By U. Kan. Ferris State University. 2018.
The American College of Rheumatology 1990 criteria for the classification of hypersensitivity vasculitis buy moduretic 50mg with visa. Long-term safety of treatment with recombinant human granulocyte colony- stimulating factor in patients with severe congenital neutropenias buy generic moduretic 50 mg line. Neurologic disease in Sjogrens syndrome: mononuclear inflammatory vasculopathy affecting the central/peripheral nervous system and muscle generic 50mg moduretic amex. Rheumatoid disease of the central nervous system with meningeal vasculitis presenting with seizure. Central nervous system involvement in systemic lupus erythematosus: a review of neuropathologic findings in 57 cases. Limitations of invasive modalities in the diagnosis of primary angiitis of the central nervous system. Primary (granulomatous) angiitis of the central nervous system: a clinical pathologic analysis of 15 new cases and a review of the literature. A multicenter, randomized, double- blind placebo- controlled trial of adjuvant methotrexate treatment for giant cell arteritis. Low-dose aspirin and prevention of cranial ischemic complica- tions in giant cell arteritis. Use of ultrasonography and positron emission tomography in the diagnosis and assessment of large-vessel vasculitis. Treatment of glucocorticoid-resistant or relapsing Takayasu arteritis with methotrexate. Gastro-intestinal tract involvement in polarteritis nodosa and Churg Straus syndrome. Palmer and Medha Singh Summary Sjgrens syndrome is a chronic autoimmune disorder, most common in adult women. Key Words: Autoimmune disease; dental caries; ocular dryness; Sjgrens syndrome; xerostomia 1. It is most common in middle-aged white women, but can occur in anyone, including children. However, early diagnosis and management are essential to prevent oral, ocular, and internal organ damage. It affects between 1 and 4 million people in the United States (9) and about 500,000 in the United Kingdom (10). However, the true prevalence may be much higher as many researchers believe that about half the cases are undiagnosed (10,11). B-cell hyperreactivity is manifest through hypergammaglobulinemia and circulating autoantibodies. It is believed that these autoantibodies can contribute to tissue dysfunction prior to any evidence of inflammation (16,18). Sufferers primarily report mild to extreme discomfort from dry eyes and/or dry mouth, but may have a variety of other signs and symptoms as well. If not treated properly and early enough, ulcers of the cornea can result, which may lead to blindness. A primary effect is salivary deficiency (known as xerostomia), which leads to dry mouth. Xerostomia can have far-reaching effects on oral health (28) and on diet and nutrition (29). Xerostomia, in turn, leads to a variety of oral problems (discussed later) with nutritional implications. Saliva is an important protective constituent of the oral cavity, and has many functions (Table 2 (23)). Saliva also provides physical and chemical protection to the oral and pharyngeal mucous membranes. Effects of Xerostomia on the Dentition Xerostomia increases the risk of developing dental caries (tooth decay). It occurs when acids are formed from the bacterial fermentation of dietary carbohydrates in the dental plaque coating teeth. The acid causes the tooth enamel demineralization that initiates the caries process (Fig. In the absence of saliva, the oral cavity loses these important protective elements, and the risk of developing dental caries increases significantly. With xerostomia, the soft tissue (gingiva) surrounding the teeth are more susceptible to bacterial infection. If the gingiva recede and newly expose the neck of the tooth, root caries may result (Fig. In the absence of saliva, acids from foods and beverages as well as from bacterial fermentation can cause severe tooth enamel demineralization (Fig. They may develop a burning sensation in the tongue, and develop tongue fissures and cracks at the corner of the mouth. The loss of the immunity provided by saliva may result in increased incidence of candidiasis and other fungal infections (Fig. The loss of the antimicrobial protection of saliva can result in increased bacterial plaque and associated gingival inflammation and recession, and mild to moderate periodontal disease (disease of the soft tissue and bone surrounding and supporting the teeth). Acids are produced on tooth surfaces as an end product of dental plaque bacterial fermentation of simple sugars; 2. Acid erosion due to fruit drinks in a xerostomic patient with Sjogrens syndrome (photo courtesy of Dr. Effects of Xerostomia on Diet and Nutrition In the absence of saliva, it becomes a challenge to chew, swallow, and even taste food (31). Difficulty masticating and lubricating food may make it difficult to eat solid foods. Patients may adapt to a primarily liquid diet that may be low in nutritional value. It is also common that people experiencing dry mouth use items such as hard candies or other slowly dissolving lozenges in an effort to increase salivation. If these items are used frequently and contain sugars, they can be major contributors to increased dental caries incidence. Frequent eating or snacking is a major risk factor for dental caries development that is increased when the oral cleansing effects of saliva are lost. Sufferers may have a dry cough, hoarseness, a decreased sense of smell, and nose bleeds. People may also report having joint or muscle pain (37), low-grade fever, increased fatigue (25), and vasculitis. The new criteria states that a person may be diagnosed as having Sjogrens syndrome if he has at least four of the following six diagnostic tests results (Table 3), including one objective measure (ie, by histopathologic examination or antibody screening) as positive (16,38).
The most distinctive clinical signs are blindness or visual abnormalities buy generic moduretic 50mg, lack of responsiveness to the environment 50mg moduretic mastercard, behavioral change order 50mg moduretic with visa, incoordination or convulsions. The pathological lesions are restricted to the cerebral cortex and characterized by loss of white matter with associated bizarre astrocytosis. The cause is unknown, but epidemiological features suggest exposure to an exogenous agent through diet or medical management (Munson 1999b). Despite abundant spiral bacteria colonization, free-ranging cheetahs have been shown to develop only mild gastritis in few cases, suggesting that a direct cause-effect is unlikely. An altered immune response to a commensal bacteria related to chronic stress is postulated (Munson, 1993, 1999a; Terio et al. In 16 cases amyloidosis was associated with glomerulosclerosis/nephrosclerosis and in 13 cases with gastritis (Munson, 1993, 1999a; Walzer, 2006). The disease was severe in about 40% of the animals older than six years, making it one of the main cause of mortality in adult cheetahs. These lesions are not clinically important, but should be recognized because they have been misdiagnosed as metastatic cancer. The cause is not known, but dietary or stress-induced metabolic changes are suspected. Only mild increase of collagen fbers and reticulin fbers were observed around the central veins and in the sinusoids (Munson, 1993, 1999a; Walzer, 2006). The viral etiology of these cases still need to be confrmed by molecular techniques. PaRa sItIc InFectIon s Massive infestation with Ascarid worms (Toxascaris leonina, Toxocara sp. Two adult cheetahs showed 271 severe parasitic pneumonia at post-mortem (Walzer, 2006). Twenty seven cubs born in fve litters from two normal dams which were sisters (Fanny and Rina) and one unrelated normal male (Fota). Similar lesions are described in a human multisystemic genetic disease known as Menkes disease, related to a defect in the copper transport proteins (Walzer, 2006). It is therefore diffcult to estimate the true prevalence of gastritis, renal failure or amyloidosis as main cause of death. Despite regular and frequent deworming, captive cheetahs tend to have signifcant Ascarid sp. Diseases of captive cheetahs (Acinonyx (Acinonyx jubatus) with and without gastritis. Journal of jubatus): results of the cheetah Research council pathology clinical Microbiology 43, 229-234. Extrinsic factors signifcantly affect patterns of disease in free-ranging and captive cheetah Walzer, C. Por consiguiente, la mortalidad relacionada con el hombre es muy signifcativa; segn el pas y el perodo de estudio, puede variar entre el 54% y el 96. Debido a su comportamiento solitario, el lince boreal tiene muy pocas oportunidades de transmitir patgenos antes del desenlace mortal o la recuperacin de la enfermedad, aunque es posible que una enfermedad de larga duracin o con un perodo prolongado de incubacin pudiese ser la excepcin a esta norma. La ausencia de anticuerpos o antgenos en los estudios de poblacin indica que las poblaciones estudiadas no haban tenido contacto reciente con estos agentes o que posiblemente la especie sea especialmente susceptible a infeccin (porque los ejemplares infectados no sobreviven), o ambos. En comparacin, una alta prevalencia indica que los agentes en cuestin no causan problemas graves de salud en la especie, sobre todo, si no se ha observado una mortalidad relacionada y las poblaciones infectadas estn estables. Por ejemplo, se han documentado prevalencias elevadas en el caso de Toxoplasma, Trichinella y cytauxzoon, que suelen ser apatognicos para el lince. La enfermedad que se diagnostica con mayor frecuencia en el lince boreal en libertad es la sarna sarcptica; no obstante, hasta ahora ni la sarna ni ninguna otra enfermedad parece ser una amenaza para las poblaciones de lince. De todos modos, las prdidas por enfermedad podran tener un impacto si se agravasen por otros problemas graves, como la caza ilegal o el deterioro del hbitat, o ambos. En este contexto, es imprescindible la colaboracin estrecha entre bilogos de campo y veterinarios, tanto en la recopilacin de datos como en su interpretacin. Thus, human-related mortality is of major importance; depending on the country and study period, it varies from 54 to 96. However, the importance of infectious diseases is probably underestimated since mortality studies mostly rely on data from lynx found dead by chance. A wide range of infectious and non-infectious diseases has been reported in Eurasian lynx. As a felid, the lynx is probably susceptible to most diseases affecting domestic cats. Nevertheless, epidemic outbreaks do not seem to occur in free-ranging populations. Because of its solitary behaviour, the Eurasian lynx has only rare opportunities to transmit pathogens before a fatal outcome or recovery from the disease although a disease with long duration and/or incubation period might represent an exception. The absence of detection of antibodies or antigens in population surveys indicate that the investigated populations either did not have any recent contact with these agents, and/or possibly, that the species is highly susceptible to infection (i. In contrast, a high prevalence is an indication that the concerned agents do not cause serious health problems in the species, especially if related mortality has not been observed and infected populations are stable. For example, high prevalences have been documented for Toxoplasma, Trichinella and Cytauxzoon, which are normally apathogenic to lynx. The disease most commonly diagnosed in free-ranging Eurasian lynx is sarcoptic mange, but neither mange nor other diseases do appear as a threat to free-ranging lynx populations so far. Nevertheless, losses due to diseases might have an impact if added to serious problems such as poaching and/or habitat destruction. Furthermore, apparently emerging problems such as congenital malformations and heart lesions in Swiss lynx underline the need for a long-term, careful health monitoring of free-living and captive populations, together with extensive sample collection for immediate or later studies. In this context, close collaboration between feld biologists and veterinarians is essential, both for data collection and interpretation. Information on causes of death and diseases of Eurasian lynx used 277 to be scarce, but interest in health aspects regarding this species clearly increased in the past decade. Health monitoring of Eurasian lynx is mainly performed by means of systematic post-mortem examinations and parasitological investigations of faecal samples. Additional data originate from physical exams of animals caught in the frame of ecological studies, and from screenings of blood samples for selected infectious agents or antibodies (serosurveys). The aims of this review are 1) to give an overview of the actual knowledge on causes T of mortality and diseases in Eurasian lynx, thus providing data on the susceptibility of Eurasian lynx to various infectious agents; 2) to discuss the importance and potential impact of infectious and non-infectious causes of mortality on free-ranging Eurasian lynx populations, and 3) to briefy assess the role of the Eurasian lynx in the epidemiology of infectious diseases. The data from Eurasian lynx can also provide useful baseline information for the planning of epidemiological surveys in Iberian lynx, and for the interpretation of data gathered in this highly endangered species. Legal shooting of Eurasian lynx that cause repeated damages on domestic livestock occasionally occurs (Ryser-Degiorgis et al. Poaching was recorded to cause 46% of the mortality of adult radio-collared lynx in Scandinavia (Andrn et al. It was reported as the most common cause of death in lynx from other countries (Jedrzejewski et al.
This antigenic map can be used to determine whether nat- urally varying amino acid sites likely changed under antibody pressure or by some other process purchase moduretic 50mg online. These alternatives can be tested by site-directed mutagen- esis discount moduretic 50 mg otc, which experimentally changes particular amino acids moduretic 50mg low cost. Athirdexperimental technique simultaneously applies antibodies to twoormoresites (Yewdell et al. This mimics host reactions in which two or more immunodominant sites gen- erate neutralizing antibodies. The frequency of escape mutants to a sin- gle antibody is about 105,sosimultaneous escape against two distinct antibodies occurs at a vanishingly low frequency of 1010. Itappears that host antibodies directed simultaneously to two or more sites can greatly reduce the chance of new escape mutants during the course of asingleinfection. Afourthexperimental method focuses on escape mutants from low- anity, subneutralizing antibodies (Thomas et al. Clearance and protection probably derive from high-anity IgA and IgG antibodies rather than low-anity IgM. This study does, however, call attention totheprocesses by which immunodominance develops within a host. The stronger antigenic sites apparently out- compete weaker sites in attracting high-anity antibodies. Sialic acid occurs as the terminal residue attached to galactose on certain carbohydrate side chains. Two commonlinkagesbetween sialic acid and galactose occur in natural molecules, the (2, 3) and (2, 6) forms. The binding site apparently evolved before the evolution of the dierent subtypes and has been retained during subsequent divergence. The human inuenza A subtypes H1, H2, and H3 derived from avian ancestors (Webster et al. Each human subtype evolved from the matching subtype in aquatic birds, for example, human H1 from avian H1. In all three subtypes, the binding anity of human lineages evolved to favor the (2, 6) linkage (Paulson 1985; Rogers and DSouza 1989; Connoretal. The evolutionary pathways dier for the human subtypes with regard to the amino acid substitutions and changes in binding that eventually led to preference for the (2, 6) form. Human sub- types H2 and H3 have substitutions at positions 226 and 228 relative to avian ancestors. Thus, dierent human lineages have followed dierent pathways of adaptation to receptor binding. Horse serum contains (2, 6)-linked sialic acid, which binds to human strains of inuenza and interferes with the viral life cycle. The horse serum therefore selects strongly foraltered binding to (2, 3)-linked sialic acid (Matrosovich et al. This substitution changed the leucine of human H3 to a glutamine residue, the same residue found in the ancestral avian H3 subtype. This substitution caused the modi- ed virus to avoid (2, 6) binding and interference by horse serum and allowed binding to (2, 3)-bearing receptors as in the ancestral avian type. They began with aduckH3isolate that had glutamine at position 226 and favored bind- ing to (2, 3) sialic acid linkages. This selection process caused replacement of glutamine at position 226 by leucine, which inturnfavoredbindingof(2, 6)-over(2, 3)-linked sialic acid. If selection of avian H1 for a change from (2, 3) to (2, 6) binding causes the same substitutions as occurred in the human H1 lin- eage, then the dierent genetic background of avian H1 compared with H3 would be implicated in shaping the particular amino acid substitu- tions. By contrast, if experimental evolution favors a change at posi- tion 226 as in H3, then the evolution of human H1 receptor binding may have followed a more complex pathway than simple selection for (2, 6)-linked sialic acid. Various steps have been proposed for adaptation of aquatic bird iso- latestohumans. These studies raise the general problem of evolutionary pathways by which pathogens change host receptors. If two or more pathogen func- tions must change simultaneously, then changes in receptor anity may be rare. The need for joint change may cause signicant constraint on amino acid substitutions in receptor binding factors. In an experimen- tal setting, one begins with a particular, dened genotype as the genetic back- ground for further analysis. One then obtains single amino acid substitutions or small numbers of substitutions derived from the original background ge- notype. Substitutions may be obtained by imposing selective pressures such as antibodies in an experimental evolution regime or by imposing site-directed or random mutagenesis. Each of these processes relates tness to dierent kinetic aspects of surface binding. First, changes in cell binding and entry aect the performance of in- tracellular pathogens. In that gure, the substitutions 190 EA, 225 GR, and 228 SGallhavestronger binding anity than the common wild type. The fact that some substitutions raise anity suggests that binding has been adjusted by selection to an intermediate rate. It may be possible to test this idea in various experimental systems by competing viruses with dierent cell binding kinetics. Those in vitro systems allow study of competition between dierent viral genotypes (Robertson et al. It would be interesting to compare the tnesses in vivo between wild type and mutants selected for higher binding anity in vitro. The second role of substitutions arises from binding that interferes with viral tness. High anity may also ag- gregate viruses in localized regions, interfering with infectious spread. Again, it would be interesting to compete variants with dierent ani- ties under various in vitro and in vivo conditions. Receptor binding sites may also be strongly selected to avoid binding molecules similar to the host-cell receptor. For example, the nonim- mune component of horse serum attracts inuenza particles that bind the (2, 6) linkage of sialic acid (Matrosovich et al. Selection fa- vors equine inuenza strains that both bind (2, 3) linkages and avoid (2, 6) linkages. Thus, host uids or host tissues dierent from the primary infection target can cull viruses from circulation.
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