Enterobiasis in the suburbs.
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Biomedical subjects
Publications and source records attributed to P Prociv.
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The youngest patient with eosinophilic meningoencephalitis to be reported from Australia, an 11-month-old girl, is presented here. The diagnosis of angiostrongyliasis was based on the exclusion of other possibilities, the strongly-positive results of serological examination and the findings of an environmental survey. Clinical signs of serious brain damage, with persistent blindness, profound mental retardation, spasticity and epilepsy more than three years later, indicate that this infection is not always as benign as is considered generally.
The clinical features of the 'Palm Island mystery disease' cannot be explained on the basis of toxocariasis, nor do they correlate with the known manifestations of algal toxicity. A detailed review of acute and chronic copper poisoning in humans and laboratory animals supports this as a possible explanation for the epidemic. The mechanisms involved in copper intoxication are discussed briefly, and a scenario is proposed to explain the occurrence and pathogenesis of the outbreak.
After the suggestion was made that the "Palm Island mystery disease" might have been an epidemic of visceral larva migrans that was caused by the flying fox parasite, Toxocara pteropodis, work was undertaken to elucidate this nematode's life-cycle and pathogenicity. Studies of infections in various laboratory animals have shown unexpectedly variable susceptibility patterns, with mice harbouring most larvae for the longest time period. However, in all susceptible animals (which include mice, guinea-pigs and suckling rats), the larvae demonstrated marked hepatotropism. Experimental infections in monkeys demonstrated that primates are susceptible to this infection, but large doses of 20,000 infective eggs produced blood eosinophilia and focal granulomatous hepatitis without clinical disease or biochemical abnormalities in the blood. It is concluded that humans are susceptible to larval infections with this nematode, but that clinical manifestations would be unlikely to develop.
Infective eggs of Toxocara pteropodis were administered to Wistar rats via oral and parenteral routes. Third-stage larvae were recovered from the livers of suckling young 8 days after oral infection, and from livers and lungs after intraperitoneal or subcutaneous inoculation of eggs. These larvae were short-lived as none were found in suckling mice killed 2 weeks post-infection. Larvae were not recovered from tissues of rats aged 22 days or more when inoculated orally, indicating that refractoriness to infection develops rapidly with growth. Small numbers of larvae were recovered from the lungs of older rats 4 days after subcutaneous but not after oral inoculation. Adult male Buffalo and Fisher rats were also totally resistant to oral infection. Hence, rats differ from mice in their susceptibility to T. pteropodis.
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Infection in mice with Toxocara pteropodis was investigated. In mice fed infective eggs, third-stage larvae hatched out and penetrated the mucosa, predominantly that of the lower intestine. They travelled via the portal vein to the liver, where they remained at least 14 months. They grew in length from 430 +/- 15 micron, at three days post infection (p.i.), to 600 +/- 50 micron, at six to nine weeks p.i., after which time growth ceased. Blood eosinophilia appeared at 28 days p.i., and eosinophil levels continued to rise gradually beyond this time. In female mice the larvae did not migrate from the liver in response to pregnancy or lactation. When infective eggs were inoculated subcutaneously or intra-peritoneally, larvae hatched out and ultimately appeared in the liver in larger numbers than seen with oral infections.
Test mice have been selectively reared for high (H) or low (L) immune responses to Nematospiroides dubius. After secondary infection with N. dubius, the L mice voided ten times as many eggs in their faeces as the H mice, and at necropsy, 71% versus 20% of the inoculum of N. dubius were recovered as adult worms from the L and H mice respectively. Furthermore, N. dubius were more fecund in the L than in H mice. High or low immune responsiveness was not restricted to N. dubius infection in these mice but was also observed during Toxocara canis infection. The migration of T. canis larvae from gut via the liver to skeletal muscle and CNS was inhibited in H versus L mice. Many more larvae were recovered from the livers of H compared with L mice which was indicative of greater immunity in the H mice. The protective immune response in H compared with L mice to both N. dubius and T. canis included pronounced eosinophilia and elevated antiparasite antibody titres.
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Findings in the Australian Grey-Headed Flying-Fox, Pteropus poliocephalus, have elucidated the life-cycle of Toxocara pteropodis. In adult bats, other than parturient females, larvae were found only in the livers. Following parturition, larvae were recovered only from mammary glands up to 2 weeks post-partum. Developing larvae were found only in the intestine of young bats from the age of two days onwards; there was no evidence of pulmonary migration. The evidence indicates that juvenile bats commence passing Toxocara eggs in their faeces at about 2 months of age and expel the worms spontaneously following weaning at about 5 months. The eggs passed in the faeces of the young bat and its mother are disseminated throughout their environment and embryonate rapidly, being infective to mice after 10 days. Under natural conditions the eggs remain viable for 6 weeks or less and are infective to bats by the oral route.
A corneal ulcer, infected with Pseudomonas aeruginosa and complicated by conjunctivitis and endophthalmitis, was treated successfully with systemic administration of ticarcillin and topical application of tobramycin. It is unlikely that carbenicillin, to which the organism was much less sensitive, would have attained sufficient tissue levels to control the infection.
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Previous studies have found a high prevalence of Isospora belli and Cryptosporidium parvum infections in African acquired immune deficiency syndrome (AIDS) patients with chronic diarrhoea. We aimed to determine the prevalence of gastrointestinal parasite in AIDS patients in hospital, not only those with diarrhoea, and to compare them with the general community. Clinically diagnosed AIDS patients in a Zambian teaching hospital were interviewed and examined, and stool specimens were studied for parasite infection. A control group was recruited from adults in a township near Lusaka. Of 90 AIDS patients (58% male), 50 (56%) had chronic diarrhoea and 9 (10%) had diarrhoea of shorter duration. In the control group (105 adults; 85% female), only one complained of diarrhoea. A variety of intestinal protozoa and helminths was found in 57% of AIDS patients and 88% of the community members. Isosporiasis was detected in 7, and cryptosporidiosis in 2, AIDS patients, all with diarrhoea, but not in any control. Strongyloides was found in 2 AIDS patients with diarrhoea and one community resident. Hospital patients with AIDS had fewer Entamoeba coli and E. histolytica infections, probably because of previous chemotherapy. We conclude that AIDS predisposes to isosporiasis and cryptosporidiosis, but not to infection with extracellular intestinal parasites, such as Entamoeba species, Blastocystis, Chilomastix, Endolimax, Ascaris and Necator.
To evaluate the role of canine hookworms in human eosinophilic enteritis (EE) in north-eastern Australia, we tested human sera in an enzyme-linked immunosorbent assay (ELISA) which incorporated antigens of adult Ancylostoma caninum. Sera from the following groups were examined: 10 patients with EE (unexplained recurrent abdominal pain and related symptoms, with peripheral eosinophilia) from Townsville and Brisbane; 2 persons known to be infected with A. caninum and 20 presumed unexposed healthy controls; 20 patients with other gastrointestinal diseases; 20 with other identified parasitic infections; and 20 with atopic conditions. High levels of specific immunoglobulin (Ig) G and IgE antibodies were found in patients with EE but not other gastrointestinal disease. Excretory-secretory (ES) products were more discriminating than somatic antigens in the ELISA and the IgG/ES-ELISA was the most specific; occasional cross-reactions could be explained on epidemiological or parasitological grounds. The IgM-ELISA was neither specific nor sensitive. We conclude that canine ancylostomiasis is a major cause of human EE in north-eastern Australia, and the pathogenesis is based probably on hypersensitivity to antigens secreted by the parasite.
This paper reports the first survey in Australia to use faecal culture to detect Dientamoeba fragilis in patients with diarrhoea. Of 3 different protozoal culture media evaluated on a case of known infection, modified Boeck & Drbohlav's medium was the most suitable. The organism could be grown from faeces stored for up to 24 h at room temperature, but for only 10 h at 4 degrees C. Culture was then used, in combination with microscopy of smears fixed with polyvinyl alcohol and trichrome-stained, to examine single stool specimens from 260 consecutive patients with diarrhoea in the city of Brisbane. D. fragilis was detected in 4 (1.5%) specimens, only 2 of which were positive by microscopy. Other protozoa were found in 36 (13.8%) specimens: Blastocystis hominis in 28 (10.8%), Giardia duodenalis in 4 (1.5%), Endolimax nana in 3 (1.2%), and Entamoeba coli in one (0.4%). One strain of Dientamoeba was cryopreserved in liquid nitrogen and recultured successfully 10 d later. Culture was more sensitive than microscopy in diagnosing D. fragilis infection and the organism, of dubious pathogenicity, was not common in patients with diarrhoea in this community. Prevalence surveys of intestinal protozoan infections should use faecal culture, and specimens should be less than 12 h old and not refrigerated. Dientamoeba strains isolated by culture can be cryopreserved.