Mother Nature always has some tricks up her sleeve.
It’s a sore point for those who care for animals or birds, but diseases and predators are there for a reason; in the wild, only enough should survive to keep the population constant. It’s highly unlikely you’d ever see a wild hen pheasant with 50-odd chicks!
The job of the gamekeeper is to avoid Mother Nature’s pitfalls, and get as many healthy birds reared and released into the food chain as they can. Netted pens have, to some extent, eliminated the impact of predators, but in doing this we have played right into Mother Nature’s hands by keeping birds at higher flocking densities than they would be in the wild. It is said that a sheep’s worst enemy is another sheep, and the same goes for our birds.
We spoke about Coccidiosis last month, and this month I want to focus on gape worms and the motile protozoans, or spirochaetes, as some people call them. In both of these diseases, the stocking density of the birds is a major factor.
When we lost the use of Emtryl several years ago, people started rearing birds at a lower density and it had a good effect. I was thinking that, as many shoots are cutting back slightly on numbers, keepers should consider spreading those remaining birds out a little.
If a bird has to walk a little further before it meets a disease, it may not complete that journey and not contact that disease. If you have spare pens it may involve a little more work, but it could reduce your mortality and give you a better result overall.
The worm, which affects both pheasants and partridge, actually consists of two worms joined together. The male is actually an appendage about six millimetres long on the side of female, which is 20 -25mm long, and he is there purely for the purpose of fertilisation.
So typically, these worms have a sort of Y-shaped appearance when found in the wind pipe. The worm has two effects on the birds: it causes impaired efficiency of breathing by obstructing the airway, or in extreme cases it can cause complete blockage and choking.
These obstructions give rise to the typical clinical signs of the disease, such as the outstretched neck and the open mouth, trouble breathing, or gaping, hence the term ‘gapes’ for the condition. The worms appear red in the trachea when it is inspected post-mortem, because they suck blood from the bird.
So how can we think about breaking the life cycle of the worm, and create an opportunity to prevent the disease? The eggs in the female that are fertilised by the conjoined male are then laid, and pass out into the pasture. There, over a period varying between seven to 14 days, they will develop into immature worms or larvae.
There may be up to three development stages in the actual egg that take it up to the larval stage three, or L3. These L3 larvae can then hatch and be picked up by the birds, or in some cases may be picked up un-hatched and hatch inside the bird.
Others may be picked up by earthworms, slugs or snails, or ‘maggots’, the larvae of the house fly or the bluebottle, and these are known as paratenic hosts. The larvae have been found to survive in earthworms for up to three years, thus providing a reservoir of infection in the ground.
The bird will eat the intermediate host as it grazes, and the L3 is finally in the body. In this microscopic form the worm develops through at least two more ‘moults’ in the bird, as the junior worm moves from the gut via the liver, to be transported in the bloodstream until it settles in the lungs.
Once in the lungs it can cause pneumonia, which is seldom recognised as a clinical disease, but can be significant. It is at this stage, approximately seven to 14 days after the initial ingestion of the larvae, that the males and females pair up and become permanently attached to each other, forming the Y-shape in which they are usually found post-mortem.
The worms then swim up into the trachea, or windpipe, and attach their mouth parts to the wall of the trachea and begins to suck blood. Research work has also shown that wild birds, particularly the crow family and other corvids such as magpies, as well as robins and starlings, can transmit the disease as they visit or overfly game bird pens.
There is also evidence to suggest that strains of Syngamus trachea from wild bird reservoir hosts may be more infective for domestic birds if they first pass through an earthworm transport host, rather than by direct infections via ingestion of L3s or eggs containing L3s.
It should be possible to reduce or eliminate infestation of the gape worm by breaking the cycle in one or more of the following ways.
1. Clean ground: moving the pens regularly will help reduce the numbers of worms on the ground.
2. Reduce the number of corvids or other birds in the area that are suspected of carrying the worms, if it is safe and legal to do so, as they are renowned carriers of the disease
3. A worming stategy: one of the few drugs licensed for use in some of our game bird species is a wormer called flubendazole, which is available as a liquid or a feed inclusion additive.
Motile protozoan parasites have long been a problem in the game bird industry, causing huge losses in some years. There are two organisms that are thought to be the main culprits, Hexamita meleagridis and Trichomonas gallinae.
Both Hexamita and Trichomonas are single-celled independent living organisms, which are propelled around by whip-like strands, or flagellae. Hexamita lives in the small intestine and has a much more frenetic action, darting around like something possessed when observed under the microscope, while Trichomonas lives in the large intestine and caecum (the blind gut) and is much slower.
In fact, some people have questioned whether it is almost a normal inhabitant of the bowel, and will only do damage when in vast numbers.
The disease signs are probably well-known throughout the industry, and include depression, fluffing up, scouring, and rapid weight loss, with weight melting away from birds in a matter of days, producing that characteristic knife-edged keel bone.
If the bowel wall of the infected birds is examined, there is surprisingly little damage to the lining of the bowel, and so it remains somewhat of a mystery as to why and how these organisms affect birds so badly and so quickly.
I unashamedly look to prevention before looking at treatment, because the prevention is often cheaper. It is almost certainly often as effective as our limited range of drugs.
We know that the disease is transmitted directly, and therefore maintaining all forms of biosecurity should help. The cleaning of drinkers and feeders, and moving drinkers and feeders to clean, dry ground will help. One of our major clients has used nipple bars in rearing pens for some years now, because the bell drinkers just got so filthy. The resting of pens, even if only for a few days, has been proven to help, as has moving to clean ground each season.
It has been long suggested that, in high doses, Oxytetracyline (OTC) would have an effect on the causal organisms. However, it is a drug which slows down the organism rather than kills it. Drugs that work in a similar way are the Chlortetracyclines and the Doxycyclines.
Tiamulin is a drug which has been used in this condition. It is available from various manufacturers, but its main drawback is that it is very bitter, and unless great care is taken to sweeten the water to remove the taste the birds may refuse to drink. Some practices use a mixture of both these drugs, and both drugs can be added to food if you are unlucky enough to have a strike of this disease after release.
In the next edition, I want to talk about a newly-identified bacterial disease, which we are currently investigating as to its effect on our birds.
Alan Pearson is a partner at Lanes Vet Group in Garstang.
The group provides a wide variety of veterinary services throughout north Lancashire. Within the 16-man group Alan, along with another partner, Lewis Thompson, provides services to all types of game bird operations, from hatcheries to small shoots.
T: 01995 602468