Parasites of Birds

This will be edited nearer the time as the bird parasites are a bit scattered between larger worm groups. I will also do one with pigs & horses. 

1. Trichostrongylus Tenuis- game birds- in particular the pheasant. Results in severe inflammation of the caecal mucosa. Highly pathogenic. 
2. Capillaria- Highly pathogenic. Ulceration of the upper GI tract, inflammation, weight loss & death. Three species:

• C.Obsignata- direct life cycle.
• C.Caudinflata/Contorta- indirect life cycle with earthworm intermediate host. 

Disease in Free Range Birds. Control= Feed BZ.


3. Poultry Ascarids

• Ascaridia Galli-> small intestine. 
• Heterakis Gallinarum-> no migration. Caeca. Cannot distinguish between this and the other ascarid via eggs. Carries histomonas meleagridis which causes blackhead disease in turkeys. 
• Low pathogenicity. 

4. Synagmus Trachea

• Common in young birds.
• Trachea. 
• Red, 2cm. 
• L3 hatches, eaten or earthworm transport host. 
• L3 to bloodstream and lungs. 
• PPP=20 days.
• Young outdoor reared flocks= problem. Mechanical blockage, asphyxia, coughing, gape, anaemia, weight loss & death. 

5. Histomonas Melegridis

• Trachea.
• Heterakis Gallinarium vector. 

6. Coccidiosis-> Eimeria Tenella

• Disease of intensification.
• Intestinal tract.
• Host specific.
• Faecal-oral transmission. 
• Cysts persist in the environment. 

Several species found in poultry- Eimeria tenella is the most important one. In turkeys, e.meleagrimitis is the most important species. 

Life Cycle

1. Oocyst unsporulated and passed into the environment via the faceces. Resistant. 
2. Sporulates-> oxygen, humidity, high temperature (27 degrees) and takes two-four days. Sporulated oocysts contain four sporocysts each containing two sporozoites. This is the infective stage. Italic= happens in the environment, rest= host. 
3. Ingested and sporozoites liberated mechanically by CO2. Sporozoites activated by trypsin/bile. Invades the enterocyte to form the trophozoite stage. 
4. Penetrates the epithelium and is taken up by macrophages in the lamina propria (villi) and resides mucosa before leaving the macrophages.
5. Binary fission (schizogony from the sporozoites). Forms schizonts. Contains merozoites. Ruptures. 
6. 2nd stage schizont- merozoites infect further epithelial cells. 
7. Macrogametocytes (females and unicellular) and microgametocytes (large number of name flagellar uninucleate organisms) fuse to form the zygote. Sexual reproduction. Cyst wall formed. Oocysts passed unsporulated in the faeces. 

Diagnosis

• Clinical signs- sometimes haemorrhagic with blood in the faeces. Listlessness, death, feeding stops, and diarrhoea. 
• PM-> caecum. Find schizont/merozoite stages. 
• Drop in food conversion rates.

Epidemiology

• Parasite- self limiting infection. Resistant oocysts in the environment. Prevent damp litter and use an ammonia based disinfectant. 
• Host- young/naive. Population of susceptible = disease @ 3-6 weeks old. 
• Immunity is good following exposure. 
• Low numbers of infective oocysts and a rapid oocyst rise. 

Pathogenesis

• Severity proportional to parasite density.
• Epithelial damage- light impairs absorption. Heavy- haemorrhage. 
• Outbreaks due to mistakes in mixing/dosing anticoccidial agent. Treatments with sulphonamide chemotherapy costly and rarely used. 

Control

• Hygiene- prevents contamination.
• Vaccinated- strong immunity and species specific. Contains all seven strains. Live, attenuated or precocious strains (only first schizont stage hence no effect). Single dose in the water at five to seven days old. 

Ionophore drugs- affect the parasite membrane:

• Broilers- eliminate disease and optimise growth & fcr. Lifetime feed prophylaxis-> switch (change drugs between batches) and shuttle (change drugs halfway through broiler life) programs. This is to not encourage drug resistance.
• Layers-> allow immunity to develop. Step down programmes, low efficacy or sub efficacy drugs. Once immunity has developed, immunity is good.