Newly hatched chicks were dosed orally with a Salmonella typhimurium wild-type strain, an S. enteritidis wild-type strain, and a genetically defined S. enteritidis aroA vaccine candidate, strain CVI3O. The S. typhimurium strain, 2391 Nalr, was virulent in newly hatched chicks and caused deaths in 7 of 20 chicks after an oral dose of 105 organisms. The S. enteritidis wild-type strain, LA5, caused death in 1 of 25 chicks and gross pathology including pericarditis and perihepatitis in 6 of the 24 survivors after an oral dose of 109 organisms. S. enteritidis aroA CVL30, attenuated by ca. 6.5 log10 in BALB/c mice, was nonvirulent when administered orally to chicks and did not cause morbidity. When newly hatched chicks were dosed, the pattern of invasion and colonization of the reticuloendothelial system by strain CVL30 was similar to that of its parent strain, LA5, irrespective of the dose. Oral inoculation of newly hatched chicks with <10 organisms of S. enteritidis LA5 or CVL3O was followed by multiplication in the cecal contents. Within 3 days of hatching, the pH of the cecal contents was reduced from ca. 7 to 5. Samples of gut contents were inoculated in vitro. The S. enteritidis strains multiplied in samples taken from the ileum and duodenum irrespective of age but multiplied in the cecal samples from newly hatched chicks only. Invasion from the gut by S. enteritidis LA5 and CVL3O was both age and dose dependent.
and popliteal arteries and similar areas in the left superficial femoral and both profunda femoris arteries. Flow to the lower legs was reduced. Treatment, including right lumbar sympathetic blockade and catheter dilatation of the right superficial femoral and popliteal arteries, restored peripheral pulses and perfusion in three days. Clinical and electromyographic evidence of right common peroneal and tibial neuropathies (presumably ischaemic) persisted. Comment These two patients developed occlusion of major arteries while taking methysergide and parenteral ergotamine for cluster headache. Arteriograms showed arterial spasm and collateral vessels, which are features of ergotism.' These signs have been described in both ergotamine and methysergide toxicity in many areas of the arterial circulation. Thrombosis may also occur.2 Ergotamine is a direct vascular smooth-muscle stimulant.3 Parenteral administration increases potency tenfold through faster and more complete absorption and raises the risk ofarterial spasm.3 Methysergide is a derivative of methylergonovine,3 independently capable of producing arterial spasm.4 Arterial spasm persisted after withdrawal of the drugs in both cases. This is typical of ergotism and presumably represents tissue binding of the drugs, since the half lives of methysergide and ergotamine are only 2-75 and 2 03 hours respectively. Accumulation in tissue also explains the delay between introduction of the drugs and the development of toxicity in these patients. Neither patient was predisposed to ergotism through fever, sepsis, hepatic disease, thyrotoxicosis, or atherosclerosis.3 Flow studies using xenon-133 indicate increased cerebral blood flow during headache.1 Pizotifen, which was also taken by the second patient, is not known to produce arterial spasm. It appears, therefore, that methysergide and parenteral ergotamine together create a particularly high risk of arterial spasm. The combination should be avoided.
Newly hatched chicks were vaccinated orally with a genetically defined Salmonella enteritidis aroA candidate, strain CVL3O. In chickens immunized with 10 or 109CFU and challenged by the intravenous route with 108 CFU of S. enteritidis 109 Nalr at 8 weeks old, there were similar reductions in colonization of the spleens, livers, and ceca of vaccinees compared with unvaccinated controls. Two groups of newly hatched female chicks were vaccinated orally with 109 CFU of strain CVL3O, and one group was revaccinated intramuscularly with 109 CFU at 16 weeks old. When challenged intravenously with S. enteritidis 109 Nalr at 23 weeks old, there was a reduction in the colonization of spleens, livers, ovaries, and ceca compared with unvaccinated controls. Inclusion of the intramuscular booster gave increased protection to the ovary, although the vaccine strain was isolated on one occasion from a batch of eggs laid at 20 weeks old. In chickens immunized with 109 CFU of strain CVL30 and challenged orally with 109 CFU of S. enteritidis 109 Nalr, there was a reduction in intestinal shedding of the challenge strain from vaccinees compared with unvaccinated controls. Circulating immunoglobulin G antibodies to lipopolysaccharide (LPS) were detected in unvaccinated controls within 7 to 10 days of oral challenge. In contrast, circulating immunoglobulin G antibodies to LPS in vaccinees were not altered by the oral challenge, which suggested that vaccination reduced or prevented invasion by the challenge strain from the gut or multiplication of the challenge strain in the tissues. Newly hatched chicks were vaccinated orally with ca. 109 CFU of strain CVL30, and 1 day later, the vaccinees and unvaccinated controls were challenged orally with l05 or 109CFU of S. enteritidis 109 Nalr. Colonization of the ceca and invasion from the gut by the S. enteritidis challenge strain was reduced in the vaccinees up to 5 days postchallenge compared with controls. In a second trial, vaccinees and controls were challenged orally with 107 or 109CFU of S. typhimurium 2391 Nalr. In contrast to the challenge with S. enteritidis, colonization of the ceca and invasion by the S.
The serological responses to Salmonella enteritidis flagella (H: g,m) and its fimbrial antigen SEF14 were evaluated as indicators of infection in chickens and to confirm serological results obtained by an ELISA using S enteritidis lipopolysaccharide (LPS) (O: 9,12) as the detecting antigen. The SEF14 antigen and flagella were extracted from S enteritidis and transferred to nitrocellulose paper for use in Western and dot blot tests. Antisera to 19 salmonella serotypes including S enteritidis were raised in rabbits and their cross reactivity to the flagellar and SEF14 antigens was evaluated. Cross reactivity with the SEF14 antigen was found in one antiserum, raised against S blegdam, and to flagella in eight of 19 antisera raised against various salmonella serotypes, most of which shared the flagellar factors g or m with S enteritidis. The intensity of cross reaction to flagella was strongest in S derby and S blegdam antisera. Antisera raised in chickens against S typhimurium and S panama did not cross react in either test, and neither did pooled sera from eight-week-old salmonella-free, broiler breeder parent chickens. Field sera from two commercial flocks with no history of salmonella infection were negative when tested by the LPS ELISA. These sera were also negative when tested by the flagellar and SEF14 blots. S enteritidis infection in a commercial laying flock was detected initially when the sera were tested by the LPS ELISA and confirmed in individual and pooled sera by the SEF14 and flagellar tests. S enteritidis PT4 was isolated from this flock post mortem.
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