Bound xenobiotic residues in food commodities of plant and animal origin

The following are extended summaries of Technical Reports which are produced at intervals by the International Union of Pure and Applied Chemistry (IUPAC). They are entirely the responsibility of IUPAC/the authors and do not necessarily reflect the views of the Editorial Board of Pest Management Science. Copyright © 2002 Society of Chemical Industry     

Prevention of pleuropneumonia in pigs by in-feed medication with sulphadimethoxine and sulphamethoxazole in combination with trimethoprim

The prophylactic effect of in-feed medication of conventional pigs with sulphadimethoxine (SDM), sulphamethoxazole (SMX), and trimethoprim (TMP) was tested by using an Actinobacillus pleuropneumoniae infection model. In each of five experiments, six pigs were given medicated feed twice daily and three pigs received antibiotic-free feed and served as positive (unmedicated, infected) controls. The following drugs or drug combinations were tested (in mg per kg feed): 500 SDM + 100 TMP, 500 SMX + 100 TMP, 125 SMX + 25 TMP, 125 SMX (alone) and 25 TMP (alone). After six days of feed medication, all animals were endobronchially inoculated with A. pleuropneumoniae in a dose of 1-3.10(4) colony-forming units (CFU). The response to the challenge in all control pigs was characterized by fever, lethargy, anorexia, reduced water consumption, and laboured breathing. At autopsy all controls manifested a fibrinous haemorrhagic pleuropneumonia. In-feed medication with 500 SDM + 100 TMP, 500 SMX + 100 TMP as well as 125 SMX + 25 TMP resulted in an effective protection against the challenge in all treated animals. After consumption of feed medicated with 125 mg per kg SMX or 25 mg per kg TMP, pleuropneumonia was evident in all challenged pigs. The results of this study indicate an in vivo potentiation of SMX and TMP in pigs against this respiratory tract pathogen.     

Ovine craniofacial malformation: A morphometrical study

Craniofacial malformation in 64 sheep was phenotypically described as mandibular distoclusion. Digital radiographs were examined in order to determine the degree of morphological changes in certain bones of the skull. Therefore, laterolateral standardised digital radiographs were used to determine anatomic reference points. Subsequently, five reference lines were defined and 16 linear and seven angular measurements were determined to describe malformations in the bones of the skull. Statistical analysis revealed a significant shortening of the rostral part of the corpus mandibulae and of the ramus mandibulae. However, the molar part of the mandible remained unchanged. These morphological changes caused premolar and molar malocclusion. No further craniofacial abnormalities, such as an elongation of the maxilla or of the incisive bone, were identified. In conclusion, the phenotypically observed mandibular distoclusion is caused by a shortening of specific parts of the mandible. This form of ovine craniofacial malformation is therefore best described as brachygnathia inferior.     

Review of literature and results from test matings of East Friesian milk sheep affected with brachygnathia inferior

Shortness of the lower jaw (brachygnathia inferior, underbite, overshot, parrot mouth) is an inborn and mostly hereditary malformation often seen in many sheep breeds. Chromosomal anomalies are generally not involved in brachygnathia inferior. Viral infections, teratogenic drugs and alkaloids of plants often lead to craniofacial malformations associated with brachygnathia inferior. A maternal deficiency of iron is discussed as a cause for brachygnathia inferior. We performed a three-year breeding trial using mainly East Friesian milk sheep affected by brachygnathic occlusion. Mating schemes included affected by affected and affected by unaffected matings. In the breeding trial, 60 lambs were born and from these 37 animals had variable degrees of brachygnathia inferior. The brachygnathic condition increased with rising age of the lambs. Extremely affected lambs showed palatine ulcers and growth retardation. Moreover, some animals had abnormal positions of the incisor teeth, distortion of the lower jaw and deformities of the external ear. Analysis of the pedigree did not support a monogenic inheritance pattern. An oligogenic inheritance including a dominant and recessive locus responsible for the major gene effects and possibly further modifying loci appeared much more likely. Other causes for brachygnathia inferior such as viral infections and anemia of the ewes could be ruled out. Chromosomal abnormalities were not evident and thus, large chromosomal defects were not associated with brachygnathia inferior.