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Q fever is a zoonosis caused by the bacterium Coxiella burnetii. One of the largest reported outbreaks of Q fever in humans occurred in the Netherlands starting in 2007; epidemiologic investigations identified small ruminants as the source. To determine the genetic background of C. burnetii in domestic ruminants responsible for the human Q fever outbreak, we genotyped 126 C. burnetii–positive samples from ruminants by using a 10-loci multilocus variable-number tandem-repeat analyses panel and compared them with internationally known genotypes. One unique genotype predominated in dairy goat herds and 1 sheep herd in the human Q fever outbreak area in the south of the Netherlands. On the basis of 4 loci, this genotype is similar to a human genotype from the Netherlands. This finding strengthens the probability that this genotype of C. burnetii is responsible for the human Q fever epidemic in the Netherlands.

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Abstract. Eighty bovine fetuses with confirmed neosporosis were used to score lesion severity and presence of parasites in brain, heart, and liver. A comparison was made between epizootic and sporadic abortion cases. The possible influence of fetal age was also investigated. Histologic lesions of multifocal encephalitis, myocarditis, and periportal hepatitis with or without focal hepatocellular necrosis were almost always observed. Neospora caninum tachyzoites were identified immunohistochemically in 85% of the brains, 14% of the hearts, and 26% of the livers. Tissue cysts were observed in 21% of the brains. Significant differences between epizootic and sporadic abortion cases were found only in the liver. Hepatic lesions were more prominent and N. caninum tachyzoites were observed more frequently and in higher numbers in epizootic cases. Examination by immunohistochemistry of the liver in addition to the brain can be highly contributive diagnostically, particularly in epizootic cases. There were no significant age-related differences except for a higher presence of tachyzoites in the hearts of younger fetuses (3-4 months gestational age).

Congenital porto‐systemic shunts in sixteen dogs and three cats are described. A major symptom was hepato‐encephalopathy. In most cases diagnosis was based on elevated venous ammonia levels, abnormal ammonia tolerance and results of operative mesenteric portography. Clinical signs, laboratory findings, results of portography, and pathologic findings in the liver and the central nervous system are described. A diagnostic schedule is proposed to aid in recognition of this syndrome.