Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sarcocystis canis n. sp. is proposed for the protozoon associated with encephalitis, hepatitis, and generalized coccidiosis in dogs. Only asexual stages are known in macrophages, neurons, dermal, and other cells of the body. The parasite is located free in the host cell cytoplasm without a parasitophorous vacuole; schizonts divide by endopolygeny. Schizonts are 5-25 x 4-20 microns and contain 6-40 merozoites. Merozoites are approximately 5-7 microns x 1 micron and do not contain rhoptries. The parasite is PAS-negative and reacts with Sarcocystis cruzi antiserum but not with Toxoplasma gondii, Neospora caninum, or Caryospora bigenetica antisera in an immunohistochemical test.
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PMID:Sarcocystis canis n. sp. (Apicomplexa: Sarcocystidae), the etiologic agent of generalized coccidiosis in dogs. 190 53

Crocodiles and ostriches are very sensitive to stress, and the ideal conditions for intensive rearing have not yet been established. Consequently, mortality is often directly linked to conditions on the farm. Crocodile and caiman pox, adenoviral hepatitis, mycoplasmosis, chlamydiosis and coccidiosis are crocodile-specific infections with reservoirs in wild populations and adult wild-caught breeding stock. Other important conditions are salmonellosis, non-specific septicaemia, trichinellosis, the nutritional diseases osteomalacia, fat necrosis and gout, as well as winter sores. The only ostrich-specific transmissible disease is libyostrongylosis. Other important conditions are Newcastle disease, avian influenza, fading chick syndrome, tibiotarsal rotation and enteritis. No cases of coccidiosis in ostriches have ever been confirmed.
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PMID:Diseases of farmed crocodiles and ostriches. 1197 14

Disseminated visceral coccidiosis (DVC) caused by Eimeria spp. was recognized as a disease entity in captive sandhill cranes (Grus canadensis) and whooping cranes (Grus americana) in the late 1970s. While most avian species of Eimeria inhabit the intestinal tract of its host, the crane eimerians, Eimeria reichenowi and Eimeria gruis, invade and multiply systemically and complete their development in both digestive and respiratory tracts. In DVC, cranes, especially chicks, may succumb to acute infections resulting in hepatitis, bronchopneumonia, myocarditis, splenitis, and enteritis. Cranes may also develop chronic, subclinical infections characterized by granulomatous nodules in various organs and tissues. This paper reviews the pathology and pathogenicity of natural and experimental DVC in sandhill and whooping cranes. Naturally infected birds appeared clinically normal, but progressive weakness, emaciation, greenish diarrhea, and recumbency before death were observed in birds administered doses > or = 10 x 10(3) sporulated oocysts per os. At necropsy, naturally infected birds had nodules in the mucosa of the oral cavity and the esophagus, and in thoracic and abdominal viscera. Experimentally infected birds necropsied less than 7 days after infection (a.i.) had no gross lesions. Birds examined later had hepatosplenomegaly, liver mottling, lung congestion and consolidation with frothy fluid in airways, and turgid intestinal tracts with hyperemic mucosa. From 28 days a.i., grossly visible granulomatous nodules were seen in the esophagus, heart, liver, cloaca, and eyelids. By light microscopy, the basic host response was a granulomatous inflammation with non-suppurative vasculitis affecting many organs and tissues. With time, multifocal aggregates of mononuclear cells, many laden with asexual coccidial stages, increased in size and number. Widespread merogony resulted in morbidity and death, particularly in birds administered 20 x 10(3) sporulated oocysts. Ultrastructural examination revealed developing asexual coccidian stages in the cytoplasm of large lymphocytes or monocytes within a parasitophorous vacuole, often indenting the nucleus. Oocysts and gametocytes were found in the intestines by 12 days a.i., and in the esophagus, trachea, bronchi, and lung by 14 days a.i., indicating that crane eimerians can complete their life cycle at these sites. Thus, DVC in cranes could be a useful animal model for the study of eimerian extra-intestinal stages and the evaluation of potential systemic anticoccidial drugs.
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PMID:Pathology and pathogenesis of disseminated visceral coccidiosis in cranes. 1522 53

For this retrospective study, infectious bursal disease virus (IBDV) was detected in 134 bursal samples that originated from flocks with conditions such as airsacculitis, tracheitis, pneumonia, septicaemia, inclusion body hepatitis, coccidiosis, and/or a history of production problems without overt clinical symptoms. Samples were from seven Canadian provinces: Ontario, Quebec, Manitoba, British Columbia, Nova Scotia, Alberta, and Newfoundland and Labrador. Viral RNA was identified in bursae with moderate to severe and acute to chronic bursal damage. The ages of the flocks from which samples were collected ranged from 3 to 63 days. Following reverse transcriptase-polymerase chain reaction the nucleotide sequence of the VP2 hypervariable region was determined and compared with sequences available in GenBank. The most common Canadian IBDV field strains were North-American variant viruses. Forty-four viruses were highly related (97.5% to 100.0%) to the US IBDV strain NC171. Moreover, 16 field viruses whose VP2 sequences were 99.2% to 100% identical to the South African 05SA8 IBDV strain appeared closely related to the NC171 group. Delaware E-related field viruses, 98.3% to 100.0% identical to the prototype virus, were identified in 33 samples. Thirty-four Canadian IBDVs showed the highest identity, 94.2% to 98.3%, to US IBDV strain 586. Five samples contained vaccine-related viruses, while two field strains showed the best match to Del A (United States) and IBDV strains SP_04_02 (Spain). Very virulent IBDVs were not detected in Canada.
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PMID:Genotyping of Canadian field strains of infectious bursal disease virus. 1789 69

We give the first published description of the pathology and molecular findings associated with adenovirus infection in lizards in Australia. A central netted dragon (Ctenophorus nuchalis) exhibited severe necrotising hepatitis with abundant intranuclear inclusion bodies within hepatocytes and rarely within intestinal epithelial cells. Polymerase chain reaction (PCR) using pooled tissues yielded an amplicon that shared strong nucleotide identity with an agamid adenovirus (EU914203). PCR on the liver of a bearded dragon (Pogona minor minor) with illthrift, coccidiosis, nematodiasis and hepatic lipidosis yielded an amplicon with strong nucleotide identity to a helodermatid adenovirus (EU914207).
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PMID:Molecular detection of two adenoviruses associated with disease in Australian lizards. 2159 45

This report reviews diseases of 1546 elasmobranchs representing at least 60 species submitted to Northwest ZooPath from 1994 to 2010. Cownose rays (Rhinoptera bonasus) (78), southern rays (Dasyatis americana) (75), dusky smooth-hounds (Mustelus canis) (74), bonnethead sharks (Sphyrna tiburo) (66), and bamboo sharks (Hemiscylliidae) (56) were the most commonly submitted species. Infectious/inflammatory disease was most common (33.5%) followed by nutritional (11.9%, mostly emaciation), traumatic (11.3%), cardiovascular (5.5%, mostly shock), and toxin-associated disease (3.7%). Bacterial infections (518/1546, 15%) included sepsis (136/518, 26%), dermatitis (7%), branchitis (6%), and enteritis (4%). Fungal infections (10/1546, 0.6%) included dermatitis (30%), hepatitis (30%), and branchitis (20%). Viral or suspected viral infections or disease processes (15/1546, 1%) included papillomatosis (47%), herpesvirus (20%), and adenovirus (7%). Parasitic infections (137/1546, 9%) included nematodiasis (36/137, 26%), ciliate infections (23%), trematodiasis (20%), coccidiosis (6%), myxozoanosis (5%), amoebiasis (4%), cestodiasis (1%), and flagellate infections (1%). Inflammation of unknown cause (401/1546, 26%) included enteritis (55/401, 14%), branchitis (9%), encephalitis (9%), and dermatitis (7%). Traumatic diseases (174/1546, 11.3%) included skin trauma (103/174, 60%), stress/maladaptation (9%), and gut trauma (7%). Toxicoses (57/1546, 4%) included toxic gill disease (16/57, 26%), gas bubble disease (19%), fenbendazole (7%), ammonia (7%), chlorine (5%), and chloramine (3%). Species trends included visceral nematodiasis in black-nosed sharks (Carcharhinus acronotus) (55%); sepsis in dusky smooth-hounds (41%), blue-spotted stingrays (36%), southern rays (36%), and wobeggong sharks (Orectolobus spp) (69%); emaciation in bamboo (33%) and bonnethead (32%) sharks and freshwater stingrays (Potamotrygon motoro) (32%); and trauma in bonnethead sharks (30%).
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PMID:A retrospective study of disease in elasmobranchs. 2352 44

Clostridium perfringens is a normal inhabitant of the intestinal tract of chickens as well as a potential pathogen that causes necrotic enteritis and colangio hepatitis. The minimum inhibitory concentration (MIC) of seven different compounds used for therapy, growth promotion or prevention of coccidiosis was determined by agar dilution method for 55 C. perfringens strains isolated from the intestines of broiler chickens. All strains showed high susceptibility to penicillin, avilamycin, monensin and narasin. Only 7.3% of the strains showed an intermediated sensitivity to lincomycin, and 49 (89.1%) were considered susceptible. For tetracycline and bacitracin, 41.8% and 47.3% of strains, respectively, were considered resistant.
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PMID:Antimicrobial susceptibility of Clostridium perfringens strains isolated from broiler chickens. 2403 55

In a large population of animals, it is normal to have some die each day from causes not related to disease, which is often referred to as natural causes. In poultry production, this phenomenon is commonly referred to as daily mortality. In egg-producing chickens, many of the natural causes of death are associated with making an egg. The causes of normal mortality in commercial egg-laying chicken flocks have been described very little to date. A commercial chicken egg farm, housing approximately two million single-comb white leghorn chickens (Gallus gallus domesticus) in 16 egg-producing flocks, was visited on a monthly basis to monitor bird health, body conditioning, skeletal integrity, and causes of daily mortality in an attempt to provide early detection of health abnormalities. A representative sample of daily mortality from each flock was necropsied to determine the cause of death. Reported herein is a summary of visits for a period of 38 mo from June 2011 to July 2014. The top 15 causes of normal mortality, in rank order of prevalence, were determined to be the following: egg yolk peritonitis, hypocalcemia, gout, self-induced molt, salpingitis, caught by spur, intussusception or volvulus (twisted intestine), cannibalism (pick out), tracheal plug, septicemia, fatty liver syndrome, internal layer, layer hepatitis, persecution, and prolapsed vent. Other causes noted were hyperthermia (during summer), trauma, coccidiosis, ovarian neoplasia, being egg bound, urolithiasis, peritonitis (not egg yolk induced), leg fracture, caught in the structure, tumor (other than ovarian origin), wing fracture, exsanguination, and cardiomyopathy.
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PMID:Causes of Normal Mortality in Commercial Egg-Laying Chickens. 2895 10