scholarly journals Exacerbation of Darier Disease under Interferon-α-2a Therapy with Clinical Signs of Lichen Nitidus

2016 ◽  
Vol 8 (2) ◽  
pp. 218-223 ◽  
Author(s):  
Ioannis Karagiannidis ◽  
Martina Brunner ◽  
Christos C. Zouboulis
Keyword(s):  
Clinical Signs ◽  
Ultraviolet B ◽  
Mechanical Trauma ◽  
Interferon Α ◽  
Trigger Factors ◽  
Gene Encoding ◽  
Darier Disease ◽  
Dyskeratosis Follicularis ◽  
Oral Corticosteroids ◽  
The Face

Darier disease/dyskeratosis follicularis is a genodermatosis characterized by brown, oily keratotic papules and plaques in the seborrheic areas of the face and chest. Responsible for the disease are mutations in the ATP2A2 gene, encoding SERCA2, a calcium pump of the sarco-/endoplasmic reticulum. Mechanical trauma, heat, humidity, ultraviolet B radiation, oral corticosteroids and lithium are known trigger factors of the disorder. We report on a 48-year-old German woman with a flare-up of Darier disease under interferon-α-2a (IFNα-2a) therapy with clinical signs of lichen nitidus. Due to the fulminant course of the eruption, we suspected IFNα as a possible trigger. To our knowledge there are no reports regarding exacerbation of Darier disease during IFNα therapy. Possible pathogenetic mechanisms are being discussed.

Tangier Disease

2016 ◽  
Author(s):  
Dominic S. Ng
Keyword(s):  
Coronary Heart Disease ◽  
Corneal Transplantation ◽  
Clinical Signs ◽  
Density Lipoprotein ◽  
Reticuloendothelial System ◽  
Cholesterol Esters ◽  
Peripheral Neuropathies ◽  
Tangier Disease ◽  
Gene Encoding ◽  
Yellow Orange

Tangier disease is characterized by profound high-density lipoprotein (HDL) deficiency in association with accumulation of cholesterol esters in tissues, especially those of the reticuloendothelial system. Clinical signs include hyperplastic, yellow-orange colored tonsils, peripheral neuropathies, and hepatosplenomegaly. The disease is caused by two mutant alleles of the ABCA1 gene encoding ATP-binding cassette subfamily A member 1. Despite severe HDL deficiency, predisposition to accelerated coronary heart disease is highly variable in affected individuals. With the exception of tonsillectomy for severe hyperplastic tonsils and corneal transplantation in rare cases of severe corneal opacification, treatments for specific manifestations are largely ineffective.

scholarly journals Dermatophytosis in companion animals: A review

2020 ◽  
Vol 13 (6) ◽  
pp. 1174-1181
Author(s):  
Alsi Dara Paryuni ◽  
Soedarmanto Indarjulianto ◽  
Sitarina Widyarini
Keyword(s):  
Immune Response ◽  
Immune Status ◽  
Companion Animals ◽  
Clinical Signs ◽  
Skin Lesions ◽  
The Face ◽  
Dermatophyte Species ◽  
Dermatophyte Infection ◽  
Age And Sex ◽  
Pro Inflammatory Cytokines

Dermatophytosis, a zoonotic disease, is caused by fungi of three main genera, namely, Micropsorum, Trichophyton, and Epidermophyton. Specific lesions of dermatophyte infections are localized in the face, legs, and/or tail. Skin lesions in infected animals demonstrate localized alopecia, erythema, and crust, which are more commonly known as ringworm. Factors that affect dermatophytosis include the dermatophyte species; virulence factors of the agent; and the immune status, age, and sex of the host. High levels of cortisol and pro-inflammatory cytokines have also been reported to play an important role in dermatophyte infection. This review aims to explore and understand factors that affect dermatophyte infection with an emphasis on the prevalence, clinical signs, pathogenesis, immune response, and the roles of cortisol and cytokines in companion animals infected by a dermatophyte.

scholarly journals Identification of lamb flocks susceptible and resistant against Brachiaria poisoning

2016 ◽  
Vol 36 (5) ◽  
pp. 383-388 ◽  
Author(s):  
Rayane C. Pupin ◽  
Gleice K.A. Melo ◽  
Rubiane F. Heckler ◽  
Tatiane C. Faccin ◽  
Camila C.B.F. Ítavo ◽  
...  
Keyword(s):  
Genetic Resistance ◽  
Clinical Signs ◽  
Giant Cells ◽  
Skin Lesions ◽  
Bile Duct Proliferation ◽  
Subcutaneous Edema ◽  
Lymphoplasmacytic Infiltrate ◽  
The Face ◽  
Resistant Group ◽  
Foamy Macrophages

Abstract: This study was designed to assess the influence of genetic resistance against brachiaria poisoning in sheep. Two groups of sheep, one identified as susceptible (formed by two ewes and one ram) and the other as resistant against brachiaria poisoning (formed by three ewes and one ram) were selected. Sheep considered susceptible were those that presented clinical signs of brachiaria poisoning at any time of their life; resistant sheep were those that even raised on Brachiaria spp. pastures, did not developed any sign of the poisoning during their life. The offspring of the two flocks (15 lambs from the sensitive flock and 9 lambs from the resistant flock) were placed into brachiaria pasture (initially Brachiaria decumbens and B. brizantha,and only B. decumbens after weaning) and followed up during two years (2013-2014). The determination of protodioscin levels in B. decumbens pasture was performed only in 2014 and revealed significant amounts of the toxic principle. Eleven lambs of the susceptible group were affected to some degree of brachiaria poisoning and six died; no lamb of the resistant group was affected. Clinical signs consisted of varying degrees of subcutaneous edema of the face and, erythema and loss of hair of the ears, crusts on the skin of ears, around the eyes and on planum nasale, scar deformation of the ears, and bilateral ocular discharge; affected lambs also sought for shadowy shelters and they were poor doers. Several sheep recovered from the condition and then relapsed. Necropsy findings in six lambs included pale mucous membranes, emaciation, dermatitis, scar deformation of the ears, large yellow livers with marked lobular pattern, and moderate infestation by Haemonchus contortus. Histologically the liver lesions were similar in all necropsied lambs but with varying degrees of severity; they were consistent with brachiaria poisoning and included architectural disruption of hepatocellular trabecula, clusters of foamy macrophages occasionally forming multinucleated giant cells, swollen and vacuolated hepatocytes, crystals or negative images of crystals in the biliary system, bilestasis, bile duct proliferation and lymphoplasmacytic infiltrate in portal triads. The skin lesions were those of photodermatitis and included epidermal necrosis, hyperkeratosis and dermal neutrophilic infiltrate. The results of this study allow to conclude that there is a genetic related resistance to brachiaria poisoning in sheep since the progeny of resistant sheep did not manifest the poisoning. The use of resistant flocks in brachiaria pastures is suggested as a valuable option for the prevention of brachiaria poisoning in sheep.

scholarly journals Enhancement of Immune Responses by an AttenuatedSalmonella entericaSerovar Typhimurium Strain Secreting anEscherichia coliHeat-Labile Enterotoxin B Subunit Protein as an Adjuvant for a LiveSalmonellaVaccine Candidate

2010 ◽  
Vol 18 (2) ◽  
pp. 203-209 ◽  
Author(s):  
Jin Hur ◽  
John Hwa Lee
Keyword(s):  
Immune Responses ◽  
Vaccine Candidate ◽  
Clinical Signs ◽  
Secretory Iga ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gene Encoding ◽  
Typhimurium Strain ◽  
Immunization Strategies ◽  
Serovar Typhimurium ◽  
Group B

ABSTRACTA plasmid harboringeltB, the gene encoding heat-labile enterotoxin (LTB), was constructed by insertion ofeltBinto an Asd+β-lactamase signal plasmid (pMMP65). This was introduced into the ΔlonΔcpxRΔasd Salmonella entericaserovar Typhimurium strain and designated the LTB adjuvant strain. LTB protein production and secretion from the strain were demonstrated with an immunoblot assay and enzyme-linked immunosorbent assay. The LTB strain was evaluated for enhancement of immunity and protection efficacy induced by a previously constructed liveSalmonellavaccine candidate. In addition, immunization strategies using the LTB strain were optimized for effective salmonellosis protection. Seventy female BALB/c mice were divided into seven groups (A to G;n= 10 mice per group). Mice were primed at 6 weeks of age and boosted at 9 weeks of age. All mice were orally challenged with a virulent wild-type strain at week 3 postbooster. Serum IgG and IgA titers from mice immunized with the LTB strain alone or with a mixture of the LTB strain and the vaccine candidate were significantly increased. The secretory IgA titers from mice immunized with the LTB strain alone or with the mixture were at least 2.2 times greater than those of control mice. In addition, all group E mice (primed with the vaccine-LTB mixture and boosted with the vaccine candidate) were free of clinical signs of salmonellosis and survived a virulent challenge. In contrast, death due to the challenge was 100% in control mice, 80% in group A mice (single immunization with the vaccine candidate), 60% in group B mice (primed and boosted with the vaccine candidate), 40% in group C mice (single immunization with the LTB strain), 30% in group D mice (primed and boosted with the LTB strain), and 30% in group F mice (primed and boosted with the vaccine-LTB mixture). These results suggest that vaccination with the LTB strain, especially when added at the prime stage only, effectively enhances immune responses and protection against salmonellosis.

Monoclonal antibody treatment of mixed cryoglobulinemia resistant to interferon α with an anti-CD20

Blood ◽  
2003 ◽  
Vol 101 (10) ◽  
pp. 3818-3826 ◽  
Author(s):  
Domenico Sansonno ◽  
Valli De Re ◽  
Gianfranco Lauletta ◽  
Felicia Anna Tucci ◽  
Mauro Boiocchi ◽  
...  
Keyword(s):  
Hepatitis C ◽  
B Cell ◽  
Clinical Signs ◽  
Mixed Cryoglobulinemia ◽  
Controlled Study ◽  
Chimeric Antibody ◽  
Interferon Α ◽  
Hcv Rna ◽  
Rapid Improvement ◽  
Antibody Treatment

Abstract A controlled study has been carried out to assess the efficacy of rituximab, a chimeric antibody that binds to the B-cell surface antigen CD20, in 20 patients with mixed cryoglobulinemia (MC) and hepatitis C virus (HCV)–positive chronic active liver disease, resistant to interferon α (IFN-α) therapy. They received an intravenous infusion of 375 mg/m2 rituximab once a week for 4 consecutive weeks. Infusion of rituximab had a good safety profile and no severe side effects were reported. Sixteen patients (80%) showed a complete response (CR), characterized by rapid improvement of clinical signs (disappearance of purpura and weakness arthralgia and improvement of peripheral neuropathy), and decline of cryocrit. CR was associated with a significant reduction of rheumatoid factor (RF) activity and anti-HCV antibody titers. Decline of IgG anti-HCV titers in the cryoprecipitates was usually associated with a favorable response (r = 0.81; P < .005). No differences in the dynamics of B-cell depletion and recovery were found between responders and nonresponders. Molecular monitoring of the B-cell response revealed disappearance/deletion of peripheral clones in the responders and great stability in the nonresponders. Rituximab had a deep impact on hepatitis C viremia; HCV RNA increased approximately twice the baseline levels in the responders, whereas it remained much the same in the nonresponders. Twelve (75%) of 16 responders remained in remission throughout the follow-up. The results indicate that rituximab has clinical and biologic activity in patients with HCV+ MC. However, in view of the increased viremia in the responders, additional modes of application and combination of rituximab with other agents need to be investigated.

scholarly journals Clostridial Enteric Infections in Pigs

2005 ◽  
Vol 17 (6) ◽  
pp. 528-536 ◽  
Author(s):  
J. Glenn Songer ◽  
Francisco A. Uzal
Keyword(s):  
Clostridium Difficile ◽  
Clinical Signs ◽  
Type A ◽  
Enteric Infection ◽  
Gene Encoding ◽  
Presumptive Diagnosis ◽  
Large Numbers ◽  
Intestinal Contents ◽  
Type C ◽  
Beta Toxin

Clostridium perfringens types A and C and Clostridium difficile are the principal enteric clostridial pathogens of swine. History, clinical signs of disease, and gross and microscopic findings form the basis for a presumptive diagnosis of C. perfringens type-C enteritis. Confirmation is based on isolation of large numbers of type-C C. perfringens and/or detection of beta toxin in intestinal contents. Diagnosis of C. perfringens type-A infection, however, remains controversial, mostly because the condition has not been well defined and because type-A organisms and their most important major (alpha) toxin can be found in intestinal contents of healthy and diseased pigs. Isolation of large numbers of C. perfringens type A from intestinal contents, in the absence of other enteric pathogens, is the most reliable criterion on which to base a diagnosis. Recently, beta2 (CPB2) toxin-producing C. perfringens type A has been linked to disease in piglets and other animals. However, implication of CPB2 in pathogenesis of porcine infections is based principally on isolation of C. perfringens carrying cpb2, the gene encoding CPB2, and the specific role of CPB2 in enteric disease of pigs remains to be fully defined. Clostridium difficile can also be a normal inhabitant of the intestine of healthy pigs, and diagnosis of enteric infection with this microorganism is based on detection of its toxins in feces or intestinal contents.

scholarly journals Fracture of the coronoid and pterygoid processes by firearms: case report

2007 ◽  
Vol 18 (2) ◽  
pp. 168-170 ◽  
Author(s):  
David Moraes de Oliveira ◽  
Ricardo José de Holanda Vasconcellos ◽  
José Rodrigues Laureano Filho ◽  
Rafael Vago Cypriano
Keyword(s):  
Ct Scan ◽  
Speech Therapy ◽  
Clinical Signs ◽  
Mouth Opening ◽  
Parotid Region ◽  
Comminuted Fracture ◽  
3D Ct Scan ◽  
The Face ◽  
The Right

A rare case of fracture of the coronoid and the pterygoid process caused by firearms is described. A 28-year-old male was hit by a bullet in the face, resulting in restricted mouth opening, difficulty in chewing and pain when opening the mouth. Clinical examination revealed a perforating wound in the right parotid region and a similar wound on the left side of the same region. A CT scan showed comminuted fracture of the left coronoid process and bilateral comminuted fracture of the pterygoid processes. Treatment was conservative, speech therapy was conducted and it was successful. Details of the clinical signs, radiology (3D-CT scan), treatment and follow-up are presented.

scholarly journals Mycobacteriosis in peafowl: Analysis of four cases

2018 ◽  
Vol 74 (1) ◽  
pp. 6001-2018 ◽  
Author(s):  
ALEKSANDRA LEDWOŃ ◽  
EWA AUGUSTYNOWICZ-KOPEĆ ◽  
PAWEŁ PARNIEWSKI ◽  
JOANNA BONECKA ◽  
MAGDALENA OSTRZESZEWICZ ◽  
...  
Keyword(s):  
Mycobacterium Avium ◽  
Clinical Signs ◽  
Mycobacterium Avium Subsp ◽  
Clinical Image ◽  
Mechanical Trauma ◽  
High Similarity ◽  
Young Bird ◽  
Pavo Cristatus ◽  
Lowenstein Jensen ◽  
Mycobacterium Avium Subsp Paratuberculosis

Peafowl (Pavo cristatus), similarly to other Galliformes, are particularly susceptible to infection by Mycobacterium avium. Peafowl differ from other Galliformes in the clinical image of the infection, with dominating respiratory signs. Occurrence of severe and sustained dyspnoea in peafowl raises suspicion of mycobacteriosis, which, however, is not always easy to confirm. In the cases described here, mycobacteria were detected in direct swabs from the trachea of two individuals, and cultures were conducted on the Löwenstein- Jensen medium. In one individual, no mycobacteria were found in tracheal swabs stained by the Ziehl-Neelsen method, despite the presence of clear clinical signs. The fourth case was a young bird submitted for necropsy. The cause of death was a mechanical trauma, but scarce caseous nodules typical of mycobacteriosis were found in the liver, spleen and lungs. The Mycobacterium avium isolates obtained from those cases were compared using (CCG)4-based PCR. A high similarity of three isolates of Mycobacterium avium subsp. avium was observed, two of which were derived from peafowl originating from the same farm, while the isolate from the fourth bird differed significantly and was identified by sequencing as Mycobacterium avium subsp. paratuberculosis..

scholarly journals Increased α-2,8-sialyltransferase 8B (ST8SIA2) expression in schizophrenia superior temporal gyrus

2018 ◽  
Author(s):  
Toni M. Mueller ◽  
Stefani D. Yates ◽  
James H. Meador-Woodruff
Keyword(s):  
Sialic Acid ◽  
Protein Expression ◽  
Superior Temporal Gyrus ◽  
Compensatory Mechanism ◽  
Nucleotide Polymorphisms ◽  
Gene Encoding ◽  
Protein Levels ◽  
Neural Cell Adhesion ◽  
The Face ◽  
The Relationship

AbstractReduced polysialylation of neural cell adhesion molecule (NCAM) in schizophrenia has been suggested to contribute to abnormal neuroplasticity and neurodevelopmental features of this illness. The posttranslational addition of sialic acid is mediated by sialyltransferases, and polysialylation (the addition of ≥ 8 α -2,8-linked sialic acid residues) is catalyzed by three enzymes: ST8SIA2 (also called STX), ST8SIA4 (also called PST), and/or ST8SIA3. ST8SIA2 and ST8SIA4 are the primary mediators of NCAM polysialylation. The gene encoding ST8SIA2 maps to schizophrenia risk locus 15q26, and single nucleotide polymorphisms (SNPs) and SNP haplotypes of the ST8SIA2 gene have been associated with schizophrenia in multiple populations. The current study in elderly schizophrenia (N = 16) and comparison (N = 14) subjects measured the protein expression of NCAM, polysialylated-NCAM (PSANCAM), and three poly-α-2,8-sialyltransferases (ST8SIA2, ST8SIA3, and ST8SIA4) in postmortem superior temporal gyrus. Although expression of NCAM, PSA-NCAM, ST8SIA3, and ST8SIA4 were not different in schizophrenia, increased protein levels of ST8SIA2 were identified. It has been reported that ST8SIA2 mutations associated with increased schizophrenia risk impair PSA-NCAM synthesis, suggesting that increased protein expression of ST8SIA2 may represent a compensatory mechanism in the face of impaired enzyme function. This interpretation is further supported by our finding that the relationship between ST8SIA2 enzyme expression and PSA-NCAM levels are different between schizophrenia and comparison subjects. Together these findings suggest a possible neurodevelopmentally-regulated mechanism which could contribute to abnormal synaptic plasticity evident in schizophrenia.

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