[Lungworm disease in dairy cattle: symptoms, diagnosis, and pathogenesis on the basis of four case reports]. / Longwormproblemen bij melkkoeien: symptomatologie, diagnostiek en pathogenese aan de hand van een viertal cases.

Clinical lungworm disease appears to occur frequently in Dutch dairy herds. Because the clinical diagnosis is difficult to make in adult cattle, the clinical diagnosis, laboratory diagnosis, differential diagnosis, therapy, and prevention are discussed in this article. In addition, four cases of lungworm disease in adult cattle are presented. The main clinical complaints were coughing, decreased milk production, and weight loss. Several lactating cows died in one herd. The disease history of four herds revealed that introduction of susceptible cows or heifers to herds with cows with subclinical patent lungworm infections had resulted in a pasture infection, leading to clinical problems in both the newly introduced and 'resident' cows of the herd. Further history analysis of the fourth herd revealed that re-introduction of lungworm infection by newly purchased cows in a lungworm free herd resulted in clinical lungworm problems in adult and young animals. The fourth case led to the conclusion that lungworm infection must have been re-introduced by cows purchased from another farm.

Nematode-trapping fungi in biological control of Dictyocaulus viviparus.

Larvae of the cattle lungworm Dictyocaulus viviparus were cultured in experimental units of 200 g cattle faeces placed in semi-transparent trays in the laboratory. In each of 4 experimental series using this experimental unit, chlamydospores (chl) of the nematode-trapping fungus Duddingtonia flagrans were admixed to half of the faecal cultures in a concentration of 50.000 chl/g. In all 4 series there was a significant reduction in the development and subsequent release of infective lungworm larvae from faecal cultures containing chlamydospores. The average reduction in larval release, caused by fungal spores, was 86%.

Evaluation of the effect of the fenbendazole sustained-release intraruminal device on the immunity of calves to lungworm.

Each of 10 set-stocked calves was given a fenbendazole sustained-release intraruminal bolus at turnout for the control of parasitic bronchitis while a group of 10 similar calves was left untreated. The respiratory rates of the control calves were not greatly increased during the grazing season, but persistent coughing was evident from early July when they all had patent lungworm infections. Only occasional coughing was reported from the bolus-treated calves except for a transient increase in its frequency in late September. In mid-August, one of the treated calves was passing lungworm larvae and when they were housed six of the 10 had patent infections. In August tracer calves picked up an average of 23.5 lungworms per day from the control paddock but only 2.1 from the paddock grazed by the treated calves. In September the corresponding figures were 7.6 and 19.2 lungworms per day, respectively, from the control and 'treated' paddocks. After housing, the post mortem worm counts after an experimental challenge with Dictyocaulus viviparus larvae were reduced by 99.2 and 98.7 per cent (P < 0.0001), respectively, for the control and bolus-treated calves in comparison with weight-matched parasite-naive calves. Thus, despite a relatively low level of challenge during the grazing season, the treated animals had developed a considerable degree of protective immunity.

Infection build-up and development of immunity in calves following primary Dictyocaulus viviparus infections of different levels at the beginning or in the middle of the grazing season.

An experiment was carried out to study the build-up of infection and development of immunity against Dictyocaulus viviparus infections in calves. Six groups of four calves were used. Groups 1-5 grazed on separate pastures and Group 6 served as a permanently housed control group. To simulate 'low' and 'very low' overwintered pasture infectivity, Groups 1 and 2 were infected experimentally six times with ten and two larvae, respectively, during the first 3 weeks on pasture in May. From the middle of July, Groups 2-4 were experimentally infected six times in 3 weeks with 10, 10 and 100 larvae, respectively, to simulate 'low' and 'moderate' pasture contamination by carriers. Group 5 served as a non-infected pasture control group. After housing of Groups 1-5 in October, all calves were treated with oxfendazole and challenged with 5000 larvae of D. viviparus to evaluate the development of immunity. The results showed a similar population build-up of lungworm infections in Groups 1-4. After the beginning of patency, 24-35 days after primary infection, an increase in faecal larval counts occurred 31-35 days later as a result of re-infection. For Group 2, this was only true when the infections with a total of 12 larvae in May were ignored, as these did not result in patent infections. Faecal larval counts were highest in Group 4, which was the only group with mild signs of lungworm disease occurring in the re-infection period. The worm counts at necropsy showed the development of immunity in Groups 1-4 but not in Group 5. This is consistent with the fact that Group 5 did not develop patent lungworm infections throughout the grazing season.

Dose-dependent pathophysiological changes in cattle experimentally infected Dictyocaulus viviparus.

In two trials five calves were each experimentally infected on three consecutive days with a total number of either 30 Dictyocaulus viviparus larvae per kg body weight (trial A) or 3 larvae/kg body weight (trial B). Five calves served as non-infected controls. Infected cattle in trial A developed severe clinical signs of dictyocaulosis and one calf died 37 days post infection (p.i.), whereas all cattle in trial B remained clinically healthy. Weight gains in both trials were not statistically different. Haemoglobin concentrations, packed cell volume (PCV), number of erythrocytes and leucocytes, blood pH and albumin concentrations were in the physiological range in all groups. Infected cattle in trial A showed increases in respiratory rates, body temperature, serum protein concentrations, and blood eosinophil counts and decreases in oxygen partial pressure. Infected cattle in trial B showed increased blood eosinophil counts. Antibody formation in infected cattle of both trials showed a similar pattern. Excretion of larvae from infected cattle reflected the different infection doses. Microbiological examinations showed an increase of facultatively pathogenic bacteria in the lung fluid.

Relationship between cytologic changes in bronchoalveolar lavage fluid and weight gain in calves with gastrointestinal nematodes and lungworms.

Two of three groups of 10 calves each were infected with either 100,000 infective larvae (L3) of Ostertagia spp. and 100,000 L3 of Cooperia spp. or with 4000 L3 of Dictyocaulus viviparus, respectively, at the age of 14 weeks. The third group was not infected. After treatment with an anthelminthic five calves from each group were challenged with either 100,000 L3 of Ostertagia spp. and 100,000 L3 of Cooperia spp. or 4000 L3 of Dictyocaulus at the age of 20 weeks. The calves were 25 weeks old when slaughtered. Total and differential cell counts were determined in bronchoalveolar lavage fluid and showed that neutrophils were the most frequent and eosinophils the least frequent cell present. There was a significant negative relationship between eosinophil levels and weight gain of the calves.

Pathophysiology of nematodiasis in cattle.

Recent detailed studies of the physiologic changes occurring in cattle infected with some of the common gastrointestinal nematodes have shown that the weight loss and reduced carcass values resulting from these infections are a consequence of major alterations in host metabolism. Dramatic changes in protein metabolism were consistently found to involve decreased muscle synthesis and increased urinary nitrogen excretion. Because of the well-recognized loss of plasma proteins into the gut lumen and cellular damage at the mucosa occurring during nematode infections of the abomasum and duodenum, it has been assumed that protein was being lost in feces or not absorbed; however, this loss has proved not to be as significant as postabsorptive protein catabolism in these infections. Only when the colon and cecum are involved in protein-losing infections is the loss of protein into the feces significant. The mechanisms by which gastrointestinal nematode infections result in such altered host metabolic states are not known, but suggestions have been made that parasites directly or indirectly alter gut hormone levels. Gut hormone changes may also be responsible for diarrhea and anorexia. Another mechanism of altering metabolism has been proposed for chronic parasitisms that stimulate macrophages. Macrophages produce a peptide called cachectin, and cachectin is thought to mediate protein and lipid catabolism. This mechanism obviously could be contributing to weight loss and anorexia whenever nematodes cause sufficient macrophage activation, including during lungworm infections, which do not have enteric involvement.

Effect of infection with lungworms (Dictyocaulus viviparus) on energy and nitrogen metabolism in growing calves.

1. Ten Friesian male calves of about 100 kg and 3 months old were reared similarly and were worm-free. From 13 weeks of age five calves received a dose of 640 infective larvae (L3) of lungworms (Dictyocaulus viviparus) twice weekly for 8 weeks to simulate continuous infection. Animals not infected were fed to the same level as the infected animals (about 1.2-1.3 kg concentrates and 1.4-1.5 kg good-quality hay/d). 2. Heat production was measured twice weekly during 48 h (days 2 and 3, and days 5 and 6) in each group of experimental animals. 3. Infection caused considerable damage to the lungs, increased respiration frequency and clearly produced antibody titres against D. viviparus. 4. Animals infected with lungworms had on average a lower rate of weight gain, reduced by 70 g/d per animal. Digestibility was not affected. Nitrogen retention was much lower in infected animals (12.0 v. 14.6 g/d per animal in controls). 5. Metabolizability of energy was slightly reduced in infected animals. Heat production as found in infected animals may be associated with an increased maintenance energy requirement of 30 kJ/kg live weight 0.75 per d or reduced partial efficiency of feed conversion above maintenance in animals infected with lungworms (58.5 v. 64.1% in the control animals). 6. It was concluded that the depression in rate of gain was related to reduced intake of feed and to decreased N retention.

Longitudinal study of the effects of lungworm infection on bovine pulmonary function.

Clinical and physiologic investigations were done weekly in 5 nonsedated Friesian calves before, during, and after an induced infection with Dictyocaulus viviparus infective larvae. Clinical, hematologic, serologic, and parasitologic findings were all compatible with the classic picture of moderate subacute verminous bronchitis. Most pulmonary function values revealed significant (P less than or equal to 0.05) changes in the 2nd or 3rd week after inoculation and maximal changes at 5 weeks after inoculation. Most marked changes included a decrease in tidal volume, dynamic lung compliance, and arterial oxygen tension, and an increase in minute ventilation, minute viscous work of breathing, and alveolar-arterial oxygen difference. Minute ventilation, dynamic lung compliance, minute viscous work of breathing, and PaO2 revealed the most homogeneous change. Conversely, maximal change of intrapleural pressure, total pulmonary resistance, and viscous work of breathing had higher variability from week to week.

Physiological effects of experimental verminous bronchitis in Friesian calves.

Pulmonary function values were measured in five Friesian calves of five months of age during the patent phase of an experimental moderate lungworm infection and were compared with the pulmonary function values recorded in four control animals. All the nine calves were free of any previous challenge with Dictyocaulus viviparus and were submitted to the same standardized conditions of body conformation, housing, feeding and procedures for pulmonary function testing. A significant increase of respiratory rate, minute ventilation, total pulmonary resistance and power of breathing and a significant decrease of tidal volume, dynamic lung compliance and PaO2 were observed in the infested animals. The absolute intrapleural pressure values were also significantly more negative. The conclusions of the statistical analysis were almost identical when predicted instead of measured pulmonary function values were used in the control group. The clinical, functional and pathological findings in the infested animals were all consistent with the picture of a lower airway obstructive disease.

Parasitological, serological and clinical effects of continuous graded levels of Dictyocaulus viviparus inoculations in calves.

To investigate the parasitological, serological, clinical and growth effects of continuous graded levels of Dictyocaulus viviparus inoculations in calves an experiment was carried out with 10 groups of 5 calves each. Calves were inoculated twice a week during a period of ten weeks. The range of the doses was 10-2560 infective larvae (L3) per inoculation. The results were analysed by linear and curvilinear regression of various traits on infection level. It is concluded that: A continuous exposure of calves to L3 of D. viviparus was followed by a continuous larval excretion at all levels; Results of the ELISA technique gave a very good reflection of the level of infection; Clinical signs and weight loss were evident before the parasitological and serological results were positive; The serological parameter and the parasitological parameters were mainly linearly related to the level of infection. The clinical parameters were mainly cubically related to the level of infection.