Some pathophysiological changes associated with infection of Eimeria zuernii in calves.

Twelve Holstein-Friesian calves were divided into two groups, one of which was infected with Eimeria zuernii. Fecal oocyst output, weight changes and various blood, cellular, protein and biochemical constituents were examined for both groups. Maximal fecal oocyst output occurred 21 days after infection. Both groups of calves gained weight in a linear fashion until day 21 postinfection when the infected group lost weight rapidly. The packed cell volume of the infected calves appeared markedly reduced. Although there was a reduction in plasma proteins it did not appear significant. There was a significant reduction in plasma Na+ and Cl- ions of the infected calves. There were no significant changes in the other blood constituents examined.     

Influence of experimental Eimeria zuernii infection on clinical blood chemistry in calves

Coccidiosis, often caused by Eimeria zuernii infection, is an important diarrhoeal disease in calves [Fitzgerald, P.R., 1980. The economic impact of coccidiosis in domestic animals. Adv. Vet. Sci. Comp. Med. 24, 121-143]. Infection trials were performed to investigate the effects of experimental E. zuernii coccidiosis on clinical blood chemistry in calves. Three groups of calves were formed: group 1 (n=14) served as uninfected control group, group 2 (n=11) was infected with 150,000 sporulated E. zuernii oocysts per calf, and group 3 (n=16) was infected with 250,000 sporulated E. zuernii oocysts per calf. Measurements throughout the prepatent and the patent period revealed a marked influence of E. zuernii infection on the following parameters: total protein, albumin, urea, bilirubin, creatine kinase, free fatty acid concentration, and cholesterol. Aberrances in these were most pronounced in group 3. No significant and/or distinct changes after infection could be detected in blood glucose concentration. E. zuernii infection impairs intestinal function and induces catabolic metabolism in affected calves. Bilirubin, urea and cholesterol concentration, and creatine kinase activity were particularly affected indicating catabolism of protein and lipids.     

Long-term effect of toltrazuril on growth performances of dairy heifers and beef calves exposed to natural Eimeria zuernii and Eimeria bovis infections

The long-term effects of a toltrazuril treatment against natural Eimeria bovis and/or Eimeria zuernii infections were investigated in comparison with diclazuril and untreated controls on two dairy (Italian Friesian breed) and two beef (Chianina breed) farms. At each trial site, 30 calves were allocated into three groups of 10 calves each: T (treated with toltrazuril), D (treated with diclazuril) and C (left untreated). For 40 weeks post-treatment, the calves were weighed and examined clinically and parasitologically. The oocyst counts as well as the number of scour days were significantly lower in the T group than in the D and C groups. Final bodyweights and body condition scores of the T group exceeded those of groups C and D. The results confirmed that toltrazuril was highly efficacious, safe and provided productive benefits in dairy and beef calves.     

Effects of inoculations with Eimeria zuernii on young calves treated with decoquinate or narasin with or without dexamethasone

Sixteen 7-week-old Holstein male calves were inoculated with sporulated oocysts of Eimeria zuernii. Four calves (controls) were euthanatized and necropsied at 14 and 20 days after inoculation (DAI). Two calves were treated with 20 mg of dexamethasone (IM) on 13, 14, and 15 DAI and euthanatized and necropsied 17 DAI and 2 calves were given similar treatments and necropsied 20 DAI. The 8 other calves were euthanatized and necropsied 20 DAI. Two were started on the anticoccidial drug decoquinate in feed 13 DAI; 2 others were given decoquinate on the same schedule plus dexamethasone on 13,14, and 15 DAI. Two calves were given the antibiotic narasin in feed beginning 13 DAI and 2 calves were given parasin on the same schedule plus dexamethasone on 13,14, and 15 DAI. All calves, except 2 controls necropsied 14 DAI and 4 calves given decoquinate, discharged moderate-to-large numbers of oocysts in feces and had moderate-to-serve changes in fecal consistency. Histologic examinations revealed large numbers of endogenous stages in tissues of calves treated or not treated with dexamethasone. Few endogenous stages were observed in tissues from calves that were given decoquinate or decoquinate plus dexamethasone. Calves given narasin or narasin plus dexamethasone had moderate-to-large numbers of endogenous stages in the tissues.     

Comparative therapeutic effect of toltrazuril, sulphadimidine and amprolium on Eimeria bovis and Eimeria zuernii given at different times following infection in buffalo calves (Bubalus bubalis)

We compared the therapeutic effect of three anticoccidial drugs (toltrazuril, sulphadimidine and amprolium) in buffalo (Bubalus bubalis) calves experimentally infected with Eimeria bovis (E. bovis) and E. zuernii oocysts (3 x 104oocyst/calf). Buffalo calves (1.5-4 month old, 70-kg body weight) were randomly allocated into 3 groups (9 calves each). Group T was experimentally infected with oocysts and treated with toltrazuril (20 mg/kg BW twice orally at a 1-week interval). Group S was experimentally infected with oocysts and treated with sulphadimidine (125 mg/kg injected IM followed by half dose for 4 successive days). Group A was experimentally infected with oocysts and treated with amprolium (50 mg/kg orally for 7 successive days). Each group had three subgroups (three calves/subgroup) to represent timing of the drug administration: 1st day of coccidia infection (FD), onset of clinical signs of coccidiosis (CC), and onset of oocyst shedding into the faeces (OS). Clinical signs, body-weight gain (BWG) and number of oocysts per gram feces (OPG) were monitored daily for 35 days post-infection (DPI). The OPG were reduced (but the BWG was not different) in the T calves compared to S and A calves. Within the same group, treatment from the 1st day of infection reduced the OPG and increased the BWG compared to the later treatment timings.     

The development of the lesions caused by second generation schizonts of Eimeria necatrix.

First generation merozoites of Eimeria necatrix were found in epithelial cells of the crypts of Lieberkühn of chicks cells appeared to migrate into the lamina propria, forming nests of second generation schizonts that extended from the external muscularis to the lamina propria of the mid-villus. On the fourth and fifth days the mature schizonts, usually still within the infected cells were dishcarged into adjacent crypts. The muscularis mucosa appeared to be repaired by the formation of new, smooth muscle cells that spliced the broken ends of the ruptured muscle. 'Ghosts' of schizonts were found in the lamina propria on the sixth day after infection.     

The pathogenesis of enteric colibacillosis in neonatal unsuckled calves.

The development of pathological lesions in the small intestine of neonatal calves is described. Seven newborn calves were challenged orally with a known enteropathogenic strain of E coli 0101k?(A) and killed at varying times after inoculation. Adhesion of bacteria to the mucosa of the small intestine was observed in all calves. A few organisms were seen in the distal small intestine at three hours after inoculation and thereafter adhesion progressed anteriorly along the intestine in calves killed from six to 36 hours. In these calves pathological changes occurred between six and 12 hours after inoculation. Villi were stunted and thickened and the epithelial surface was irregular. A further calf, anaesthetised from five-and-a-half to 10 hours after inoculation and repeatedly sampled from the distal small intestine, developed similar lesions abruptly at nine hours after inoculation. Villus and crypt lengths in the challenged calves were compared with those in three normal uninoculated control calves.     

Coccidiosis causes diarrhea in calves in the pasture. Pasture coccidiosis caused by Eimeria alabamensis

A severe outbreak of diarrhoea in young (age 18-20 month) cattle 14 days after their first turnout is described. In the manure large numbers Eimeria alabamensis oocysts were found. This infection is considered as a case of coccidial diarrhoea in (older) calves at pasture.     

The involvement of polymorphonuclear leukocytes in the pathogenesis of bronchopneumonia in calves. III. Granulocyte activation by platelets.

The influence of platelets and platelet lysate on superoxide anion production and beta-glucuronidase release from neutrophils was investigated. Neither the suspension of unstimulated platelets from healthy calves nor its lysate had any influence on O2- production and enzyme release On the other hand, a great rise in superoxide anion production and beta-glucuronidase release was observed in the case of platelets from bronchopneumonic calves. It is suggested that platelets of bronchopneumonic calves can activate polymorphonuclear leukocytes, causing their degranulation and aggravating superoxide anion production.     

The involvement of polymorphonuclear leukocytes in the pathogenesis of bronchopneumonia in calves. VII. Granulocyte activation by arachidonic acid.

Arachidonic acid-induced granulocyte activation was studied in calves. Both in healthy and in bronchopneumonic animals, neutrophil stimulation with 67 microM arachidonic acid caused a rise in granulocyte exocytosis. This event, however, was much more intense in granulocytes from diseased calves. Fatty acids were found to stimulate granule exocytosis from granulocytes. Oleic acid possessed the weakest while dihomo-gamma-linoleic acid showed the strongest activity of this type. It is suggested that arachidonic acid may be an important mediator of calf bronchopneumonia.     

Experimental Eimeria bovis infection in calves: a histopathological study.

Eight male holstein calves, four to six weeks of age, were infected with 100,000 sporulated oocysts of a culture containing Eimeria bovis. The calves were injected with steroids on days 13, 14 and 15 and killed on days 16, 18, 19, 20, 21, 22, 24 and 26 postinfection. The lesions caused by experimental E. bovis infection in the small and large intestines are characterized by a diphtheritic typhilitis and colitis. Severe lesions were also seen in the last metre of the ileum in a calf killed 19 days after infection. Most of the damage of the intestinal mucosa is caused by the sexual stages. There is destruction and loss of epithelial cells with subsequent exposure of lamina propria and formation of diphtheritic membranes.     

The pathogenesis of Trypanosoma congolense infection in calves. V. Quantitative histological changes.

Calves infected with Trypanosoma congolense TREU 112 had generalized microvascular dilation which was most prominent in the liver and the mesentery; there also was increase in cellularity in the lung with significant alveolar thickening and accumulation of hemosiderin-bearing cells in the alveolar septa, focal accumulations of lymphocytes primarily at the corticomedullary junction of the kidneys and a well developed glomerulonephritis, likely membranoproliferative. Reticuloendothelial changes were marrow hyperplasia with an erythroid shift, moderate hemosiderosis and moderate dysthrombopoiesis, marked thymic cortical atrophy, hypersplenism and enlarged nodes with reduced cellular density, paracortical atrophy and medullary sclerosis.     

The involvement of polymorphonuclear leukocytes in the pathogenesis of bronchopneumonia in calves. IV. Myeloperoxidase activity.

Stable oxidant and hypochlorous acid production in neutrophils of bronchopneumonic calves was investigated. The production of these compounds was much more intense in neutrophils of diseased calves than in the control cells. The production of stable oxidants and hypochlorous acid was restrained by free radical scavengers. Functional response of neutrophils was inhibited by cyclooxygenase products and stimulated by lipoxygenase products of the arachidonic acid cascade. Superoxide anion production is not connected with the degranulation process (beta-glucuronidase release), and the two events are under different control mechanisms.     

The pathogenesis of Trypanosoma congolense infection in calves. IV. The kinetics of blood coagulation.

Blood coagulation studies showed there was a pronounced thrombocytopenia and hypofibrinogenemia in Holstein calves infected with Trypanosoma congolense TREU 112. There was also ineffective thrombopoiesis characterized by an increased megakaryocytic mass, reduced uptake of 35S-methionine into peripheral blood platelets and a normal platelet lifespan. There was an increased uptake of isotopic label into fibrinogen and a shortened half life indicating a consumptive error with increased peripheral use of fibrinogen. No consistent abnormalities were found in ethanol gelation, partial thromboplastin time, clot retraction and lysis or plasminogen assay. Fibrin split products were rarely detected. These findings suggest that in the chronic form of bovine trypanosomiasis there is a partially compensated consumption coagulopathy.     

Conjunctival lesions caused by Moraxella bovis in gnotobiotic calves

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.