Morphogenesis and Migration of Ascaris suum Larvae Developing to Fourth Stage in Swine

Douvres, F. W.; Tromba, F. G.; Malakatis, George M.

doi:10.2307/3277198

Cited by 115 publications

(44 citation statements)

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“…It is of interest to note that few large larvae of 1,000 µm or longer were recovered on day 3 and 7 from the livers of chickens. The length of larvae on day 4 in the livers of experimentally infected pigs was 533 µm to 619 µm [6] and on day 3 in mice was 386.7 ± 121.1 µm [7]. Permin et al [13] investigated the VLM in chickens infected with A. suum and reported that no liver lesions were found macroscopically on the organs on day 7 after first infection.…”

Section: Similar To the Visceral Larval Migrans (Vlm) Of Toxocara Canmentioning

confidence: 99%

Hepatic Lesions Caused by Migrating Larvae of <i>Ascaris suum</i> in chickens

Yoshihara¹,

Hattori²,

Nishizono³

et al. 2008

The Journal of Veterinary Medical Science

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ABSTRACT. 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. KEY WORDS: Ascaris suum, chickens, visceral larval migrans.J. Vet. Med. Sci. 70(10): 1129-1131, 2008 Similar to the visceral larval migrans (VLM) of Toxocara canis (T. canis) infection [3], Ascaris suum (A. suum) infection in humans has been reported in Japan [2,8,10,11,15]. It was considered that at least three human cases were caused by eating fresh raw meat and liver from cattle or chickens [2,8,10]. These reports suggest that chickens may play an important role in the zoonotic transmission of A. suum. To clarify the VLM of A. suum larvae in infected chickens, an investigation was carried out on the distribution of larvae and the pathological changes in the livers.Fresh A. suum eggs were obtained from female worms at a local abattoir. Embryonation of the eggs was performed as described by Tsuji et al. [16]. A total number of 65 male broiler chickens aged about 20-days old were used. Initially, groups A (chickens infected with a single dose of A. suum) and B (chicken infected two successive dose) of 30 chickens each received 10,000 eggs and were kept in cages. The same number of eggs were given again to chickens of group B 17 days after the first dose. On days 1, 3, 7, 14, and 21 after the first or second infection, six chickens from each group were sacrificed by cervical dislocation. Larvae were collected from the liver (lobus dexter), lung, pectoral muscle (musculus pectoralis profurdus; about 30 g), and the duodenum (without contents and mucus) using the Baerman method. The contents and mucus of the duodenum were fixed separately in 5% formalin solution and examined microscopically. A video micrometer was used for the measurement of the length of larvae. Statisitical analysis of differences in larval counts between both groups on the same day after first or second infection was done using Statisitica (Stat Soft, Tulsa, OK, U.S.A., P<0.05). The liver (lobus sinister) was investigated macroscopically and fixed in 10% buffered formalin solution. Paraffin sections were stained with hematoxylin and eosin (HE) or with Azan. To examine the lesion in repeatedly infected animals, remaining 5 chickens (group C) were infected with 10,000 eggs twice weekly for five weeks and sacrificed 7 days after the final infection.No clinical signs were observed in any of the infected chickens during the study period. Table 1 shows the distribution of A. suum larvae in chickens of groups A and B. Larvae were ...

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Section: Similar To the Visceral Larval Migrans (Vlm) Of Toxocara Canmentioning

confidence: 99%

Hepatic Lesions Caused by Migrating Larvae of <i>Ascaris suum</i> in chickens

Yoshihara¹,

Hattori²,

Nishizono³

et al. 2008

The Journal of Veterinary Medical Science

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“…Furthermore, some of these 247 juveniles had earlier passed larvae in their faeces. Worm loss may have resulted from fruit ingestion, or may have been comparable with massive A.suum infections in pigs which fail to result in patent infections (Schwarz, 1959;Douvres et al, 1969). immediately after the death of the bat, larvae were consistently within inflammatory foci, whereas in bats dead for some time prior to autopsy, larvae were usually "free" in tissues.…”

mentioning

confidence: 99%

“…suum infections in pigs which fail to result in patent infections (Schwarz, 1959;Douvres et al, 1969). immediately after the death of the bat, larvae were consistently within inflammatory foci, whereas in bats dead for some time prior to autopsy, larvae were usually "free" in tissues.…”

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confidence: 99%

“…A similar pattern to this may occur in ascaridoid infections (see Discussion, Chapter 5). However, a massive dose of A_^ suum eggs fed to pigs precipitates such an aggressive immune response to migrating larvae that they are all lost through the faeces, sometimes without successfully establishing a patent infection (Schwartz, 1959;Douvres et al, 1969). In piglets fed lower doses of eggs, the number of adult worms establishing is inversely related to the dose (Roneus, 1971;Andersen et al, 1973).…”

mentioning

confidence: 99%

“…In pigs fed A. suum eggs, most larvae pass via the portal vein to the liver, then through the lungs to the trachea. A very small proportion penetrate mesenteric lymphatics (Roberts, 1934), and possibly reach the lungs, although Douvres et al (1969) considered that most in lymphatics were not capable of proceeding. However, at least some T.…”

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confidence: 99%

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Toxocara pteropodis Baylis, 1936 : life-cycle, epizootiology and zoonotic potential

Prociv¹

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The aim of this study was to establish whether a human epidemic of hepato-enteritis, the "Palm Island mystery disease", could have been a manifestation of nematode visceral larva migrans caused by the flying fox parasite, Toxocara pteropodis. An assessment of the risk of human exposure to such an infection, and of its pathogenicity, required collection of data from field and laboratory studies.The life-cycle was elucidated in Pteropus poliocephalus, the predominant flying fox in the Brisbane region. Adult worms develop in the intestines of suckling juveniles, and infections may become patent in bats as young as 35 days. About 50% of juveniles develop patent infections, and each harbours an average of 1 adult male worm and 2 adult females. These worms are voided spontaneously before the bats leave their summer camps.Each female worm produces about 25,000 eggs per day, most of which are shed into the environment of the summer camp. Eggs become infective from 10 days after voiding; few remain viable longer than 6 weeks. As very little fruit remote from the camps was found contaminated with eggs, adult bats probably become infected in the camps by licking foliage and grooming during wet weather. Eggs ingested by bats hatch in the intestine and the released third-stage larvae penetrate the mucosa to reach the liver via the portal vein. These larvae may remain indefinitely in the liver, where they grow over 3 months from a length of about 420 jim to about 600 pm. In male bats, hepatic larvae gradually accumulate, but in females many leave the livers at the time of parturition and pass through the mammary glands to reach the juvenile intestines in the first 3 weeks after birth. Many developing intestinal larvae, predominantly males, are expelled spontaneously in the faeces of suckling bats. This explains the low average worm burdens in patent infections and their unequal sex representation.Virtually all adult male P_^ poliocephalus harbour larvae in their livers; in adult females the prevalence and intensity of hepatic infection 11 is lower. In the P. alecto and P_^ conspicillatus populations of northern Queensland, the prevalence pattern of T_^ pteropodis appears to be similar whereas in southern P_^ alecto, and in P_^ scapulatus, infection is much less common. T. pteropodis was also found in Pteropus specimens from New Guinea, Indonesia and India. Nematodes from Rousettus sp. from the Philippines, and poorly-preserved type specimens of Toxocara cynonycteridis, from a Rousettus sp. in Burma, were very similar to, if not identical with, T. pteropodis.On detailed examination, T_^ pteropodis had some features distinct from those of other members of the genus. The relatively thick egg-shell may protect against desiccation. The second moult occurs in the egg. Thirdstage larvae grow in the livers of definitive (and some abnormal) hosts.Adult worms have cephalic surface features which may be unique, and do not possess a cervical alar "supporting bar" typical of the genus.Experimental mammals other than bats exhibit v...

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Nematoda: Ascaris lumbricoides

Dold

2012

Immunity to Parasitic Infection

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Morphogenesis and Migration of Ascaris suum Larvae Developing to Fourth Stage in Swine

Cited by 115 publications

References 9 publications

Hepatic Lesions Caused by Migrating Larvae of <i>Ascaris suum</i> in chickens

Hepatic Lesions Caused by Migrating Larvae of <i>Ascaris suum</i> in chickens

Toxocara pteropodis Baylis, 1936 : life-cycle, epizootiology and zoonotic potential

Nematoda: Ascaris lumbricoides

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