Pasteurella anatipestifer infection in commercial meat-type turkeys in California

A disease outbreak characterized by respiratory signs, occasional neurologic signs, and increased mortality in commercial meat turkeys from four separate companies in central California was investigated in the late summer and early fall of 1986. The disease syndrome affected turkeys from 6 to 15 weeks of age and caused a severe fibrinous pericarditis, perihepatitis, and airsacculitis. Bacteriologic and serologic examinations as well as virus- and chlamydia-isolation attempts initially failed to implicate an etiologic agent. Eventually culture attempts were made in a 5% CO2 incubator, resulting in isolation of Pasteurella anatipestifer. The disease syndrome was reproduced in young turkeys and broiler chicks inoculated with the organism.     

Spondylitis in turkeys associated with experimental Pasteurella anatipestifer infection.

Nine previously vaccinated turkeys were inoculated intravenously with Pasteurella anatipestifer, and blood samples were taken periodically to evaluate the potential of chronically infected turkeys to serve as reservoirs of infection for blood-feeding arthropod vectors. Vertebral osteomyelitis (spondylitis), as yet unreported in the literature in association with infection with the organism, was found in the thoracic vertebrae of five out of nine inoculated turkeys, and P. anatipestifer was isolated from the thoracic vertebrae of three of the five. The organism was isolated from the peripheral blood of six turkeys 24 hours postinoculation and from the peripheral blood of one turkey 7 days postinoculation. The organism was also isolated from the heart blood of two birds at necropsy--from one at 21 days and, following an intramuscular injection of dexamethasone, from the other turkey at 38 days postinoculation.     

Dermal necrosis caused by Pasteurella multocida infection in turkeys

Severe dermal necrosis caused by Pasteurella multocida Serotype 1 was diagnosed in three dressed turkey carcasses and two live turkeys from a commercial flock. The dressed carcasses were among several condemned at a processing plant. The isolate, P. multocida Serotype 1, produced progressive dermal necrosis when experimentally inoculated into injured skin of turkeys. The organism was reisolated from the dermal lesions. The turkey houses were found to be infested by mice; the skin injury and infection with P. multocida probably originated from mouse bites.     

鸭疫巴氏杆菌病的预防与治疗

鸭疫巴氏杆菌(Pasteurella anatipestifer,PA)病是家鸭、火鸡和多种禽类的一种高度接触性传染病,又称为新鸭病、鸭败血症、鸭疫综合征、传染性浆膜炎、鸭疫里雷默氏杆菌(Riemerella anatipestifer,RA)病。鸭疫巴氏杆菌病于1932年由Hendrickson J M.首次报道,我国郭玉璞等于1982年在北京首次报道,并对本病病原菌进行了分离和鉴定。     

武汉地区鸭疫巴氏杆菌的分离鉴定

２０００年３～５月,对送检于华中农业大学兽医院的病鸭进行病理剖检及细菌分离鉴定,确定送检病例５０％以上由鸭疫巴氏杆菌（ＰＡ）引起,其发病日龄为７～５０日龄。从病鸭的脑脊液、心血、肝等均易分离到ＰＡ。药敏试验显示所有菌株对氯霉素高度敏感。此次试验结果说明,在武汉地区鸭疫巴氏杆菌确已存在,并已成为严重危害当地养鸭业的重要疾病之一。     

鸭传染性浆膜炎免疫研究进展

鸭传染性浆膜炎是由鸭疫里氏杆菌(RA)又名鸭疫巴氏杆菌引起的一种严重危害雏鸭的传染病。本病呈急性败血症或慢性过程，以纤维素性心包炎、肝周炎、气囊炎、脑膜炎和干酪性输卵管炎为特征。1～8周龄雏鸭易感，恶劣环境条件可诱发此病。死亡率最高可达75％。慢性经过的鸭主要表现脑膜炎症状，即斜颈，生长缓慢成僵鸭，给养鸭业造成巨大的损失。　　药物防治是我国目前控制该病的主要措施。虽然药敏试验表明该菌对多种药物敏感，但实际防治效果并不理想；加上肉鸭在养殖全程均对该菌易感，要达到较好的治疗效果，必须反复投药，既增加了成本…     

Pasteurella multocida recovered from live turkeys: prevalence and virulence in turkeys

Swabs of the oropharynges of 801 live turkeys (621 meat birds and 180 breeders), collected from 15 flocks that had experienced an outbreak of fowl cholera and from 12 non-outbreak flocks, were screened for the presence of Pasteurella multocida. Turkeys from outbreak flocks were sampled within 2 to 9 weeks of the outbreak. Forty-nine isolates of P. multocida were recovered from turkeys in 11 of the outbreak flocks, and none were recovered from turkeys in non-outbreak flocks. Isolation rates varied from 0 to 72% of turkeys sampled in a flock. Nineteen isolates were tested for virulence by injecting them intravenously into turkeys, and 14 were lethal. Results demonstrated that for purposes of disease control, meat birds in fowl-cholera-outbreak flocks should be considered carriers of potentially virulent P. multocida for the life of the flock.     

Molecular epidemiology of Pasteurella multocida in turkeys.

Pasteurella multocida isolated from turkeys during an outbreak of fowl cholera was characterized by serotype and heterogeneity of genes encoding rRNA (ribotype) to investigate the epidemiology of the organism. Isolates were collected between October 1985 and July 1986. The M9 or Clemson University fowl cholera vaccine-like strain was detected in 17% of the flocks with fowl cholera. One particular strain, isolated only from breeder flocks, was recovered from 7 of the 10 breeder flocks examined in this study. Intracompany transmission appeared to be common, implying a failure in biosecurity. Circumstantial evidence indicated that in the field; the incubation period of P multocida in a turkey flock may be between 2 to 7 weeks. Wildlife did not appear to be an important reservoir of P multocida for turkeys during this study period. Ribotyping results tended to discount several of the possible interflock transmissions, as suggested by examination of serotyping results alone; however, serotyping in combination with ribotyping proved helpful in understanding the epidemiology of P multocida in turkeys.     

Acute airsacculitis in turkeys inoculated with Pasteurella multocida

Thirty female turkeys, inoculated into the caudal thoracic air sacs with Pasteurella multocida were examined from 0 to 6 hours post-inoculation (PI). The air sac reacted rapidly and intensely with exudation of heterophils. Circulating leukocyte and thrombocyte numbers remained normal except for an absolute lymphopenia by 6 hours PI. P. multocida was initially isolated from blood at 3 hours PI. Total cell counts increased markedly in air sac lavage fluids by 1.5 hours PI and continued to increase until 6 hours PI. Heterophils predominated in lavage fluids (greater than 94%), with macrophages comprising the remaining cells. Microscopically occasional heterophils were present within air sac blood vessels and perivascularly by 0.5 hour PI. They became more numerous by 1.5 and 3 hours PI when transepithelial migration into the air sac lumen was seen. By 6 hours PI, there was diffuse, severe swelling of air sac epithelium and mesothelium, and bacteria were located in air sac interstitium. Ultrastructurally, endothelial and air sac epithelial cells were swollen and vacuolated Interdigitating processes of air sac epithelial cells were separated. These results indicate that air sacs can be the portal of entry for P. multocida into the systemic circulation, probably via damaged air sac epithelium.     

Protection of ducklings with a broth-grown Pasteurella anatipestifer bacterin

Pasteurella anatipestifer (PA) serotypes 1, 2, and 5 grew to high densities in tryptic soy broth and tryptose broth (TB) when the media were continuously shaken or aerated. Growth in 100 ml to 15 liters of TB exceeded an absorbance of 1.0 at a wavelength of 525 nm (about 0.7 for a 1/3 dilution) and contained more than 10(10) colony-forming units per ml. A bacterin was prepared from the three serotypes of PA grown in aerated TB. Two subcutaneous injections of this bacterin protected 70% to 85% of ducklings against experimental challenge with each of the three PA serotypes, which killed 90% to 100% of unimmunized controls. The bacterin could be diluted 1/5 without decreasing protection below 80%. Field studies on Long Island duck farms in 1980 and 1981 demonstrated significant reductions in mortality with the use of the broth-grown PA bacterin.     

Immune defence mechanism against blood-borne Pasteurella multocida in turkeys

Humoral and cellular immune defence factors involved in controlling blood-borne Pasteurella multocida were investigated in turkeys by the passive transfer of immune serum or by the treatment with macrophage-activating agents. The treated and untreated birds were intravenously inoculated with a virulent strain of P multocida, and the viable bacteria in the blood, liver and spleen were counted. In untreated birds, the bacteria were rapidly removed from the blood, and the majority were recovered from the liver and spleen 120 minutes after inoculation. Neither the transfer of immune serum nor the treatment with macrophage-activating agents significantly influenced the clearance rate of bacteria from the blood. The number of bacteria recovered from the liver 120 minutes after inoculation was slightly lower in the birds treated with macrophage-activating agents and significantly lower in those given immune serum than in the untreated birds. None of the treatments, however, significantly changed the number of bacteria recovered from the spleen 120 minutes after inoculation. The results suggest that the phagocytes in the liver, but not in the spleen, play a crucial role in the intravascular defence against P multocida in the presence of specific antibodies.     

Prevalence and characteristics of Pasteurella multocida in commercial turkeys

The oropharyngeal regions of 680 meat turkeys and 55 breeder turkeys from nine outbreak farms, three history-outbreak farms, and 19 nonoutbreak farms in Ohio, Indiana, and Pennsylvania were cultured to determine the prevalence of Pasteurella multocida in turkeys. Pasteurella multocida was recovered from 32 out of 105 turkeys belonging to outbreak farms. Pasteurella multocida was not recovered from either history-outbreak or nonoutbreak farms. Characterization via capsular and somatic serotyping, biotyping, restriction endonuclease analysis, and antimicrobial susceptibility testing was performed on all recovered P. multocida isolates. Pasteurella multocida serotype A:1 and somatic serotype 1 with an un-typable capsular serogroup (UT:1) were the most common serogroups found. All isolates belonged to biotype P. multocida ssp. multocida. EcoRI, HpaII, and HindIII restriction enzyme digestions identified three, five, and five restriction fragment length polymorphism profiles, respectively. A majority of the isolates were susceptible to amikacin, ampicillin, ceftiofur, cephalothin, enrofloxacin, florfenicol, gentamicin, neomycin, novobiocin, oxacillin with 2% NaCl, sarafloxacin, tilmicosin, and trimethoprim with sulphadiazine and resistant to clindamicin, penicillin, tiamulin, and tylosin.