A case of mammary sparganosis due to infection with Spirometra mansoni

2019 ◽  
Vol 25 (4) ◽  
pp. 712-715
Author(s):  
Jun Zuo ◽  
Hai Gang Feng ◽  
Sha Sha Xie ◽  
Jun Tao Yang
Keyword(s):  
Parasitology ◽  
1994 ◽  
Vol 109 (5) ◽  
pp. 611-621 ◽  
Author(s):  
Y. Kong ◽  
Y.-B. Chung ◽  
S.-Y. Cho ◽  
S.-Y. Kang

When immunoglobulin G (IgG) was incubated with Spirometra mansoni plerocercoid (sparganum), it was cleaved into Fab and Fc fragments. Fab/c fragments were also hydrolysed. The digestion was accelerated by dithiothreitol (DTT), indicating that cleavage of IgG heavy chain was due to a cysteine protease secreted into the medium. The responsible enzyme, of Mr 27 (± 0·8) kDa, was purified by a series of thiopropyl affinity, Sephacryl S-300 HR and DEAE-anion exchange chromatographies, either from worm extracts or from excretory–secretory products (ESP). The purified, thiol-dependent protease showed an optimal activity at pH 5·7 with 0·1 M sodium acetate but was active over the pH range 4·5–8·0. Its activity was inhibited completely by 10−5 M L-trans-epoxysuccinylleucylamido(4-guanidino) butane (E-64) and 1 mM iodoacetamide (IAA), but by only 53% using the specific cathepsin L inhibitor, Z-Phe-Phe-CHN2 (5 × 10−5 M). Partial NH2-terminal amino acid sequence was Leu-Pro-Asp-Ser-Val-Asn-Trp-Arg-Glu-Gly-Ala-Val-Thr-Ala-Val which showed 80% homology to human cathepsin S. Immunoblot analysis showed that sera from infected patients exhibited IgE antibody reaction. It is proposed that cleavage of immunoglobulin by an excreted–secreted, cathepsin S-like, allergenic protease is a mechanism of immune evasion used by the sparganum.


2014 ◽  
Vol 113 (9) ◽  
pp. 3511-3516 ◽  
Author(s):  
Jing Cui ◽  
Tong Wei ◽  
Li Na Liu ◽  
Xi Zhang ◽  
Xin Qi ◽  
...  

2004 ◽  
Vol 59 (3-4) ◽  
Author(s):  
IDALIA VALERIO ◽  
BEATRÍZ RODRÍGUEZ ◽  
MISAEL CHINCHILLA

Parasitology ◽  
1994 ◽  
Vol 108 (3) ◽  
pp. 359-368 ◽  
Author(s):  
Y. Kong ◽  
Y.-B. Chung ◽  
S.-Y. Cho ◽  
S.-H. Choi ◽  
S.-Y. Kang

SUMMARYIn the pathogenesis of sparganosis, proteases have been considered to play important roles in tissue migration and parasite feeding. Several bands of proteolysis were observed when crude extracts of Spirometra mansoni plerocercoid (sparganum) were examined using gelatin substrate gel at neutral pH, of which two proteases of 198 and 104 kDa were purified by two chromatographic steps, and a 36 kDa protease was purified by gelatin-affinity and DEAE–anion exchange chromatography. All the purified proteases exhibited optimal activity at pH 7·5 and 0·1 M Tris–HCI. Proteolytic activities at 198 and 104 kDa were inhibited specifically by serine protease inhibitors, and 4-(amidinophenyl)methansulfonyl fluoride (APMSF, 0·5 m) and N-α–p–tosyl-L-lysine chloromethyl ketone (TLCK, 1 mM), which strongly suggested that these two proteases were trypsin-like proteases. The activity of the 36 kDa protease was inhibited by N-tosyl-l-phenylalanine chloromethyl ketone (TPCK, I mM) and chymostatin (0·1 mM), and was potentiated in 10 mM Ca2+ which showed that the protease had a chymotrypsin-like property. All the proteases were Schiff(PAS) positive. Proteases of 198 and 104 kDa degraded collagen completely within 24 h. The 36 kDa enzyme cleaved human recombinant interferon-γ (rIFNγ) and bovine myelin basic protein. In addition, all the purified proteins elicited strong antibody responses in the infected patients.


Author(s):  
C.N. Sun ◽  
J.J. Daly ◽  
H.J. White ◽  
A.L. Barron

Mueller and Strano have reported finding virus-like particles lining the walls of excretory ducts in plerocercoid (sparganum) larvae of the pseudophyllidean tapeworms, Sparganum proliferum, from a human host, and Spirometra mansonoides and Spirometra mansoni, from animal hosts. Although human sparganosis caused by these species is distributed world-wide, only 50 cases have been officially reported in the United States. A sparganum in a nodule from the outer aspect of the right thigh of a 30 year-old male in Arkansas has recently been described which is believed to be either S. mansonoides or S. mansoni. Since the previously studied material of these two species were from non-human hosts, this worm afforded the opportunity to examine a non-proliferating sparganum from a human host for the presence of virus particles.The worm, which was 90 mm long and 1 mm wide, was fixed in neutral buffered formalin and post-fixed with buffered 2% osmium tetroxide.


2016 ◽  
Vol 53 ◽  
pp. 41-45 ◽  
Author(s):  
Qing Hong ◽  
Jieping Feng ◽  
Haijuan Liu ◽  
Xiaomin Li ◽  
Lirong Gong ◽  
...  

2012 ◽  
Vol 87 (3) ◽  
pp. 257-270 ◽  
Author(s):  
J. Finsterer ◽  
H. Auer

AbstractCerebral involvement in parasitoses is an important clinical manifestation of most of the human parasitoses. Parasites that have been described to affect the central nervous system (CNS), either as the dominant or as a collateral feature, include cestodes (Taenia solium (neurocysticerciasis), Echinococcus granulosus (cerebral cystic echinococcosis), E. multilocularis (cerebral alveolar echinococcosis), Spirometra mansoni (neurosparganosis)), nematodes (Toxocara canis and T. cati (neurotoxocariasis), Trichinella spiralis (neurotrichinelliasis), Angiostrongylus cantonensis and A. costaricensis (neuroangiostrongyliasis), Gnathostoma spinigerum (gnathostomiasis)), trematodes (Schistosoma mansoni (cerebral bilharziosis), Paragonimus westermani (neuroparagonimiasis)), or protozoa (Toxoplasma gondii (neurotoxoplasmosis), Acanthamoeba spp. or Balamuthia mandrillaris (granulomatous amoebic encephalitis), Naegleria (primary amoebic meningo-encephalitis), Entamoeba histolytica (brain abscess), Plasmodium falciparum (cerebral malaria), Trypanosoma brucei gambiense/rhodesiense (sleeping sickness) or Trypanosoma cruzi (cerebral Chagas disease)). Adults or larvae of helminths or protozoa enter the CNS and cause meningitis, encephalitis, ventriculitis, myelitis, ischaemic stroke, bleeding, venous thrombosis or cerebral abscess, clinically manifesting as headache, epilepsy, weakness, cognitive decline, impaired consciousness, confusion, coma or focal neurological deficits. Diagnosis of cerebral parasitoses is dependent on the causative agent. Available diagnostic tools include clinical presentation, blood tests (eosinophilia, plasmodia in blood smear, antibodies against the parasite), cerebrospinal fluid (CSF) investigations, imaging findings and occasionally cerebral biopsy. Treatment relies on drugs and sometimes surgery. Outcome of cerebral parasitoses is highly variable, depending on the effect of drugs, whether they are self-limiting (e.g. Angiostrongylus costaricensis) or whether they remain undetected or asymptomatic, like 25% of neurocysticerciasis cases.


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