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Biomedical subjects

L R Ash

Publications and source records attributed to L R Ash.

At least 37 records · Page 2Linked to original sources
PubMed1986

First report of Angiostrongylus cantonensis in Puerto Rico.

From January to April 1984, 63 Rattus rattus and 40 R. norvegicus were trapped in northeastern Puerto Rico and examined for Angiostrongylus cantonensis adults. Nineteen (47.5%) of the R. norvegicus and 10 (15.9%) of the R. rattus were infected, giving an overall infection rate of 28.2%. Four species of terrestrial snails and one species of brown slug were examined for A. cantonensis larvae. Two snail species, Subulina octona and Aquebana belutina, were found infected with third stage larvae of A. cantonensis. These larvae were harvested and inoculated per os into adult white mice. Immature adult worms were found in the brain tissue of all mice inoculated. This is the first report in the rat and snail populations of Puerto Rico.

Angiostrongylus↗
PubMed1983

Analysis of Brugia pahangi microfilariae surface carbohydrates: comparison of the binding of a panel of fluoresceinated lectins to mature in vivo-derived and immature in utero-derived microfilariae.

A fluoresceinated lectin binding assay was employed to detect carbohydrates on the sheath and cuticle of mature in vivo-derived, and immature in utero-derived Brugia pahangi microfilariae. The sheath of mature microfilariae bound concanavalin A and wheat germ agglutinin, indicating the presence of N-acetylglucosamine and glucose or mannose. In addition to binding concanavalin A and wheat germ agglutinin, the sheath of in utero-derived microfilariae also bound Limulus polyphemus agglutinin, peanut agglutinin, Ricinus communis agglutinin-I, and soybean agglutinin, indicating the presence of the additional sugars galactose, sialic acid, and N-acetylgalactosamine. There was no evidence of cuticle carbohydrates, as none of the tested fluoresceinated lectins bound to either mature or immature exsheathed microfilariae. The significance of these results in terms of the survival of microfilariae in the mammalian host, and development to third-stage larvae in the mosquito vector, is discussed.

Acetylgalactosamine↗
PubMed1983

Parameters influencing the susceptibility of neonate mice to infection with Brugia pahangi.

A total of 307 young mice between less than 1 day (neonate) and 4 wk after birth were inoculated either subcutaneously or intraperitoneally with infective larvae of Brugia pahangi to determine the best protocol for the establishment of patent infections. For both male and female neonates, i.p. infection produced higher adult worm burdens than did s.c. infection. Although the numbers of adult worms harbored by male and female mice were not statistically different, male mice were more prone to develop a patent infection; no neonate female mice became microfilaremic , whereas seven of 113 i.p.-infected male mice developed microfilaremia. More female adult worms were recovered, on the average, than were male worms, regardless of the age of mice used for infection. However, the younger the mice were at infection, the higher were the numbers of male worms recovered. A high number of gravid female worms were recovered from amicrofilaremic mice. Adult female and male worms harvested from amicrofilaremic mice, implanted into the peritoneal cavity of jirds (Meriones unguiculatus), did not produce microfilariae although approximately 50% of the jirds contained gravid female parasites. Jirds implanted with worms from microfilaremic mice did, however, contain peritoneal microfilariae. It appeared that amicrofilaremic mice irreversibly damaged female worms to the extent that worms could survive and appear healthy, but could not release microfilariae.

Aging↗
PubMed1983

Characterization of the exposed carbohydrates on the sheath surface of in vitro-derived Brugia pahangi microfilariae by analysis of lectin binding.

Adult female Brugia pahangi were maintained metabolically active in vitro for up to 35 days in Click's medium supplemented with 10% horse serum. For the first 14 to 18 days microfilariae were released into culture. Although these in vitro-derived microfilariae were morphologically identical to in vivo-derived microfilariae, they could be differentiated by their characteristic of binding to a panel of fluorescein-conjugated lectins. The results suggest that maturation and release of microfilariae are correlated with glycosidic alterations on the sheath surface.

Animals↗
PubMed1983

Karyotypes of Brugia pahangi and Brugia malayi (Nematoda: Filarioidea).

Using air-dried preparations of the testis and ovary, karyotypes were analyzed and compared to each other in two species of filarial parasites, Brugia pahangi and B. malayi. Both species had a diploid number of 10 chromosomes and were karyotypically very similar. C-banding analyses disclosed that the sex-determining mechanism of these species was of the XY-XX type, where the X chromosome was the largest, and the Y chromosome was of medium-size.

Animals↗
PubMed1982

Inhibition of adherence and cytotoxicity by circulating immune complexes formed in experimental filariasis.

Peritoneal exudate cells (PEC) from normal jirds (Meriones unguiculatus) showed adherence of Brugia pahangi microfilariae, and subsequent cytotoxicity in the presence of antimicrofilarial antisera. Heat inactivation of the antisera diminished both adherence and cytotoxicity, but readdition of fresh normal jird sera only partially restored the reactions. Macrophages were the predominant adherent cell type. Circulating immune complexes precipitated with polyethylene glycol (PEG) from the sera of jirds with an 8-month infection inhibited both of these reactions. Complement consumption by the precipitated complexes was found not to be the cause of inhibition. Blocking of adherence and cytotoxicity by circulating immune complexes may be preventing the trapping of microfilariae in vivo, and may play a role in the persistence of microfilaraemia in the jird.

Animals↗
PubMed1981

Sequential determination of circulating immune complexes in experimental filariasis.

Levels of circulating immune complexes were measured in jirds (Meriones unguiculatus) infected with the filarial nematode Brugia pahangi during an 11-month infection. Using 16 infected and 8 control animals, we found three general trends, which correspond to events in the life cycle of the filarial worm in the host, in all individually infected jirds. These were (i) an initial peak of immune complexes at 2 weeks postinfection, (ii) a drop to a minimum postinfection value near the beginning of patency, and (iii) a gradual increase in immune complex levels beginning at the time of peak adult worm size and continuing to a maximum value at approximately 10 months postinfection. Microfilarial levels and hemagglutination assay titers to adult worm antigens did not correlate with immune complex levels.

Animals↗
PubMed1981

Further studies on the development of Wuchereria bancrofti in laboratory animals.

In an attempt to obtain a small animal laboratory model for Wuchereria bancrofti Mongolian gerbils and hamsters were infected with third-stage larvae of strains of the parasite from Indonesia and China. Gerbils were necropsied at 7 to 591 days and larvae recovered up to 219 days. The third molt occurred on or before 10 days and worms found after 14 days were in the fourth stage. More worms were recovered early in the infection (7 to 30 days) than in older infections. The worms were usually recovered from the testes, pelt and carcass and heart and lungs. An adult male worm was recovered on one occasion from the lung of a gerbil at 92 days. The parasite was also found to develop in hamsters with results similar to those in gerbils. Gerbils and hamsters were given antithymocyte sera before and after infection and more worms were recovered and the worms larger in size in some treated animals. Continued studies with geographic strains of W. bancrofti in various animals should be encouraged in order to find a small laboratory animal model for the parasite.

Animals↗
PubMed1980

The lymphatic pathology of Brugia pahangi in the Mongolian jird.

We studied the sequence of histopathologic changes associated with Brugia pahangi (Nematoda: Filarioidea) infections in lymphatic vessels in the spermatic cord of the Mongolian jird (gerbil), Meriones unguiculatus. Intravascular granulomas caused mainly by disintegrating worms were seen in 67% of jirds necropsied on, or after, 35 days postinoculation, whereas none of 20 jirds examined before this day showed dying larvae. These granulomas usually evolved without vascular occlusion. Other granulomatous foci, often with a thrombuslike core, sometimes harbored microfilariae or microfilarialike materials. The perilymphatic cellular infiltrate consisted mostly of eosinophils, lymphocytes, and plasma cells. Large numbers of eosinophils were seen in the early weeks, but later declined, while lymphocytes increased to become the predominant cell in old infections. Irregular fibrosis of some valves and portions of the lymphatic walls were seen as early as the 2nd wk postinoculation. Lymphatic changes in the jird are similar to those described in other hosts infected with filariae, but remained moderate. Living worms appeared to be the stimulus for many observed changes. Most pathologic alterations were well established by 3 or 4 mo and showed little qualitative change during the remaining 4 mo of the study.

Animals↗
PubMed1980

Circulating immune complexes in experimental filariasis.

Circulating immune complexes have been investigated in jirds (Meriones unguiculatus) infected with the filarial nematode Brugia pahangi. Two-month-old male jirds were inoculated with seventy-five B. pahangi infective larvae into the left groin. At 8 months post-infection, sera of individual animals from a group of seventeen infecteds and seventeen age-matched controls were analysed for immune complexes by (1) a solid-phase C1q binding assay (Clq-SP) and (2) precipitation with 3.5% polyethylene glycol followed by binding of 125I-labelled rabbit anti-jird Ig antiserum (PEG). A significant increase in the level of circulating immune complexes was shown in the infected group as compared with the controls for both assays, with a P value = 0.005 for PEG and P = 0.001 for Clq-SP. Using the mean of the control group +/- 2 s.d. as the upper limit of the normal range, 24% of the infected group had elevated immune complex levels by the PEG assay, and 41% were elevated in the C1q-SP assay. A high degree of variability was noted in the levels of immune complexes among individual animals in the infected group by each test. No correlation between immune complex levels and numbers of circulating microfilariae was found in either assay.

Animals↗
PubMed1979

Experimental transmission of Wuchereria bancrofti to monkeys.

Infective larvae of Wuchereria bancrofti from laboratory-raised Culex pipiens fatigans and Aedes togoi mosquitoes fed on human volunteers in Jakarta, Indonesia (J strain) and Kinmen Island, China (K strain) were introduced into Taiwan monkeys (Macaca cyclopis) by subcutaneous inoculation, by foot puncture, or by permitting infected mosquitoes to feed weekly on the monkeys. Some animals were splenectomized and others were treated with varying regimens of immunosuppressants. Necropsy was done on monkeys that died or were killed and the entire bodies were examined for worms. A total of 78 monkeys (43 males and 35 females) were exposed to infection and parasites were found in 29% of the females and 63% of males. In infections of 38 days or less worms were recovered from the testes of males and the pelt, carcass and lymph nodes of both sexes, but after 42 days of infection most worms were in the testes of males, and a few were recovered from lymph nodes and carcasses of females. Worms recovered at 8-11 days were third-stage, those found between 14 and 38 days fourth-stage, and ones found between 42 and 103 days were young adults. After 148 days most were adults and microfilariae were seen in the uteri of female worms at 160 days and later. The parasites continued to grow in size with time. Microfilariae were detected in the blood of nine monkeys between 8 and 18 months and the patent period varied from 5-21 months. Microfilarial densities were low and erratic, and periodicity could not be determined. The effectiveness of methods of administering infections and the value of various treatment regimens seem uncertain; monkey antilymphocytic sera, however, appeared to have some influence. Parasites were found in 36% of the Taiwan monkeys given the J strain and 54% of those given the K strain. A limited number of M. mulatta (3), M.irus (fascicularis) (3) and Aotus trivirgatus (4) were also given infective larvae and adult W. bancrofti were recovered from the testes of one male M. mulatta and one male M. irus; uterine microfilariae were found in one female worm from the latter monkey. A. trivirgatus were negative. Low numbers of infective larvae recovered from mosquitoes fed on patent monkeys were introduced intermittently into seven clean monkeys and one became microfilaremic between 11 and 17 months postinoculation.

Aedes↗
PubMed1979

Ultrastructure of the rectum of infective-stage Wuchereria bancrofti (Nematoda: Filarioidea).

The authors have examined the ultrastructure of the rectum of infective-stage Wuchereria bancrofti by transmission electron microscopy. Our observations show that the rectum is divided into anterior and posterior segments. The cells of the anterior rectum appear to be derived from the microfilarial R (rectal) cells described by other authors. In both stages, these cells show voluminous nuclei, abundant mitochondria, and small cytoplasmic processes which contain fibrillar components. Amorphous material associated with these processes appears throughout the larval rectum and may protrude from the anus as the rectal plug. In the specimens examined, a patent lumen could not be traced completely through the anterior rectum. The posterior rectum has no counterpart in published accounts of microfilarial ultrastructure and probably arises during larval morphogenesis; it is lined with invaginated body cuticle, overlaid by a single layer of epithelial cells which may be of hypodermal origin.

Animals↗