Effects of leucocyte extract, levamisole and sulphadimidine on natural coccidial infections (Eimeria spp.) in young lambs

The efficacy of leucocyte extract (LE) and sulphadimidine in preventing coccidiosis in naturally infected lambs on pasture was evaluated in 3 separate experiments, whereas the prophylactic effect of levamisole was studied in 1 of the experiments. LE prepared from ewes immune to coccidia (Eimeria spp.) was administered either intravenously or intraperitoneally to young lambs 7, 5, or 2 days before they were turned out on pastures contaminated with coccidia. In all experiments, LE failed to transfer protective immunity to the lambs against the first coccidial infection on pasture. The LE preparations used apparently had an immunosuppressive effect, which resulted in more severe clinical signs of coccidiosis in the recipients. The lambs given LE showed a higher incidence of diarrhoea, a poorer weight gain, a higher mortality, and a higher oocyst output than the untreated control lambs. In lambs treated with sulphadimidine at 200 mg/kg on days 12, 13, and 14 after turnout there was a reduced severity of the coccidial infections in all experiments. The sulphadimidine-treated lambs had better weight gains and passed fewer oocysts than the controls during the third and fourth week after turnout, but some of them developed diarrhoea. Lambs treated with levamisole at 2 mg/kg 2 days before turnout, at turnout, and 2 days after turnout were more severely affected by the first coccidial infection on pasture than the controls.To study the lambs’ immunity against a heavy challenge infection with coccidia as compared with their immunity against the natural reinfection on pasture, some of the lambs from the original groups (untreated, sulphadimidine-treated, LE-treated) were each inoculated with 2 mill. Eimeria spp. oocysts about 6 weeks after turnout. The oocyst counts of the challenged lambs, except the LE-treated lambs, increased to a new peak 19–20 days after challenge. The challenge infection caused a softening of the faeces and a marked depression in weight gain in all challenged groups of lambs, mainly between days 10 and 17 after challenge. The lambs were thus only partially immune to coccidia after the first coccidial infection on pasture. The lambs treated with either LE or sulphadimidine in connection with the first coccidial infection on pasture were not appreciably more susceptible to the challenge infection than the untreated lambs.     

Ovine coccidiosis: studies on the pathogenicity of Eimeria ovinoidalis and E. crandallis in conventionally-reared lambs, including possible effects of passive immunity

No pathogenic effect was detected in lambs when 10(4) oocyts of each species were inoculated before 72 h of age. At 4 weeks of age the combined inoculum caused diarrhoea and weight loss, the severity being roughly proportional to the size of the inoculum. Even 1000 oocysts of each species caused diarrhoea; the pathogenic effect was attributable mainly to E. ovinoidalis. Hyperimmunization of ewes during pregnancy (by repeated inoculation of massive doses of oocysts) reduced the effects of oocyst inoculation in their progeny. Levamisole administration during pregnancy increased the birthweight of lambs.     

Dose-response effects of diclazuril against pathogenic species of ovine coccidia and the development of protective immunity

Twin lambs at pasture with their ewes, were divided into seven groups of 10 lambs. One group of 10 lambs served as a non-infected, untreated control. Five groups of 10 lambs were infected with 10,000 oocysts of Eimeria crandallis and 10,000 oocysts of Eimeria ovinoidalis when they were 3 weeks old (day 21 of the study). This produced a good level of infection with high oocysts production and diarrhoea in the lambs. Fourteen days after the primary, artificial challenge (day 35) four of these groups were treated with oral diclazuril at 0.25, 1.0, 2.0 or 4.0mg/kg. Diclazuril treatment was highly effective, dramatically reducing symptoms of diarrhoea and reducing faecal oocyst output by 79.7%, 97.3%, 99.4% and 99.5% respectively in the treated groups within four days. Two weeks post-treatment, and 28 days after the primary coccidial challenge (day 49 of the study), five groups of lambs were re-challenged with 100,000 oocysts of E. crandallis and 100,000 oocysts of E. ovinoidalis (secondary challenge). A group of lambs which had received neither the primary coccidia infection, nor drug treatment (susceptible controls) were also given the secondary challenge. All lambs given the secondary challenge produced high numbers of coccidia and exhibited varying degrees of diarrhoeic faeces. The lambs, which had previously received the higher doses of diclazuril at 2.0 and 4.0mg/kg, developed clinical signs of coccidiosis. These lambs were completely susceptible despite having received the early primary immunising infection of coccidia on day 21. The effects of the secondary challenge were more severe in the groups dosed with the two highest levels of diclazuril than in the susceptible control lambs, which had presumably been exposed to continued low levels of pasture contamination and had acquired a limited degree of immunity from this exposure. It would appear that treatment at the higher dose levels not only eliminated most of the oocysts from the primary challenge but also adventitious infection derived from the grazing paddocks. In contrast, lambs which had received the two lower drug levels of diclazuril (0.25 and 1.0mg/kg) whilst producing large numbers of oocysts, had only transient diarrhoea following secondary challenge. It was concluded that when used as a metaphylactic treatment, diclazuril works rapidly and is effective within four days of administration. Overall, a single dose of diclazuril at either 0.25-1.0mg/kg appears to be highly effective in the control of coccidiosis in young lambs at pasture whilst allowing the development of protective immunity against subsequent heavy coccidia challenge.     

Pulmonary lesions in lambs experimentally infected with ovine adenovirus 5 strain RTS-42

Twelve lambs were inoculated transtracheally and intranasally with Mastadenovirus ovi 5 strain RTS-42 and killed sequentially. Pulmonary lesions were studied by light and electron microscopy. Four lambs served as sham inoculated controls. Pulmonary lesions consisted of multifocal areas of bronchiolitis and alveolitis associated with necrosis and sloughing of isolated type I and type II alveolar epithelial cells and nonciliated bronchiolar epithelial cells. This was followed rapidly by hyperplasia of the remaining epithelium and repair of the damage. A cellular infiltrate of neutrophils and macrophages began at 2 days after inoculation, peaked at 4 days after inoculation, gradually diminished until minimal at 12 days after inoculation, and was resolved at 21 days after inoculation. Surfactant was abundant and, along with debris, was removed from the alveoli by macrophages. Clinical disease was not seen, but lesions were believed to be sufficient to allow bacteria to colonize the lungs and cause severe disease.     

Toxic effects for lambs of cytotoxic necrotising factor from Escherichia coli

The lethal effect, clinical signs and lesions caused by the intravenous inoculation into six lambs (seven to 10 days old) of a partly purified preparation of cytotoxic necrotising factor (CNF) from Escherichia coli, strain BM2-1, were investigated. Two control preparations were also tested in two lambs each: (i) the same as above but heated for one hour at 60 degrees C, a treatment which inactivates CNF and preserves residual endotoxic activity; and (ii) purified material from a CNF-defective mutant of BM2-1. Whereas none of the lambs in either of the control groups died or showed significant clinical signs or lesions, all the lambs inoculated with partly purified CNF developed severe clinical signs starting six hours after inoculation which consisted mainly of neurological signs and mucoid diarrhoea. The most striking lesions were oedema and haemorrhages in the central nervous system, and foci of coagulation necrosis in the myocardium. Mucus hypersecretion in the gastrointestinal tract was not associated with cellular inflammation.     

开食料补饲日龄对羔羊瘤胃和小肠组织形态的影响

为研究开食料补饲日龄对羔羊瘤胃和小肠组织形态的影响,选用72只体重接近的湖羊初生公羔(双羔,初生重3.51±0.52 kg),随机分为2组,7或42 d补饲开食料,每组36只羔羊。分别在14,28,42,56,70和84 d每组各屠宰6只羔羊,采集瘤胃和小肠组织样品。结果表明:42 d时7 d补饲组瘤胃背囊和腹囊乳头高显著高于42 d补饲组(P<0.05),42 d时7 d补饲组瘤胃腹囊乳头宽有大于42 d补饲组的趋势(P=0.053),42 d时7 d补饲组背囊肌层厚显著高于于42 d补饲组(P<0.05);28和42 d时7 d补饲组十二指肠和回肠绒毛长均显著高于42 d补饲组(P<0.05),42 d时7 d补饲组回肠隐窝深显著低于42 d补饲组(P<0.05),42 d时7 d补饲组十二指肠和回肠绒毛长和隐窝深比显著高于42 d补饲组(P<0.05)。结论 7 d补饲有利于瘤胃组织形态发育和42 d前小肠粘膜发育。     

Pathology in the ovine foetus caused by an ovine pestivirus

Homogenised tissues or tissue culture supernatant fluid containing a noncytopathic pestivirus obtained from a lamb with a neurologic form of border disease, were inoculated into ewes at different stages of pregnancy. Foetal death occurred in 9 ewes of those inoculated between 19 and 47 days of pregnancy while 3 ewes did not lamb. Eight of the foetuses were aborted between 77 and 132 days of pregnancy; of these 6 were autolysed or mummified and one had arthrogryposis. The one full-term dead lamb had a hairy birth coat and lissencephalic micrencephaly. Foetal death occurred in only 7 of 14 ewes inoculated between 57 and 72 days of pregnancy. Four of these ewes aborted between 77 and 108 days of pregnancy and 3 gave birth to full-term, dead, hairy lambs. The remaining 7 ewes gave birth to live hairy lambs with severe inco-ordination. All lambs carried to term and aborted foetuses or lambs that could be examined had a range of intracranial malformations including focal leucomalacia, micrencephaly, hydranencephaly, porencephaly, lissencephaly and cerebellar hypoplasia. Some lambs also had skeletal abnormalities including arthrogryposis, scoliosis and brachygnathia inferior. The pestivirus isolate used in these trials produced more severe effects on the ovine foetus than previously observed in similar inoculation trials using pestivirus isolates from border disease lambs without nervous signs.     

Experimental models of porcine post-weaning colibacillosis and their relationship to post-weaning diarrhoea and digestive disorders as encountered in the field

The aim of this study was to develop a reliable model system of porcine post-weaning colibacillosis, and in doing so to assess the primary relationship of enterotoxigenic Escherichia coli to post-weaning diarrhoea and digestive disorders as encountered in the field. Six sequential experiments were carried out using 168 SPF piglets weaned into an optimal controlled environment at 28 days of age. The piglets were allocated to 23 treatment groups, 17 of which were inoculated either orally or intragastrically with enterotoxigenic strains of E. coli (LT+, STI+, STII+) possessing adhesive factors including K88 (F4). The piglets were challenged either once (Day 4 post-weaning) or on several days post-weaning, with the challenge load for each inoculation varying from 10(8) to 10(12) CFU.Overall 14.5% of inoculated pigs developed severe illness and died: these had lesions in their digestive tracts typical of colibacillosis. Diarrhoea occurred on at least 1 day in 50% of inoculated pigs, but was transient (1.7 days on average), appeared very soon after challenge (sometimes within half a day), and was accompanied by signs of depression and low weight gain. Generally a prompt recovery then occurred. In the second 2 weeks post-inoculation daily weight gain reached the same level in most inoculated groups of pigs as in the uninoculated controls. Only a small number of pigs developed a chronic enteritis lasting several days, as is typically observed in field cases. Diarrhoea was more common in the piglets that were tested adhesive positive to the K88 fimbriae receptor, but the disorders were no more severe in these animals. The response of all pigs depended primarily on the inoculum used, and especially on the challenge load. Although enterotoxigenic E. coli are clearly important in the aetiology of post-weaning diarrhoea, other factors are also required for the production of the chronic post-weaning digestive disorders and ill-thrift that are commonly encountered in commercial piggeries.     

Effects of intranasal inoculation with Bordetella bronchiseptica, porcine reproductive and respiratory syndrome virus, or a combination of both organisms on subsequent infection with Pasteurella multocida in pigs

OBJECTIVE: To determine effects of intranasal inoculation with porcine reproductive and respiratory syndrome virus (PRRSV) or Bordetella bronchiseptica on challenge with nontoxigenic Pasteurella multocida in pigs. ANIMALS: Seventy 3-week-old pigs. PROCEDURE: In experiment 1, pigs were not inoculated (n= 10) or were inoculated with PRRSV (10), P. multocida (10), or PRRSV followed by challenge with P. multocida (10). In experiment 2, pigs were not inoculated (n = 10) or were inoculated with B. bronchiseptica (10) or PRRSV and B. bronchiseptica (10); all pigs were challenged with P. multocida. Five pigs from each group were necropsied 14 and 21 days after initial inoculations. RESULTS: Pasteurella multocida was not isolated from tissue specimens of pigs challenged with P. multocida alone or after inoculation with PRRSV. However, in pigs challenged after inoculation with B. bronchiseptica, P. multocida was isolated from specimens of the nasal cavity and tonsil of the soft palate. Number of bacteria isolated increased in pigs challenged after coinoculation with PRRSV and B. bronchiseptica, and all 3 agents were isolated from pneumonic lesions in these pigs. CONCLUSIONS AND CLINICAL RELEVANCE: Infection of pigs with B. bronchiseptica but not PRRSV prior to challenge with P. multocida resulted in colonization of the upper respiratory tract and tonsil of the soft palate with P. multocida. Coinfection with PRRSV and B. bronchiseptica predisposed pigs to infection of the upper respiratory tract and lung with P. multocida. Porcine reproductive and respiratory syndrome virus and B. bronchiseptica may interact to adversely affect respiratory tract defense mechanisms, leaving pigs especially vulnerable to infection with secondary agents such as P. multocida.     

Experimental microcyst sarcocystis infection in lambs: pathology

Six 34- to 42-day-old lambs raised in coccidia-free conditions were inoculated with 70,000 sporocysts derived from sheep heart with microscopic sarcocysts. Fever and mild anorexia occurred between 25 and 33 days after inoculation. A transient anaemia was most marked 32 days after inoculation. Lambs were killed and examined 14, 25, 33, 42, 60 and 81 days after inoculation. Gross lesions were absent. First and second generation meronts were present in endothelial cells at 25 and 33 days after inoculation. Meronts were most numerous in kidney glomeruli. Developing sarcocysts were rare at 42 days after inoculation. Sarcocysts with a primary cyst wall 2 to 3 micron thick composed of palisade projections were common at 60 and 81 days after inoculation in striated muscle and brain. Mild to severe striated muscle myositis and non-suppurative encephalitis or encephalomyelitis with glial nodules were observed 25 to 81 days after inoculation. Sarcocyst frequency varied considerably; it was highest in myocardium, M vastus intermedius, M vastus medialis, M extensor carpi radialis and tongue muscle and was lowest in M masseter.     

Transmissible congenital demyelinating encephalopathy of lambs

Twenty-two fetal lambs were inoculated in utero with tissue suspension prepared from lambs born with weakness, incoordination and clonic tremor. Clinically, affected newborn lambs had clonic tremor, were generally weak and had abnormally pigmented hairy fleece. The inoculation resulted in a disseminated encephalomyelitis with secondary teratologic changes in a significant number of fetuses. The mononuclear inflammatory changes were most obvious 14 days after inoculation, after which there was rapid resolution. Changes seen at birth were chronic astrocytosis with neuron loss in the spinal cord and cerebellar dysplasia. Single radioimmunodiffusion studies showed consistently low IgG in infected fetuses and high IgG in lambs at birth.     

The effect of transfer factor treatment on two challenge infections of Haemonchus contortus in immuno-competent 7-month-old lambs

A number of immuno-competent Blackface lambs were infected with 10,000 Haemonchus contortus third stage larvae and were later challenged with a second dose of 10,000 H. contortus third stage larvae. One group of lambs was treated with dialysed transfer factor prior to the second challenge dose. Histological changes in the abomasal wall, reductions in abomasal worm burdens at slaughter and faecal egg counts monitored throughout the experiment suggested the presence in some animals of an innate resistance, a "self curing" effect, an enhancement of this "self curing" effect in the transfer factor treated group and a response in one transfer factor treated animal comparable to "classical self cure".     

Experimental infection of fetal and newborn Suffolk sheep with scrapie virus

Fetal (n = 21) and newborn (n = 7) Suffolk sheep were inoculated with scrapie virus isolated from other Suffolk sheep. Twenty fetuses, 76 to 109 days of gestational age, were inoculated IM in the neck through the uterine wall and were examined for virus 47 to 322 days later by mouse inoculation. Scrapie virus was not detected before 254 days of age; only traces of virus were detected in 3 of 7 lambs examined thereafter (2 at 254 days of age and 1 at 322 days of age). Virus was limited to the supra-pharyngeal, prescapular, and mesenteric lymph nodes. Seven lambs were inoculated into the palatine tonsils with scrapie virus as newborns (3 to 12 days old) and were examined for virus when they were 147 to 210 days old. Virus was not detected in the lymphoreticular tissues or terminal portion of ileum of any lamb. Failure to find scrapie virus in these lambs and in most lambs inoculated as fetuses might indicate few had became infected. However, if most lambs and fetuses had become infected, the long zero phase of the infection could have accounted for failure to find scrapie virus in many of them examined too soon after inoculation. The limited findings of this study indicate that efforts to demonstrate prenatal or neonatal transmission of scrapie by detecting virus are hampered by the slowness of its replication.     

ENTERITIS IN FOALS INDUCED BY ROTAVIRUS AND ENTEROTOXIGENIC ESCHERICHIA COLI

Colostrum-deprived, colostrum-fed or suckling foals were orally inoculated with foal rotavirus and enterotoxigenic Escherichia coli derived from a calf. Neither agent given alone caused diarrhoea in foals aged 1 or 2 days, although with rotavirus, 2 of the 3 inoculated foals became depressed 3 days after inoculation and all 3 were excreting rotavirus in the faeces. Inoculation of both agents induced diarrhoea in colostrum-deprived, colostrum-fed or suckling foals aged up to 16 days. There was an apparent age-related resistance to diarrhoea which developed between 2 and 3 weeks of age. It was related to failure of rotavirus to establish apparent infection in older foals and was independent of preinoculation maternal antibody.     

A MUCOSAL DISEASE VIRUS AS A CAUSE OF ABORTION HAIRY BIRTH COAT AND UNTHRIFTINESS IN SHEEP

A condition resembling border disease has been transmitted by the inoculation of pregnant ewes with material from affected lambs. Forty-nine merino ewes, mated to merino rams 7 to 87 days previously, were inoculated with an homogenate of brain, spinal cord and spleen from affected lambs. Mummified foetuses, abortions and stillbirths were observed, and lambs with hairy birth coats were born to ewes inoculated between days 12 to 70 of gestation. A mucosal disease virus (MDV), present in the original material, was recovered from the aborted foetuses and lambs. Attempts to induce passive protection using bovine anti-serum to the C24V strain of MDV were not successful. The condition was also transmitted by inoculation of pregnant ewes with a cell culture supernatant prepared from tissue cultures that had been inoculated with an organ homogenate pool. MDV was present in the supernatant and was recovered from aborted foetuses and lambs. It is suggested that a condition in sheep in Australia resembling border disease is due to the infection of the pregnant ewe by a mucosal disease virus.     

Studies on the response of ewes to live chlamydiae adapted to chicken embryos or tissue culture.

Ewes infected before gestation with chicken embryo or tissue culture adapted chlamydial strain B-577 were challenge inoculated with the homologous strain at four to 18 weeks of gestation. The ewes responsed with group specific complement fixing antibody titers of 1:8 to 1:256 by the second week after initial infection. A secondary antibody response in the surviving challenge inoculated ewes occurred at the time of lambing and reached titers of 1:32 to 1:256 by the second week after parturition. Group specific complement fixing antibodies did not appear to play a significant role in resistance to chlamydial infection. Ewes infected with the chicken embryo adapted strain B-577 excreted chlamydiae in their feces 60 days after inoculation. However, chlamydiae were not recovered from feces of ewes infected with the tissue culture adapted strain B-577. Placentas of ewes challenge inoculated by the intravenous route were consistently infected. Chlamydiae were recovered from placentas, some fetuses and lambs. In two instances when challenge inoculation was given by the intramuscular route, infection was detected only by the direct fluorescent antibody method.     

Experimental infection of pregnant ewes with bovine viral diarrhea virus type-2 (BVDV-2): effects on the pregnancy and fetus

The reproduction effects of bovine viral diarrhea virus type-2 (BVDV-2) infection were investigated in ewes inoculated with a non-cytopathic BVDV-2 isolate at three stages of gestation. Virus inoculation was followed by a transient viremia, accompanied by a transient and mild hyperthermia and nasal discharge in a few animals. Some ewes were sacrificed at different time-points after virus inoculation to study the kinetics of fetal infection. Infectivity and viral antigens were detected in placentomes from day 7 to 36 post-inoculation (pi) and in fetal fluids and tissues between days 10 and 28 pi. Cardiac petechial hemorrhages and hemoperitoneum accompanied by a severe fibrinous ulcerative placentitis were observed in fetuses examined at days 21, 28 and 36 pi. Inoculation of ewes at days 55-60 of gestation resulted in a prolonged virus replication in placentomes and fetal tissues; ewes that were allowed to proceed with pregnancy had 77% of abortions or fetal and perinatal deaths. Seven stillbirths, unviable and viable lambs born to these ewes were virus-positive at birth. Infectious virus was repeatedly isolated from leukocytes of two lambs up to 2 and 6 months of age, indicating they were persistently infected. Ewes inoculated at days 65-70 of gestation had 66.6% of fetal and perinatal losses. Three viable lambs born to these ewes were healthy, BVDV antibody-positive and virus-negative. A transient viral replication in placentomes and in a few fetal tissues, followed by the rise of fetal neutralizing antibodies and virus clearance was the result of inoculating ewes at days 120-125 of gestation. Lambs born to these ewes were healthy, antibody-positive and virus-negative. These results demonstrate that the biology of BVDV-2 infection in pregnant sheep is essentially similar to that of BVDV-1 in pregnant cattle and sheep. These features make this species an attractive animal model for studying the pathogenesis of congenital BVDV-2 infection.     

Activity of an anti-inflammatory drug against cryptosporidiosis in neonatal lambs

The efficacy of the anti-inflammatory drug Bobel-24 against experimental infection by Cryptosporidium parvum was evaluated in neonatal lambs. The animals were treated by oral administration of the drug at 50 or 500 mg/kg of body weight. The prophylactic/therapeutic treatment was started 4 h before inoculation of the lambs with oocysts and was continued for eight consecutive days. The therapeutic treatment was initiated at the onset of diarrhoea, after confirmation of infection, and was continued for six consecutive days. Infection was monitored by daily examination of faecal samples from the first day until 30 days post-inoculation. The criteria considered in evaluating development of the infection and the drug activity were: oocyst shedding, presence of diarrhoea and weight gain at 15 and 30 days post-inoculation. Bobel-24 was effective as a prophylactic/therapeutic treatment at the lowest dose (50 mg/kg of body weight); in the group treated with this dose of drug there was a longer prepatent period, a shorter patent period and a lower intensity of oocyst excretion than in the untreated control group, and the differences were all statistically significant (P<0.05). Moreover, one animal did not excrete oocysts, and two lambs had diarrhoea, for only 1 and 2 days. In the group treated with the higher dose of the drug, the diarrhoea lasted for a significantly shorter period (P<0.05) than in the untreated group.     

Studies on Mycoplasma mycoides subsp. mycoides (LC) in lambs and calves.

Six cesarean-derived lambs were inoculated either with 4.5 X 10(4), 4.5 X 10(6) or 4.5 X 10(8) Mycoplasma mycoides subsp. mycoides intratracheally. One animal receiving the intermediate dose died four days post-inoculation, the two receiving the high dose died six days postinoculation, while one receiving the low dose died eight days postinoculation. The two surviving lambs were challenged on day 20 postinoculation with 1 X 10(8) organisms subcutaneously and 2 X 10(9) organisms intravenously. One animal died eight days following this challenge while the other survived and was killed. Six conventionally reared lambs challenged with 90 to 8500 organisms by intranasal and intraocular instillation failed to become infected. Three conventionally reared calves were each inoculated with 1 X 10(8) organisms by each of intratracheal, subcutaneous and intravenous routes. They were killed 20 days post-inoculation without having shown any clinical signs.     

Evaluation of Campylobacter jejuni colonization of the domestic ferret intestine as a model of proliferative colitis

Forty 3- to 17-week old domestic ferrets, including 2 gnotobiotes, were inoculated orally and/or rectally with 10(6) to 10(9) colony-forming units of 1 or more of 4 strains of Campylobacter jejuni, 3 of mink and 1 of human origin. Feeding or gavage of any of the 4 strains, in milk or broth, with or without preinoculation sodium bicarbonate treatment to neutralize stomach acid, induced colonization in 38/40 ferrets; diarrhea lasted 2 to 4 days in conventional kits, 6 days in gnotobiotes. Bacteremia was detected in 4 of 18 tested, 2 to 5 days after inoculation. Two strains caused no more severe disease or prolonged colonization after 3 serial IV passages in kits than they did before passage. Multiple inoculations with a given strain resulted in progressively briefer colonization and milder disease, but subsequent inoculation with a different strain induced colonization and gastrointestinal disease similar to a primary infection. Five kits inoculated rectally after 4 previous homologous inoculations were resistant to colonization as well as to disease. Agglutinin titers of ferrets inoculated orally or rectally once were low or undetectable, but increased in response to repeated inoculation. Pretreatment with a 1% formalin enema caused mild colon irritation without clinical or histologic evidence of proliferative colitis in ferrets concurrently inoculated orally and/or rectally, whether or not they had preexisting antibodies to any strain of C jejuni. Histologic examination of tissues revealed leukocytic infiltration of intestinal lamina propria in 29 of 35 infected kits and 5 of 8 noninfected controls, and cryptosporidiosis in 5 infected kits plus 1 control.(ABSTRACT TRUNCATED AT 250 WORDS)