates of Haemophilus paragallinarum were shown to constitute a new serovar within the presently termed serogroup II. Because of the likelihood that new serovars will continue to be established, we propose a rationalization of the nomenclature of the Kume scheme. Under this altered scheme, the three recognized serogroups I, II, and III are renamed A, C, and B, respectively. Within each of the serogroups, the serovars are numbered sequentially, allowing new serovars to be added in numerical order. Thus, the nine currently recognized Kume serovars are termed A-1, A-2, A-3, A-4, B-1, C-1, C-2, C-3, and C-4.
Diabetes interferes with reproductive function in laboratory animals. Previous studies in female diabetic rats have not resolved if the reproductive abnormalities observed are at the hypothalamic, pituitary and/or ovarian level. The interaction of the gonadal and adrenal axes has not been studied in the diabetic female rat. The purpose of this study is twofold: first, to determine the level of dysfunction in the hypothalamic-pituitary axis caused by diabetes in the adult female rat controlling for stage of the estrous cycle, and, second, to evaluate basal corticosterone secretion in female diabetic rats. Sixty cycling 40-day-old female rats were randomly assigned to 3 groups; control (n = 32), diabetic (n = 14), and diabetic insulin-replaced animals (n = 14). The level of hyperglycemia in each group was documented by glycosylated hemoglobin levels and biweekly blood glucoses. Three weeks after induction of diabetes, pituitary luteinizing hormone (LH) responsiveness following an i.v. injection of gonadotropin-releasing hormone (GnRH) was assessed in representative diestrous rats from each group. All animals were sacrificed in either diestrus or proestrus for determination of GnRH concentration in the hypothalamus, LH and follicle-stimulating hormone (FSH) content in pituitary and LH, FSH, estradiol and corticosterone in serum. Uterine weight to body weight ratios (a bioassay for estrogen) were also calculated. Hypothalamic GnRH concentration was significantly lower in diabetic versus control diestrous rats. Basal pituitary and serum gonadotropin levels were not different between any groups. GnRH-stimulated serum LH levels were higher in diabetic vs. control and diabetic insulin-treated animals. LH surges occurred in the control and diabetic insulin-replaced but not the diabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)
Ninety-five isolates of Haemophilus paragallinarum were classified serologically by a hemagglutinin serotyping scheme, and the results were compared with results from agglutinin serotyping of the same isolates. Of the isolates, 65 were from Australia, 5 were from Japan, 6 were from the Federal Republic of Germany, 7 were from the United States, and 12 were from South Africa. Seven hemagglutinin serovars, HA-1 to HA-7, corresponding to agglutinin serovars A (HA-1, HA-2, and HA-3), C (HA-4, HA-5, and HA-6), and B (HA-7) have been described. Only one of the seven hemagglutinin serovars was found among the Australian isolates. This was serovar HA-5, comprising 49 isolates. Fifteen Australian isolates, all from southeast Queensland and northern New South Wales, were found to belong to a new hemagglutinin serovar. This was designated HA-8 and represented a fourth subgroup of agglutinin serovar A. Of the 95 isolates examined, only 1 did not produce a hemagglutinating antigen and was nonserotypeable by the hemagglutinin system. This compared favorably with the agglutinin scheme, which serotyped only 60 of the 95 isolates, with 29 nonserotypeable and 6 autoagglutinating.
Treatment of the somatostatin (SRIF)-producing TT cell line with 1,25 dihydroxyvitamin D3 (1,25 D3) lowered intracellular SRIF mRNA and peptide concentration. In separate experiments, the cAMP analog 8-(4-chlorophenylthio)-cAMP stimulated a rapid increase in SRIF mRNA content of the TT cells and SRIF peptide secretion. To determine whether 1,25 D3 could inhibit either the transcriptional or secretory effects of cAMP, TT cells were pretreated with 1,25 D3 for 4 days followed by treatment with the cAMP analog. Pretreatment with 1,25 D3 inhibited the cAMP-mediated increase of SRIF mRNA, but had no effect on the secretory response. We conclude that the ability of 1,25 D3 to silence SRIF gene expression is more potent than cAMP enhancer activity but that 1,25 D3 has no effect on that portion of the cAMP-dependent pathway which regulates peptide secretion.
IgG antibodies to insulin are present in insulin-treated patients and are detected in the prodrome of untreated type I diabetes. Sporadic reports of autoantibodies to insulin suggest that they are also present in other disorders. To establish the incidence of insulin autoantibodies in other endocrine and autoimmune diseases an ELISA was used to examine sera from 529 subjects with no prior insulin therapy. These untreated patients included: normal controls (adults and children), newly-diagnosed type I diabetes, first-degree relatives of diabetics, type II diabetes, Graves' hyperthyroidism, and systemic lupus erythematosus. As a positive control group, 280 insulin-treated patients were studied. Measurement of IgG antibodies by direct binding to insulin coated plates was complicated by differences between adult and pediatric populations and by overlap of binding between treated and untreated subjects. Competitive inhibition with excess soluble human insulin overcame these problems and permitted identification of insulin specific binding. Using this approach insulin antibodies were most frequent in insulin-treated diabetics (98%) and in type I diabetics (37%) prior to treatment. The absolute numbers of subjects with insulin autoantibody in the other groups differed depending upon whether a cut-off for binding (mean + 2SD of controls) or for insulin inhibition of binding (45%) was used. Regardless of the criteria used there were subjects (2-24%) in all groups tested with circulating insulin-specific IgG autoantibody detected by ELISA. These low level antibodies detected in solid phase assays may be part of the normal immune repertoire.
To determine their capacity to host Brucella abortus, face flies were examined 1 to 120 hours after feeding on broth containing bacteria and bovine erythrocytes. Brucella abortus was cultured in large numbers from whole flies for 12 hours after feeding, but not after 72 hours. Histologic analysis showed that brucellae were rapidly taken into the midgut, sequestered from erythrocytes, transiently stored, and shed in the feces; there was no evidence of bacterial replication within epithelial cells. Immunoperoxidase and immunogold techniques revealed that most brucellae in the gut were confined to the lumen by the peritrophic membrane, that brucellae were degraded in secondary lysosomes of midgut epithelial cells, and that intact brucellae passed into connective tissues surrounding the midgut. Bacterial excretion without midgut replication is consistent with transient, but not long-term, insect transmission in nature.
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Primigravid swine were vaccinated orally with a live enterotoxigenic Escherichia coli (ETEC) strain that produces pilus antigen K99. The titers of K99 antibody in colostrum and milk of vaccinates remained higher than those of nonvaccinated controls through the first lactation after vaccination (4 weeks). Some control swine had low titers of K99 antibody in colostrum or developed low titers of K99 antibody in milk during lactation. Lacteal K99 antibody titers of vaccinates dropped to control levels during the second lactation, 6 months after vaccination. Pigs suckling vaccinates and controls were equally susceptible to challenge exposure to K99+ ETEC during the second lactation. Orally vaccinated swine given a parenteral booster vaccination (with killed K99+ ETEC) during their second gestation had K99 antibody in milk through their second lactation. During the second lactation, these orally vaccinated parenterally revaccinated swine had higher titers of K99 antibody in postcolostral milk than did nonvaccinated controls, controls given only the parenteral booster injection, or controls vaccinated parenterally during both gestations.
We utilized the TT cell, a human C-cell line derived from a medullary thyroid carcinoma, to study the effects of 1,25-dihydroxyvitamin D3 on cell growth and expression of the calcitonin gene. The growth rate of cells treated for 8 days with 1,25-dihydroxyvitamin D3 did not differ significantly from control or 24,25-dihydroxyvitamin D3 treated cells. Total RNA was isolated, and calcitonin and calcitonin gene-related peptide (CGRP) levels were measured by hybridization. 1,25 D3 lowered calcitonin and CGRP mRNA levels in a time- and dose-dependent fashion; 24,25 D3 had no effect. Northern blots revealed a decrease in the mature mRNA as well as the common precursor forms, indicating a transcriptional effect of 1,25 D3.
Moraxella bovis was instilled into the conjunctival sac of gnotobiotic calves and corneas were sampled serially after infection. Lesions developed in seven of eight infected calves, but were absent in a noninfected control calf. Histologically, M. bovis was first seen in foci of swollen epithelium and within basal epithelial cells adjacent to ulcers. Corneal ulcers were severe in later stages of infection; fibrin deposits, neutrophils, and bacteria were present in the stromas. Examination of early lesions by scanning electron microscopy showed M. bovis in pits on the surfaces of dark epithelial cells, enmeshed in degenerate epithelial cells and within erosions and an ulcer; in later samples, bacteria were rare. Ultrastructurally, M. bovis was seen in surface pits in superficial epithelial cell processes and within swollen epithelial cells. In stroma, M. bovis was frequently seen among collagen fibrils, within neutrophil phagosomes, and associated with cellular debris. This study demonstrates that a virulent strain of M. bovis can invade bovine corneal epithelial cells and can cause keratitis in the absence of injurious ultraviolet irradiation or other known predisposing environmental factors.
Hemolytic Moraxella bovis was instilled into the conjunctival sac of gnotobiotic calves, and conjunctivae were sampled serially after infection. Bilateral lesions developed in seven of eight infected calves. Histologically, M. bovis was first seen within swollen epithelial cells near the lid margins and occasionally within superficial epithelium in other areas. Conjunctival erosions and ulcers were seen in later stages. Scanning electron microscopy showed M. bovis in pits on surfaces of epithelial cells and in erosions on palpebral conjunctivae; lesions were prominent near lid margins. By transmission electron microscopy, M. bovis was seen within swollen epithelial cells near lid margins; many epithelial cells had undergone cytolysis. This study demonstrates that virulent M. bovis can invade bovine conjunctival epithelial cells and cause conjunctivitis in the absence of injurious ultraviolet irradiation or other predisposing environmental factors.