Case report: protein-losing enteropathy caused by Mesocestoides vogae (syn. M. corti) in a dog.

An eight-year-old, neutered, female Shetland Sheepdog presented with a 6-week history of small intestinal diarrhea. Regenerative anemia, hypoproteinemia, and an increased plasma C-reactive protein concentration were detected on blood examination. Fecal examination and abdominal radiography were unremarkable. Abdominal ultrasonography showed diffusely hyperechoic mucosa in the small intestine. Gastroduodenoscopy, performed under general anesthesia, revealed mucosal edema and increased granularity in the duodenum and jejunum. Histopathological examination of the endoscopically biopsied small intestinal mucosa revealed tapeworm infection. A single administration of a combined anthelmintic drug (5mg/kg praziquantel, 14.4 mg/kg pyrantel pamoate, and 15 mg/kg febantel) was successful for deworming, and the dog fully recovered. The parasites were removed from stored frozen duodenal mucosa and morphologically identified as Mesocestoides sp. immature adult worms. Mitochondrial (mt) 12S rDNA and mt cytochrome c oxide subunit 1 genes were amplified from the parasites. DNA sequence analysis showed that the genes shared 100% identity with those of reported M. vogae (syn. M. corti). This is the first reported case of protein-losing enteropathy caused by M. vogae in a dog.

An indigenous case of intestinal capillariasis with protein-losing enteropathy in Korea.

We encountered an indigenous case of intestinal capillariasis with protein-losing enteropathy in the Republic of Korea. A 37-year-old man, residing in Sacheon-si, Gyeongsangnam-do, admitted to the Gyeongsang National University Hospital (GNUH) due to long-lasting diarrhea, abdominal pain, anasarca, and weight loss. He recalled that he frequently ate raw fish, especially the common blackish goby (Acanthogobius flavimanus) and has never been abroad. Under the suspicion of protein-losing enteropathy, he received various kinds of medical examinations, and was diagnosed as intestinal capillariasis based on characteristic sectional findings of nematode worms in the biopsied small intestine. Adults, juvenile worms, and eggs were also detected in the diarrheic stools collected before and after medication. The clinical symptoms became much better after treatment with albendazole 400 mg daily for 3 days, and all findings were in normal range in laboratory examinations performed after 1 month. The present study is the 6th Korean case of intestinal capillariasis and the 3rd indigenous one in the Republic of Korea.

Reactive arthritis, psoriasiform lesions and protein loosing enteropathy secondary to Strongyloidiasis.

Reactive arthritis is associated with demonstrable infection at a distant site without evidence of sepsis at the affected joint(s). We present a rare case reactive arthritis where no bacterial or chlamydial infections could be established, rather larvae of Strongyloides stercoralis could be demonstrated in the stool and duodenal biopsy. Reactive arthritis, psoriasiform lesions and malabsorption with hypoproteinaemia, responded to successful treatment with antihelminthic drugs. Early recognition and adequate treatment for gastrointestinal infections and infestations before complications is important.

Interaction of Ostertagia and Nematodirus species in sheep and the potential of serum fructosamine determination in monitoring gastrointestinal parasitism.

Serum fructosamine concentration falls with an increase in plasma protein turnover. Since this increase is a feature of gastrointestinal parasite infection at all sites, a falling serum fructosamine level may be of general application in the interpretation of parasite-related events. The circulating fructosamine level was investigated in the lamb as an indicator of protein-losing gastroenteropathy associated with two parasites at different sites, Ostertagia circumcincta (abomasum) and Nematodirus spathiger (small intestine). Infection with 10,000 N spathiger infective larvae daily for seven weeks produced only slight clinical signs, and only a small change in serum fructosamine levels. 2500 O circumcincta L3 daily gave no clinical signs in most animals, but serum fructosamine was more strongly affected in this group. Concurrent infection with both organisms caused some degree of diarrhoea in all lambs, and a sustained fall in serum fructosamine, more accentuated than that observed in either of the single infection groups, supporting the value of serum fructosamine determination in monitoring gastrointestinal parasitism.

Protein losing enteropathy: an unusual presentation of intestinal schistosomiasis.

A patient presenting with features suggestive of malabsorption syndrome is described who had florid intestinal schistosomiasis on peroral biopsy of the jejunum. Liver biopsy and rectal biopsy also revealed schistosomal ova. Biochemical studies revealed severe hypoproteinaemia and hypoalbuminaemia, caused by a protein losing enteropathy. This is the first reported case of protein losing enteropathy caused by intestinal schistosomiasis.

Enteropatia perdedora de proteínas causada por estrongiloidíase maciça na infância: relato de um caso / Protein losing enteropathy caused by massive strongyloidiasis in infancy: a case report

Em situaçöes anormais perda protéica, de causa primária ou secundária, pode ocorrer em qualquer nível do trato gastrintestinal. Dentre as doenças parasitárias, perda protéica intestinal tem sido descrita em giardíase, filariose, paracoccidioidomicose, esquistossomose, amebíase e tricuríase. Näo é do conhecimento dos autores relatos na literatura de perda protéica intestinal associada a estrongiloidíase na infância. O presente trabalho descreve um caso de perda protéica intestinal num paciente de 20 meses com infestaçäo maciça por Strongiloides stercoralis. O paciente tinha história de diarréia intermitente, desnutriçäo e edema de pés e pernas. Parasitológico de fezes revelou Ascaris lumbricoides, Giardia lamblia e Strogiloides stercoralis. A albumina sérica era de 1,78 g%; D-xilose na 1ª hora de 8,7 mg%; curva de sobrecarga de triglicérides com incremento de 11,6 mg%. A biópsia de intestino delgado mostrou atrofia vilositária parcial e processo granulomatoso em lâmina própria por ovos e larvas de nematódeos. Ovos e larvas de estrongilóides estavam presentes no suco jejunal. O teste da cromoalbumina marcada mostrou perda protéica de 3.2 g/dia. As alteraçöes morfológicas e funcionais do intestino delgado reverteram parcialmente com a erradicaçäo do parasita