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Outbreaks of H5N1 highly pathogenic avian influenza (HPAI) occurred in various types of domestic poultry in Thailand during 2004-05. H5N1 viruses were also detected in humans and other mammalian species. Infections were mainly detected in backyard chickens and domestic ducks. The geographic distribution of the 2004 outbreaks was widespread throughout Thailand; most outbreaks occurred in the Central Region, the southern part of the Northern Region, and the Eastern Region. In 2005, the H5N1 outbreaks continued and showed a clustered pattern in four provinces in the southern part of the Northern Region and in one province in the Central Region. H5N1 HPAI outbreaks caused serious socioeconomic consequences to the poultry industry, the social community, farmers' livelihood, and human health. After key measures were implemented, the incidence of the outbreaks declined remarkably in 2005.

Pasteurella multocida group B, serotype 3, was isolated from sinusitis-affected khaki Campbell ducks. To study the role of P. multocida in sinusitis, commercial khaki Campbell ducks were experimentally infected with P. multocida alone or combined with Escherichia coli. In Expt. 1, experimental ducks were infected with P. multocida intranasally or ocularly. A comparison was done by intranasal inoculation with pooled nasal discharge from the affected ducks or phosphate-buffered saline. The ducks intranasally inoculated with the nasal discharge or P. multocida showed sinusitis. In Expt. 2, E. coli alone or a combination of P. multocida and E. coli was intranasally inoculated into experimental ducks. The ducks intranasally inoculated with the combination of P. multocida and E. coli had sinusitis, the same as found in the field but less severe than that of the field cases. Pasteurella multocida was already present in litter/floor of duck farms. We concluded that P. multocida played a role in induction of sinusitis. However, the sinusitis in ducks may be initiated by poor management, especially in the brooding period of ducks.

Attempts to reproduce malabsorption syndrome (MAS) by oral inoculation with several different combinations including intestinal homogenate, reovirus, and hemolytic Escherichia coli obtained from MAS-affected chickens and intestinal homogenate from healthy chickens (healthy homogenate) were performed in 1-day-old specific-pathogen-free (SPF) broilers. The MAS homogenate, serving as a positive control, induced weight gain depression and intestinal lesions such as cystic crypts of Lieberkuhn, villus atrophy, and lymphoid and/or granulocytic infiltration. The healthy homogenate, the formalin-treated MAS homogenate, the formalin-treated healthy homogenate, and phosphate-buffered saline caused neither weight gain depression nor intestinal lesions. We were able to reproduce both weight gain depression and intestinal lesions by inoculation of reovirus either combined with the formalin-treated MAS homogenate or combined with healthy homogenate. Surprisingly, when hemolytic E. coli was added to the combination of reovirus with formalin-treated MAS homogenate, this did not cause weight gain depression although this combination caused the described intestinal lesions. Identical results were obtained with the combination of formalin-treated MAS homogenate with hemolytic E coli or the combination of reovirus with hemolytic E. coli. The intestinal lesions were more severe and developed faster by combinations including reovirus and formalin-treated MAS homogenate. This study indicates that a combination of enteropathogenic reovirus with other agents or substances that are present in an intestinal homogenate from MAS-affected and healthy chickens can induce MAS in SPF broilers. Escherichia coli is not essential for induction of weight gain depression but can play a role in development of intestinal lesions. Furthermore, intestinal lesions alone will not always result in weight gain depression.

Five malabsorption syndrome (MAS) homogenates from The Netherlands and Germany were used to reproduce MAS in broilers. We studied the histopathology after inoculation of 1-day-old broiler chicks and the agents that might be involved. Generally, the MAS homogenates induced signs that differed in severity and pathobiology. We could distinguish and classify the inoculated groups best by histopathology: proventriculitis, lesions in the small intestines in combination with proventriculitis, or lesions of the small intestines only. Lesions in the small intestine had more impact on weight gain depression than lesions in the proventriculus. In three out of five inoculated groups, microscopic lesions of the pancreas were found. Reovirus was detected in the inoculated groups by virus isolation and seroconversion, and reoviral antigen was detected by immunohistochemistry of the small intestine. Also, enteroviruslike particles were detected in three of the five inoculated groups, although not in the most affected group. Additionally, bacteriophages and bacteria (hemolytic Escherichia coli, Pasteurella hemolytica, and Enterococcus durans) were isolated from inoculated chicks. The role these agents play in pathogenesis of MAS is still unsolved.