Anthelmintic tolerance in free-living and facultative parasitic isolates of<i>Halicephalobus</i>(Panagrolaimidae)

Fonderie, Pamela; Bert, Wim; Hendrickx, Frederik; Houthoofd, Wouter; Moens, Tom

doi:10.1017/s0031182012000558

Cited by 19 publications

(16 citation statements)

References 36 publications

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“…Most affected animals deteriorated (16,17,19,21,22,30) despite treatment, and the presence of live worms at autopsy suggests that the anthelmintic treatment was ineffective. In vitro susceptibility testing using microagar larval developmental tests (MALDTs) has been used to assess the effects of thiabendazole and ivermectin on the hatching rate and larval development of H. gingivalis (48). Thiabendazole at concentrations of 10 to 100 g/ml showed a dose-dependent inhibition effect on the hatchability of eggs.…”

Section: Case Reportmentioning

confidence: 99%

“…Nonetheless, PCR-based sequencing of DNA from brain biopsy material and CSF could potentially assist in diagnosis. Treatment has not been described in human cases, but pharmacokinetic studies (48,49) suggest that treatment with ivermectin or thiabendazole administered parenterally may not be effective because of poor killing effect per se and inability to achieve therapeutic levels in CNS. Nucleotide sequence accession number.…”

Section: Case Reportmentioning

confidence: 99%

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First Human Case of Fatal Halicephalobus gingivalis Meningoencephalitis in Australia

et al. 2015

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h Halicephalobus gingivalis (previously Micronema deletrix) is a free-living nematode known to cause opportunistic infections, mainly in horses. Human infections are very rare, but all cases described to date involved fatal meningoencephalitis. Here we report the first case of H. gingivalis infection in an Australian human patient, confirmed by nematode morphology and sequencing of ribosomal DNA. The implications of this case are discussed, particularly, the need to evaluate real-time PCR as a diagnostic tool. CASE REPORTA 74-year-old lady from a regional town in the Eyre Peninsula of South Australia with a 4-day history of mental state deterioration, fever, and a loss of coordination was transferred to the Royal Adelaide Hospital. She was moderately immune suppressed by methotrexate and etanercept treatment for rheumatoid arthritis and had a history of diabetes. During the admission, her conscious state deteriorated rapidly, requiring mechanical ventilation and admission to the intensive care unit (ICU). Subsequently, she developed signs of brainstem involvement and exhibited a loss of corneal and gag reflexes. She was administered benzylpenicillin, ceftriaxone, and aciclovir for presumptive meningoencephalitis of bacterial or viral etiology. Cerebrospinal fluid (CSF) obtained by lumbar puncture demonstrated 280 ϫ10 6 polymorphonuclear leukocytes (PMN)/liter, 18 ϫ10 6 mononuclear lymphocytes/liter, elevated CSF protein of 1.59 g/liter, and CSF glucose of 3.3 mmol/ liter; aerobic and anaerobic bacterial culture results were negative, as were PCR results for Streptococcus pneumoniae, Neisseria meningitidis, herpes simplex virus, and varicella-zoster virus. CSF India ink stain and cryptococcal antigen lateral flow assay (Immy, Inc., Norman, OK, USA) results were negative. Magnetic resonance imaging (MRI) of the brain exhibited a left-predominant, asymmetrical meningeal enhancement in the frontoparietal cortex, without any detectable brainstem changes. Two days later, repeated lumbar punctures showed a marked elevation of PMN to 2,500 ϫ10 6 cells/liter and 34 ϫ10 6 mononuclear cells/liter, with no bacteria detected upon Gram staining. CSF stained with DiffQuick (Alere, Brisbane, Australia) showed 99% PMN with very few eosinophils. CSF protein was markedly elevated (5.46 g/liter), and CSF glucose was 1.3 mmol/liter. Microscopic examination of 100 l of unstained CSF was performed after centrifugation at 700 ϫ g for 10 min, but no amoebic trophozoites were detected. With a suspicion of parasitic infection, given the unexplained high PMN counts, the antimicrobial treatment strategy was changed to liposomal amphotericin B, sulfadiazine, pentamidine, and azithromycin to target protists such as amoebae and Toxoplasma gondii. CSF was subjected to PCR for Naegleria fowleri, Acanthamoeba sp., and Balamuthia mandrillaris, but all test results were negative. No anti-Strongyloides serum antibody (IgG) was detected in an enzyme-linked immunosorbent assay using somatic larval antigens from Strongyloides ratti (Bordier Affinity Pr...

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Section: Case Reportmentioning

confidence: 99%

Section: Case Reportmentioning

confidence: 99%

First Human Case of Fatal Halicephalobus gingivalis Meningoencephalitis in Australia

et al. 2015

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“…However, H gingivalis may be able to opportunistically colonise the host in different ways. Possible infection routes include oral infection via ingestion of contaminated food facilitated by lacerations of the buccal mucosa (Ferguson and others 2008), transplacental transmission from mare to foal (Wilkins and others 2001), percutaneous through open wounds (Dunn and others 1993), or through the respiratory tract (Fonderie and others 2012). …”

Section: Discussionmentioning

confidence: 99%

Parasitic nephritis and meningoencephalomyelitis in a horse

Brown

Elsheikha

Turner³

2014

Vet Record Case Reports

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A 10-year-old horse developed ataxia and incoordination and was submitted for necropsy after euthanasia. The main gross postmortem finding was of bilateral renal masses, and a renal carcinoma had been suspected. Also, nematodes were present in histological sections of the cervical spinal cord. The microscopic feature was marked granulomatous inflammation, in both kidneys and local lymph nodes, and the clinical and morphologic features of this case resemble those observed in other reports of Halicephalobus gingivalis infection in horses. Aspects of the pathogenesis and pathology are discussed. Infection with H gingivalis should be included in the differential diagnosis of horses with acute neurological disease. However, lesions of H gingivalis are likely to be present in other organs that may be clinically inapparent. Owing to the widespread geographic distribution of H gingivalis and its zoonotic potential, this parasite poses a risk to animal and human health.

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“…Treatment with thiabendazole or albendazole may be useful, as they have been found to improve signs and symptoms in some cases of severe neurologic disease caused by Toxocara canis [15]. However tolerance of these parasites to ivermectin and thiabendazole even at very high concentrations has been observed [16]. Non-disseminated equine halicephalobosis from a para-orbital granuloma was treated with ivermectin and surgical excision, but it is unclear which intervention resulted in clinical resolution [17].…”

Section: Contents Lists Available At Sciencedirectmentioning

confidence: 99%

Fatal human eosinophilic meningo-encephalitis caused by CNS co-infection with Halicephalobus gingivalis and West Nile virus

Anwar

Gokozan

Ball

et al. 2015

Parasitology International

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Anthelmintic tolerance in free-living and facultative parasitic isolates ofHalicephalobus(Panagrolaimidae)

Cited by 19 publications

References 36 publications

First Human Case of Fatal Halicephalobus gingivalis Meningoencephalitis in Australia

First Human Case of Fatal Halicephalobus gingivalis Meningoencephalitis in Australia

Parasitic nephritis and meningoencephalomyelitis in a horse

Fatal human eosinophilic meningo-encephalitis caused by CNS co-infection with Halicephalobus gingivalis and West Nile virus

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