Infectious laryngotracheitis (ILT) is an important respiratory disease of chickens and annually causes significant economic losses in the poultry industry world-wide. ILT virus (ILTV) belongs to alphaherpesvirinae and the Gallid herpesvirus 1 species. The transmission of ILTV is via respiratory and ocular routes. Clinical and post-mortem signs of ILT can be separated into two forms according to its virulence. The characteristic of the severe form is bloody mucus in the trachea with high mortality. The mild form causes nasal discharge, conjunctivitis, and reduced weight gain and egg production. Conventional polymerase chain reaction (PCR), nested PCR, real-time PCR, and loop-mediated isothermal amplification were developed to detect ILTV samples from natural or experimentally infected birds. The PCR combined with restriction fragment length polymorphism (RFLP) can separate ILTVs into several genetic groups. These groups can separate vaccine from wild type field viruses. Vaccination is a common method to prevent ILT. However, field isolates and vaccine viruses can establish latent infected carriers. According to PCR-RFLP results, virulent field ILTVs can be derived from modified-live vaccines. Therefore, modified-live vaccine reversion provides a source for ILT outbreaks on chicken farms. Two recently licensed commercial recombinant ILT vaccines are also in use. Other recombinant and gene-deficient vaccine candidates are in the developmental stages. They offer additional hope for the control of this disease. However, in ILT endemic regions, improved biosecurity and management practices are critical for improved ILT control.

The effect of crude aflatoxin (AF) on the growth, performance, and immune response of turkeys and broilers was studied. Crude AF, produced from a natural outbreak of Aspergillus flavus on corn, was ground and mixed in rations to contain either 0, 100, 200, 400, or 800 ppb of aflatoxin B1 (AFB1). Turkeys (Experiment 1) and broilers (Experiment 2) were used in identical experimental designs. In each, 200, 14-day-old birds were divided equally by sex into five groups of 40 and were fed one of five AF diets for 35 days. In Experiment 1, crude AF greater than or equal to 400 ppb was highly toxic to turkeys. These levels produced signs and lesions of aflatoxicosis as well as a significant decrease in weight gain and feed conversion during 5 weeks. In addition, microscopic lesions, indicative of aflatoxicosis, were evident as low as 100 ppb, and significant decreases in cell-mediated immunity were noted in the 200 ppb group birds. Experiment 2 indicated that chickens were less susceptible to crude AF than turkeys. Neither morbidity nor mortality occurred in broilers. Gross lesions consistent with AF toxicity were evident in birds given 800 ppb and microscopic lesions were observed in birds given 100 ppb. Feed conversion was significantly increased in the 800 ppb broilers only. Cell-mediated immunity, measured by a delayed hypersensitive skin test, was significantly decreased in broilers receiving AF at 200 ppb or greater. Neither humoral immunity nor the development of the acquired immunity to Newcastle disease or fowl cholera vaccination were decreased in turkeys or broilers given AF.

Seven-day-old conventional broilers were inoculated either orally or intratracheally (IT) with 2.5 X 10(5), 5.0 X 10(5), or 2.0 X 10(6) oocysts of Cryptosporidium baileyi (32 birds for each dosage level per group; 192 birds total). Thirty-two birds served as unninoculated controls. Mean weekly weight gain and feed conversion were determined during a 5-week period. Carcass pigment was graded using a Roche Color Fan. Fecal oocysts were calculated from random cage samples 6, 8, 11, 13, 15, 18, 20, 22, and 25 days after inoculation (DAI). Effects of C. baileyi on immune responses were examined for Newcastle disease virus-hemagglutination inhibition (NDV-HI) antibody, infectious bursal disease virus-enzyme-linked immunosorbent assay (IBDV-ELISA) antibody titers and delayed hypersensitivity (DH) in half of the birds in each group. Disease or death from cryptosporidiosis did not result from oral inoculation of C. baileyi. Signs of respiratory disease, consisting of rales, sneezing, and dyspnea were observed in all IT-inoculated birds 7 to 21 DAI. Seven deaths occurred in the IT-inoculated groups 14 to 21 DAI. At necropsy, lung parenchyma was gray, firm, and wet in the ventral region. Air sacs contained a foamy, white to gray, mucoid fluid. Histologic lesions in the air sacs and bronchi were epithelial hyperplasia, discharge of mucocellular exudate to the mucosal surface, thickening of the mucosa by cellular infiltrates, loss of cilia, and dilation of mucous glands. Weight gains for IT-inoculated birds were lower (P less than .05) than controls from 14 to 21 DAI, although weight gains for the 5-week period were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Tenuazonic acid, a toxic metabolite produced by various Alternaria species was found to be toxic to young chickens. Tenuazonic acid given in the diet at 10 Mg of toxin/g of feed or by daily esophageal intubation at the levels of 1.25 or 2.50 mg of toxin/kg of body weight to 3-weekold broilers for 3 weeks resulted in decreased weight gain and lowered feed efficiency during the second and third weeks of toxin administration. Although no morbidity or mortality was noted in chickens receiving toxin by either route, marked gross and microscopic lesions were evident in various tissues of birds receiving toxin by either method. The majority of chickens receiving toxin by esophageal intubation developed either all or several of the following lesions: enlarged and mottled spleen, slight erosions of the gizzard, hemorrhage in the intestinal lumen and on the surface of the heart, edema of the myocardium, and hemorrhage with bruising in the musculature of the thigh. Broilers receiving toxin in the feed showed no gross hemorrhages, although gizzard erosion with pale and mottled spleens was evident. Microscopically, congestion of blood vessels and hemorrhage was evident in all grossly affected tissues as well as in the kidneys and liver. One-week-old White Leghorns receiving either 1.25 or 2.50 mg toxin/kg body weight daily by esophageal intubation for 3 weeks also had lower weight gain and feed efficiency as well as similar pathologic changes as seen with broilers receiving toxin by esophageal intubation.

Purified aflatoxin B1 (AFB1) or AFB1 plus aflatoxin B2 (AFB2) was given daily for 5 weeks in gelatin capsules to 2-week-old feather-sexed broilers. In Experiment 1, pure AFB1 was given in doses equivalent to the quantity of toxin received, if diets containing either 0, 200, 500 or 1000 ppb of AFB1 were consumed. In Experiment 2, pure AFB1 or AFB1 plus B2 was administered in capsules in doses equivalent to the quantity of toxin received, if diets containing either 0, 100, 200, or 400 ppb of AFB1 were consumed. In Experiment 1, pure AFB1 greater than or equal to 500 ppb was only mildly toxic. These levels produced a significant decrease in the 5-week weight gain and microscopic lesions indicative of alfatoxicosis. No morbidity, mortality, or effects on feed conversion or immune responses, however, were noted in birds given pure AFB1 at these levels. Gross liver lesions indicative of aflatoxin toxicity occurred at the 1000 ppb only. Results of Experiment 2 were similar to the first. Weight gain and feed conversion were not affected for broilers receiving pure AFB1 as low as 200 ppb. No morbidity, mortality, or gross lesions were evident in birds given either pure AFB1 or AFB1 plus AFB2 as high as 400 ppb. However, cell-mediated immunity as measured by a delayed hypersensitive skin test was significantly affected in birds receiving 400 ppb AFB1 plus AFB2. No effects on humoral immunity or the development of acquired immunity to Newcastle disease or fowl cholera vaccination were noted.