Production of Antibody in Mammary Gland of Pregnant, Non-Lactating and Lactating Cows, Evoked by Polyvalent Antigen with Reference to Dosage and Frequency of Immunization

Sixteen cows were used in a series of experiments to test dose, route and frequency responses in the production of milk and serum agglutinins to a spectrum of 9 proven bovine pathogens. The bacterial species were: Pasteurella multocida (2 isolates), Escherichia coli, Staphylococcus aureus, Staphylococcus albus, Streptococcus sp., Corynebacterium sp., Salmonella enteriditis, and Aerobacter aerogenes. Primary immunizations were made either through the teat canal or intramuscularly. “Booster” injections were made through the teat canal. Agglutinins in the blood appeared only after a week or more. In the milk, titers were recorded in 1 or 2 days following primary immunization. Variation of titer in the blood and milk was somewhat independent. In all but 1 cow, antibody was produced against each organism in milk and blood serum. Udder inflammation was observed in the experiments when a 15-day interval separated immunizations. Inflammation was minimal in the experiments employing the 7-day interval of immunization. A positive Whiteside test was observed following most injections, even where no other clinical signs of reaction were seen. The findings are discussed in relation to the previous literature.     

Clinical and Pathological Observations on the Experimental Passage of Swine Dysentery

The length of incubation for 36 eight and 12 week old swine in eight experimental passages averaged 11 days and ranged from five to 24 days. The duration of diarrhea for 24 of these swine averaged 6.4 days and ranged from two to 19 days. The consistent macroscopic lesion was a colitis and, subsequently, a typhlitis. In the swine euthanized on the first day of diarrhea, the colitis was most intense in the coils near the apex of the colon and, frequently, these swine had a hyperemia of the fundus of the stomach. The amount of visible blood in the colon varied. Organisms identified microscopically and ultrastructurally as spirochetes were observed commonly in the feces and the mucosal glands of the colon of swine with a diarrhea, but not in the adjacent mesenteric lymph nodes. These spirochetes which were the most numerous on the first day of diarrhea, could not be isolated and propagated in vitro. Swine which recovered naturally or were medicated at the height of a diarrhea, developed a resistance to swine dysentery. Colon from infected swine remained infectious when stored at -77°C for nine months but not when stored at -16°C. Feces from infected swine were not infectious after lyophilization and storage at -12°C.     

Experimental Studies on the Pathogenesis of Corynebacterium equi Infection in Foals

Four month-old foals were infected orally with 75 mL of a suspension of 5.0 × 10⁸ Corynebacterium equi per mL. Two foals were killed after ten days and had scanty number of C. equi in the caeco-colic lymph nodes. No C. equi were recovered from the other two foals, killed 20 days after infection. No gross pathological change was detected in these four foals, although mild microscopic lesions were seen in the ileum of one foal. Results of lymphocyte blastogenesis using peripheral blood lymphocytes and C. equi antigens showed, however, that lymphocytes became sensitized to C. equi following this challenge.

In a second experiment four month-old foals were given orally the same dose of organisms but on five consecutive days. Two foals were killed ten days after infection and showed mild histological changes in the large bowel mucosa and C. equi could be recovered from all intestinal lymph nodes cultured. In one of these foals moderate numbers of C. equi were present in the bronchial lymph node. Of the other two foals, one died after 22 days with severe ulcerative enterocolitis and intestinal lymphadenitis. Only one small pulmonary abscess was detected despite large numbers of C. equi in the lungs. The other foal developed similar intestinal changes and was euthanized 25 days after infection. No C. equi were detected in the lungs or bronchial lymph node. Lymphocyte blastogenesis in these animals showed a rapid rise in response to C. equi antigens.

These studies suggest that C. equi pneumonia in foals does not always arise from an intestinal infection, that minor intestinal infection causes a cellular immune response and that massive exposure of the bowel over a sustained period is necessary to induce intestinal lesions.

     

Ascaris suum Infection in Calves I. Clinical Signs

Clinical signs consistent with those of atypical interstitial pneumonia (AIP) were induced in calves sensitized with infective Ascaris suum eggs at seven to 20 weeks of age and challenged at three-week intervals one or more times. These signs usually appeared on the sixth or seventh day postinfection and reached maximum severity between the tenth and 13th days following infection. Prominent signs were: dyspnea, often with expiratory grunt, coughing, mouth breathing and emphysema as well as increased respiration and heart rates. In general, the intensity of signs was dependent upon dose size, although a single small dose resulted in acute signs and death in one calf. Intermittent coughing and vesicular sounds were induced in calves given A. suum eggs continually over prolonged periods. No respiratory abnormalities resulted from challenge with Toxocara canis after sensitization with A. suum. Antihistamine therapy did not alter the clinical signs in A. suum infected calves.     

Reinfection of Yearling Calves with Ascaris suum

Naturally occuring outbreaks of Ascaris suum infection in calves have usually beeen found in animals nine to 12 months of age. The circumstances surrounding these outbreaks suggest that yearling calves are either particularly susceptible to a primary exposure to A. suum or react strongly to A. summ after sensitization early in life to this or some related ascarid. To determine the effect of reinfection with A. suum nine to 12 months after varying levels of exposure to this nematode, six calves were inoculated with 200,000 to 9,000,000 eggs. Neither death nor, in general, severe clinical signs resulted from reinfection. All calves were examined 15 days after reinfection with pathological changes noted only in the lungs and consisting of emphysema, alveolar wall thickening as well as accumulations of fibrin, eosinophils and hemorrhage in the lumina of alveoli. The findings suggested that exposure to A. suum early in life is not a factor in the development of disease in calves infected at one year of age. It was also found that the eosinophilia that develops following a primary infection with A. suum evidently persists for at least one year.     

Infectivity of Cryptosporidium parvum isolated from asymptomatic adult goats to mice and goat kids.

An experimental study was carried out in neonatal goat kids to examine the infectivity of Cryptosporidium oocysts, pattern of oocyst shedding and morphological changes in the intestine during the infection. Cryptosporidium oocysts isolated from adult asymptomatic goats, and identified as C. parvum by polymerase chain reaction (PCR) were used in this study. Of three 4-day-old goat kids, two were orally infected with C. parvum oocysts (10(5) oocysts in 10 ml PBS/kid). One goat kid given 10 ml PBS only by the oral route served as a control. Cryptosporidium oocysts were detected in the faeces of one infected kid on day 3 post-inoculation (pi) whereas in the other 6 days pi. The faecal oocyst counts gradually increased and the peak counts in the two kids were 2 x 10(6)g(-1) (on day 12 pi) and 3.2 x 10(6)g(-1) (on day 14 pi). The increase in faecal oocyst output coincided with diarrhoea in an infected kid from days 10-17 pi. Although the oocyst excretion declined gradually after the peak, both infected kids excreted oocysts until euthanized on days 20 and 22 pi. Light and scanning electron microscopic investigations of the ileum revealed the endogenous stages on the brush border of the enterocytes, infiltration of neutrophils and mononuclear cells into the lamina propria, atrophy, stunting and fusion of villi. For purposes of comparison, goat Cryptosporidium oocysts were inoculated orally (10(3) oocysts/mouse) to eight, 1-week-old mice. All experimental mice excreted oocysts from day 3 pi, and four infected mice continued to excrete oocysts up to day 42 pi. The experimental infection described in goat kids resembled the natural disease in terms of oocyst excretion, clinical signs and intestinal pathology. The ability of oocysts excreted by asymptomatic goats, to infect goat kids and mice is likely to have a major impact on the epidemiology of cryptosporidiosis in livestock and man.     

捻转血矛线虫重组H11抗原山羊免疫保护性试验

以重组H11-1、H11-2及H11-1与H11-2混合物分别免疫山羊后,ELISA检测发现血清抗体均在首次免疫后14 d达到较高水平,在第2次免疫后10 d达到高峰。用10 000只捻转血矛线虫第3期幼虫攻击山羊后,对不同免疫组山羊排出虫卵数、虫卵孵化率和成虫数的统计分析结果表明,免疫组与对照组间差异不显著,但免疫组雌虫数显著少于对照组,这对防治捻转血矛线虫病可能会起一定的作用。     

Early Development of and Pathology Associated with Strongylus edentatus

Pony foals inoculated with infective Strongylus edentatus larvae were monitored for clinical signs and selected blood changes and were examined at necropsy from two to 56 days postinfection. Larvae penetrated the intestine and reached the liver intravenously before 40 hours postinfection. Occasional thrombi and larval tracks associated with the intima of cecal and colic veins suggested aberrant paths. Larvae in the liver doubled in width between seven and 15 days postinfection and a sudden increment in circulating eosinophils occurred between 11 and 15 days. These changes were probably associated with the third molt. At 30 days fourth stage larvae were migrating in the liver; at 42 days they were present in the hepatorenal ligament.

White foci were observed in the liver from two to 56 days. They contained mononuclear cells and eosinophils and later necrotic cores of eosinophils. By one month foci were overshadowed by tortuous tracks of migrating larvae. Aberrant larvae in the lungs were confined in granulomas. Massive granulomas in the wall of the cecum and colon contained small larvae which were probably inhibited by antibody associated with the third molt. Severe disruption of omental architecture and adhesions involving the intestine occurred several weeks after infection.

     

Some Clinical and Hematological Features of Virus Enteritis of Mink

Twenty-six, ten-week-old mink were infected by force feeding by pipette 2 ml of a tissue suspension containing a Wisconsin strain of mink enteritis virus. Four days later, diarrhea and partial or complete loss of appetite developed simultaneously in all of the animals. Squinting and occasional vomiting were also observed. By the sixth day after inoculation, all of the mink were anorectic and weak. Anorexia persisted for 48 to 96 hours. Diarrhea and vomiting continued until the eighth to ninth day after exposure. For the first two days after the appearance of diarrhea, the feces contained large quantities of mucus and intestinal casts were seen frequently in the droppings. Thereafter, the feces consisted mostly of yellowish green, watery fluid and contained no casts. Some of the animals died on the eighth day after infection. Those which survived were severely dehydrated and debilitated, but resumed eating and achieved complete clinical recovery within the next five to six days.

Leukopenia, i.e., total leukocyte count of less than 5,000 cells per mm³ of blood, was found in seven of nine mink examined during the height of the disease. Leukopenic animals were deficient in both lymphocytes and neutrophils.

     

Prophylaxis using paromomycin of natural cryptosporidial infection in neonatal kids

The chemoprophylactic effects of paromomycin sulfate against natural cryptosporidiosis in young kids were investigated. Two studies were carried out using two groups of 18 and 12 animals in two pens. In each pen, kids were allocated to treated or control groups. The treatment consisted of oral paromomycin given at 100 mg kg⁻¹ body weight day⁻¹ for 11 consecutive days from 2 days of age. All kids were weighed at 2, 6 and 10 days of age. Infection was monitored by collecting fecal samples and staining fecal smears every 3–4 days from days 4 or 5 to days 15 or 19. The results clearly showed the efficacy of paromomycin in reducing cryptosporidial oocyst output. Moreover, paromomycin prevented clinical signs and mortality.     

Ascaris suum Infection in Calves II. Circulating and Marrow Eosinophil Responses

An increment in the number of circulating eosinophils occurred between the 11th and 14th days after infection with Ascaris suum and this increase was generally greater after a challenge infection. Continual infection with small numbers of A. suum eggs over prolonged periods resulted in circulating eosinophil levels which fluctuated and were dose-dependent. The per cent marrow eosinophils always increased after a primary infection and a greater increase usually followed a challenge infection. The maximum increment of marrow eosinophils occurred between the tenth and 12th days and preceded the rise in circulating eosinophils by 36 hours. Antihistamine therapy did not alter eosinophil responses to A. suum. Circulating eosinophilia was not usually reflected by drastic changes in differential white cell counts. However, an increase in total white cell count often followed infection with A. suum and frequently parallelled changes in eosinophil counts. Hemoglobin and P.C.V. values remained within normal limits in A. summ infected calves.     

Oral treatment of avian lead intoxication with meso-2,3-dimercaptosuccinic acid.

The efficacy of meso-dimercaptosuccinic acid (DMSA) (succimer) in treating avian lead intoxication was studied in a retrospective, nonrandomized, longitudinal study. Nineteen birds with moderate to high blood lead concentration and neurologic signs compatible with lead toxicity were treated with DMSA (30 mg/kg p.o., b.i.d.; n = 15) for a minimum of 7 days. In cases with severe neurologic signs, DMSA was supplemented with a single dose of edetate calcium disodium (<50.0 mg/kg of body weight i.m.; n = 4). Blood lead concentrations were measured two or more times (before and after treatment). Median blood lead concentration decreased (87%), neurologic signs were resolved, and there were no apparent adverse secondary effects.     

Antibody-mediated enhancement of disease in feline infectious peritonitis: Comparisons with dengue hemorrhagic fever

Non-immune kittens passively immunized with feline serum containing high-titered antibodies reactive with feline infectious peritonitis virus (FIPV) developed a more rapid disease after FIPV challenge than did kittens pretreated with FIPV antibody-negative serum. Antibody-sensitized, FIPV challenged—kittens developed earlier clinical signs (including pyrexia, icterus, and thrombocytopenia) and died more rapidly than did non-sensitized, FIPV-challenged kittens. Mean survival time in sensitized kittens was significantly (P < 0.05) reduced compared to non-sensitized kittens (mean ± SEM, 10.0 ± 0.6 days vs. 28.8 ± 8.3 days, respectively). Lesions induced included fibrinous peritonitis, disseminated pyogranulomatous inflammation and necrotizing phlebitis and periphlebitis. FIPV antigen, immunoglobulin G, complement (C3) and fibrinogen were demonstrated in lesions by immunofluorescence microscopy.The pathogenesis of dengue hemorrhagic fever (DHF) in persons bears striking resemblance to that of FIP in experimental kittens. In both FIP and DHF, non-neutralizing antibody may promote acute disease by enhancement of virus infection in mononuclear phagocytes or by formation of immune complexes, activation of complement and secondary vascular disturbances.     

Four distinct neurologic syndromes in Marek's disease: effect of viral strain and pathotype

A chronological study of central nervous system disorders induced by Marek's disease virus (MDV) has been conducted. Neurologic clinical signs were recorded daily for individual chickens of two genetic lines after inoculation of 13 serotype 1 MDV strains representing all three pathotypes. In addition to classical transient paralysis (TP) previously described by many workers, and acute TP, described in the companion paper, we have identified for the first time two other neurologic syndromes, persistent neurologic disease (PND) and late paralysis (LP). PND designates birds that showed a variety of neurologic signs (ataxia, torticollis, and nervous tics) after recovery from paralysis (12-15 days postin-oculation [DPI]) that either persisted through the observation period or presented a cyclic pattern. LP was a rare syndrome characterized by the late onset of the paralytic stage (about 20 DPI), perhaps indicating occasional failure of the initial intraabdominal inoculation to induce infection. Clinical signs and histopathologic alterations of the brain were also evaluated sequentially in chickens of two genetic lines after inoculation with two MDV strains (virulent MDV and very virulent plus MDV). Although clinical response differed greatly among treatment groups, types of lesions (endotheliosis, mononuclear perivascular cuffing, vasculitis, vacuolization, and increase in cellularity of the neuropil) were similar. However, early onset of lesions (by 6 days) appeared to be associated with a greater severity of clinical signs. We also found that neurologic response was greatly influenced by viral pathotype (virulence). This study thus confirms that the central nervous system is an important target organ for MDV resulting in several distinct clinical manifestations and suggests that neurologic responses in antibody-free chickens might be a useful criterion for virus pathotyping.     

Pharmacokinetics of meloxicam in adult goats and its analgesic effect in disbudded kids

Ingvast‐Larsson, C., Högberg, M., Mengistu, U., Olsén, L., Bondesson, U., Olsson, K. Pharmacokinetics of meloxicam in adult goats and its analgesic effect in disbudded kids. J. vet. Pharmacol. Therap. 34 , 64–69. The pharmacokinetics and analgesic effect of the nonsteroidal anti‐inflammatory drug meloxicam (0.5 mg/kg) in goats were investigated. In a randomized, cross‐over design the pharmacokinetic parameters were investigated in adult goats (n = 8) after single intravenous and oral administration. The analgesic effect was evaluated in kids using a randomized, placebo controlled and blinded protocol. Kids received meloxicam (n = 6) once daily and their siblings (n = 5) got isotonic NaCl intramuscularly while still anaesthetized after cautery disbudding and injections were repeated on three consecutive days. In the adult goats after intravenous administration the terminal half‐life was 10.9 ± 1.7 h, steady‐state volume of distribution was 0.245 ± 0.06 L/kg, and total body clearance was 17.9 ± 4.3 mL/h/kg. After oral administration bioavailability was 79 ± 19%, C_max was 736 ± 184 ng/mL, T_max was 15 ±5 h, although the terminal half‐life was similar to the intravenous value, 11.8 ± 1.7 h. Signs of pain using a visual analogue scale were smaller in kids treated with meloxicam compared with kids treated with placebo on the first day after disbudding, but subsequently no difference in pain was noticeable. Plasma cortisol and glucose concentrations did not differ between the two groups.     

Development of Clinical Signs and Occurrence of Feline Corona Virus Antigen in Naturally Infected Barrier Reared Cats and Their Offspring

The onset and pattern of the clinical signs of feline corona virus (FCoV) infection in cats were studied in a setting behind an isolation barrier. Two FCoV-seropositive cats were the source of the infection, and 3 barrier reared cats–initially FCoV-seronegative–were the recipients. The first clinical sign in the recipients appeared 11 days after contact with the source of infection. After 2 years 1 male and 1 female of the recipients started to breed. Their offspring developed clinical signs of disease at an age of 4-5 weeks. A pattern of recurring upper respiratory tract signs and conjunctivitis at intervals of about 4 months was observed in both the recipients and their offspring, while CNS dependent signs and wasting remained or got worse, once developed. Once demonstrated, FCoV antigen persisted in membrana nictitans throughout the investigation, and was found in all cats but 4 (90%). The offspring died during 2 periods, around the first week of life (9/37), and at 3-5 months of age (5/25). For comparison 3 offspring were euthanised at an age of 1 day and 16 offspring at an age of 3-6 months. FCoV antigen was demonstrated in all organs investigated (100%) from offspring dying during the first period, and in 97% from those dying during the second period. For the offspring euthanised during the same 2 periods the corresponding findings were 95% and 85%. Offspring euthanized between 9 and 17 months (4 kittens) had antigen in 67% of all investigated organs. The incidence of FCoV antigen in almost every organ in the investigated newborn kittens suggests an intrauterine infection. The demonstration of FCoV antigen in all euthanised cats, suggests a persistant infection. Virus was cultivated from membrana nictitans, that was FCoV antigen positive in the M3 test.     

Enzootic ataxia and caprine arthritis/encephalitis virus infection in a New England goat herd [corrected

Ataxia was diagnosed in kids from a New England goat herd. Concurrent infection with the caprine arthritis/encephalitis (CAE) virus contributed to the development of hind limb ataxia and weakness in one of the kids. Six kids from this herd had signs of hind limb ataxia and paralysis. Detailed evaluation of 2 of the affected kids revealed low liver and serum copper concentrations and spinal cord demyelination. One kid also had histologic changes in the CNS and lungs, compatible with a diagnosis of CAE. Serum copper concentration was determined in affected goat kids and their dams and was compared with serum copper concentration in clinically normal kids and their dams from the same herd. Serum copper concentration also was measured in dams and kids in a control herd that had no history of ataxia. The mean serum copper concentration in affected kids was 0.125 microgram/ml, compared with 0.45 microgram/ml in unaffected kid herdmates. Kids from the control herd had mean serum copper concentration of 0.6 microgram/ml. Mean serum copper concentration in dams of kids with neurologic signs also was low (0.25 microgram/ml), compared with that (0.5 microgram/ml) in dams of clinically normal kids of the affected herd and that (0.95 microgram/ml) in dams of kids of the control herd. Results of a serologic survey (by use of agar gel immunodiffusion) of the affected herd for CAE indicated that 69.5% of the goats were seropositive. Dietary copper intake was determined to be adequate in this goat herd; therefore, copper deficiency appeared to be conditioned by an interfering substance. However, a search for interfering substances was unrewarding.     

Surgical technique, postoperative complications and outcome in 14 dogs treated for hydrocephalus by ventriculoperitoneal shunting

Objective: To report frequency and type of complications, and outcome in dogs with severe neurologic signs secondary to internal, suspected obstructive hydrocephalus treated by ventriculoperitoneal (VP) shunting. Study Design: Case series. Animals: Dogs (n=14). Methods: Medical records (2001–2006) was reviewed for dogs that had VP shunting. Inclusion criteria were complete medical record, progressive forebrain signs unresponsive to medical treatment, normal metabolic profile, negative antibody titers and/or cerebrospinal PCR for Toxoplasma gondii, Neospora caninum, and canine distemper virus, magnetic resonance images of the brain, confirmed diagnosis of VP shunting, and follow‐up information. Results: Hydrocephalus was idiopathic in 5 dogs and acquired (interventricular tumors, intraventricular hemorrhage, inflammatory disease) in 9 dogs. Four dogs developed complications 1 week to 18 months postoperatively, including ventricular catheter migration, infection, shunt under‐drainage, kinking of the peritoneal catheter, valve fracture, and abdominal skin necrosis. Three of these dogs had 1 or more successful revision surgeries and 1 dog was successfully treated with antibiotics. All, but 1 dog, were discharged within 1 week of surgery, and had substantial neurologic improvement. Median survival time for all dogs was 320 days (1–2340 days), for dogs with idiopathic hydrocephalus, 274 (60–420) days and for dogs with secondary hydrocephalus, 365 (1–2340) days. Conclusions: VP shunting was successful in relieving neurologic signs in most dogs and postoperative complications occurred in 29%, but were resolved medically or surgically.     

Immunization with Eimeria ninakohlyakimovae-live attenuated oocysts protect goat kids from clinical coccidiosis

Caprine coccidiosis, affecting mainly young goat kids around the weaning period, is worldwide the most important disease in the goat industry. Control of caprine coccidiosis is increasingly hampered by resistances developed against coccidiostatic drugs leading to an enhanced need for anticoccidial vaccines. In the current study we conducted an oral immunization trial with live attenuated sporulated Eimeria ninakohlyakimovae oocysts. Sporulated E. ninakohlyakimovae oocysts were attenuated by X-irradiation technique. The experimental design included a total of 18 goat kids divided into the following groups: (i) animals immunized with attenuated E. ninakohlyakimovae oocysts at 5 weeks of age and challenged 3 weeks later with non-irradiated homologous oocysts (group 1); (ii) animals infected with non-attenuated E. ninakohlyakimovae oocysts at 5 weeks of age and challenged 3 weeks later with non-attenuated homologous oocysts (group 2); (iii) animals primary-infected with untreated E. ninakohlyakimovae oocysts at 8 weeks of age (control of the challenge infection, group 3); (iv) non-infected control animals (group 4). Goat kids immunized with live attenuated E. ninakohlyakimovae oocysts (group 1) excreted significantly less oocysts in the faeces (95.3% reduction) than kids infected with non-attenuated ones (group 2). Furthermore, immunization with live but attenuated oocysts resulted in ameliorated clinical coccidiosis compared to goat kids infected with untreated oocysts (group 2) and resulted in equally reduced signs of coccidiosis after challenge infection compared to acquired immunity driven by non-attenuated oocysts. Overall, the present study demonstrates for the first time that live attenuated E. ninakohlyakimovae oocysts orally administered showed almost no pathogenicity but enough immunogenicity in terms of immunoprotection. Importantly, vaccinated animals still shed low amounts of oocysts, guaranteeing environmental contamination and consecutive booster infections to sustain ongoing immunity.