Angiostrongylus cantonensis is a bursate nematode parasite that causes eosinophilic meningitis (or meningoencephalitis) in humans in many parts of the world. The genomic data from A. cantonensis will form a useful resource for comparative genomic and chemogenomic studies to aid the development of diagnostics and therapeutics. We have sequenced, assembled and annotated the genome of A. cantonensis. The genome size is estimated to be ∼260 Mb, with 17,280 genomic scaffolds, 91X coverage, 81.45% for complete and 93.95% for partial score based on CEGMA analysis of genome completeness. The number of predicted genes of ≥300 bp was 17,482. A total of 7737 predicted protein-coding genes of ≥50 amino acids were identified in the assembled genome. Among the proteins of known function, kinases are the most abundant followed by transferases. The draft genome contains 34 excretory-secretory proteins (ES), a minimum of 44 Nematode Astacin (NAS) metalloproteases, 12 Homeobox (HOX) genes, and 30 neurotransmitters. The assembled genome size (260 Mb) is larger than those of Pristionchus pacificus, Caenorhabditis elegans, Necator americanus, Caenorhabditis briggsae, Trichinella spiralis, Brugia malayi and Loa loa, but smaller than Haemonchus contortus and Ascaris suum. The repeat content (25%) is similar to H. contortus. The GC content (41.17%) is lower compared to P. pacificus (42.7%) and H. contortus (43.1%) but higher compared to C. briggsae (37.69%), A. suum (37.9%) and N. americanus (40.2%) while the scaffold N50 is 42,191. This draft genome will facilitate the understanding of many unresolved issues on the parasite and the disorder it causes.
Kimura's disease (KD) is an uncommon chronic inflammatory condition of unknown aetiology involving subcutaneous tissue, presenting as a tumor like lesion with a predilection for the head and neck region. Clinically it is often confused with parotid tumor with lymph node metastasis. It is difficult to diagnose before tissue biopsy. Fine needle aspiration cytology has only limited value. Unless the pathologists are aware of this entity, it might be misdiagnosed. Surgery, radiotherapy and steroid therapy have been tried but none is proved best and recurrence is common. Three cases of KD seen in our hospital and the problems encountered in them are presented.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia/diagnosis*
We present three cases of Acquired Platelet Dysfunction with Eosinophilia (APDE). The importance of recognising this benign condition, which usually does not require any specific therapy, is stressed to avoid the pitfalls of diagnosing more serious bleeding disorders in children presenting with ecchymosis.
Kimura disease (KD) is a rare benign chronic inflammatory disease that presents as a nodule mostly involving deep subcutaneous tissue of the head and neck region with frequent regional lymphadenopathy and peripheral blood eosinophilia. KD shares some clinical and histopathological similarity with angiolymphoid hyperplasia with eosinophilia (ALHE). Consequently, KD and ALHE were once considered variants of the same disease spectrum. We present here rare cases of Kimura disease and ALHE involving the eyelid and lacrimal gland and discuss their differential features.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia/diagnosis*
Brugia malayi and Wuchereria bancrofti infections cause lymphatic filariasis in Malaysia. About 2.5 million people live in endemic areas of filariasis, of whom 5% have microfilaraemia and probably twice as many are infected. There is a wide clinical spectrum of response to the infection. While some have asymptomatic microfilaraemia, others have episodic attacks of fever, lymphadenitis, retrograde lymphangitis and lymphoedema. Elephantiasis is a late complication. Tropical pulmonary eosinophilia and other forms of occult filariasis are due to hyper allergic reactions to microfilarial antigens. Parasitological and serological tests aid in confirming the clinical diagnosis. The drug of choice is diethylcarbamazine citrate.
Kimura's disease is rare chronic inflammatory disease with a distinct clinicopathological entity. It has three major components; inflammatory, vascular and fibrosis. It has to be considered as a differential diagnosis in young patient presenting with head and neck swelling. Although of unknown aetiology many hypothesis has been postulated. Inflammation is the most prominent and predominating characteristic in this disease. Although reported to be predominant in Asian literature regarding this disease is scanty. We report a complete clinical-radiological and pathological picture of this disease.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia
Kimura's disease is a chronic inflammatory disorder of unknown etiology commonly seen among orientals and characterized histologically by lymphatic follicles, vascular proliferation, and marked eosinophilic infiltration. It has a predilection for the head and neck region. The lesion is benign but can be mistaken to be a malignant lesion.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia/drug therapy*; Angiolymphoid Hyperplasia with Eosinophilia/pathology; Angiolymphoid Hyperplasia with Eosinophilia/surgery*
We would like to highlight an unusual clinical presentation of Kimura's disease, a rare, benign, idiopathic condition, usually seen as swelling and lesions of the head and neck region and commonly affecting young men of Asian descent. It is rare for this disorder to present with lesions on other parts of the body, especially the lower limbs. We report a 27-year-old man who presented with a large mass located at the inguinal region and extending down to the upper thigh. Due to the large size of the mass (28 x 18 cm), our provisional diagnosis was a soft tissue sarcoma. Open biopsy showed that the lesion was benign.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia
Kimura’s disease (KD) is a rare, benign chronic inflammatory disease of unknown aetiology, typically presents in the Orientals as subcutaneous masses in the head and neck region that could be easily misdiagnosed as a malignant tumour, leading to unnecessary radical surgery or intensive cytotoxic therapy. It has been mainly reported in the Chinese and Japanese literature. It is difficult to diagnose before tissue biopsy and fine needle aspiration cytology (FNAC) has limited value. Hence, unless the pathologists are aware of this entity, it might be mistaken as a malignant lesion. We encountered a case of KD in a Malay patient presenting as a parotid mass that was initially diagnosed as Hodgkin’s lymphoma (HL). This disorder should be suspected in young male Asian patients presenting with a painless unilateral mass in the head and neck region with associated hypereosinophilia.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia
Quantitation of serum immunoglobulin M, G, A, D and E levels was carried out in Malaysians with Brugia malayi infections. Results showed highly elevated levels of IgM and IgE as well as moderately elevated levels of IgG. These were most significant in patients with tropical pulmonary eosinophilia or elephantiasis. Serum IgE levels were extremely high in microfilaraemic patients (6,060 +/- 3,958 IU ml) probably due to a constant antigenic stimulation by dead and dying microfilariae.
The distribution of anti-toxoplasma antibodies among the aborigines in Malaysia and its association with other soil transmitted infections and eosinophilia were studied. A total of 415 serum samples were collected and tested by IFA test. Overall prevalence was 10.6%, lower than previously reported. The antibody titers showed a unimodal distribution peaking at 1:8 dilution. There was a higher proportion of high antibody titer (> 1:128) in the adult compared to the children with no significant difference in prevalence rate by sex. The pattern of infection does not differ from other soil transmitted infections and there was no association between raised Toxoplasma antibodies with eosinophilia.
The association of mast cells with typical lesions of Kimura's disease was investigated by quantitative methods after immunohistochemical staining for Factor VIII-related antigen and counterstaining with toluidine blue. Formalin-fixed, paraffin-embedded, tissue sections from 9 confirmed cases of Kimura's disease were examined after staining to estimate mast cell and blood vessel densities by counting 100 random fields under oil immersion. There was a statistically significant increase of both mast cells and blood vessels in Kimura's disease (p<0.01) compared with normal skin and reactive lymph node controls. However, as far as the individual Kimura's disease lesion is concerned, there was generally no correlation between areas with mast cell increase and the degree of vascularity. Moreover, when lesions of less than 1 year's duration were compared with older lesions, there appeared to be a relative decrease in mast cells and a concomitant increase in vascularity in the latter. These results confirmed that mast cells are associated with Kimura's disease, and suggest that they may be involved in its early pathogenesis, although its possible role in angiogenesis may not be direct.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia/metabolism; Angiolymphoid Hyperplasia with Eosinophilia/pathology*
The diverse clinical syndromes characterized by asthmatic symptoms, transient pulmonary infiltrates, and eosinophilia have tended to obscure the specific association of one such entity with filarial infections. Serum IgE levels were determined before and after therapy in a group of well-characterized patients with tropical eosinophilia (TE), studied earlier in Singapore. The mean serum IgE level in 14 cases before treatment with diethylcarbamazine was 2,355 ng. per milliliter, with a trend but statistically nonsignificant decrease in levels to 600-1,000 ng. occurring 8 to 12 weeks after therapy. Leukocyte and eosinophil counts showed a rapid reduction after treatment, and although mean complement-fixing (cf) titers to Dirofilarial antigen tended to decrease, they were not significantly reduced until 5 to 6 weeks. The historical development of evidence supporting the filarial etiology of TE was reviewed. Many basic questions engendered by the clinical syndrome of tropical eosinophilia make it an excellent model for study of the immunopathology of parasitic infections.
Seven members of a 15-man U.S. military team that had operated in rural Malaysia developed an acute illness consisting of fever, myalgias, bronchospasm, fleeting pruritic rashes, transient lymphadenopathy, and subcutaneous nodules associated with eosinophilia, elevated erythrocyte sedimentation rate, and elevated levels of muscle creatinine kinase. Sarcocysts of an unidentified Sarcocystis species were found in skeletal muscle biopsies of the index case. Albendazole ameliorated symptoms in the index case; however, his symptoms persisted for more than 5 years. Symptoms in 5 other men were mild to moderate and self-limited, and 1 team member with laboratory abnormalities was asymptomatic. Of 8 team members tested for antibody to Sarcocystis, 6 were positive; of 4 with the eosinophilic myositis syndrome who were tested, all were positive. We attribute this outbreak of eosinophilic myositis to accidental tissue parasitism by Sarcocystis.
The principal etiologic agent of human eosinophilic meningitis, Angiostrongylus cantonensis, was first detected in rats in Canton, China in 1933. The first human case was detected on Taiwan in 1944. Epidemic outbreaks were noted on Ponape (E. Caroline Is.) from 1944 to 1948. The disease may present as transient meningitis or a more severe disease involving the brain, spinal cord and nerve roots, with a characteristic eosinophilia of the peripheral blood and CSF. Since 1961 it has been known that human infections are usually acquired by purposeful or accidental ingestion of infective larvae in terrestrial mollusks, planaria and fresh-water crustacea. There is no effective specific treatment. The African land snail, Achatina fulica played an important role in the panpacific dispersal of the organism: it will be important in Africa in the future as well. Rats were, and will continue to be the principal agents of expansion of the parasite beyond the Indopacific area. During and just after WWII the parasite was introduced, and/or spread passively from South and Southeast Asia into the Western Pacific islands and eastward and southward through Micronesia, Melanesia, Australia and into Polynesia, sequestered in shipments of war material and facilitated by post-war commerce. In the 1950s numerous cases were identified for the first time on Sumatra, the Philippines, Taiwan, Saipan, New Caledonia, and as far east as Rarotonga and Tahiti. Then cases were detected in Vietnam, Thailand, Cambodia, Java, Sarawak, the New Hebrides, Guam and Hawaii during the 1960s. Subsequently in the Pacific Basin the disease has appeared on Okinawa, other Ryukyu islands, Honshu, Kyushu, New Britain, American Samoa and Western Samoa, Australia, Hong Kong, Bombay, India, Fiji and most recently in mainland China. The parasite in rats now occurs throughout the Indopacific Basin and littoral. Beyond the Indopacific region, the worm has been found in rodents in Madagascar (ca 1963), Cuba (1973), Egypt (1977), Puerto Rico (1984), New Orleans, Louisiana (1985) and Port Harcourt, Nigeria (1989). Human infections have now been detected in Cuba (1973), Réunion Island (1974) and Côte d'Ivoire (1979) and should be anticipated wherever infected rats of mollusks have been introduced. Caged primates became infected in zoos in Hong Kong (1978) and New Orleans and Nassau, Bahamas (1987). The use of mollusks and crustacea as famine foods, favored delicacies and medicines has resulted in numerous outbreaks and isolated infections. Economic and political instability, illicit trade, unsanitary peridomestic conditions and lack of health education promote the local occurrence and insidious global expansion of parasitic eosinophilic meningitis.(ABSTRACT TRUNCATED AT 400 WORDS)
Matched MeSH terms: Eosinophilia/diagnosis; Eosinophilia/etiology*; Eosinophilia/prevention & control
The term 'tropical' refers to the region of the Earth lying between the Tropic of Cancer and the Tropic of Capricorn. Located between these equatorial parallels demarcating the Torrid Zone are several underdeveloped and developing countries: Thailand, the Philippines, Malaysia, Singapore, Indonesia, southern India, Sri Lanka, Brazil, Cuba, Ethiopia, Sudan and Nigeria, to name but a few considered to be 'tropical'. The climate in most of these countries is characterized by high temperatures and high humidity. The tropical climate and general state of socio-economic underdevelopment in such countries provide an ideal environment for pathogenic organisms, their vectors and intermediate hosts to flourish. Furthermore, the cultural habits and educational background of the people living in such countries expose them to pathogens and, when these people become infected, they readily become reservoirs for, or carriers of, those organisms. Ultimately, the adverse socioeconomic conditions of underdeveloped countries impede attempts to eradicate or control tropical diseases.
Kimura disease presents as benign lesion and is commonly present among the Asian population. It
is a disease with a favourable prognosis and a peak age of onset in the third decade. It is a chronic
inflammatory disorder of unknown etiology that involves the lymph nodes and subcutaneous
tissues of the head and neck region. We report a case of a 15-year-old boy with multiple Kimura
lymphadenopathies involving the left posterior auricular region as well as the anterior and posterior
triangles of the neck.
Matched MeSH terms: Angiolymphoid Hyperplasia with Eosinophilia