Sylvatic trichinosis in British Columbia: potential threat to human health from an independent cycle.

The results of a 3-year study of trichinosis in British Columbia wild-life, based on the testing of more than 9,000 tissue specimens from a large variety of animal species, indicated that trichinosis is widespread among wild mammals in the southern and central parts of British Columbia. This continuing survey has established that the disease is carried by at least 15 species of terrestrial mammals including 3 species of rodents. The finding of Trichinella spiralis in ground squirrels and nonsynanthropic mice may be the first reported in North America. Although trichinosis appears to be eradicated in domestic pigs in British Columbia, a sylvatic cycle of the disease continues to exist independently and poses a potential threat to human health. It is possible for human beings to contract trichinosis by consuming inadequately cooked meat from certain wildlife species, especially bears, as well as meat products (such as pork or beef sausage) to which game meat has been added; several local outbreaks were caused by this source. Another hazard of unknown potential is the spread of trichinosis from the wild animal reservoir--from rodents in particular--to domestic pigs and thus to man.

Fusariotoxicosis from barley in British Columbia. I. Natural occurrence and diagnosis.

Clinical sickness was observed in domestic ducks, geese, horses and swine during October 1973. All species showed upper alimentary distress with mortalities occurring in the geese. Barley derived from a common source had been fed. Examination of the barley revealed invasion by Fusarium spp and detection of a high level of dermatitic fusariotoxins.

Fusariotoxicosis from barley in British Columbia. II. Analysis and toxicity of syspected barley.

Fusariotoxin T-2, a trichothecene, was tentatively identified in barley samples which caused field outbreaks of mycotoxicosis in British Columbia. Geese died when fed the contaminated barley experimentally but mice were little affected after long term feeding. The methods used in the laboratory for trichothecene extraction and identification of T-2 toxin are described.

Ascaris suum infection in calves. 3. Pathology.

Gross changes in the lungs of Ascaris suum- infected calves consisted of atelectasis and hemorrhagic foci, edema and emphysema, frequently with bullae. Prominent microscopic lung lesions were edema and emphysema of the interlobular septa with large numbers of eosinophils within and around lymphatics, peribronchiolar lymphoid nodules and parasitic granulomas. Many of the microscopic features were consistent with those found in atypical interstitial pneumonia. Changes in the alveoli were atelectasis, the exudation of plasma proteins, mononuclear cells and eosinophils, and alveolar wall thickening. Lesions found later included fibrosis and fetalization of the alveolar walls. Plasma cells and neutrophils were not common. Challenge with Toxocara canis after sensitization with A. suum resulted in the lungs developing a few areas of atelectasis. Migration of T. canis to lungs of calves is slower than A. suum. A. suum larvae were always found in bronchi, bronchioles and alveoli of calves that died. Lesions were observed in the liver but not the kidney of A. suum infected calves; both lung and liver lesions tended to resolve with time.

Ascaris suum infection in calves. I. Clinical signs.

Clinical signs consistent with those of atypical interstitial pneumonia (AIP) were induced in calves sensitized with infective Ascaris suum eggs at seven to 20 weeks of age and challenged at three-week intervals one or more times. These signs usually appeared on the sixth or seventh day postinfection and reached maximum severity between the tenth and 13th days following infection. Prominent signs were: dyspnea, often with expiratory grunt, coughing, mouth breathing and emphysema as well as increased respiration and heart rates. In general, the intensity of signs was dependent upon dose size, although a single small dose resulted in acute signs and death in one calf. Intermittent coughing and vesicular sounds were induced in calves given A. suum eggs continually over prolonged periods. No respiratory abnormalities resulted from challenge with Toxocara canis after sensitization with A. suum. Antihistamine therapy did not alter the clinical signs in A. suum infected calves.

Ascaris suum infection in calves. II. Circulating and marrow eosinophil responses.

An increment in the number of circulating eosinophils occurred between the 11th and 14th days after infection with Ascaris suum and this increase was generally greater after a challenge infection. Continual infection with small numbers of A. suum eggs over prolonged periods resulted in circulating eosinophil levels which fluctuated and were dose-dependent. The per cent marrow eosinophils always increased after a primary infection and a greater increase usually followed a challenge infection. The maximum increment of marrow eosinophils occurred between the tenth and 12th days and preceded the rise in circulating eosinophils by 36 hours. Antihistamine therapy did not alter eosinophil responses to A. suum. Circulating eosinophilia was not usually reflected by drastic changes in differential white cell counts. However, an increase in total white cell count often followed infection with A. suum and frequently parallelled changes in eosinophil counts. Hemoglobin and P.C.V. values remained within normal limits in A. summ infected calves.