Pluronic poisoning in a herd of dairy calves

Of 32 calves given an unknown amount of a pluronic bloat mixture with their milk, 28 died in convulsions over 24 hours. Supportive therapy was unsuccessful. Concentrations of pluronic present in abomasal and rumenal contents supported a diagnosis of pluronic poisoning.     

Copper poisoning in a dairy herd fed a mineral supplement

Copper poisoning in a dairy herd resulted in the death of 9 of 63 (14%) adult Holstein cows. Clinical signs were acute anorexia, weakness, mental dullness, poor pupillary light reflexes, and scant nasal discharge. These were followed by recumbency, chocolate-colored blood, jaundice, and death. Four animals exhibited signs of hyperesthesia and/or rumen stasis prior to death. At necropsy there was generalized icterus of body tissues, with the liver appearing orange and the kidneys dark blue. Histologically, there was accumulation of hemosiderin in Kupffer cells, and severe to moderate hepatocellular necrosis in all cases. Ammonium molybdate added to the ration, combined with the cessation of mineral supplementation, arrested the outbreak.

These cases illustrate significant mortality, due to copper poisoning, in adult cattle fed a low-dose mineral dietary supplement for over two years. Dietary copper intake of the herd (on a dry matter basis) was 37.5 mg/kg for lactating cows and 22.6 mg/kg for dry cows.

     

Case study of copper poisoning in a British dairy herd

Following the initial diagnosis of chronic copper poisoning (CCP), the copper (Cu) status of a British dairy herd was investigated. Eight fatal cases of CCP were identified over a 17-month period, from December 1999 to May 2001, involving seven Jersey cows and one Holstein-Friesian; seven cows were dry when CCP occurred. Case diagnostic criteria were necrotising hepatopathy associated with abnormally high liver and kidney Cu concentrations. Analysis of the ration for the high-yielding Jersey cow group revealed about 50 mg Cu/kg dry matter intake (DMI). Risk factors predisposing to fatal CCP were Jersey breed, previous high yield, first two weeks of the dry period and moderately high dietary Cu (greater than 40 mg Cu/kg DMI).     

Carbamate poisoning in a dairy goat herd: Clinicopathological findings and therapeutic approach

Abstract

CASE HISTORY: Approximately 1 hour after the consumption of carnations from a nearby glasshouse 55 animals from a dairy goat herd exhibited signs of possible poisoning.

CLINICAL FINDINGS: Upon clinical examination affected animals exhibited signs of salivation, tympany, tachypnoea, polydipsia, urination, diarrhoea, bradycardia, miosis, tremor and convulsions. As poisoning from an acetylcholinesterase-inhibiting insecticide was suspected, treatment with atropine sulphate was initiated at a dose of 0.3 mg/kg bodyweight. The treatment was repeated for some animals that relapsed, and was effective in all cases, with the exception of one goat kid that died.

DIAGNOSIS: Necropsy of the goat kid showed pulmonary oedema and congestion of internal organs. Toxicological analysis of stomach contents and liver of the dead animal, as well as of the carnations, revealed high concentrations of carbamates.

CLINICAL RELEVANCE: Carbamate poisoning after consumption of polluted feedstuffs or glasshouse products can be fatal for dairy goats. Atropine sulphate, at 0.3 mg/kg, can be useful in treating this condition.     

Monensin toxicosis in a dairy herd

An acute onset of illness was reported in a lactating dairy herd in Canada in which monensin had been incorporated in error in its ration at almost 10 times the prescribed level. All of the lactating cows became lethargic, were inappetant, developed diarrhea, and had decreased milk production from 28 kg/cow/day, the day before exposure, to 23 kg/cow/day, 3 d later. Within 9 d, all animals recovered from the incident and milk production returned to previous levels.     

Phosphorus deficiency in a dairy herd

Phosphorus deficiency was diagnosed in a 90 cow seasonal supply dairy herd which showed low milk production, ill-thrift, infertility and osteophagia. Serum inorganic phosphorus and pasture phosphorus levels were low, pasture Ca:P ratios high and soil phosphorus levels very low; the soil phosphate retention value was 96%. The deficiency, which had probably existed for several years, was considered to be due to inadequate annual phosphate fertiliser applications on a high phosphate retaining soil. Phosphorus deficiency may have been exacerbated by the application of lime without phosphate several months before the onset of severe clinical disease. The finding of low sodium levels in pasture samples suggested that sodium deficiency may have co-existed and contributed to the clinical picture. Treatment, comprising bone flour dusting of pasture, water trough supplementation and phosphorus-containing injections, appeared to induce ovarian activity in anoestrous cows and suppress osteophagia, though controlled treatment trials were not performed. No improvement was noted in milk production or cow condition. Increased annual super-phosphate and reduced potassium applications were recommended, together with the monitoring of pasture and soil macro elements and serum phosphorus levels. A decision on whether to supplement with sodium would be based on the results of pasture monitoring, since a direct animal test is not currently available. It is suggested that phosphorus deficiency may not be uncommon in dairy herds in some North Island districts; based on the present case, the decline in New Zealand superphosphate quality in the 1970's and recently published data which has shown a high proportion of pasture phosphorus deficient sites in some North Island areas.     

Mycoplasmal mastitis in a dairy herd

In October 1985, mycoplasmas were isolated from bulk tank milk samples in a large Florida dairy (greater than 1,400 lactating cows). At that time, measures to isolate and control the spread of infection were instituted. In an initial screening test, Mycoplasma bovis was isolated from 21 of 153 milking string samples (milk from all quarters of 10 cows/string). Composite quarter milk samples from all quarters of every individual lactating cow in the herd were obtained for culture in November 1985 and December 1985. In October, 88 of 1,535 (5.7%) cows were identified as Mycoplasma-positive. An additional 31 Mycoplasma-infected cows were identified in December. The dairy elected to maintain the infected cows in a separate Mycoplasma-positive subherd, which would be milked at the end of each milking session. Seven additional Mycoplasma-positive cows were identified at initiation of lactation. All newly identified infected cows were transferred to the Mycoplasma-positive subherd. After segregation of Mycoplasma-positive cows, bulk tank milk samples obtained routinely from the main herd remained culture negative throughout the study. From February 1986 to October 1986, quarter milk samples were obtained monthly from cows in the Mycoplasma-positive subherd. Any cow that developed clinical mastitis or substantial decrease in milk production was, at the discretion of the herdsman, culled. Of the 126 cows in the subherd, 22 (17.5%) were culled for mastitis, 35 (27.8%) were culled for low production, and 9 (7.1%) were culled for other reasons. Of the remaining 60 cows, 16 (12.7% of the 126 cows) were Mycoplasma-positive on the basis of results from one or more samples obtained after February 1986.(ABSTRACT TRUNCATED AT 250 WORDS)     

Aldicarb toxicosis in a dairy herd

Aldicarb, an extremely toxic carbamate, caused sudden death of several lactating Holstein cows. Confirmation of this toxic agent as the cause of death was hindered by its rapid breakdown in biological tissue. Therefore, aldicarb was not detected in rumen contents of some of the dead cows, and brain acetylcholinesterase values were essentially normal. The analyses were conducted 2 to 4 days after death of the cows. Rapid testing of tissue samples is necessary if a carbamate insecticide is suspected.     

Effect of terbufos poisoning on the blood cholinesterase and hematological values in a dairy herd

This report describes the effects of a sublethal dose of terbufos (counter 15G formulation) in a dairy herd. Ingestion of terbufos depressed whole blood cholinesterase activity. No recovery of this enzyme was evident until 30 days after ingestion after which a constant rate (0.65%/day) increase was observed.

There was a good correlation between blood cholinesterase levels and clinical signs. Normal cholinesterase levels were reached at approximately 150 days after exposure. Cholinesterase levels in animals, ill prior to exposure, were slow to recover, while levels of healthy cattle surpassed those of control animals. Anemia was observed in some cows at approximately 30 days after exposure. The degree of anemia paralleled the severity of poisoning. The increase in packed cell volume paralleled the return of blood cholinesterase activity.

     

Neospora abortion epidemic in a dairy herd

Neospora caninrm is a protozoan closely related to Toxoplasma gonclii. It was discovered only a few years ago, but it is now recognised as one of the most common and important causes of abortion in cattle. Brain lesions characteristic of Neospora infection have been found in about 25% of aborted foetuses submitted to diagnostic laboratories in New Zealand and overseas⁽¹⁾⁽²⁾. Average abortion rates due to Neospora on New Zealand farms have been estimated at 7% of pregnancies compared with 4% due to other causes⁽¹⁾. The upper range of abortion rates for Neospora was 17–30% compared to only 7–10% for other causes, showing that the economic effects of Neospora abortions on the more severely affected farms can be devastating.