So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

Human biochemical genetics

Avian pathogenic Escherichia coli (APEC) cause aerosacculitis, polyserositis, septicemia and other mainly extraintestinal diseases in chickens, turkeys and other avian species. APEC are found in the intestinal microflora of healthy birds and most of the diseases associated with them are secondary to environmental and host predisposing factors. APEC isolates commonly belong to certain serogroups, O1, O2 and O78, and to a restricted number of clones. Several experimental models have been developed, permitting a more reliable evaluation of the pathogenicity of E. coli for chickens and turkeys. Hence, virulence factors identified on APEC are adhesins such as the F1 and P fimbriae, and curli, the aerobactin iron sequestering system, K1 capsule, temperature-sensitive hemagglutinin (Tsh), resistance to the bactericidal effects of serum and cytotoxic effects. Experimental infection studies have shown that the air-exchange regions of the lung and the airsacs are important sites of entry of E. coli into the bloodstream of birds during the initial stages of infection and that resistance to phagocytosis may be an important mechanism in the development of the disease. They have also demonstrated that F1 fimbriae are expressed in the respiratory tract, whereas P fimbriae are expressed in the internal organs of infected chickens. The role of these fimbrial adhesins in the development of disease is not yet, however, fully understood. The more recent use of genetic approaches for the identification of new virulence factors will greatly enhance our knowledge of APEC pathogenic mechanisms. Diagnosis of APEC infections is based on the clinical picture, lesions and isolation of E. coli. This may be strengthened by serotyping and identification of virulence factors using immunological or molecular methods such as DNA probes and PCR. Approaches for the prevention and control of APEC infections include the control of environmental contamination and environmental parameters such as humidity and ventilation. Antibiotherapy is widely used, although APEC are frequently resistant to a wide range of antibiotics. Vaccines containing killed or attenuated virulent bacteria protect against infection with the homologous strain but are less efficient against heterologous strains. Hence, vaccination for colibacillosis is not widely practised because of the large variety of serogroups involved in field outbreaks.

https://hal.archives-ouvertes.fr/hal-00902571/document

Avian pathogenic escherichia coli (apec)

Research on ascites occurring in meat-type chickens reared at moderate and low altitude has shown that the pathogenesis is similar to that of the high altitude disease. Pulmonary hypertension (PH) caused by increased blood flow or increased resistance to flow in the lung results in right ventricular hypertrophy (RVH), valvular insufficiency, increased venous pressure and ascites. The structure of the avian heart, with its thin-walled right ventricle and muscular right atrioventricular valve, allows PH to induce heart failure quickly. The sudden increase in pulmonary hypertension syndrome (PHS) in meat-type chickens in the 1980s was associated with a rapid increase in growth rate and feed conversion. This was a result of a combination of genetic selection for fast-growing, heavy broilers with low feed conversion and a more dense, high caloric, pelleted food that supplied all the nutrients required for rapid growth and encouraged a high nutrient intake. PHS in meat-type chickens is usually primary pulmonary hypertension, that is, PH that occurs without evidence of prior heart or lung disease that could account for the increase in blood flow or resistance to flow that results in the increased pressure in the pulmonary arteries. The lungs of birds are firm and fixed in the thoracic cavity and they do not expand to draw air into the lung. The blood and air capillaries form a rigid network that allows only minimal expansion of the blood capillaries when more blood flow is required. Air is moved through the lung by abdominal movement which draws air in and out of the air sacs. The anatomy and physiology of the avian respiratory system are important in the susceptibility of meat-type chickens to PHS. The small stature of the modern meat-type chicken, the large, heavy breast mass, the pressure from abdominal contents on air sacs, and the small lung volume compared to body weight, may all be involved in the increased incidence of PHS. There is limited space for blood flow in the avian lung. Factors that increase blood flow or increase resistance to flow are additive. Increased blood viscosity caused by the polycythaemia of hypoxia, or increased erythrocyte rigidity of high Na (+), are more likely to produce PH in fast-growing than in slow-growing birds. Increased flow due to cold exposure is also additive. Ascites caused by PH is a production-related disease at low altitude. It can be prevented easily by restricting growth rate. It is possible that some meat-type chickens of the phenotype we have created have reached the limit of blood flow through their lungs and that future improvements in growth rate will only be possible if the lung and abdominal cavity capacities are enlarged.

https://www.tandfonline.com/doi/pdf/10.1080/03079459308418934

Ascites in poultry

Factors Regulating Bone Maturity and Strength in Poultry

Rapid growth problems: ascites and skeletal deformities in broilers

Summary Male progeny from two commercial sire strains, were fed on a high energy or low energy diet and kept at an environmental temperature of 23 C or 13°C after day 22 to day 57. In the cold 42.4% of strain A and 29.6% of strain B died from right ventricular failure (RVF) and ascites secondary to pulmonary hypertension (PH) prior to day 57. Of the birds surviving to day 57, 9.4% (strain A) and 6.4% (strain B) had RVF and ascites. In the warm, 17.3% (A) and 7.4% (B) died from RVF and ascites before day 57 and 4.6% and 3.2%, respectively had ascites at day 57. Chickens on the high energy diet were significantly heavier at day 56 than those on the low energy diet, particularly those kept in the cold. However, chickens on the latter diet had better weight gain between days 42 and 56, again more marked in cold conditions. The higher metabolic rate elicited by cold would increase oxygen consumption and blood flow in these broilers which, because of their rapid growth, already had a high metabolic rate. The ca...

https://www.tandfonline.com/doi/pdf/10.1080/03079458908418641

The effect of cold and dietary energy on right ventricular hypertrophy, right ventricular failure and ascites in meat‐type chickens

Summary One hundred commercial male broiler chickens were grown to 27 days in four floor pens on a commercial diet containing 0.14% sodium (Na+). From day 6 each pen received different levels of sodium chloride (NaCl) in the drinking water; 0.0%, 0.15% (0.06% Na+), 0.3% (0.12% Na+) and 0.6% (0.24% Na+). Eight chicks from each group were killed at 13, 20 and 27 days and examined for right ventricular hypertrophy (RVH) and right ventricular failure (RVF). By day 27 as little as 0.06% added Na+ caused two cases of RVH and one case of RVF with ascites, typical of the ascites caused by RVF in commercial broilers. RVH, RVF and ascites developed earlier in broilers on higher levels of Na+.

https://www.tandfonline.com/doi/pdf/10.1080/03079458708436353

The effect of increased sodium in the drinking water on right ventricular hypertrophy, right ventricular failure and ascites in broiler chickens

Percent hemoglobin oxygen saturation was measured with a pulse oximeter in 6-week-old slow-growing (light) and fast-growing (heavy) male broiler chickens and those with ascites from right ventricular failure (RVF). Pulse rate and percent oxygen saturation were read from the ulnar artery just proximal to the carpus. Percent oxygen saturation was significantly (P less than or equal to 0.0001) higher in light chickens (mean 91.6%) than in heavy chickens (mean 86.0%), and the percent oxygen saturation was significantly (P less than or equal to 0.0001) higher in both groups with normal hearts than in the group with RVF from valvular insufficiency (mean 62.1%). All RVF chickens and those with normal hearts were confirmed at necropsy. Light chickens were males with leg deformity or stunting and were 20-50% lighter than the heavy chickens.

R. J. Julian

Papers

Ascites in poultry

Rapid growth problems: ascites and skeletal deformities in broilers

The effect of cold and dietary energy on right ventricular hypertrophy, right ventricular failure and ascites in meat‐type chickens

The effect of increased sodium in the drinking water on right ventricular hypertrophy, right ventricular failure and ascites in broiler chickens

Blood oxygen concentration of fast-growing and slow-growing broiler chickens, and chickens with ascites from right ventricular failure.