Biomedical subjects
M D Ruff
Publications and source records attributed to M D Ruff.
Life cycle and biology of Eimeria lettyae sp. n. (Protozoa: Eimeriidae) from the northern bobwhite, Colinus virginianus (L.).
A new species of coccidium, Eimeria lettyae sp. n. (Protozoa: Eimeriidae) was recovered from feces of the northern bobwhite, Colinus virginianus (L.), from Pennsylvania and Florida. Oocysts measured 21.1 microns (16.4 to 25.8) by 17.2 microns (14.1 to 21.2); index (L/W ratio) = 1.22. Oocysts lacked a micropyle, residuum, and polar granules. Sporozoites penetrated the upper 1/2 of the villi, then moved to the lamina propria at the base of the villi. There were five asexual generations, all of which developed above the nucleus of the host cell. Meronts measured 9.4 X 7.0 microns, 18.6 X 11.2 microns, 11.8 X 10.1 microns, 7.1 X 6.2 microns, and 20.2 X 12.8 microns, respectively. These matured at 32, 40, 48, 56, and 72 hr postinoculation (PI) and contained 12, 50+, 24 to 36, 12 to 24, and 50+ merozoites, respectively. Infection was most intense in the duodenum although some gamonts were found in the ileum and ceca. The prepatent period was 88 to 91 hr PI. Sporulation time was 18 hr at 25 C. The peak of oocyst production was broad and extended from 4 days PI through 14 days PI. Oocysts were passed for at least 67 to 76 days PI. Eimeria lettyae sp. n. did not infect chickens (Gallus domesticus), domestic turkeys (Meleagris gallopavo), ring-necked pheasants (Phasianus cochicus), chukar partridge (Alectoris graeca), or Japanese quail (Coturnix coturnix). Immunizing bobwhite with E. lettyae sp. n. did not protect against challenge with E. dispersa. Immunizing bobwhites 25 times with 10(2) or 10(3) sporulated oocysts of E. lettyae did not entirely eliminate oocyst production following challenge with the same species.
Pathogenicity of coccidia in Japanese quail (Coturnix coturnix japonica).
Coccidia were recovered from a field outbreak in commercially raised Japanese quail from South Carolina. After propagation in unmedicated quail, the culture was identified as a mixture of approximately 65% Eimeria uzura, 33% E. tsunodai, and 2% E. taldykurganica. Several pure cultures of E. uzura were obtained by single oocyst isolation. A micropyle was not present in all oocysts; thus, it is not a reliable taxonomic characteristic for identification of E. uzura. Neither the mixed culture nor the E. uzura isolates were infective for Bobwhite quail, Chukar partridge, pheasants, chickens, or turkeys. Seventeen-day-old quail were inoculated with various doses of sporulated oocysts ranging from 5 x 10(2) to 5 x 10(5) of the mixed culture and 1 x 10(3) to 1 x 10(6) of E. uzura. The rate of weight gain was depressed at 3 or 4 days postinoculation (DPT) with as few as 5 x 10(2) oocysts/quail of the mixed culture. As few as 1 x 10(3) oocysts of E. uzura produced a weight loss. Some individual quail had depressed packed cell volume and plasma pigment compared with levels in the uninoculated controls. Plasma protein was not affected. Young quail (3 days old at inoculation) were more susceptible than 17-day-old quail. Infection did not adversely affect body weights of adult quail, although egg production was reduced. Mortality was seen only with the mixed culture (100 and 8% in 3- and 17-day-old quail given 5 x 10(5) oocysts, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Changes in liver glycogen of broilers during coccidiosis.
Liver glycogen levels of broilers with Eimeria acervulina, E. Brunetti, or E. tenella fell during the acute phase of the infection with the maximum effect at 5-6 days post-inoculation (DPI). During the early recovery phase (6-8 DPI), liver glycogen levels in the E. acervulina-infected birds increased to levels up to 3 times greater than those found in uninoculated control birds. A lesser increase was occasionally seen in E. tenella-infected birds. Pair feeding studies showed that the decrease in liver glycogen was not related to the amount of feed consumed. The magnitude of the glycogen overshoot at 7 DPI was not related to the depression of weight gain at 5 and 6 DPI. When feed was withheld from birds, liver glycogen levels of uninoculated control birds fell rapidly within 1 h after feed withdrawal. In birds infected with E. acervulina, liver glycogen levels remained high even after 3 h starvation. Injection of glucagon indicated that glycogen could be mobilized in both infected and uninfected birds.
Eimeria acervulina and Eimeria tenella infections in ochratoxin A-compromised broiler chickens.
A 2 x 6 factorial experimental design was used to evaluate the effects of coccidial infections in ochratoxin A-compromised chicks. Ochratoxin A was incorporated into the feed at the dose levels of 0, .5, 1.0, 2.0, 4.0, and 8.0 micrograms/g toxin in feed (ppm), and fed to the birds from 1 day of age. Birds from each treatment were inoculated with either Eimeria acervulina or Eimeria tenella at 14 days of age. Ochratoxin A decreased the severity of lesions caused by both E. acervulina and E. tenella but did not prevent infection. Packed cell volume, hemoglobin concentration, relative weight of the kidney, and plasma protein levels were altered in a manner consistent with the independent effects of ochratoxicosis and coccidiosis. A combination of ochratoxin A and either species of coccidia produced a greater decrease in body weights, increase in feed conversions, and decrease in plasma carotenoid levels than either disease alone. The relative weight of the liver and level of plasma uric acid were altered in a manner that was dependent on the species of coccidia used. These data indicate that ochratoxin A and coccidial infections can interact to limit broiler performance and that some responses are directly related to the species of coccidia.
Reduced intestinal absorption in broilers during Eimeria mitis infection.
The absorption of glucose and L-methionine was as much as 52% less in the intestine of broilers inoculated with 2 strains of Eimeria mitis than in the intestine of noninoculated controls. This malabsorption was observed in the region of, and caudad to, the yolk sac diverticulum. Malabsorption was greater in birds given 500,000 sporulated oocysts than in those given 50,000 sporulated oocysts/bird. Depigmentation of the plasma was also considered an indication of malabsorption. Gross lesions were not evident in the intestine of these infected birds, even though histopathologic sections showed the presence of numerous parasites. Body weight was also less in inoculated birds, but PCV and plasma protein concentrations were not affected.
Effects of coccidiosis on the electrophoretic pattern of serum proteins in chickens.
The electrophoretic distribution of serum proteins was measured in chickens inoculated with sporulated oocysts of Eimeria acervulina, E. tenella, and E. maxima. Total serum protein decreased on day 5 and 7 postinoculation (PI) with all three species. However, the changes produced in the individual serum protein fractions differed with the species. In serum from E. acervulina-infected birds, all protein components decreased quantitatively; the largest decrease was in the alpha globulins. The overall percent distribution of the globulins was similar to that of uninoculated controls, except for a decrease in the alpha globulins. In E. tenella-infected chickens, albumin decreased (both quantitatively and in percent distribution), but the alpha 1, beta, and gamma 1 globulins increased. In E. maxima-infected chickens, only albumin and alpha 1 globulin decreased quantitatively; the amounts of alpha 2, beta, or gamma globulins did not change. These changes were transitory and had disappeared by day 10 PI.
Eimeria meleagrimitis, E. adenoeides, and E. dispersa: severity of infection and changes in the intestinal mucosa of the turkey.
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Composition of heart, liver, and skeletal muscle from broilers with coccidiosis.
Infection with Eimeria acervulina, Eimeria brunetti, or Eimeria tenella affected the composition of the breast, thigh, heart, and liver of 3 or 4-week-old broilers. Liver glycogen was significantly increased at 6 and 8 days postinoculation (PI) with E. acervulina. Conversely, liver glycogen was decreased at 4 and 6 days PI with E. tenella and was unaffected by infection with E. brunetti. The levels of RNA and lipid in the liver were decreased with E. acervulina but unchanged with E. tenella. Both species decreased RNA levels in the breast. None of the three coccidial species had any effect on the moisture, ash, protein, or DNA content of the tissues.
Analysis of liver glycogen in chicks.
The glycogen levels in homogenates from livers from 3- to 4-week-old broilers were measured using alkaline digestion and ethanol precipitation followed by direct hydrolysis with amyloglucosidase. Glycogen was determined with glucose oxidase. Glycogen levels were not affected by rapid freezing in liquid nitrogen and storage at -10 C. Glycogen was stabile at 4 C for at least 1 hr; however, at room temperature, over 50% of the glycogen was lost within 1 hr. Homogenization with .05 M ethylenediaminetetraacetate (EDTA) prevented this loss. Liver glycogen decreased rapidly (within 1 hr) after feed withdrawal and was sometimes undetectable within 2 hr. There was considerable variation in glycogen levels among individual birds. Liver glycogen levels were up to 50% higher at 1100 than at 0800 hr.
Physiological basis of Eimeria tenella-induced mortality in individual chickens.
Chickens dying from Eimeria tenella infection revealed four major physiological stresses before death: (1) hypothermia, (2) depletion of carbohydrate stores, (3) metabolic acidosis, and (4) renal tubule-cell dysfunction. These stresses were less pronounced in chickens surviving the infection. Similar stresses could not be demonstrated in pair-feeding trials, in which uninfected chickens were fed only the amount consumed by infected chickens. Prolonged starvation of uninfected chickens only slightly altered the indicators used in assessing the stresses. The variability of previously reported plasma glucose values, in part, may be due to whether the birds tested were those on the verge of death or those that, ultimately, would survive the infection.
Total intestinal absorption of glucose and L-methionine in broilers infected with Eimeria acervulina, E. mivati, E. maxima or E. brunetti.
The in vitro absorption of glucose and L-methionine in the intestine of broiler chickens was measured 7, 14 and 21 days post-inoculation (p.i.) with sporulated oocysts of Eimeria acervulina, E. mivati, E. maxima or E. brunetti. The small intestine of each bird was divided into 8 regions of equal length and absorption was measured on 3 tissue disks of equal size from each region. The absorption rate of each substrate with each coccidial species was measured based on (1) an equal area from each region, (2) an equal weight from each region, (3) the total absorption in each region, and (4) the total potential absorption in the intestine. Comparisons of absorption rate of equal areas in each intestinal region demonstrated that infected birds at 7 days p.i. absorbed significantly less substrate per unit area in the regions of maximum infection than uninfected controls. Malabsorption was less apparent when the weight of the region was used as the unit of measurement. Compensatory absorption was seen in some uninfected regions with E. acervulina. The total potential intestinal absorption at 7 days p.i. was reduced with E. mivati, E. maxima and E. brunetti but not with E. acervulina. At 14 days p.i., total L-methionine and glucose absorption in some regions of the intestine was significantly increased with E. acervulina but not with E. mivati, E. maxima or E. brunetti. No absorption differences were seen at 21 days p.i. with any species.
Eimeria meleagrimitis Tyzzer in turkeys: the life cycle and effects of inoculum size and time on severity of infection and intestinal distribution.
Developmental stages of Eimeria meleagrimitis Tyzzer were found throughout the intestine and ceca of turkeys given inocula ranging from 10(4) to 7.5 x 10(5) sporulated oocysts/bird. Infection initially occurred in the duodenum and upper jejunum but later moved down the intestine and into the ceca. The speed with which the infection moved into these areas was rougly proportional to the inoculum size. Heaviest infections were in the ileum, neck of the cecum, and large intestine. The life cycle consisted of 5 asexual generations before gametogony, a 6th asexual generation developing simultaneously with gametogony. First- and 2nd-generations were located along the sides of villi in the upper intestine rather than in the crypts of Lieberkühn, as previously described in England for this species. Transitory first-generation stages that were abnormally large and usually degenerate were found in the neck of the cecum.
Physiological effects of gentian violet on broiler chickens.
The effects of dietary gentian violet upon certain physiological parameters of broiler chickens were studied. Gentian violet exhibited no effect upon growth rates or feed conversion ratios at dietary levels of 16, 32, or 64 micrograms/g. In vitro intestinal absorption of methionine and glucose was also unaltered. Dietary gentian violet significantly increased hemoglobin concentration without an effect on packed cell volume. Furthermore, commercial gentian violet containing preparations, when incorporated into the diet, resulted in increased intestinal absorption of Fe59 but this increase was dependent upon type of inert carrier used. Dietary gentian violet alleviated some of the growth suppression caused by dietary aflatoxin; however, no effect was observed on plasma pigmentation. These data suggest that dietary gentian violet possesses effects other than those for which it has been traditionally employed.
Relationship of restricted feeding and medication to coccidiosis control.
Hubbard breeder pullets were fed a complete pullet developer ration on an ad libitum (AL) or restricted feeding (RF) regimen. The ration either was unmedicated or contained .0125% amprolium, .0125% clopidol, or .0110% monensin. The relationship between the feeding schedule and coccidial infection was determined on the basis of 1) efficacy of the medication in controlling a single infection in susceptible pullets and 2) the development of immunity to subsequent challenge inoculation after a series of immunizing inoculations. Cage-reared, susceptible pullets were inoculated with sporulated oocysts of either. Eimeria tenella, 2 strains of E. acervulina, or E. maxima. With all three medications, the infection with a least one species was more severe, as measured by intestinal lesion score, in the RF pullets than in the corresponding AL pullets. Other pullets were kept for three weeks in floor pens that contained coccidial oocysts to allow natural infection and immunity to develop. The pullets were then transferred to suspended cages to prevent reinfection and fed an unmedicated ration. After one week, the pullets were challenged with the same coccidial strain as that used for immunizing. All pullets initially exposed to coccidia and given no medication were resistant to challenge inoculation. Control pullets are exposed to coccidia during rearing were susceptible to challenge. The administration of anticoccidial drugs (especially monensin) by ad libitum feeding interfered with development of immunity under these conditions, but, when the same drugs were given with a restricted feeding regimen, they did not interfere with development of immunity.
Anticoccidial activity of narasin in broiler chickens reared in floor pens.
The anticoccidial activity of the ionophore narasin was tested in 3 floor-pen experiments. Narasin was tested at levels of 40, 60, 80, 100, or 120 ppm and compared against feeding ration containing 80, 100, or 121 ppm monensin or no medication. Feeding at all levels of narasin significantly prevented coccidiosis-induced mortality and improved weight gains and feed conversion ratios compared with the same parameters in groups given unmedicated feed. Protection with narasin was equal to or slightly greater than the protection obtained with monensin. The reduction in intestinal lesion scores was greater with narasin medication than with monensin. Analysis of pooled data from these trials indicated that a level between 48 and 96 ppm narasin would provide the optimum, depending on whether maximum weight gain or optimum feed conversion ratio was desired. Testing for coccidial immunity using the immunity challenge technique indicated that, based on the parameters of weight gain and lesion scores, even levels as low as 40 ppm narasin had enough efficacy to significantly reduce the amount of immunity which developed in medicated birds compared with the level of immunity developed in birds receiving unmedicated feed.
Anticoccidial activity of narasin in battery raised broiler chickens.
The anticoccidial activity of the ionophorus antibiotic narasin was tested against six species of coccidia (Eimeria acervulina, Eimeria mivati, Eimeria maxima, Eimeria necatrix, Eimeria brunetti, and Eimeria tenella) in battery-raised broilers. Feeding ration medicated with 60, 80, or 100 ppm narasin significantly improved weight gains during the periods of D 0 to D7 and D 0 to D 14 (D 0 = day of inoculation with sporulated oocysts), compared with the weight gains in corresponding inoculated groups fed unmedicated feed. A similar protective effect of the medication was seen with feed conversion ratios (feed consumed/bird weight) and coccidiosis-induced mortality. With most species studied, 40 and 60 ppm narasin was not as efficacious as 80 or 100 ppm. The maximum numerial improvement in weight gain and feed conversion ratio was with 80 ppm narasin. Gross intestinal lesion scores were reduced by medication compared with the scores in birds fed unmedicated feed. The overall trend was for a larger reduction in lesion score with higher drug levels. Narasin at 80 or 100 ppm was generally more effective in controlling individual or mixed species infections of coccidia than 99 ppm monensin.
Eimeria dispersa, E. adenoeides, and E. meleagrimitis: intestinal mucosal disruption in turkeys as seen with scanning electron microscopy.
Tissues from the digestive tract of turkeys infected with Eimeria dispersa, E. adenoeides, or E. meleagrimitis were compared with tissues from uninfected controls as seen with light microscopy (LM) and scanning electron microscopy (SEM). Six regions were examined--duodenum, jejunum, ileum, cecal neck, cecal pouch, and large intestine. Although LM showed large numbers of E. dispersa in the epithelial cells, SEM usually showed little mucosal disruption. Occasionally the surface of duodenum and jejunum, as seen with SEM, was convoluted and disrupted. In one bird, some parasite-induced damage was found with either LM or SEM in the duodenum and jejunum of turkeys given E. adenoeides oocysts. Although LM showed parasites in the rest of the digestive tract of all E. adenoeides infected birds, SEM showed only a localized sloughing of the mucosa in the cecal pouch. The most extensive damage to the villar surface was caused by E. meleagrimitis. Infections often disrupted the villar tips, especially in the small intestine and cecal neck. Localized areas of pitting were often found on individual villi. All 3 species produced oocyst extrusion sites, especially in the ileum and the ceca.