Pathological changes in the brains of rabbits experimentally infected with Angiostrongylus cantonensis after albendazole treatment: histopathological and magnetic resonance imaging studies

Wang, Lian-Chen; Jung, Shih‐Ming; Chen, Chien-Chuan; Wong, Ho-Fai; Wan, Dinah-Pingni; Wan, Yung‐Liang

doi:10.1093/jac/dki430

Cited by 39 publications

(28 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The major pathological damages in human CNS induced by A. cantonensis infection include; (1) meningitis with a predominance of eosinophils and plasma cells; (2) multiple microcavities, tortuous tracks, and microscopic hemorrhage surrounded by inflammatory cells and neuron lesions in the brain and spinal cord parenchyma; (3) granulomatous response to the dead worms; (4) nonspecific vascular reactions, thrombosis, and aneurysm formation [ 42 , 44 ]. In A. cantonensis -infected mammalian brains (permissive host rats and nonpermissive hosts, including mice, rabbits, and guinea pigs), similar pathological changes were also found in CNS [ 23 , 24 , 28 , 29 , 45 , 46 ]. In this study, plaque-like lesions also showed in various regions in infected animals.…”

Section: Discussionmentioning

confidence: 87%

Neuronal Apoptosis: Pathological Basis of Behavioral Dysfunctions Induced by Angiostrongylus cantonensis in Rodents Model

et al. 2017

View full text Add to dashboard Cite

Angiostrongylus cantonensis invades the central nervous system (CNS) of humans to induce eosinophilic meningitis and meningoencephalitis and leads to persistent headache, cognitive dysfunction, and ataxic gait. Infected mice (nonpermissive host), admittedly, suffer more serious pathological injuries than rats (permissive host). However, the pathological basis of these manifestations is incompletely elucidated. In this study, the behavioral test, histological and immunohistochemical techniques, and analysis of apoptotic gene expression, especially caspase-3, were conducted. The movement and motor coordination were investigated at week 2 post infection (PI) and week 3 PI in mice and rats, respectively. The cognitive impairs could be found in mice at week 2 PI but not in rats. The plaque-like lesion, perivascular cuffing of inflammatory cells, and dilated vessels within the cerebral cortex and hippocampus were more serious in mice than in rats at week 3 PI. Transcriptomic analysis showed activated extrinsic apoptotic pathway through increased expression of TNFR1 and caspase-8 in mice CNS. Immunohistochemical and double-labeling for NeuN and caspase-3 indicated the dramatically increased expression of caspase-3 in neuron of the cerebral cortex and hippocampus in mice but not in rats. Furthermore, western-blotting results showed high expression of cleaved caspase-3 proteins in mice but relatively low expression in rats. Thus, extrinsic apoptotic pathway participated in neuronal apoptosis might be the pathological basis of distinct behavioral dysfunctions in rodents with A. cantonensis infection. It provides the evidences of a primary molecular mechanism for the behavioral dysfunction and paves the ways to clinical diagnosis and therapy for A. cantonensis infection.

show abstract

Section: Discussionmentioning

confidence: 87%

Neuronal Apoptosis: Pathological Basis of Behavioral Dysfunctions Induced by Angiostrongylus cantonensis in Rodents Model

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Several dogs in the historical cohort worsened despite treatment with glucocorticoids, possibly due to this phenomenon. Clearly, mechanical damage due to migrating larvae and inflammation secondary to the appropriate host immune response both contribute to neural damage [43,66,81-85]. Which of the two is the more significant depends on (i) the age, species and breed of the infected host, (ii) the number of larvae ingested and the time course over which infection occurs, (iii) the physical dimensions of the spinal cord and nerve roots.…”

Section: Discussionmentioning

confidence: 99%

Twenty two cases of canine neural angiostrongylosis in eastern Australia (2002-2005) and a review of the literature

Lee

Smaller

et al. 2012

Parasites Vectors

View full text Add to dashboard Cite

Cases of canine neural angiostrongylosis (NA) with cerebrospinal fluid (CSF) evaluations in the peer-reviewed literature were tabulated. All cases were from Australia. A retrospective cohort of 59 dogs was contrasted with a series of 22 new cases where NA was diagnosed by the presence of both eosinophilic pleocytosis and anti- Angiostrongylus cantonensis immunloglobulins (IgG) in CSF, determined by ELISA or Western blot. Both cohorts were drawn from south east Queensland and Sydney. The retrospective cohort comprised mostly pups presented for hind limb weakness with hyperaesthesia, a mixture of upper motor neurone (UMN) and lower motor neurone (LMN) signs in the hind limbs and urinary incontinence. Signs were attributed to larval migration through peripheral nerves, nerve roots, spinal cord and brain associated with an ascending eosinophilic meningo-encephomyelitis. The contemporary cohort consisted of a mixture of pups, young adult and mature dogs, with a wider range of signs including (i) paraparesis/proprioceptive ataxia (ii) lumbar and tail base hyperaesthesia, (iii) multi-focal central nervous system dysfunction, or (iv) focal disease with neck pain, cranial neuropathy and altered mentation. Cases were seen throughout the year, most between April and July (inclusive). There was a preponderance of large breeds. Often littermates, or multiple animals from the same kennel, were affected simultaneously or sequentially. A presumptive diagnosis was based on consistent signs, proximity to rats, ingestion/chewing of slugs or snails and eosinophilic pleocytosis. NA was diagnosed by demonstrating anti- A. cantonensis IgG in CSF. Detecting anti- A. cantonensis IgG in serum was unhelpful because many normal dogs (20/21 pound dogs; 8/22 of a hospital population) had such antibodies, often at substantial titres. Most NA cases in the contemporary series (19/22) and many pups (16/38) in the retrospective cohort were managed successfully using high doses of prednisolone and opioids. Treatment often included antibiotics administered in case protozoan encephalomyelitis or translocated bacterial meningitis was present. Supportive measures included bladder care and physiotherapy. Several dogs were left with permanent neural deficits. Dogs are an important sentinel species for NA. Human cases and numerous cases in tawny frogmouths were reported from the same regions as affected dogs over the study period. Electronic supplementary material The online version of this article (doi:10.1186/1756-3305-5-70) contains supplementary material, which is available to authorized users.

show abstract

“…Both experimental infection studies and isolated reports indicate that killing the worms may exacerbate inflammation and increase the severity of the disease (164,291). Prednisolone (60 mg/kg of body weight/day for 2 weeks) and albendazole (15 mg/kg twice a day [b.i.d.]…”

Section: Treatmentmentioning

confidence: 99%

Update on Eosinophilic Meningoencephalitis and Its Clinical Relevance

2009

View full text Add to dashboard Cite

SUMMARY Eosinophilic meningoencephalitis is caused by a variety of helminthic infections. These worm-specific infections are named after the causative worm genera, the most common being angiostrongyliasis, gnathostomiasis, toxocariasis, cysticercosis, schistosomiasis, baylisascariasis, and paragonimiasis. Worm parasites enter an organism through ingestion of contaminated water or an intermediate host and can eventually affect the central nervous system (CNS). These infections are potentially serious events leading to sequelae or death, and diagnosis depends on currently limited molecular methods. Identification of parasites in fluids and tissues is rarely possible, while images and clinical examinations do not lead to a definitive diagnosis. Treatment usually requires the concomitant administration of corticoids and anthelminthic drugs, yet new compounds and their extensive and detailed clinical evaluation are much needed. Eosinophilia in fluids may be detected in other infectious and noninfectious conditions, such as neoplastic disease, drug use, and prosthesis reactions. Thus, distinctive identification of eosinophils in fluids is a necessary component in the etiologic diagnosis of CNS infections.

show abstract

Pathological changes in the brains of rabbits experimentally infected with Angiostrongylus cantonensis after albendazole treatment: histopathological and magnetic resonance imaging studies

Abstract: Pathological changes in the brains of the treated rabbits are more severe than those without albendazole treatment, suggesting that the drug may not be very suitable for the treatment of cerebral angiostrongyliasis.

Cited by 39 publications

References 21 publications

Neuronal Apoptosis: Pathological Basis of Behavioral Dysfunctions Induced by Angiostrongylus cantonensis in Rodents Model

Neuronal Apoptosis: Pathological Basis of Behavioral Dysfunctions Induced by Angiostrongylus cantonensis in Rodents Model

Twenty two cases of canine neural angiostrongylosis in eastern Australia (2002-2005) and a review of the literature

Update on Eosinophilic Meningoencephalitis and Its Clinical Relevance

Contact Info

Product

Resources

About