Occurrence of Campylobacter spp. in young gulls, duration of Campylobacter infection and reinfection by contact.

Two groups of three week old Herring Gulls (Larus argentatus) were held to observe the carrier state with Campylobacter. All 27 birds of group I excreted Campylobacter jejuni biotype III when they were caught from their colony. Four weeks later all but one were negative, indicating that the carrier state lasts until about the seventh week of life, with self-elimination if infection with another Campylobacter species is prevented by housing in a closed environment as in this study. Only one bird became reinfected one year later when gulls from group I were brought into contact with gulls from group II, consisting of ten freshly caught gulls, four of which were infected with the same biotype of Campylobacter, indicating that there might be some kind of immunity protection against infection with the same biotype of Campylobacter spp.     

Pathogenicity of Campylobacter jejuni for turkeys and chickens.

A Campylobacter jejuni isolate obtained from a turkey liver, designated C101, and a C. jejuni isolate obtained from the feces of a chicken, designated C111, were used to inoculate their respective hosts. Isolate C101 depressed weight gain by 20% when inoculated into newly hatched poults or 4-day-old poults. It also caused death, hepatic necrosis, and generalized hemorrhages in turkey embryos. The chicken-derived isolate, C111, did not reduce weight gain in newly hatched chicks, but it did induce mortality in chicken embryos. The supernatant of the cultures of both C. jejuni isolates also caused mortality in embryos.     

Experimental infection of specific pathogen-free pigs with Campylobacter: excretion in faeces and transmission to non-inoculated pigs

Campylobacter species are leading agents of human bacterial gastroenteritis and consumption of food of animal origin is a major source of infection. Although pigs are known to frequently exhibit high counts of Campylobacter in their faeces, more information is needed about the dynamics of this excretion. An experimental trial was conducted to evaluate the faecal excretion of Campylobacter by 7-week-old specific pathogen-free piglets inoculated per os with three Campylobacter strains (one C. coli isolated from a pig, one C. coli and one C. jejuni from chickens) alone or simultaneously (5x10(7)CFU/strain). Non-inoculated pigs were housed in adjacent pens. Pigs were monitored for 80 days for clinical signs and by bacteriological analysis of faeces. Pigs inoculated with porcine C. coli or with a mix of the three strains excreted from 10(3) to 10(6)CFU/g of faeces with a slight decrease at the end of the trial. Animals inoculated with poultry C. coli or C. jejuni strain excreted a lower quantity and some of them stopped excreting. At the end of the trial, only C. coli was detected in the faeces of pigs inoculated simultaneously with the three bacteria. Moreover, the transmission of Campylobacter was noticed between pens for the two C. coli strains and all the neighbouring animals became shedders with a level of excretion similar to the inoculated pigs. Intermittence in the Campylobacter excretion was also observed. Finally, our study highlighted a host preference of Campylobacter, namely C. coli seems to have a higher colonization potential for pigs than C. jejuni.     

The infection of turkey poults with Histomonas meleagridis by contact with infected birds or contaminated cages

The conditions under which infection with Histomonas meleagridis could spread from directly inoculated turkey poults to uninoculated poults without the aid of invertebrate hosts or vectors was investigated in several experiments. In three experiments in battery cages, uninoculated poults were commingled with directly infected birds on pine-shaving litter. Directly exposed birds were inoculated per cloaca with H. meleagridis by means of a plastic pipette tip attached to a 10-ml syringe or orally gavaged with fresh cecal droppings from donor turkeys 4 days postinoculation (PI). Of the cloacally inoculated controls in these experiments, 31 of 44 (70.5%) birds had severe lesions ofhistomoniasis at 14 days PI, whereas none of the orally gavaged birds became infected. Histomoniasis developed in 11 of 36 (30.5%) birds allowed to commingle with inoculated birds. In other treatments, poults were allowed only contact with droppings from directly inoculated birds after the infected birds were removed from the cages. This was done for a single period of 1 hr or repeated five times. Four of 32 birds (12.5%) became infected in this way after the single exposure, whereas only four of 44 birds (9.1%) exposed five times developed lesions. In a comparison of floor materials, 35 of 35 control birds inoculated per cloaca developed severe liver and cecal lesions, irrespective of litter. Uninoculated birds allowed to commingle with infected birds on paper or pine shavings became severely infected in all cases (12/12 and 12/12 birds, respectively), whereas only 33% of those on wire-floored cages became infected (4/12). These results suggest that transmission of infection is more likely to occur as a result of direct contact between birds than from contact with litter or fecal material.     

Immunohistochemical identification of Campylobacter fetus in natural cases of bovine and ovine abortions

An immunohistochemistry (IHC) procedure for the detection of Campylobacter fetus antigens using an avidin-biotin complex technique was performed on formalin fixed bovine and ovine fetal tissues from 26 natural cases of Campylobacter spp. abortion (four ovine and 22 bovine). The species of Campylobacter isolated included C. fetus ssp. venerealis from 13 bovine fetuses, C. fetus ssp. fetus from two ovine and one bovine fetus, Campylobacter jejuni from seven bovine fetuses, Campylobacter lari from two ovine fetuses and an unspeciated Campylobacter species in one bovine fetus. Histologic lesions identified in the aborted fetuses included placentitis, serositis, pneumonia, gastroenteritis, hepatitis and encephalitis. Campylobacter fetus antigens were identified by IHC in 13 of 13 bovine fetuses from which C. fetus ssp. venerealis was isolated and in two of two ovine fetuses from which C. fetus ssp. fetus was isolated. The IHC stains were negative in tissues from seven bovine fetuses from which C. jejuni was isolated, one bovine fetus infected with C. fetus ssp. fetus, one bovine fetus infected with the unspeciated Campylobacter and two ovine fetuses infected with C. lari. In positive cases, the IHC stain most frequently identified bacteria in the lung and gastrointestinal tract. The C. fetus IHC procedure performed on formalin fixed tissues is a practical tool for the diagnosis of natural cases of ovine and bovine abortion caused by C. fetus.     

Campylobacter jejuni infection in the ferret: an animal model of human campylobacteriosis

Campylobacter infection in weanling ferrets (Mustela putorius furo) was studied as an animal model for enteric campylobacteriosis in persons. The screening of fecal cultures on selective campylobacter media showed that Campylobacter jejuni/coli was not present in the normal enteric flora. Intragastric feeding of a mixture of cat feed and 2.5 X 10(8) C jejuni isolated from ferrets with naturally occurring proliferative colitis was accomplished. All ferrets (n = 8) became infected on 3 days after they were inoculated, and at 5 to 7 days, they had bile-tinged, liquid feces with excessive mucus and blood. Ferrets gradually recovered from the diarrhea, and feces were normal 10 to 14 days after inoculation was done. Feces contained C jejuni at 14, 23, 28, 39, 46, 60, 91, 101, 109 and 144 days. In the second experiment, weanling ferrets initially were treated with 10% sodium bicarbonate, and 1 X 10(10) C jejuni organisms were administered in the cat feed. Diarrhea with fecal leukocytes and occult blood with occasional mucus appeared in almost all of the 21 ferrets from days 4 through 7. Campylobacter jejuni was isolated from the blood of 11 ferrets between 3 hours and 14 days after they were inoculated. Campylobacter jejuni bactericidal antibodies were present in serum samples at 14 days, with titers of 1:16 to 1:32. Intestinal lesions including cellular infiltration with mononuclear and polymorphonuclear leukocytes were in the lamina propria of the pyloric mucosa and small intestine of infected and control ferrets. The colon of 3 infected ferrets had small focal infiltrates of neutrophils on the lamina propria; one ferret had perivascular cuffing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antibiotic aerosolization: the effect on experimentally induced Alcaligenes rhinotracheitis in turkeys

Oxytetracycline hydrochloride was delivered by aerosol twice daily for 3 days to uninfected turkeys and to turkeys experimentally inoculated with Alcaligenes faecalis. The clinical, microbiological, and histological changes in the upper respiratory tracts were studied. No lesions were observed in the tracheas of uninoculated poults exposed to the aerosol. In experimentally infected poults, clinical signs included ocular and nasal discharges and open-mouthed breathing. Histologic lesions included progressive bacterial colonization of ciliated epithelium, loss of cilia, depletion of mucin from goblet cells, and accumulation of inflammatory cells within the tracheal lumen. Aerosolization of oxytetracycline effected a temporary decrease in bacterial colonization and a delay in clinical signs and histologic lesions in infected treated poults compared with untreated infected poults. Bacterial colonization and histologic lesions in the tracheas of both treated and untreated infected poults were similar by 4 days after the treatment was discontinued. This study indicates additional research with bactericidal antibiotics is needed to further evaluate antibiotic aerosolization as a treatment for alcaligenes rhinotracheitis.     

Effect of two commercial vaccines to Campylobacter fetus subspecies on heifers naturally challenged

Efficacy of two commercial vaccines containing Campylobacter fetus subspecies on heifers naturally challenged by service with an infected bull was tested. Sixteen heifers were vaccinated parentally two times with 3 weeks as interval, eight with commercial vaccine A and the other eight with commercial vaccine B. Eight other heifers were used as unvaccinated controls. Forty days after the first vaccine dose, the heifers were served by an infected bull during 60 days. Measure of systemic immune response and identification of the microorganism from genital secretions by culture and immunofluorescent antibody test (IFAT) were done. Vaccinated and control heifers had a poor reproductive performance (pregnancy rates were 2/8, 3/8 and 0/8 in groups A, B and C, respectively) and were infected by both methods during breeding time and after it. Moreover, one heifer in the groups B and C remained infected until 300 days post-breeding time. Neither vaccinated nor control heifers had an important increment of systemic antibody level. Only, they had a slight increment of antibody level after the breeding period and it may be because of natural stimulus by the infected bull during the copula. Culture and IFAT yielded high correlation on identification of C. fetus subspecies.     

Phage therapy reduces Campylobacter jejuni colonization in broilers

The effect of phage therapy in the control of Campylobacter jejuni colonization in young broilers, either as a preventive or a therapeutic measure, was tested. A prevention group was infected with C. jejuni at day 4 of a 10-day phage treatment. A therapeutic group was phage treated for 6 days, starting 5 days after C. jejuni colonization of the broilers had been established. Treatment was monitored by enumerating Campylobacter colony forming units (CFU) and phage plaque forming units (PFU) from caecal content. Counts were compared with control birds not receiving phage therapy. A clear 3 log decline in C. jejuni counts was initially observed in the therapeutic group, however, after 5 days bacterial counts stabilized at a level 1 log lower than that of the control group. Colonization of C. jejuni in the prevention group was delayed by the treatment and after an initial 2 log reduction, colonization stabilized within a week at levels comparable to the therapeutic group. The CFU and PFU counts displayed opposing highs and lows over time, indicative of alternating shifts in amplification of bacteria and phages. There were no adverse health effects from the phage treatment. Two different phages were combined as therapeutic treatment of Campylobacter positive chickens challenged at the age approaching broiler harvest. This again resulted in a significant decrease in Campylobacter colonization. We conclude that phage treatment is a promising alternative for reducing C. jejuni colonization in broilers.     

Decreased osmotic fragility of red blood cells of Eimeria adenoeides-infected turkeys

The osmotic fragility of red blood cells (RBC) from Eimeria adenoeides-infected turkey poults was compared with that of RBC from control and water-deprived poults. At different hypotonic NaCl concentrations, lysis of RBC from infected poults was 10 to 35% less on day 4 postinoculation (PI) and 50 to 65% less on day 7 PI than that of controls. Red blood cells of poults deprived of water for 3 days were also resistant to lysis; the percent lysis was roughly the same as that of RBC from infected poults at day 7 PI. Incubating control RBC in plasma from infected poults, in extracts of infected ceca, or at different pH levels did not increase their resistance to lysis, suggesting that neither a stabilizing factor in the plasma that had rapid effect on the RBC nor a transient shift in blood pH was involved. Mean RBC size differed little among infected, water-deprived, and control poults (14.0-14.2 X 8.0-8.1 X 3.8 microns). However, although 3.5% of RBC population of control and water-deprived poults were immature (mid to late polychromatic erythrocytes), only 0.4% of the RBC of infected poults were immature. The data suggest that reduced water intake as well as other factors may be involved in the decreased osmotic fragility of RBC from poults infected with E. adenoeides.     

The occurrence of Campylobacter species in Hungarian broiler chickens from farm to slaughter

The reported number of human enteric diseases caused by thermotolerant campylobacters increased in the last few decades worldwide. The microorganism gets into the food chain mostly with poultry meat or meat products. We are not aware of the way the campylobacters infect the broiler flocks, and there is little information about the real prevalence, about the reaction of thermotolerant campylobacters to the environmental factors and about the possibilities of elimination of the bacteria from the food chain. As a part of the long study, samples were collected from a broiler flock from the first day of life to the slaughter of the animals, in summer and in winter. In the summer period, at the first two sampling days (days 0 and 12) all of the samples were negative. At day 26, one cloaca sample, one sample from the surface of the wall near the ventilation aperture and an insect-sample were positive. At day 42, we found Campylobacter spp. on every sampling point at the slaughterhouse. In the winter period, we could not find Campylobacter spp. either from 0 day old, or from 10- and 31-day-old chickens, but we found them at 42 days of age on the slaughter plant. At the slaughtering place, 93.3% of the live birds were infected with Campylobacter spp., and at the end of the processing line, the infection rate was 100%. We could isolate campylobacters from the hands of the workers and from the processing environment as well. Out of the positive samples, 95.5% was contaminated with Campylobacter jejuni.     

Effect of egg storage upon the survival of Campylobacter jejuni in laboratory-infected fertile poultry eggs

Fertile eggs were infected by Campylobacter jejuni in the laboratory by a temperature differential method of inoculation, which resulted in up to 10% of the hatched birds carrying C. jejuni in the intestine. When infected eggs were stored for 5 1/2 days before incubation, the infection rate of the eggs had decreased to 20% or less when set, and no infected chicks were hatched. Inoculation of eggs after 8 days in storage also failed to yield infected chicks. In all cases, the hatch ratio was no different from that of uninfected control eggs.     

Blackhead disease in turkeys: direct transmission of Histomonas meleagridis from bird to bird in a laboratory model

The spread of Histomonas meleagridis infections through groups of turkeys in the absence of the cecal worm vector (Heterakis gallinarum) was studied in a battery cage model. Battery-reared poults were exposed at 2 wk of age by commingling with infected birds into cages that had the floor lined with paper. One treatment received no exposure, whereas other birds were commingled with two, three, or four birds/cage (25%, 37.5%, or 50%) inoculated per cloaca with cultured H. meleagridis (200,000/bird). Inoculated birds died at 7-13 days postinoculation (DPI) showing typical liver and cecal lesions of histomoniasis. By 14 DPI, 87.5% of the directly inoculated birds died or had severe lesions of histomoniasis. Turkeys commingled with two, three, or four infected birds became infected at the rate of 72%, 80%, or 75%, respectively. In another experiment, two birds/cage (25%) were inoculated with Histomonas from culture and allowed to commingle with other birds for 1, 2, 3, or 4 days. Two of 12 (16.7%) birds had minor cecal lesions after contact with inoculated birds for 1 day, but 87.5%-100% became infected if inoculated birds remained in the cage for 2-4 days. Contemporaneous inoculation with cecal coccidia (Eimeria adenoeides) as a predisposing factor in blackhead infections was studied using the model. Turkey poults directly inoculated with Histomonas were allowed to commingle for 5 days with uninoculated birds that had received inoculation with 0, 10(3), or 10(4) sporulated oocysts. The coccidian infection appeared to interfere with transmission of blackhead infection by 7 DPI, as suggested by lessened severity of cecal lesions and a lower percentage of infected birds. These studies confirm that histomoniasis is transmitted readily from directly exposed young turkeys to others in the absence of the cecal worm vector, and that this phenomenon can be reproduced in battery cages as an experimental model.     

Evidence for bursal involvement in the pathogenesis of hemorrhagic enteritis of turkeys

The pathogenesis of hemorrhagic enteritis in turkey poults infected with hemorrhagic enteritis virus (HEV) at 3 days or at 2 or 5 weeks of age was compared with pathogenesis in poults that had been chemically bursectomized neonatally and exposed to cell-culture-propagated virus at 2 or 5 weeks of age. Conventional poults exposed to HEV at 2 or 5 weeks developed clinical disease, and mortality ranged from 38% to 100%. In addition to the splenic and intestinal lesions usually seen with HEV infection, the pancreas, bursa of Fabricius, and thymus were also affected. In contrast, although they were free from detectable maternal antibody, poults infected with HEV at 3 days of age failed to develop clinical disease or mortality; however, virus was demonstrated by histological and electron microscopic examinations in spleens of these poults. Neonatal chemical bursectomy completely prevented the clinical signs, gross lesions, and mortality induced by HEV in poults at 2 or 5 weeks of age. These findings strongly suggest that an intact bursa is necessary for HEV to induce disease in turkeys.     

Use of an enzyme-linked immunosorbent assay to measure antibody levels in turkey breeder hens, eggs, and progeny following natural infection or immunization with a commercial Bordetella avium bacterin

Twelve large white turkey hens were immunized with a commercially available Bordetella avium bacterin. Hens and eggs were tested using an enzyme-linked immunosorbent assay (ELISA) to determine the response to the bacterin. Three hundred poults were then obtained from two commercial flocks, the hens of one flock having been immunized with the same bacterin used on the group of 12 turkeys. Titers of the poults were monitored for 7 weeks, and poults were challenged by exposure to infected poults at 1, 7, 14, and 21 days post-hatch. Hens produced an antibody response following immunization, with a parallel antibody response being detected in eggs. Maternal antibodies were present in poults from immunized hens. Poult titers declined to near the level of poults from unimmunized hens by 14 days of age. Poults from immunized hens challenged at 1 and 7 days were resistant to development of clinical disease and gross lesions, whereas all poults from unimmunized hens exhibited clinical signs and gross lesions. After 14 days, the resistance of both groups to development of clinical disease, became near equal, neither group being affected as severely as the unimmunized hens challenged at days 1 and 7. Six commercial turkey breeding flocks and their progeny that had not been vaccinated for B. avium and had no history of B. avium infection were evaluated with the B. avium ELISA. There were variations between the flocks, with poult titers reflecting those found in the hens.     

Role of litter in the transmission of Campylobacter jejuni

Autoclaved or non-autoclaved used broiler litter that was experimentally contaminated with Campylobacter jejuni was capable of infecting specific-pathogen-free chicks maintained in modified Horsfall isolators. Artificially infected chicks became fecal shedders of C. jejuni, resulting in contamination of both autoclaved and non-autoclaved used broiler litter. Fecal shedding of C. jejuni by litter-reared, artificially infected chicks persisted for at least 63 days after chicks were transferred to an isolation unit with a wire floor, which prevented coprophagy. C. jejuni was consistently recovered from water and litter in units housing directly and indirectly infected birds, indicating environmental contamination. These experiments demonstrate the potential role of litter in the perpetuation and transmission of C. jejuni infection in commercial chickens.     

Turkey origin reovirus-induced immune dysfunction in specific pathogen free and commercial turkey poults

Recently, pathogenesis studies, using genetically distinct turkey-origin reoviruses (TRVs), revealed that poults infected with certain TRV isolates had moderate to severe bursal atrophy, suggesting virus-induced immune dysfunction. In order to characterize the effect of TRV infection on the turkey immune system, classical assays were undertaken to quantify the humoral and cell-mediated immune responses in small Beltsville and broad-breasted white poults infected with the TRV isolate NC/SEP-R44/03. A marked effect on the cutaneous basophil hypersensitivity response, and on the antibody response to Newcastle disease virus (NDV) exposure, was noted in commercial and specific pathogen free (SPF) poults inoculated with NC/SEP-R44/03 at three days of age. Moderate to severe bursal atrophy, similar to that noted previously in SPF poults, occurred in commercial poults inoculated at three days of age. This immune dysfunction and bursal atrophy was not present in commercial poults inoculated at three weeks of age.     

A trial of biosecurity as a means to control Campylobacter infection of broiler chickens

We ran a controlled intervention trial to assess whether the risk of a broiler flock becoming infected with Campylobacter could be reduced by biosecurity measures. These were a standard method of cleansing and disinfecting the poultry house prior to stocking, and a standard hygiene protocol followed by all personnel who entered the study house during the flock's life. Thirty-nine flocks were allocated to intervention or control groups in a ratio of 1:2. Intervention flocks were asked to follow the specified biosecurity measures; all flocks were monitored weekly for Campylobacter infection. Analysis of infection at 42 days of age and over the life of the flock showed that the risk of thermophilic Campylobacter infection of broilers was reduced by over 50% in intervention flocks. Parts of the intervention identified as significant in the univariable analysis included twice weekly replenishment of boot dip disinfectant; potential independent risk factors identified included the location of ventilation fans and daily sanitisation of the water supply. The non-random allocation of 10 flocks to the control group may have introduced some study bias (the effect of which is discussed in the paper).     

鸡弯曲菌性肝炎的病理学研究

对30例40日龄自然感染弯曲菌性肝炎鸡的肝脏、胆囊及主要脏器进行了眼观、病理组织学、肝脏的透射电镜、胆囊的扫描电镜和透射电镜的观察.根据病变特点分为急性肝炎和亚急性肝炎.30例患鸡肝脏石蜡切片应用免疫过氧化物酶染色,空弯菌的检出率为100%;肝脏断面触片应用石炭酸复红稀释液及Warthin-Starry染色时,可检出弧形、弯曲状或螺旋状病菌.提出了以肝脏肉眼变化,结合肝断面触片石炭酸复红稀释液染色检出弯曲菌,作为宰后快速检验方法.