Studies on the pathogenesis of Salmonella typhimurium and Salmonella choleraesuis var kunzendorf infection in weanling pigs

Twenty-six 4-week-old pigs were randomly allotted to 4 groups: group 1--orally inoculated with Salmonella typhimurium; group 2--orally dosed with S choleraesuis; and groups 3 and 4, with surgically constructed intestinal loops--loops inoculated with either S typhimurium or S choleraesuis. One pig each from groups 1 and 2 was killed at 8, 12, 24, 48, 72, 96, and 120 hours after inoculation. One pig each from groups 3 and 4 was killed at 2, 4, 6, 8, 12, and 24 hours after intestinal loop inoculation. Inoculation of S typhimurium resulted in acute enterocolitis of variable severity, whereas inoculation of S choleraesuis resulted initially in septicemia followed by formation of large necrotic and ulcerative lesions in the colonic mucosa. The most consistent systemic lesion of S choleraesuis infection was interstitial pneumonia and multifocal hepatic necrosis. Salmonella typhimurium and S choleraesuis were ultrastructurally within enterocytes of ligated ileal loops. Intracellular bacteria were morphologically intact, occurred free in the cytoplasm and membrane bound, and caused no detectable cytotoxic effect to the cell. Both S typhimurium and S choleraesuis penetrated the intestinal mucosa and were isolated from mesenteric lymph nodes at 2 hours after inoculation.     

Experimental infection of weanling pigs with Salmonella typhisuis: effect of feeding low concentrations of chlortetracycline, penicillin, and sulfamethazine

Clinical and pathologic variables of Salmonella typhisuis infections were studied in weanling pigs. The influence of daily feeding of low concentrations of chlortetracycline, penicillin, and sulfamethazine on S typhisuis infection also was determined. Ten pigs (group 1) given feed containing low concentrations of chlortetracycline, penicillin, and sulfamethazine when orally inoculated with S typhisuis became pyretic, developed a mild neutrophilia, and had increased serum agglutinating antibody titers, but were clinically normal. Lesions were not present, and S typhisuis was not isolated from 2 group-1 pigs that were killed and necropsied on postinoculation day 8. Then, the antimicrobial agents were withdrawn from the feed of the remaining 8 pigs for 6 days. The pigs were reinoculated with S typhisuis on postinoculation day 16 and developed mild clinical disease with sustained high rectal temperatures. Severe necrotizing typhlocolitis and ulcerative proctitis were found at necropsy in all 8 of the pigs. Similar findings were induced in 7 additional pigs (group 2) that were concurrently inoculated with S typhisuis, but that had no previous exposure to S typhisuis. Successful isolation of S typhisuis required special care and media.     

Colonization of reproductive organs and internal contamination of eggs after experimental infection of laying hens with Salmonella heidelberg and Salmonella enteritidis

Internal contamination of eggs laid by hens infected with Salmonella enteritidis has been a prominent international public health issue since the mid-1980s. Considerable resources have been committed to detecting and controlling S. enteritidis infections in commercial laying flocks. Recently, the Centers for Disease Control and Prevention also reported a significant association between eggs or egg-containing foods and S. heidelberg infections in humans. The present study sought to determine whether several S. heidelberg isolates obtained from egg-associated human disease outbreaks were able to colonize reproductive tissues and be deposited inside eggs laid by experimentally infected hens in a manner similar to the previously documented behavior of S. enteritidis. In two trials, groups of laying hens were orally inoculated with large doses of four S. heidelberg strains and an S. enteritidis strain that consistently caused egg contamination in previous studies. All five Salmonella strains (of both serotypes) colonized the intestinal tracts and invaded the livers, spleens, ovaries, and oviducts of inoculated hens, with no significant differences observed between the strains for any of these parameters. All four S. heidelberg strains were recovered from the interior liquid contents of eggs laid by infected hens, although at lower frequencies (between 1.1% and 4.5%) than the S. enteritidis strain (7.0%).     

环磷酰胺对断奶仔猪免疫功能的影响

本试验旨在探讨环磷酰胺(CY)对断奶仔猪免疫功能的影响。选取12头(28±3)d的杜×长×大断奶仔猪,随机分为对照组和CY组。第1天和第7天,给CY组仔猪注射50mg/kg BW的CY,对照组仔猪注射等量的生理盐水;第7天和第14天,前腔静脉采血待测;第14天,测定迟发型超敏反应。结果表明:(1)CY可降低第7天断奶仔猪的中性粒细胞数量(P0.1)及第14天白细胞、淋巴细胞、中性粒细胞(P0.05)和单核细胞数量(P0.1);(2)CY可降低第14天牛血清白蛋白抗体水平(P0.05);(3)CY可降低第7天干扰素-γ水平(P0.05)。本研究结果表明,CY可抑制断奶仔猪的免疫功能。     

早期断奶仔猪蛋白质营养研究进展

早期断奶最大障碍在于仔猪的消化机能不健全而对饲料的要求特别高。本文结合早期断奶仔猪消化生理特点,介绍了仔猪断奶后氨基酸营养的需要和各种蛋白质饲料原料的营养价值,为调制由母乳过渡到仔猪日粮且不影响仔猪生长率的蛋白质饲粮提供参考。     

Controlling Salmonella infection in weanling pigs through water delivery of direct-fed microbials or organic acids: Part II. Effects on intestinal histology and active nutrient transport

The objective of this study was to evaluate the effects of water-delivered, direct-fed microbials (DFM) or organic acids on intestinal morphology and active nutrient absorption in weanling pigs after deliberate Salmonella infection. Pigs (n = 88) were weaned at 19 ± 2 d of age and assigned to 1 of the following treatments, which were administered for 14 d: 1) control diet; 2) control diet + DFM (Enterococcus faecium, Bacillus subtilis, and Bacillus licheniformis) in drinking water at 10(9) cfu/L for each strain of bacteria; 3) control diet + organic acid-based blend (predominantly propionic, acetic, and benzoic acids) in drinking water at 2.58 mL/L; and 4) control diet + 55 mg/kg carbadox. Pigs were challenged with 10(10) cfu Salmonella enterica var Typhimurium 6 d after commencement of treatments. Pigs (n = 22/d) were harvested before Salmonella challenge and on d 2, 4, and 8 after challenge. Duodenal, jejunal, and ileal mucosal tissues were sampled for measurement of villus height and crypt depth. Jejunal tissue was sampled for determination of active nutrient absorption in modified Ussing chambers. Duodenal villus height was greater in pigs fed in-feed antibiotic before infection (P < 0.05). Jejunal crypts were deeper in DFM- and acid-treated pigs on d 4 after infection compared with all other treatments (P < 0.05). Salmonella infection resulted in a linear decrease in phosphorus (P < 0.001) and glucose (P < 0.05) active transport, and an increase (P < 0.001) in glutamine uptake immediately after challenge. Salmonella infection reduced basal short-circuit current (I(sc)); however, water-delivered DFM or organic acid treatments caused greater basal I(sc) on d 2 after challenge than did carbadox. Carbachol-induced chloride ion secretion was greatest in negative control pigs before infection (P < 0.01) and DFM-treated pigs (P < 0.05) after infection. In conclusion, both the DFM and acidification treatments induced increases in basal active ion movement and jejunal crypt depth, which could be interpreted as responses consistent with increased Salmonella pathology, but none of the additives markedly affected intestinal absorptive and secretory function in response to Salmonella challenge.     

Studies of the pathogenesis of Rhodococcus equi infection in foals

Pyogranulomatous pneumonia was induced in Thoroughbred foals by intranasal challenge with freeze-dried cultures of Rhodococcus equi (previously Corynebacterium equi). The incubation period was about 18 days and clinical signs were not seen for a further week. There were marked seasonal and individual foal differences in responses to infection. Elevations in serum caeruloplasmin oxidase activity and copper concentrations appeared to be sensitive indicators of infection. Serum zinc concentrations and serum alpha-mannosidase and alkaline phosphatase activities fell in the more severely infected foals. Use of trace elements and trace element-related parameters along with faecal culture for R. equi could prove useful for early diagnosis of field cases.     

The pathology and pathogenesis of Salmonella stanley infection in experimental chicks

Experimental infection with Salmonella stanley was produced by oral, intravenous and intramuscular routes in day-old chicks. The earliest evidence of the presence of the organisms was in duodenal mucosa six hours after oral infection. Following oral infection the organisms were detected in the duodenum from six hours to five days, in the caecum from 12 hours to nine days, liver, spleen and blood from 24 hours to seven days. The resistance to infection was found to be significant after 10 days old, but not up to six days old. The work confirmed that the survival time of birds given S stanley by the intravenous or intramuscular routes was inversely proportional to the dose up to a maximum beyond which the survival time was not further decreased by dose increase. The presence of S stanley in tissues and blood was detected by isolation and by the fluorescent antibody technique.     

Effects of a Quillaja saponaria extract on growth performance and immune function of weanling pigs challenged with Salmonella typhimurium

Ninety-six pigs (initially 8.9 kg and 24 d of age) were used in a 28-d experiment to determine the effects of Quillaja saponaria extract (QS) on weanling pig growth performance and immune function in response to enteric disease challenge with Salmonella typhimurium (ST). Experimental treatments were arranged in a 2 x 4 factorial with main effects of disease challenge (control vs ST-challenge) and dietary addition of QS (0, 125, 250, or 500 mg/kg). Pigs were fed QS diets for 14 d and then challenged orally with ST or sterile media. There were no differences in ADG or ADFI among dietary treatments, but gain/feed ratio (G/ F) was depressed (P < 0.06) in pigs fed 250 mg/kg QS. ST-challenge reduced ADG (P < 0.05), ADFI (P < 0.05), and G/F (P < 0.05) 1 wk after challenge. Daily estimates revealed reductions in feed intake in ST-infected pigs on d 2 to 5 following infection (P < 0.05), and rectal temperature was increased maximally 2 d following infection (P < 0.05). There was a marked decline in serum IGF-I during the 6 d after ST-infection (P < 0.05). ST-challenge produced a rise (P < 0.05) in serum haptoglobin on d 7 after challenge, and serum alpha1-acid glycoprotein (AGP) in ST-challenged pigs also was elevated (P < 0.05) above controls on d 7 and 14 after challenge. Serum immunoglobulin (Ig) M increased (P < 0.05) over time in both groups, and serum IgM of ST-challenged pigs was greater than controls on d 7 after challenge (P < 0.05). Serum IgG was not affected by enteric disease challenge; however, on d 7 and 14 after disease challenge, serum IgG for both groups was greater (P < 0.05) than on d 0. Dietary QS had no significant influence on any of the end points used to characterize the acute phase response to ST-challenge. Phagocytic cell function was depressed in pigs fed 250 (P < 0.05) and 500 (P < 0.05) mg/kg as compared to pigs fed 125 mg/kg QS. Yet, there was no difference in phagocytic function among pigs fed 0, 250, or 500 mg/kg QS. We conclude that this model of enteric disease invokes an acute phase response accompanied by decreases in feed intake and serum IGF-I. Furthermore, dietary QS, at the levels fed in this study, appears to offer little benefit to growth performance or immune function in the presence or absence of ST-challenge.     

Desferoxamine and iron dextran in acute Salmonella cholerae-suis infection in pigs

Serum iron (SI)-related and hematologic changes were evaluated in a herd of weaned pigs inoculated with a strain of Salmonella cholerae-suis, causing 83% mortality within 22 days after inoculation was done. Serum iron concentrations decreased to 35% of base-line values 2 days after inoculation was done, but recovered to near base line subsequently. Total SI-binding capacity (TIBC) decreased gradually for 14 days after inoculation was done. Transferrin (TF) concentrations decreased to near half the base line throughout the postinoculation observation period. The calculated SI saturation coefficient decreased to half the base line, but recovered to or above the base-line value subsequently. Combined observations of SI, TIBC, TF, and SI saturation coefficient concentrations indicated that there was higher saturation of host iron-binding proteins and recruitment of additional iron-binding systems subsequent to 2 days after inoculation was done. Day 2 after inoculation seemed to be a critical period for host iron metabolism. Injection of supplemental iron dextran simultaneously with Salmonella infection resulted in lower mortality of iron-injected pigs (P less than 0.005). A highly significant negative correlation was observed between SI concentration and rectal temperatures after pigs were inoculated with Salmonella (r = -0.54; P less than 0.0001). Hemoglobin concentrations, mean corpuscular volume, and mean corpuscular hemoglobin were not significantly affected by Salmonella infection or iron injection concurrent with Salmonella infection.(ABSTRACT TRUNCATED AT 250 WORDS)     

Immunofluorescence studies on the pathogenesis of hemagglutinating encephalomyelitis virus infection in pigs after oronasal inoculation

Hemagglutinating encephalomyelitis virus (HEV; also designated vomiting and wasting disease virus) was inoculated oronasally in 14 colostrum-deprived pigs at the day of birth. Anorexia and vomition were seen after 4 days. Pigs were killed at different times after inoculation, and the results of the examination by immunofluorescent antibody technique revealed that the epithelial cells of nasal mucosa, tonsils, lungs, and small intestine served as sites of primary viral replication. After the local replication near the sites of entry, the virus spread via peripheral nervous system to the CNS. During the incubation period, viral antigens were detected in the trigeminal ganglion,the inferior vagal ganglion, the superior cervical ganglion, the intestinal nervous plexuses, the solar ganglion, and the dorsal root ganglia of the lower thoracic region. In the brain stem, the infection started in the trigeminal and vagal sensory nuclei and spread to other nuclei and to the rostral part of the brain stem. In later stages of the infection, viral spread into the cerebrum, cerebellum, and spinal cord was sometimes also observed. Viral replication in nervous plexuses of the stomach was not present during the incubation period, but was detected in all except 1 of the pigs that were ill when killed. The question whether the vomition is induced centrally by viral replication in the brain stem or is due to viral replication in peripheral nervous tissues remains unanswered.