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Birds
Despite the routine inclusion of anticoccidial drugs in the feed of reared game birds, coccidiosis remains one of the commonest conditions diagnosed in game birds submitted to Disease Surveillance Centres of SAC and Regional Laboratories of VLA. This probably reflects the relatively low inclusion rate of these drugs in the feed and the potential for large numbers of coccidial oocysts to build up and persist in game bird rearing and release pens.
Between 2002 and 2010, 93% of all submissions of pheasants (Phasianus colchicus) in which a diagnosis of coccidiosis was made occurred in the months of June, July and August. In partridges (red-legged partridges Alectoris rufa, grey partridges Perdix perdix and other unspecified partridges) diagnoses of coccidiosis tended to persist into September, with 75% of all positive submissions in 2002-2010 occurring in June to August and a further 16% in September (Figure 5 - see top right-hand side). The wider temporal spread in partridges compared with pheasants is probably due to differences in the rearing and releasing practices. Pheasants are often released around six weeks of age, but partridges are usually retained in their rearing accommodation for longer and released at around twelve weeks of age.
The number of diagnoses of coccidiosis in pheasants and partridges increased between 2004 and 2007, but has remained relatively constant since 2007 (Figure 6 - see top right-hand side).
Captive birds
A ten-month-old male Temminck’s tragopan (a bird of the pheasant family naturally found in Asia) developed a strange gait, became recumbent and died. The female bird of the pair had died two weeks earlier after showing similar signs. Postmortem examination revealed a severe myopathy affecting the superficial and deep pectoral muscles and the muscles of the upper leg. Affected muscles were heavily infiltrated by white and green streaks, visible on the surface and cut surface (figure 7 - see top right-hand side). Histopathology demonstrated a severe degenerative myopathy, with swelling, fragmentation and necrosis of muscle fibres. Proteinaceous fluid was present between the muscle fibres, and areas of fibrocyte proliferation, mononuclear cell infiltration and early mineralisation were noted. Similar subacute changes were seen in the myocardium. The cause remains unclear but given the specialised nature of the diet of such birds, a nutritional myopathy was suspected.
Wild birds
This month further deaths in mute swans (Cygnus olor) were investigated. One of three mute swans submitted from a wildlife rehabilitation centre had severe necrotic enteritis from which Clostridium perfringens was isolated. Another bird had no obvious necrotic enteritis but marked enlargement of the liver and spleen, with multiple miliary necrotic foci in both organs. Similar lesions in the liver and spleen have been seen in flock outbreaks of necrotic enteritis in mute swans previously (Necrotic enteritis in mute swans associated with cyanobacterial toxins, Veterinary Record 154, pages 575-576). The third bird from this site had multiple white nodules in the air sacs and lungs from which Aspergillus fumigatus was isolated.
Three yellowhammers (Emberiza citronella) submitted for necropsy were thin with extensive caseous necrosis of the crop wall. Trichomonosis was suspected but could not be confirmed due to carcase autolysis. Trichomonosis was also considered to be the cause of necrotic oesophagitis in a chaffinch (Fringilla coelebs) and of a caseous mass in the oral cavity of a tawny owl (Strix aluco). Infection with Escherichia albertii (previously referred to as E coli O86 profile) caused the death of a siskin (Carduelis spinus).
Very large numbers of roundworms (Contracaecum species) were found in the proventriculus and gizzard of a thin cormorant (Phalacrocorax carbo) from the north of Scotland. Similar findings were made in a thin shag (Phalacrocorax aristotelis) submitted from southwest Scotland. The heavy parasitic burdens probably contributed to the deaths of both birds.

