Schistosomiasis in Hamsters: The Relationship of Egg Concentration in the Liver to Disease

Erickson, D. G.; Jones, Clarence E.; Tang, Douglas B.

doi:10.4269/ajtmh.1974.23.449

Cited by 7 publications

(5 citation statements)

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“…This association between duration of infection and the ability of worms to migrate to the bladder could be the result of increasingly severe pathological changes in the host. Thus, portal hypertension (Erickson, Jones & Tang, 1974) might in turn cause generalized distention of blood vessels or the development of porto-systemic anastamoses, and the latter has been implicated in the occasional migration of S. haematobium to the bladder in Green Monkeys (Sulaiman, Hakim & Amin, 1982). If the barrier to vesicular migration is removed by the development of portal hypertension, it would be expected that hosts with large numbers of eggs in the liver would have worms in the bladder more frequently than lightly infected hosts.…”

Section: Discussionmentioning

confidence: 99%

“…Smaller experimental animals do suffer a greater degree of hepatic pathology, because even lightly infected animals suffer comparatively intense infections. Erickson et al (1974) found that the percentage of the liver of hamsters that was occupied by granulomas with comparable egg densities was similar for 8. haematobium, S. mansoni and S. japonicum infections. However, von Lichtenberg, Erickson & Sadun (1973) described qualitative differences in the host response that suggested that the greatest damage occurred with 8. japonicum infections and the least with S. haematobium.…”

Section: Host Pathologymentioning

confidence: 92%

“…Extensive calcification of eggs in human tissues is the rule (Cheever et al 1977;Smith et al 1974Smith et al , 1975 but is not frequently seen in experimental animals. Extensive calcification of eggs does occur in chimpanzees (Sadun et al 1970) and gibbons (Kuntz et al 1975) but not in baboons (Cheever et al 1974;Soliman, Cheever, Kuntz & Myers, 1974;Webbe et al 1974) or hamsters (Erickson et al 1974;von Lichtenberg et al 1973). Cheever (1985) considered that calcification is not related to duration of infection since it occurs within a year in gibbons (Kuntz, Cheever, Myers, Young & Moore, 1975) but not at all in baboons (Cheever et al 1974), and is probably a host-specific response.…”

Section: Host Pathologymentioning

confidence: 99%

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The host—parasite relationship ofSchistosoma haematobiumin CBA mice

1988

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The host-parasite relationships of two geographical isolates of Schistosoma haematobium in CBA mice are described and compared to previous reports on this parasite in other experimental hosts and in man. The mean percentage establishment of worms in mice was 17% and was not affected by the age or sex of the host. Adult worm burdens remained constant over 20 weeks, but were reduced after 18 months of infection. Male and female worms reached mean maximum lengths of 4.78 and 5.9 mm respectively. Egg laying commenced 9.5 weeks after infection and eggs accumulated in the tissues throughout the period of infection. A large increase in the rate of egg accumulation occurred coincidental with the appearance of eggs in the bladder of some mice. Faecal eggs were first observed in some mice at 12.5 weeks and most mice excreted a few eggs by 17 weeks p.i. (post-infection). Eggs were not found in the urine of infected mice. Excreted eggs and eggs isolated from the livers of infected mice hatched, but the resulting miracidia were unable to infect appropriate snail hosts. The development of hepatic granulomas and egg-induced pathology in the bladder of mice is described.

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Section: Discussionmentioning

confidence: 99%

Section: Host Pathologymentioning

confidence: 92%

Section: Host Pathologymentioning

confidence: 99%

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The host—parasite relationship ofSchistosoma haematobiumin CBA mice

1988

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“…In this study the golden hamster was chosen as an experimental model since it is susceptible to S. haemato bium infection, it is small enough to permit examination of a large number of infected animals for an extended period of time and due to the fact that the distribution of the adult worms in the host circulation is similar to that reported in man [13,14]. Hamsters were infected with an Egyptian strain of 5. haematobium.…”

Section: Discussionmentioning

confidence: 99%

<i>Schistosoma haematobium</i><i>-</i>lnducedGlomerular Disease: An Experimental Study in the Golden Hamster

Sobh

Moustafa

Ramzy

et al. 1991

Nephron

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Information regarding glomerular lesions related to Schistosoma haematobium infection in man or animal are extremely lacking and disputed. The objective of this experimental study was to investigate glomerular lesions in S. haematobium-infected golden hamsters. In this work, 53 hamsters were infected with S. haematobium cercariae and 18 animals of similar age and sex served as controls. Hamsters were infected either with 50,200,300,400 or 600 cercariae and sacrifïed after 8, 9, 10,14,18, 24 or 32 weeks. Infected and control hamsters were subjected to laboratory examinations including serum creatinine, serum albumin, total protein, serum cholesterol, total urine protein as well as histopathologic evaluations. Kidney biopsies were examined by light microscopy, indirect immunofluorescence and by electron microscopy. Significant proteinuria, hypoalbuminaemia and hypercholesterolaemia were observed in all but 5 S. haematobium-infected, but in none of the control hamsters. Renal impairment was observed in 5 hamsters. Histopathologic evaluations showed IgG, circulating anodic antigen and circulating cathodic antigen deposits in the renal glomeruli. By electron-microscopic examination, these deposits were seen mainly in the subendothelial, mesangial and paramesangial areas. Amyloid deposits were also seen in the renal glomeruli, tubular basement membrane and in the interstitium. A correlation was found between the extent of amyloid deposition and the duration but not the intensity of schistosomal infection. We have concluded that S. haematobium infection can lead to glomerulopathy in golden hamsters.

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“…The study comprised two separate but simultaneously conducted experiments and the criteria used included the size and reproductive capacity (tissue egg counts) of the established S. mansoni worm burden and wet liver and spleen weights in groups of mice previously exposed to cercariae of T. szidati as compared with groups o£ previously non-exposed mice. According to ERICKSON et al (1974), GROVE & WARREN (1976), TIBOLDI (1979) and others, wet liver and spleen weights are valuable parameters for assessment of the relative severity of hepatosplenic murine schistosomiasis.…”

mentioning

confidence: 99%