Anatomical studies of maxillary cheek teeth infundibula in clinically normal horses.

REASONS FOR PERFORMING STUDY: Although clinical disorders of equine maxillary cheek teeth (CT) infundibula are common, anatomical knowledge of these structures is poor. HYPOTHESIS: Anatomical examinations of sectioned CT infundibula will better define their shapes and sizes and allow identification of infundibular cemental variations and changes. MATERIAL AND METHODS: Cheek teeth were extracted post mortem from 33 horses, aged 3-30 years, without a clinical history of dental disease. The CT were sectioned longitudinally in the bucco-palatal plane through the widest aspects of both infundibula. The infundibular surfaces were then assessed morphologically, including by measurements of areas of cemental variations and changes. Specimens from selected teeth were examined histologically. RESULTS: Infundibular length and infundibular surface area, and infundibular length as a proportion of dental crown length progressively decreased with age, e.g. infundibular length was up to 89 mm after eruption to 2 mm in one older horse. Triadan 06 and 09 positions had significantly shorter CT and therefore infundibula, than the other 4 Triadan positions. Only 11.7% of infundibula were filled completely with normal appearing cementum, 8.2% of infundibula (especially the 09 position) had complete cemental caries; 22.6% of infundibula had areas with cemental hypoplasia and the remaining 57.5% of infundibulae had a variety of other cemental appearances, including the presence of central defects, localised occlusal caries and cemental discolourations. Histology showed the presence of an apical blood supply to infundibular cement in younger horses. CONCLUSIONS: Anatomical variations of CT infundibular cement are very common and some changes, such as areas of localised cemental hypoplasia, may predispose to the development of infundibular caries. POTENTIAL RELEVANCE: This more complete description and quantification of CT infundibular anatomy should allow more rational assessment and treatment of equine CT infundibular disorders.

Efficacy of an injectable combination anthelmintic (nitroxynil+clorsulon+ivermectin) against early immature Fasciola hepatica compared to triclabendazole combination flukicides given orally or topically to cattle.

The objective was to compare the efficacy against artificially induced 2- and 4-week old early immature triclabendazole-susceptible liver flukes (Fasciola hepatica) of an injectable combination of nitroxynil, clorsulon and ivermectin with oral and pour-on combination formulations containing triclabendazole. Groups of yearling Angus or Angus cross cattle were confirmed fluke free before being artificially infected with 500 Sunny Corner strain triclabendazole-susceptible liver fluke metacercariae. Two or four weeks after infection, cattle were treated with the test combination Nitromec (10.2mg/kg nitroxynil, 2.0mg/kg clorsulon, 0.2mg/kg ivermectin), or oral Flukazole C+Se (triclabendazole/oxfendazole/Selenium), oral Fasimec C (triclabendazole/ivermectin) or Genesis Ultra Pour-On (triclabendazole/abamectin). At intervals cattle were weighed, faecal sampled for liver fluke egg counts and blood sampled for liver serum enzyme analysis. Cattle were slaughtered 14 weeks after infection for recovery of adult flukes; fluke egg counts and liver pathology assessment. All cattle increased in body weight by 0.4-0.8kg/day but there were no significant differences between control and treated groups or between the treatment groups. Geometric mean 14-week fluke egg counts and total fluke counts for all treatments, were significantly less (p<0.05) than the control group, except for the group treated with Genesis Ultra Pour-On, 2 weeks after infection. Nitromec treatment of 2-week old flukes was 83% and 95% effective as assessed by 14-week egg and fluke counts, respectively, compared to Flukazole C; 96% and 99%, Fasimec C; 70% and 46%, and Genesis Pour-On, which was ineffective, with egg and fluke count reductions of 0% and 8%, respectively. Against 4-week old flukes, Nitromec treatment was 88% and 99% effective when assessed by 14-week egg and fluke counts, respectively, with Flukazole C; 98% and 99%, Genesis Pour-On; 98% and 82% and Fasimec C; 91% and 61% effective, respectively. Group mean levels of the bile duct-associated enzyme gamma glutamyl transpeptidase (GGT) and the parenchymal associated enzymes, aspartate amino-transferase (AST) and glutamate dehydrogenase (GLDH) increased above the normal range 8 and 11 weeks after infection in the untreated control animals and the group treated 2 weeks after infection with Genesis Pour-On. The groups treated with Fasimec at 2 or 4 weeks after infection, also had elevated enzyme levels. The use of liver-associated enzyme assay is supported as supplementary indicators of fluke-induced pathology.

Presence of Mycobacterium avium subspecies paratuberculosis in suspensions of ovine trichostrongylid larvae produced in faecal cultures artificially contaminated with the bacterium.

A reference strain of Mycobacterium avium subspecies paratuberculosis was added to faecal larval cultures of Haemonchus contortus, Ostertagia circumcincta and Trichostrongylus colubriformis. Samples of the larvae produced were cultured for the presence of the bacterium in modified BACTEC 12B medium, both before and after exposure to gamma irradiation. The water used to wash the larvae off the faecal cultures was also tested for the presence of the bacterium. Positive growth was confirmed as M. avium subspecies paratuberculosis by IS900 polymerase chain reaction and restriction endonuclease analysis of the product. M. avium subspecies paratuberculosis was detected in the unirradiated larval suspensions and wash waters of all three nematode species, and in the irradiated H. contortus larval suspension.

Evaluation of a laboratory test to detect resistance to closantel in Haemonchus contortus.

OBJECTIVE: To evaluate a laboratory test for closantel resistance in Haemonchus contortus. PROCEDURE: Field isolates of H contortus, known to be resistant to closantel, were tested in the assay. In addition, mixtures of closantel-susceptible and closantel-resistant laboratory reference strains were tested to develop a method of predicting the proportion of resistant worms in a sample from the field. RESULTS: The assay correctly identified as resistant all of the closantel-resistant field isolates of H contortus. It also identified one isolate with an in vivo efficacy of 98% as having emerging resistance. Testing of the mixtures of laboratory reference strains revealed that an isolate would be classified as resistant when it consists of about 25% or more resistant worms. Test samples that are not fully susceptible yet contain less than 25% resistant worms may be classified as emerging resistance. CONCLUSION: The in vitro migration assay is a sensitive method of detecting closantel resistance in H contortus.

Molecular genetic and morphological analyses of the African wild dog (Lycaon pictus).

African wild dog populations have declined precipitously during the last 100 years in eastern Africa. The possible causes of this decline include a reduction in prey abundance and habitat; disease; and loss of genetic variability accompanied by inbreeding depression. We examined the levels of genetic variability and distinctiveness among populations of African wild dogs using mitochondrial DNA (mtDNA) restriction site and sequence analyses and multivariate analysis of cranial and dental measurements. Our results indicate that the genetic variability of eastern African wild dog populations is comparable to that of southern Africa and similar to levels of variability found in other large canids. Southern and eastern populations of wild dogs show about 1% divergence in mtDNA sequence and form two monophyletic assemblages containing three mtDNA genotypes each. No genotypes are shared between the two regions. With one exception, all wild dogs examined from zoos had southern African genotypes. Morphological analysis supports the distinction of eastern and southern African wild dog populations, and we suggest they should be considered separate subspecies. An eastern African wild dog breeding program should be initiated to ensure preservation of the eastern African form and to slow the loss of genetic variability that, while not yet apparent, will inevitably occur if wild populations continue to decline. Finally, we examined the phylogenetic relationships of wild dogs to other wolf-like canids through analysis of 736 base pairs (bp) of cytochrome b sequence and showed wild dogs to belong to a phylogenetically distinct lineage of the wolf-like canids.

Imaging the ovine heparin-protamine interaction with 111In-protamine.

Protamine reversal of heparin anticoagulation occasionally induces the release of thromboxane into plasma with catastrophic pulmonary hypertension. To examine the site of neutralization, we labeled protamine sulfate with 111In and compared activity scans after administration of labeled protamine in unheparinized and heparin-anticoagulated sheep. Protamine administration in sheep without prior heparinization did not cause thromboxane release, pulmonary hypertension, or significant leukopenia, and 111In-protamine was rapidly cleared from the lungs (half time 0.48 +/- 0.08 min). Neutralization of heparin anticoagulation by labeled protamine produced elevated plasma thromboxane, pulmonary vasoconstriction, leukopenia, and prolonged pulmonary clearance of 111In-protamine (half time 3.32 +/- 0.43 min). In rats, protamine reversal of heparin anticoagulation did not induce either thromboxane synthesis or pulmonary hypertension, and 111In-protamine cleared rapidly from the lungs. Thus the ovine heparin-protamine reaction produces concomitant pulmonary sequestration of heparin-protamine complexes, thromboxane release, and pulmonary vasoconstriction; this did not occur in the rat. The lung specificity of the reaction and interspecies differences suggest that ovine pulmonary intravascular macrophages may be activated by heparin-protamine complexes to release thromboxane and provoke acute pulmonary vasoconstriction.

Nafamstat mesilate attenuates pulmonary hypertension in heparin-protamine reactions.

Rapid protamine reversal of heparin anticoagulation in awake sheep caused, after 1 min, a approximately 15-fold increase of arterial plasma thromboxane B2 (TxB2) levels, a 4-fold rise of pulmonary vascular resistance (PVR), a 2-fold rise of pulmonary arterial pressure, and after 3 min, a 2-fold rise of ovine arterial plasma complement C3a levels (P less than 0.05). Infusion of nafamstat mesilate (FUT-175), a protease and complement pathway inhibitor, before protamine reduced these increases by approximately 60-90% (P less than 0.05). FUT-175 did not modify heparin + protamine-induced leukopenia, suggesting that FUT-175 incompletely blocked C5a production. We also learned that infusing protamine first and heparin 5 min later did not increase either plasma C3a or TxB2 levels or PVR while the activated clotting time increased only minimally. Thus, in awake sheep, the sequence of heparin and protamine infusion influences complement activation and pulmonary vasoconstriction. FUT-175 pretreatment reduces thromboxane release and pulmonary vasoconstriction probably by limiting complement activation.

Effects of recombinant human tumor necrosis factor alpha, lymphotoxin, and Escherichia coli lipopolysaccharide on hemodynamics, lung microvascular permeability, and eicosanoid synthesis in anesthetized sheep.

We infused recombinant human tumor necrosis factor alpha (rhTNF alpha), lymphotoxin (rhLT), and Escherichia coli 0111:B4 lipopolysaccharide (LPS) into anesthetized sheep with a lung lymph fistula to compare their effects on systemic and pulmonary hemodynamics, lung lymph dynamics, and eicosanoid release. rhTNF alpha (25-150 micrograms/kg, n = 6 sheep), but not rhLT (25 micrograms/kg, n = 3), rapidly increased lung lymph and plasma levels of 6-keto-prostaglandin F1 alpha (6-k-PGF1 alpha) and caused profound systemic vasodilation and hypotension. Meclofenamate pretreatment (10 mg/kg) of three other sheep given 25 micrograms/kg rhTNF alpha prevented the increase of lymph and plasma 6-k-PGF1 alpha levels, systemic vasodilation, and the early (less than 2 hrs) but not the late (4-6 hours) hypotension caused by rhTNF alpha. LPS (1 micrograms/kg, n = 11) induced a briefer increase of lymph 6-k-PGF1 alpha levels than did rhTNF alpha while plasma 6-k-PGF1 alpha levels did not increase. LPS induced more gradual hypotension than did rhTNF alpha but did not cause systemic vasodilation. LPS and rhTNF alpha, but not rhLT, increased lymph thromboxane B2 (TXB2) levels during the first hour of study, whereas only LPS acutely increased plasma TXB2 levels. LPS caused acute pulmonary vasoconstriction and greater acute pulmonary artery hypertension than did either rhTNF alpha or rhLT. Whereas LPS-treated sheep required less fluid transfusion than rhTNF alpha-treated sheep to maintain mean systemic arterial pressure greater than 50 mm Hg, LPS infusion caused a greater increase of lung lymph protein clearance. rhTNF alpha caused minimal alterations of lung microvascular permeability. We conclude that eicosanoid mediators contribute importantly to differences of systemic and pulmonary hemodynamics caused by these agents in sheep. rhTNF alpha cannot account for all of the LPS-induced hemodynamic, lung lymph, and eicosanoid responses in sheep.

Effect of platelet depletion on lung vasoconstriction in heparin-protamine reactions.

In six awake sheep the control heparin-protamine reaction was associated with a 150-fold rise in arterial plasma thromboxane B2 (TxB2) levels, a 4.5-fold increase in pulmonary vascular resistance, a 20% decrease in cardiac output, a 30% decrease in arterial PO2, and a 30% reduction in arterial white blood cell concentrations. Depletion of 99% of circulating platelets by antibodies did not prevent either acute and severe pulmonary hypertension or increased plasma TxB2 levels induced by heparin-protamine administration. We produced sheep platelet aggregation in vitro with bovine thrombin and measured marked TxB2 release (36.3 +/- 16.3 ng/10(9) platelets). In contrast, neither heparin, protamine, nor heparin-protamine complexes over a 10,000-fold range of concentrations induced platelet aggregation and release of thromboxane in vitro. Therefore sheep platelets are not the source of thromboxane production associated with acute pulmonary hypertension during the heparin-protamine reaction, and other cells must produce the thromboxane.

Factors associated with surfactant treatment response in infants with severe respiratory distress syndrome.

In a prospective, randomized study of 18 infants treated with bovine surfactant (surfactant TA, Tokyo Tanabe Co, Tokyo) for severe respiratory distress syndrome, a lasting response was found in 12 infants (66%), a transient response was found in two (11%), and no response was found in four (22%) when arterial to alveolar PO2 ratios were used to define responses during the first 48 hours after treatment. In contrast, three of 23 control infants (13%) had a transient or lasting "response" to sham treatment (Pediatrics 1987;79:31-37). To determine whether maldistribution of surfactant could explain lack of response or a transient response, surfactant TA was mixed with technetium-99m sulfur colloid (approximately 300 mu Ci per infant), and eight infants with severe respiratory distress syndrome were treated six to 58 hours after birth. Scintigraphy of the lungs was performed three to 15 hours after treatment. Although a lasting response was observed in three infants, a transient one in three, and no response in two, no gross maldistribution of the radioactive label was found. Either lung received from 37% to 62% of the total radioactivity. During the past 3 years, in all infants with severe respiratory distress syndrome who were treated with surfactant (n = 29), poor or transient responses were associated with early patent ductus arteriosus and air leaks (pulmonary interstitial emphysema and pneumothoraces). Pathophysiologic conditions associated with respiratory distress syndrome are more likely to explain suboptimal responses after surfactant treatment than gross maldistribution of surfactant in the lungs.

East African cheetahs: evidence for two population bottlenecks?

A combined population genetic and reproductive analysis was undertaken to compare free-ranging cheetahs from east Africa (Acinonyx jubatus raineyi) with the genetically impoverished and reproductively impaired south African subspecies (Acinonyx jubatus jubatus). Like that of their south African counterparts, the quality of semen specimens from east African cheetahs was poor, with a low concentration of spermatozoa (25.3 X 10(6) per ejaculate) and a high incidence of morphological abnormalities (79%). From an electrophoretic survey of the products of 49 genetic loci in A. jubatus raineyi, two allozyme polymorphisms were detected; one of these, for a nonspecific esterase, shows an allele that is rare (less than 1% incidence) in south African specimens. Estimates of polymorphism (2-4%) and average heterozygosity (0.0004-0.014) affirm the cheetah as the least genetically variable felid species. The genetic distance between south and east African cheetahs was low (0.004), suggesting that the development of genetic uniformity preceded the recent geographic isolation of the subspecies. We propose that at least two population bottlenecks followed by inbreeding produced the modern cheetah species. The first and most extreme was ancient, possibly late Pleistocene (circa 10,000 years ago); the second was more recent (within the last century) and led to the south African populations.

The decline of the Serengeti Thomson's gazelle population.

The population of Thomson's gazelles in the Serengeti National Park, Tanzania has declined by almost two thirds over a 13 year period. In the early 1970s, numbers stood at 0.66 million animals but had decreased to less than 0.25 million animals in 1985 as estimated by 5 different censuses using two different counting techniques. Predation, interspecific competition and disease are all factors that could have contributed to this decline, and at least one of these factors, predation, could now prevent the Thomson's gazelle population from increasing.

Comparison of ultrashort-lived iridium-191m with technetium-99m for first pass radionuclide angiocardiographic evaluation of right and left ventricular function in adults.

Ultrashort-lived iridium-191m (Ir-191m, physical half-life = 5.0 seconds) has been used in angiocardiography, primarily in pediatric patients. A theoretical obstacle to more widespread use of Ir-191m is the belief that its physical half-life is too short to permit evaluation of left ventricular function in adult patients. To evaluate its usefulness in adults, first pass ejection fractions of the left and right ventricles determined with use of Ir-191m and technetium-99m (Tc-99m) were compared in 33 adult patients. An osmium-191m----iridium-191m (Os-191----Ir-191m) generator was employed to deliver doses of 150 to 250 mCi (5.5 to 9.2 GBq) of Ir-191m for intravenous injection. The whole body radiation absorbed dose with Ir-191m was 15 to 25 mrad. High quality angiocardiograms were obtained with both Tc-99m and Ir-191m. Total counts per image for the right ventricle were 51,000 +/- 8,000 (mean +/- SD) for Ir-191m and 30,000 +/- 8,000 for Tc-99m. The left ventricular counts were comparable for both radiotracers (25,000 +/- 7,000 for Ir-191m and 25,000 +/- 8,000 for Tc-99m). Right ventricular ejection fractions were similar: 44 +/- 8% for Ir-191m and 47 +/- 9% for Tc-99m. The correlation coefficient was 0.93 with a standard deviation of the regression of 3.1% ejection fraction units. The left ventricular ejection fractions were also similar: 45 +/- 14% for Ir-191m and 46 +/- 13% for Tc-99m. The left ventricular ejection fraction correlation coefficient was 0.96 with a standard deviation of the regression of 3.7%.(ABSTRACT TRUNCATED AT 250 WORDS)