Estimate of economic impact of fowl cholera in turkeys in Georgia in 1986

Information gathered from cases of fowl cholera (FC) in commercial turkey flocks through case records, flock records, and telephone and mail surveys was used to estimate disease costs. The cost to the Georgia commercial turkey industry in 1986 from preventive measures, treatment of outbreaks, and production losses from the disease was estimated at $634,545. The cost of FC per kg of live production was estimated to be $0.015.     

Characteristics of fowl cholera outbreaks in turkeys in Georgia in 1986

Information was gathered from 64 cases of fowl cholera (FC) in turkey flocks through diagnostic case records, flock records, and telephone and mail surveys. Forty-five cases came from flocks of commercial turkeys, of which 15 were presented twice, and four came from mature breeder flocks. The prevalence of FC was 18.0% of commercial flocks and 14.7% of breeder flocks at risk. The average age at first diagnosis of FC was 90 days in commercial turkey flocks and 32 weeks 5 days in breeder flocks. Acute mortality was the most common presenting complaint, with a 0.37% average mortality in commercial flocks on the day of first presentation, 0.80% in commercial flocks presented a second time, and 0.43% in breeder flocks. Pasteurella multocida was cultured from 69.8% of the 361 tissue samples submitted from these cases. Novobiocin, penicillin, and chlortetracycline (CTC) had the greatest in vitro activity against isolates. Serotype 3-cross-4 was found in all 18 commercial flocks from which isolates were typed. All breeder flocks and 88.6% of commercial flocks were vaccinated before disease onset. Flocks were treated for an average of 14.3 days, most commonly with high levels of sulfadimethoxine and/or CTC. Body weights of affected birds were comparable to those of birds in unaffected flocks, but mortality and feed efficiency were worse.     

Possible genetic variation in resistance of turkeys to erysipelas and fowl cholera

Natural disease outbreaks of erysipelas and fowl cholera occurred in several lines of turkeys maintained for genetic studies. There were line differences in mortality during both outbreaks, suggesting that there is genetic variation in resistance to these diseases. A line developed by selection for increased egg production had a higher mortality rate from fowl cholera than did the randombred control line from which it was developed. Both the egg line and its control line had a lower mortality rate in the erysipelas outbreak than did a line selected for increased growth rate. Both diseases induced high mortality in a line selected for increased growth.     

Soluble fractions of Pasteurella multocida: their protective qualities against fowl cholera in turkeys

Soluble fractions of Pasteurella multocida strain P1059 were extracted from a single source by four methods, and their immunogenicity was evaluated by challenge exposure in turkeys. The fractions were extracted by 1) heating in 2.5% NaCl, 2) 0.5M potassium thiocyanate, 3) 1.0M sodium salicylate, and 4) prolonged stirring in formalin solution followed by pelleting (LPS-protein antigen). Eighty percent to 90% of infected turkeys were protected in two trials by vaccination with the saline extract or LPS-protein antigen, whereas less consistent protection was associated with the other two preparations. Endotoxin content was the highest in LPS-protein antigen, followed by KSCN, Na salicylate, and saline extract in that order. The four fractions contained at least one common antigen, which had previously been shown to be a surface-protective antigen.     

A descriptive study of fowl cholera in California meat turkeys: August 1985-July 1986

One hundred sixty meat-turkey premises in California were monitored for outbreaks of fowl cholera from August 1985 through July 1986. Nearly 27 million turkeys in 720 flocks were at risk during the year. Fifty-three flocks of approximately 3 million turkeys on 34 different premises experienced confirmed fowl cholera outbreaks. The epidemic curve for the year indicated that the majority of outbreaks occurred in the late summer and fall, particularly in October. The incidence of outbreaks during this time was not significantly associated with seasonal variation in the size of the turkey population. The mean flock age at outbreak was 10.8 weeks, with a range of 5-18 weeks.     

Relationship of increased fowl cholera outbreaks in turkeys with high environmental temperatures.

The relationship of an increase in fowl cholera outbreaks in turkeys with an increase in environmental temperatures during June, July, August, and September between 1959 and 1992 was analyzed. High environmental temperatures were found to be influential in the development of fowl cholera in turkeys. When the average monthly maximum environmental temperatures for 5 mo of July and 7 mo of August during the 13 yr between 1967 and 1979 were above 30.5 C, there was a significantly (P < 0.05) higher number of fowl cholera outbreaks in turkeys for each month than during the same months when the average maximum temperatures were below 30.5 C. To test the hypothesis that an increase in fowl cholera outbreaks was preceded by an increase in temperature, the pre- and postoutbreak temperatures for 46 selected outbreak clusters occurring between 1959 and 1992 were averaged. Both the average maximum and minimum temperatures for the latter 9 days of the preoutbreak period were highly significantly (P < 0.001) higher than those of the average cluster outbreak day and the following four postoutbreak days. Also, for the nine individual days of the latter pre-outbreak period, the daily average maximum temperature was significantly (P < 0.05) higher for 3 days and partially significantly (P < 0.10) higher for 3 days than that of the average cluster outbreak day, and the daily average minimum temperature was significantly (P < 0.05) higher for 2 days and partially significantly (P < 0.10) higher for 1 day than that for the average cluster outbreak day.     

Attenutated live fowl cholera vaccine. III. Laboratory and field vaccination trials in turkeys and chickens

Administered via the drinking water, M-3-G, an attenuated strain of Pasteurella multocida of serotype 1, was found to immunize turkeys and chickens against fowl cholera. Immunity was tested by challenging birds intramuscularly, by palatine cleft swab, or orally after 3 vaccinations. No reactions to vaccination were noted in 390 turkeys in 12 laboratory trials, nor in 20,245 vaccinated in field trials. Chickens showed no vaccination reactions, and immunity was elicited by challenge in a laboratory trial and in face of natural outbreaks in the field, where 11,600 chickens were vaccinated. No vaccination reactions were noted, although most birds involved in the trials were carrying Mycoplasma spp. Immunity was found to last about 10 weeks after the last vaccination. The immunizing properties of M-3-G are compared with the CU strain.     

DNA fingerprinting of plasmid-containing serotype A: 3,4 Pasteurella multocida isolated from cases of fowl cholera in chickens and turkeys

The live, attenuated vaccine strains of Pasteurella multocida have been hypothesized to be responsible for homologous serotype outbreaks of fowl cholera on farms that use the commercial vaccines. We have further hypothesized that the naturally occurring Clemson University (CU) vaccine strain may be transformed to virulence by the acquisition of plasmid DNA. To test this hypothesis, we obtained seven homologous serotype (A:3,4) P. multocida isolates, all plasmid bearing, that were cultured from fowl cholera cases in vaccinated flocks and compared the isolates with the CU reference vaccine by molecular methods. Restriction fragment length polymorphisms (RFLPs) were detected by DNA/DNA hybridization with labeled probes specific for the cya, aroA, and rrn genes of P. multocida. The RFLPs obtained from BglII-digested genomic DNA probed with cya demonstrated no differences among the isolates. Although three isolates probed with aroA showed a RFLP identical to the vaccine strain, five isolates were distinctly different. Isolates probed with rrn grouped into three different restriction patterns that were dissimilar from that of the vaccine strain. Therefore, we have shown that these fowl cholera isolates are different from the CU vaccine strain and that these outbreaks were not vaccine related.     

Pathogenesis of fowl cholera: influence of encapsulation on the fate of Pasteurella multocida after intravenous inoculation into turkeys

The role of the capsule in the pathogenesis of fowl cholera was studied in turkeys. Avian Pasteurella multocida P-1059 was used in an encapsulated form, an enzymatically decapsulated form, and a mutant form lacking capsule-productivity (strain T-325). These forms were inoculated intravenously into normal or immune turkeys, and the numbers of viable bacteria in the blood, liver, and spleen were enumerated over a 120-minute period. Both normal and immune birds rapidly removed all three forms of organisms from the blood-stream at similar rates and trapped in the liver and spleen. In the liver of normal birds, the non-encapsulated mutant T-325 was readily inactivated, but the encapsulated P-1059 strain was not. When the decapsulated form of P-1059 was used, the bacterial counts in the liver temporarily decreased at 60 minutes PI. In immune birds, all three forms of organisms were equally inactivated in the liver. In the spleen, however, the bacterial numbers did not change throughout 120 minutes PI with all three forms of organisms in both normal and immune turkeys. The results indicated that the blood-borne P. multocida were readily trapped by reticuloendothelial phagocytes. The trapping process was not affected by encapsulation of the organism or by the immune status of turkey. Both factors, however, appeared to greatly influence the subsequent killing of P. multocida by hepatic, but not splenic, phagocytes.