Seminal vesicle and coagulating gland growth induced by intraperitoneal inoculation of fungi in mice

The effect of fungi on the growth of body organs in mice was investigated. Single, intraperitoneal injections of yeasts (Cryptococcus albidus, Saccharomyces cerevisiae, Schizosaccharomyces octosporus) or molds (Aspergillus niger, Geotrichum candidum, Mucor haemalis) induced an increase in the mass of seminal vesicles and coagulating glands independent of whole body weight changes in mice.     

Airway hypersensitivity induced by Ascaris suum extract in New Zealand Romney sheep

Sheep from local farms with and without previous exposure to pigs were tested for their skin and airway responses to a commercial Ascaris suum antigen. There was an immediate reaction to intradermal injection of the antigen in 90% of 101 sheep. A bronchial provocation test by aerosol of the same antigen was undertaken on 43 of the sheep with a positive skin reaction. About 70% of sheep showed an immediate airway response to the antigen as an aerosol, reflected as a significant increase in airway resistance and/or decrease of dynamic lung compliance. The mean peak airway resistance and mean lowest dynamic lung compliance were 165% above and 61% below their baselines, respectively. No significant changes were recorded when the same animals were given an aerosol of phosphate buffered saline. Similarly, no correlation was found between the degree of skin reaction and the magnitude of bronchoconstriction (p>30.05). The sheep with previous exposure to pigs showed no significant differences in airway responses to antigen challenge, although they showed significantly greater skin reactions than those without exposure to pigs. These results indicate that the majority of Romney sheep in the Manawatu have a natural skin and airway sensitivity to A. suum antigen and may therefore be used as an animal model to study human airway hypersensitivity. The origin of this sensitivity has yet to be determined.     

Airway hypersensitivity induced by Ascaris suum extract in New Zealand Romney sheep

Sheep from local farms with and without previous exposure to pigs were tested for their skin and airway responses to a commercial Ascaris suum antigen. There was an immediate reaction to intradermal injection of the antigen in 90% of 101 sheep. A bronchial provocation test by aerosol of the same antigen was undertaken on 43 of the sheep with a positive skin reaction. About 70% of sheep showed an immediate airway response to the antigen as an aerosol, reflected as a significant increase in airway resistance and/or decrease of dynamic lung compliance. The mean peak airway resistance and mean lowest dynamic lung compliance were 165% above and 61% below their baselines, respectively. No significant changes were recorded when the same animals were given an aerosol of phosphate buffered saline. Similarly, no correlation was found between the degree of skin reaction and the magnitude of bronchoconstriction (p>0.05). The sheep with previous exposure to pigs showed no significant differences in airway responses to antigen challenge, although they showed significantly greater skin reactions than those without exposure to pigs. These results indicate that the majority of Romney sheep in the Manawatu have a natural skin and airway sensitivity to A. suum antigen and may therefore be used as an animal model to study human airway hypersensitivity. The origin of this sensitivity has yet to be determined.     

猪蛔虫研究进展

猪蛔虫病是仔猪常见的多发性寄生虫病 ,可导致仔猪的腹泻、消瘦、贫血、出血、生长不良 ,并易引起其它疾病的继发 ,严重的导致仔猪死亡。本病流行和分布极为广泛 ,对我国养猪业造成的损失较为严重。其病原体为寄生于猪小肠中的蛔科 (Ascaridae)大型线虫。猪蛔虫属专性寄生 ,它既不寄生于马属动物 ,也不寄生于反刍动物。有时猪蛔虫可能误入非专性宿主体内 ,但不能发育为成虫。本文就近年来国内外猪蛔虫的研究进展作一综述。目前 ,人们对猪蛔虫的研究主要集中在以下几个方面 :1　蛔虫的呼吸机制和代谢这是猪蛔虫研究的热点。 Kita等 [1] 研究…     

Influence of an experimental infection of Ascaris suum on performance of pigs

Thirty-two pigs (average 26.6 kg live weight) were individually housed and fed to study the effect of an infection of Ascaris suum (either 0, 600, 6,000 or 60,000 A. suum eggs/pig) on performance of growing-finishing pigs. Increasing the level of A. suum infection produced linear (P less than .07) and quadratic (P less than .09) effects on final weight, weight gain and average daily gain. Feed to gain ratio and number of A. suum worms recovered from the intestines of pigs at slaughter increased linearly (P less than .01) with increasing doses of A. suum eggs. Pigs receiving 60,000 A. suum eggs were 13% less (P less than .01) efficient than the noninfected controls. In each of two trials, eight crossbred barrows (15.7 kg in trial 1 and 16.1 kg body weight in trial 2) were examined for the effects of two levels of A. suum infection (0 and 20,000 eggs/pig) on digestibility coefficients for dry matter, crude protein and gross energy. The infection did not affect (P greater than .05) digestibility coefficients during the first two collection periods (d 6 through 10 and 19 through 23). However, digestion coefficients for dry matter, crude protein and gross energy obtained from the total collection period on d 33 through 37 postinfection were greater (P less than .01) for control pigs than for pigs given 20,000 A. suum eggs each. Also, N retention was greater (P less than .05) for control pigs than for infected pigs.     

Immunity of swine to Ascaris suum

Swine were hyperimmunized to Ascaris suum by giving multiple oral inoculations of embryonated eggs. Sera and lymphocyte lysate from these pigs were administered parenterally to 4-week-old pigs. The latter animals were no more resistant to larval migration than control pigs receiving sera or lymphocyte lysate from non-immunized pigs. Other pigs were infected with transmissible gastroenteritis (TGE) virus, allowed to recover and challenged with embryonated ascarid eggs. They likewise were no more resistant to ascarid larval migration than control pigs.     

Ascaris suum infection in pigs sensitizes lymphocytes but suppresses their responsiveness to phytomitogens

The effect of Ascaris suum infection and treatment with fenbendazole on the blastogenic response of peripheral blood lymphocytes to A. suum antigens and to three phytomitogens was assayed by the lymphocyte transformation technique. Repeated infections with A. suum led to the development of sensitized lymphocytes primarily responding to egg hatching fluid antigen. Treatment with fenbendazole decreased the number of specific sensitized lymphocytes, but favorably increased the resistance of pigs to reinfection. Immunity to reinfection did not correlate with the strength of the blastogenic response to A. suum antigens. Repeated infection with A. suum negatively affected the development of the blastogenic response to phytomitogens in the pigs, leading to a partial depression of the responsiveness of lymphocytes and to the partial suppression by serum. Responses to pokeweed mitogen were affected more than the responses to concanavalin A and phytohemagglutinin.     

Characterization of isolated porcine intestinal mucosal mast cells following infection with Ascaris suum

Porcine intestinal mucosal mast cells (IMMC) were isolated from intestinal tissues of swine by enzymatic digestion and density gradient separation. Helminth-free swine and swine exposed to the nematode parasite, Ascaris suum, were used as a source of intestinal tissue. Up to 40% of the isolated intestinal cells stained metachromatically with toluidine blue pH 3.0, indicating the presence of IMMC. The histamine content of this cell population ranged from 2.9-8.9 pg per toluidine blue-positive IMMC, regardless of the animal source. Enrichment procedures that increased the proportion of toluidine blue-positive IMMC from the isolated intestinal cell population correlated with an increase in the amount of histamine detected in the cell population, indicating that toluidine blue-positive IMMC were the major source of histamine in this heterogeneous cell population. However, only cells isolated from the intestines of parasite-exposed swine released histamine in vitro after mixing with antigens derived from A. suum. Cells from the intestines of both helminth-free and parasite-exposed swine did not release histamine after mixing with a non-parasite hapten-protein molecule DNP-human serum albumin, but did release greater than 90% of their total histamine after lysis with Triton X-100 or with the Ca2+ ionophore (A23187). The stimulus for acquired responsiveness of IMMC to A. suum antigens in vitro was parasitic infection in vivo because helminth-free swine maintained in confinement on concrete yielded IMMC that specifically released histamine in the presence of parasite antigens only after 3 weeks of daily experimental inoculations with A. suum eggs. IMMC isolated from the entire length of the small intestines of infected pigs were responsive to antigens in vitro, but the relative number of IMMC isolated and their level of histamine release decreased from the anterior to the posterior end. IMMC isolated from infected swine were also stimulated to release histamine in vitro by viable second stage larvae of A. suum and by treatment with anti-swine immunoglobulin. Responsiveness to both parasite antigens and anti-immunoglobulin were totally eliminated, however, by a brief treatment of the cells with acidic buffer, suggesting that an acid-dissociable cell-bound antibody molecule was responsible for specific antigen-induced histamine release by IMMC.     

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.     

Mature Ascaris suum in naturally infected calves

In two small farms in Sweden young calves were found to be naturally infected with Ascaris suum. One of the calves expelled mature worms with the faeces, one had a great number of worms in the ductus choledochus and two others had worms in the intestine. Most of the worms were mature and at the egg-producing stage. The morphology of the eggs and the adult worms indicated that these parasites were A. suum and that Toxocara (syn. Neoascaris) vitulorum could be excluded.     

Hepatic lesions caused by migrating larvae of Ascaris suum in chickens

Group A consisted of chickens infected with a single dose of Ascaris suum and group B of chickens infected with two successive doses. At days 1, 3, 7, 14 and 21 after the first or second infection dose, six chickens from each group were sacrificed. In both groups, larvae were recovered from the livers on days 1, 3, and 7 and lungs on days 3 and 7. No larvae were detected in chickens on day 14. Clear white lesions were noticed only on the livers from chickens of group B at day 7 but had disappeared at day 14. A comparison with group B showed mild histological changes that developed relative to the livers from group A.     

The development of Ascaris suum in calves.

To determine the development of Ascaris suum after a primary and a secondary infection, 18 calves were inoculated with 2,000,000 infective eggs and examined from 18 hours to 13 days postinfection. At 18 hours larvae were recovered from the wall of the abomasum, duodenum and jejunum. They were found in small intestine lymph nodes on the third day, in the liver at five days and were most abundant in the lungs on days 7 and 9. The pattern of recovery of larvae from the lung between days 5 and 13 postinfection was similar after a primary or a secondary infection. Slower growth of larvae following a secondary infection was the only evidence of resistance to A. suum. There were no pathological changes observed in the alimentary canal. White foci were found on the surface of the liver as early as the third day. The rapid decline in the number of A. suum in the lungs after the ninth day was considered to be related to immobilization or death of larvae soon after the reaction to them commences.     

Ascaris suum Infection in Calves III. Pathology

Gross changes in the lungs of Ascaris suum- infected calves consisted of atelectasis and hemorrhagic foci, edema and emphysema, frequently with bullae. Prominent microscopic lung lesions were edema and emphysema of the interlobular septa with large numbers of eosinophils within and around lymphatics, peribronchiolar lymphoid nodules and parasitic granulomas. Many of the microscopic features were consistent with those found in atypical interstitial pneumonia. Changes in the alveoli were atelectasis, the exudation of plasma proteins, mononuclear cells and eosinophils, and alveolar wall thickening. Lesions found later included fibrosis and fetalization of the alveolar walls. Plasma cells and neutrophils were not common. Challenge with Toxocara canis after sensitization with A. suum resulted in the lungs developing a few areas of atelectasis. Migration of T. canis to lungs of calves is slower than A. suum. A. suum larvae were always found in bronchi, bronchioles and alveoli of calves that died. Lesions were observed in the liver but not the kidney of A. suum infected calves; both lung and liver lesions tended to resolve with time.     

The protective effect of developmental stages in an Ascaris suum infection in the guinea pig

The capacity of various developmental stages of Ascaris suum to induce a protective immune response in the guinea pig model was evaluated. Larvated eggs, second, third or fourth stage larvae were injected into guinea pigs by either the suncutaneous, intramuscular, ear vein or mesenteric vein route. Animals were challenged with a mesenteric vein injection of artificially hatched infective larvae of A. suum. Second stage larvae produced the highest degree of immunity and fourth stage larvae produced the least protection comparing all routes of administration. The most effective route of immunization for all the developmental stages was the mesenteric vein. Antibody titer as assessed by indirect hemagglutination was not correlated with the degree of protection.