The presence of pinworms (Enterobius sp.) in the mesenteric lymph nodes, liver and lungs of a chimpanzee, Pan troglodytes

1990 ◽  
Vol 64 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Guang-Wen Zhang ◽  
Xiang-Rui Ji ◽  
Donald P. McManus

ABSTRACTThis report describes a case of fatal enterobiasis caused by Enterobius sp. in the mesenteric lymph nodes, lymphatic vessels of mesentery, blood vessels of the liver and lungs of a chimpanzee from Qingdao Zoo, China. Based on pathological findings, it is likely that the pinworms obtained access to these organs via the lymphatic or haematogenous pathway. As far as we are aware, this is the first reported case of Enterobius sp. in the mesenteric lymph nodes and blood vessels of the lungs and veins of the hepatic triad in a chimpanzee.

2007 ◽  
Vol 56 (3) ◽  
pp. 233-241 ◽  
Author(s):  
Marleen I. Verstege ◽  
Fiebo J. W. ten Kate ◽  
Susanne M. Reinartz ◽  
Cornelis M. van Drunen ◽  
Frederik J. M. Slors ◽  
...  

Dendritic cells (DCs) are key cells in innate and adaptive immune responses that determine the pathophysiology of Crohn's disease. Intestinal DCs migrate from the mucosa into mesenteric lymph nodes (MLNs). A number of different markers are described to define the DC populations. In this study we have identified the phenotype and localization of intestinal and MLN DCs in patients with Crohn's disease and non-IBD patients based on these markers. We used immunohistochemistry to demonstrate that all markers (S-100, CD83, DC-SIGN, BDCA1-4, and CD1a) showed a different staining pattern varying from localization in T-cell areas of lymph follicles around blood vessels or single cells in the lamina propria and in the MLN in the medullary cords and in the subcapsular sinuses around blood vessels and in the T-cell areas. In conclusion, all different DC markers give variable staining patterns so there is no marker for the DC.


2021 ◽  
pp. 102-110
Author(s):  
Hryhorii Zon ◽  
Lyudmyla Ivanovska ◽  
Illia Zon ◽  
Tion Matthew Terzungwe

Aim of the study: to examine the pathological changes in dogs that died due to confirmed intestinal yersiniosis and parvoviral enteritis and establish trends for characteristic organ lesions for both diseases in comparison, then evaluate our findings with the existing published material of sufficient evidence quality regarding differential postmortem diagnosis of spontaneous intestinal yersiniosis and parvoviral enteritis in dogs. Materials and methods: the study examined the cases of 25 dogs from 2 month to 1.3 y.o. of various breed, gender that died due to either confirmed Canine parvoviral enteritis (CPV) infection or intestinal yersiniosis and subsequently divided into two groups based on their diagnosis. The definitive diagnosis has been confirmed by performing rapid ELISA diagnostics (SensPERT®, VetAll Laboratories, Kyunggi-Do, Korea) for CPV and serological tests for Y. enterocolitica sera AT were performed using yersiniosis antigens from the "Component set for serological diagnosis of animal yersiniosis" (Kharkiv, NSC IEKVM, TS 46.15.091-95) in accordance with the "Interim guidelines for the use of a set of components for serological diagnostics". A dilution of 1: 200 has been considered as the diagnostic titer. After the definitive diagnosis had been confirmed, the animals were divided into two groups, depending on diagnosis: CPV (n=14) or IY (n=11). The autopsies of twenty randomly (10 from each group) selected dog corpses have been conducted utilizing standard methodology. Results: according to the results of autopsy of dogs afflicted by CPV, the main pathological changes were found in the small intestine – catarrhal-desquamative inflammation (in 100 % of cases), serous-hemorrhagic mesenteric lymphadenitis (90 %) large intestine (70 %) in the stomach (60 %), in the liver (50 %), in other organs – less than 40 percent of cases and most notably caused lung damage (edema and local atelectasis) in 90 % of the animals in the study, which was not the case for intestinal yersiniosis with only 20 % incidence of lung damage. Conclusions: Spontaneous intestinal yersiniosis in dogs was pathologically manifested by pronounced catarrhal-desquamative processes mainly in the stomach and small intestine (70, 100 and 80 % of cases, respectively), inflammation of the mesenteric lymph nodes (90 %) and large intestine (80 %), dystrophy and congestive processes in the liver (80 %). Low incidence and type of lung damage (congestive hyperemia in 20 % of reviewed cases compared to 90 % of local atelectasis add edema in CPV group) was noteworthy. Cases of 25 animals that died due to either confirmed CPV or Y. enterocolitica infection were analyzed, and 20 animal corpses were autopsied during study. Dogs that died from intestinal yersiniosis had significantly higher frequency of pathological findings in kidney (200 %) and liver (60 %) in particular. Changes in stomach and large intestine were also more frequent. At the same time, we observed a lower frequency of pathological changes in spleen (33 % lower), heart (25 % lower) and the lowest frequency was in lungs (77 % lower) presented by edema and local atelectasis in animals afflicted by yersiniosis compared to CPV. Incidence and manifestation of pathological findings was mesenteric lymph nodes and abdominal cavity were similar, and could not be considered during posthumous diagnostics.


Author(s):  
Osman Selçuk Aldemir ◽  
Meral Aydenizöz ◽  
Özlem Ateşoğlu

In this study was aimed to investigate spread and pathological findings of Linguatula serrata nymphs in mesenteric lymph nodes (MLNs) in sheep. A total of 1000 MLNs from 140 sheep (125 male and 15 female) were collected from a commercial (Konet) abattoir. Fourteen of 140 sheep (10%) were infested with nymph stages of L. serrata.Infested lymph nodes were swollen, firm, edematous, many yellowish-white pinpoint and with congestion. In histopathological examinations, these nodules were consist of one or more nymphal stages of L. serrata and these were surrounded by infiltration mononuclear cells and neutrophyl leucocyte. Lymphoid follicules were hyperplastic and sinus catarrh was also observed in medulla.


2001 ◽  
Vol 120 (5) ◽  
pp. A183-A183
Author(s):  
H KOBAYASHI ◽  
H NAGATA ◽  
S MIURA ◽  
T AZUMA ◽  
H SUZUKI ◽  
...  

Author(s):  
Carolin Wiechers ◽  
Mangge Zou ◽  
Eric Galvez ◽  
Michael Beckstette ◽  
Maria Ebel ◽  
...  

AbstractIntestinal Foxp3+ regulatory T cell (Treg) subsets are crucial players in tolerance to microbiota-derived and food-borne antigens, and compelling evidence suggests that the intestinal microbiota modulates their generation, functional specialization, and maintenance. Selected bacterial species and microbiota-derived metabolites, such as short-chain fatty acids (SCFAs), have been reported to promote Treg homeostasis in the intestinal lamina propria. Furthermore, gut-draining mesenteric lymph nodes (mLNs) are particularly efficient sites for the generation of peripherally induced Tregs (pTregs). Despite this knowledge, the direct role of the microbiota and their metabolites in the early stages of pTreg induction within mLNs is not fully elucidated. Here, using an adoptive transfer-based pTreg induction system, we demonstrate that neither transfer of a dysbiotic microbiota nor dietary SCFA supplementation modulated the pTreg induction capacity of mLNs. Even mice housed under germ-free (GF) conditions displayed equivalent pTreg induction within mLNs. Further molecular characterization of these de novo induced pTregs from mLNs by dissection of their transcriptomes and accessible chromatin regions revealed that the microbiota indeed has a limited impact and does not contribute to the initialization of the Treg-specific epigenetic landscape. Overall, our data suggest that the microbiota is dispensable for the early stages of pTreg induction within mLNs.


1997 ◽  
Vol 169 (5) ◽  
pp. 1253-1255 ◽  
Author(s):  
K N Chintapalli ◽  
C C Esola ◽  
S Chopra ◽  
A A Ghiatas ◽  
G D Dodd

Sign in / Sign up

Export Citation Format

Share Document