Listeria monocytogenes septicemia was diagnosed in a 6-day-old Thoroughbred foal. Primary clinical signs included fever, depression, diarrhea, and respiratory distress. Hematologic abnormalities included leukopenia, neutropenia, degenerative left shift, and hyperfibrinogenemia. Clinical chemistry and blood gas abnormalities included metabolic acidosis, hypoxemia, hypocapnia, hypoglycemia, and hyponatremia. Despite aggressive therapeutic intervention and intensive care, the foal died within 12 hours of admission. A postmortem examination was performed, and the primary gross lesion was bilaterally severe, focally extensive bronchopneumonia. Histopathology revealed severe subacute multifocal suppurative bronchopneumonia with necrotizing vasculitis and intralesional coccobacilli. Cultures of blood collected at admission and immediately prior to death were positive for L. monocytogenes, as were cultures obtained from lung and liver at necropsy. Immunohisto-chemical examination of formalin-fixed tissues revealed abundant intra- and extracellular L. monocytogenes antigen within the lung and intravascularly in multiple organs.
Between January 1997 and March 1998, 11 cases of H7N2 avian influenza (nonpathogenic) were diagnosed at the Laboratory of Avian Medicine and Pathology, Kenneth Square, PA. These cases involved either commercial leghorn laying hens or leghorn pullets raised in Pennsylvania. Grossly and histologically, the most striking lesion associated with disease was salpingitis, usually with edema and occasionally with oviduct necrosis. Fluid, fibrinous, and egg yolk material in the peritoneum (egg yolk peritonitis) as well as pulmonary congestion and pulmonary edema were also frequently seen. Oviduct lesions have rarely been described in association with avian influenza infections in previous outbreaks. Mortality in affected houses was mild to moderate (less than 4% total mortality during the outbreak), with concurrent mild to moderate egg production declines (2%-4% at the time of disease onset).
Encephalomycarditis virus recovered from a pig mortality in New South Wales was used to produce experimental infections. Of 34 pigs exposed, 17 died and a further 7 were found to have severe heart lesions when killed. Deaths occurred from 2 to 11 days after exposure with a mode of approximately 3 days. Ten of 11 pigs exposed by intramuscular injection died and the remaining pig was killed after 28 days and found to have severe resolving heart lesions. Of 15 pigs exposed per os to various doses of virus, 6 died, 4 were killed and found to have severe heart lesions and 5 were apparently not infected. Intranasal exposure of 8 pigs resulted in 1 death and 4 pigs with mild to severe heart lesions. Different doses of virus and routes of exposure did not substantially influence the character of the lesions. Lesions were similar to those found previously in field cases, and virus was recovered from all of 19 animals examined with severe acute lesions of 10 days standing or less.
Substantial pig mortalities due to heart disease caused by EMC virus infection are described. The majority occurred in 1970 in conjunction with a rodent plague, but retrospective diagnosis of occasional similar mortalities in previous years was possible. Mortality rates in pigs aged 3 to 16 weeks ranged from a few percent to over 50% and the rate was generally highest in younger animals. It is likely that a considerable proportion of cases was sub-clinical. Focal or diffuse pale areas occurred in the myocardium, the wall of the conus arteriosus being most severely affected. In a few animals, resolving lesions were present. Encephalomyocarditis virus was consistently recovered from pigs with acute heart lesions, but not from those in which myocardial fibrosis had commenced. The virus was demonstrated in rodents, although the dependence of pig disease on rodent-derived virus could not be established. Because of similarities between EMC and FMD myocarditides in pigs, specific diagnosis by virus isolation and identification should be obtained whenever possible.
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