Rotavirus A Associated with Clinical Disease and Hepatic Necrosis in California Pigeons (Columba livia domestica)

2019 ◽  
Vol 63 (4) ◽  
pp. 651 ◽  
Author(s):  
Julia Blakey ◽  
Beate Crossley ◽  
John K. Rosenberger ◽  
Daniel Rejmanek ◽  
Milos Markis ◽  
...  
2021 ◽  
Vol 49 (01) ◽  
pp. 22-27
Author(s):  
Volker Schmidt ◽  
Michael Kümpel ◽  
Kerstin Cramer ◽  
Michael Sieg ◽  
Maxi Harzer ◽  
...  

Abstract Objective Pigeon rotavirus A (RVA) isolates of genotype G18P[17] are causing disease outbreaks and fatalities in pigeon lofts in Australia, Germany, Belgium, Denmark and USA since 2016. Most disease outbreaks have been reported from juvenile pigeons (Columba livia forma domestica). However, reports on RVA-associated disease outbreaks in fancy pigeons in connection with fancy pigeon shows in Germany are rare. Material and methods Overall 18 pigeons (16 fancy pigeons and one racing pigeon from 9 pigeon fanciers, as well as one feral pigeon from a rescue center) were sent in for routine diagnostic necropsy including histopathologic, parasitologic and microbiologic examinations. Molecular biologic examinations for detection of RVA, circovirus, Usutu virus, West Nile virus and Chlamydia psittaci were also carried out on all pigeons. An accompanying questionnaire filled in by the senders was used to generate basic information on the affected pigeon lofts. Results Disease outbreaks in juvenile and adult pigeons were reported 7–14 days after fancy pigeon shows. One fancier who had previously vaccinated his pigeons with an autogenous pigeon RVA vaccine, noted no morbidity and mortality among his pigeons and thus sent in a healthy pigeon for diagnostic purposes. Reported clinical signs in the other pigeons were regurgitation, green slimy diarrhea, anorexia, apathy and death after 24 hours. Hepatic necrosis and detection of pigeon RVA isolates of genotype G18P[17] confirmed disease outbreaks caused by pigeon RVA in all pigeons, except for the vaccinated pigeon. Besides pigeon circovirus, which was detected in 15 of 18 pigeons, all other pathogens were singular findings. Conclusion and clinical relevance In disease outbreaks following fancy pigeon shows in juvenile and adult pigeons diagnostics should include pigeon RVA of genotype G18P[17].


PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0203853 ◽  
Author(s):  
Christina McCowan ◽  
Sandra Crameri ◽  
Ayfer Kocak ◽  
Songhua Shan ◽  
Mark Fegan ◽  
...  

2020 ◽  
Author(s):  
Diederik Strubbe ◽  
Roel Haesendonck ◽  
Elin Verbrugghe ◽  
Luc Lens ◽  
Richard Ducatelle ◽  
...  

AbstractWidespread endemism of host-adapted pathogens poses a heavy burden on animal and human health. Mechanisms underpinning long-term host pathogen co-existence and concurrent costs are poorly understood. We use infections in pigeons with pathogenic, pigeon adapted Salmonella Typhimurium to explain how host and pathogen trade-offs and benefits sustain long-term pathogen endemism. An experimentally infected group of pigeons that was studied for 15 months showed that pathogen persistence decreased host condition and reproductive success, but conferred protection against Salmonella-induced clinical disease. The relevance of these findings was confirmed in nature, where this pathogen was shown to widely occur in feral pigeons (Columba livia), yet without clinical disease. Pathogen transmission and long-term persistence were associated with intermittent faecal shedding, which markedly increased during crop feeding and natural stress periods. Exploiting host specific traits in the presence of protective host population immunity thus facilitates long-term co-existence, be it at a significant reproductive cost.


1995 ◽  
Vol 24 (3) ◽  
pp. 475-483 ◽  
Author(s):  
P. De Herdt ◽  
R. Ducatelle ◽  
Cindy Lepoudre ◽  
G. Charlier ◽  
H. Nauwynck

Author(s):  
W.T. Collins ◽  
Charles C. Capen ◽  
Louis Kasza

The widespread contamination of the environment with PCB, a compound used extensively by industry in hydraulic and heat transfer fluids as well as plasticizers and solvents in adhesives and sealants, has resulted in detectable tissue levels in a large portion of the human population, domestic animals, and wildlife. Intoxication with PCB produces severe hepatic necrosis, degeneration of lymphoid tissues and kidney, skin lesions, decreased reproductive performance, reduced feed efficiency, and decreased weight gain. PCB also has been reported to reduce the binding of thyroid hormone to serum proteins and enhance the peripheral metabolism of thyroxine with increased excretion of thyroxine-glucuronide in the bile (Bastomsky, Endocrinology 95: 1150-1155, 1974).The objectives of this investigation were (1) to investigate the histopathologic, histochemical, and ultrastructural changes in thyroid FC produced by the acute (4 week) and chronic (12 week) administration of low (50 ppm) and high (500 ppm) doses of PCB to rats, (2) to correlate these alterations to changes in serum immunoreactive thyroxine concentration, and (3) to investigate the persistence of the effects of PCB on the thyroid gland.


Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.


Author(s):  
Becky Jackson

Preliminary investigation has indicated similarity in hepatic ultrastructural morphology in nutritional deprivation, and cyanide induced hepatic necrosis. Analysis of hepatic tissue has indicated disruption of intracellular membranes, specifically, reduction in rough endoplasmic reticulum (RER) mitochondrial integrity, and glycogen stores. An increase in smooth endoplasmic reticulum (SER) portion was observed.To further investigate the apparent equivalence of necrotic morphology, ultrastructura1ly, BDF1 mice were subjected to senescence, nutritional deprevation, potassium cyanide (KCN) induced toxemia, and acetaminophen induced toxemia. Controls were utilized to ellucidate non-necrotic hepatocellular normals. U1trastructura1 investigation of controls (Fig. 1) shows densely granular RER, abundant glycogen stores, and morphologically normal mitochondria. Subjects with acetaminophen induced necrosis exhibit reduced normal RER with increased levels of dialated, vesicular RER in apparent conversion to SER (Fig. 2), loss of mitochondrial integrity, and glycogen store reduction. Senescent subjects exhibit a pronounced increase in SER and loss of glycogen store. (Fig. 3). Investigation of the senescent SER at high magnification (Fig. 5) indicates that the SER is arising from degranulating and vesiculating RER.


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