[Preliminary note on the phlebotomus of the Bamako-Mali region. Presence of Phlebotomus sergenti, Parrot 1917].
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The Nat Health files. Sick as a parrot.
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State Medicine↗
Index of Suspicion. Case 2. Pseudoparalysis of Parrot caused by congenital syphilis.
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[The taxonomic status of Phlebotomus sergenti Parrot, 1917, vector of Leishmania tropica (Wright, 1903) and Phlebotomus similis Perfiliev, 1963 (Diptera - Psychodidae). Morphologic and morphometric approaches. Biogeographical and epidemiological corollaries].
A morphological and morphometrical study of the closely related taxa Phlebotomus (Paraphlebotomus) sergenti et P. (Paraphlebotomus) similis confirms their specific taxonomic status. Differential characters between these two species are discussed. Males differ by the aspect of the basal process of the coxite which is curved and narrow in the first species whereas straight and thick for the latter. The P. similis process is bigger and tuffer and its style is longer than those of P. sergenti. Females differ by the morphology of the armature of the pharynx and by the number of rings of the spermatheca. Distribution areas of these species are described. P. similis is a North-Eastern Mediterranean species (from Yugoslavia to western Turkey and Azerbaïdjan). P. sergenti is present from Canary Islands (Spain) to India. From these data, the settlement of Paraphlebotomus in the Mediterranean basin may have occurred during the Miocene age. From an Asiatic common ancestor, two migration routes are proposed. One, north of the Paratethys Sea, may be responsible for the isolation of P. similis. The other, south of the Paratethys and Tethys Seas, may have contributed to the individualisation of P. sergenti. The authors consider P. similis as a suspected vector of Leishmania tropica.
Animals↗
Cranial neural crest cell migration in cockatiel Nymphicus hollandicus (Aves: Psittaciformes).
Parrots have developed unique jaw muscles in their evolutionary history. The M. pseudomasseter, which completely covers the lateral side of the jugal bar, is regarded as a jaw muscle unique to parrots. In a previous study, I presented a hypothesis on the relevance of modifications in the regulation of cranial neural crest cell (NCC) development to the generation of this novel jaw muscle based on histological analyses (Tokita [2004] J Morphol 259:69-81). In the present study, I investigated distribution and migration patterns of cranial neural crest cells (NCCs) through parrot embryogenesis with immunohistochemical techniques to further understand the role of cranial NCCs in the evolution of the M. pseudomasseter, and to provide new information on the relative plasticity in cranial NCC migration at early stages of avian development. The basic nature of cranial NCC development was mostly conserved between chick and parrot. In both, cranial NCCs migrated from the dorsal tip of the neural tube in a ventral direction. Three major populations were identified in their cranial NCCs. Migration pathways of these cells were almost identical between chick and parrot. The principal difference was seen in the relative timing of cranial NCC migration. In the parrot, cranial NCC migration into the first pharyngeal arch was more advanced than in the chick at early stages of development. Such a temporal shift in cranial NCC migration might influence architectural patterning of parrot jaw muscles that generates new muscle like M. pseudomasseter.
Animals↗
Pharmacokinetics of ceftiofur sodium in exotic and domestic avian species.
The pharmacokinetics of ceftiofur sodium were determined in domestic chicks, turkey poults, adult cockatiels (Nymphicus hollandicus), and adult orange-winged Amazon parrots (Amazona amazonica) after subcutaneous (chicks and turkey poults and intramuscular (i.m.) dosing (cockatiels and Amazon parrots). Turkey poult data were best fit to a single exponential model with disappearance half-lives (t1/2) of 8.6, 7.4 and 5.6 h after doses of 0.12, 0.24 and 0.48 mg ceftiofur free acid equivalents (CFAE)/poult, respectively. Data from chicks were best fit to a biexponential model with primary and secondary half-lives of 2.2 and 7.5, 3.7 and 6.8, and 3.8 and 5.3 h after doses of 0.04, 0.08 and 0.16 mg CFAE/chick, respectively. Cockatiel and Amazon parrot data were best fit to a biexponential model with primary and secondary half-lives of 0.28 and 2.5, and 0.93 and 7.9 h, respectively, after doses of 10 mg CFAE/kg body weight. The maximum concentration (Cmax) and area under the concentration time curve (AUC) in chicks and poults were dose-proportional. The Cmax for cockatiels was 5.2 micrograms/mL and for Amazon parrots was 11 micrograms/mL. Clearance in cockatiels and Amazon parrots were 11.3 and 3.8 mL/min/kg, respectively, and reflected the much greater AUC seen in Amazon parrots. Clearance values of ceftiofur were similar in chicks and Amazon parrots, slightly greater in turkey poults and greatest in cockatiels. These results indicate that pharmacokinetic differences must be considered when establishing dosage regimens for different avian species.
Animals↗
Flow cytometric analysis of nuclear DNA for sex identification in three psittacine species.
OBJECTIVE: To evaluate flow cytometric analysis for sex identification in 3 psittacine species, establish reference values for blood cell DNA content for each species, and determine effects of sample storage on DNA content. ANIMALS: 36 orange-winged Amazon parrots, 41 budgerigars, and 39 cockatiels. PROCEDURE: Blood samples were stained and analyzed by use of flow cytometry to measure cellular DNA content. Samples were analyzed immediately after collection and after being stored at 4 C for 48 and 72 hours. RESULTS: Mean DNA content (picograms per cell) was 3.248 for Amazon parrots, 2.702 for budgerigars, and 2.946 for cockatiels; DNA concentrations in samples analyzed immediately overlapped in a male and a female Amazon parrot and among 19 cockatiels. For budgerigars, DNA overlap between sexes was not detected in samples analyzed immediately or after storage for 72 hours. Sex was identified correctly in 94.4% of Amazon parrots, 100% of budgerigars, and 51.3% of cockatiels. For both sexes, DNA content in samples analyzed immediately was significantly different from that of stored samples. CONCLUSIONS AND CLINICAL RELEVANCE: Flow cytometric analysis was accurate for sex identification of Amazon parrots and budgerigars. Sample storage at 4 C for 48 or 72 hours caused variability in DNA content.
Animals↗
Antibody response to and maternal immunity from an experimental psittacine beak and feather disease vaccine.
Adult umbrella cockatoos, Moluccan cockatoos, African grey parrots, and a yellow-headed Amazon parrot were inoculated IM or SC with beta-propiolactone-treated psittacine beak and feather disease (PBFD) virus. Thirty- to 45-day-old African grey parrot, umbrella cockatoo, and sulphur-crested cockatoo chicks also were vaccinated with the same inoculum. The hemagglutination inhibition (HI) and agar-gel diffusion tests were used to assay for post-vaccination development of anti-PBFD virus antibodies. All adult vaccinates seroconverted and had increases in HI and precipitating antibodies. The vaccinated chicks had increased concentrations of HI antibodies, but precipitating antibodies could not be detected. To demonstrate that chicks from vaccinated hens are protected from PBFD virus challenge, 3 African grey parrot chicks and 2 umbrella cockatoo chicks from vaccinated hens and 1 African grey parrot chick and 1 umbrella cockatoo chick from nonvaccinated hens were exposed to purified PBFD virus. Chicks from the vaccinated hens remained clinically normal during the 50-day test period. Chicks from the nonvaccinated hens developed clinical and histologic lesions of PBFD. Infected tissues from these birds were confirmed to contain viral antigen, using immunohistochemical staining techniques. The PBFD virus was recovered from the affected birds. These findings indicate that adult and 30- to 45-day-old psittacine birds will seroconvert following vaccination with beta-propiolactone-treated PBFD virus. Also, hens inoculated with beta-propiolactone-treated PBFD virus produce chicks that are, at least temporarily, resistant to virus challenge.
Animals↗
Salmonella enteritidis infection in two species of psittaciformes.
In 1990, Salmonella enteritidis phage type 4 was recovered from two young (less than 20-week-old) lilac-crowned Amazon parrots (Amazona finschi Schlater), one in Tennessee and one in Kansas. The parrot from Tennessee was treated for a plugged naris and anorexia before the S. enteritidis infection was discovered. The parrot from Kansas exhibited signs of septicemia and died within 24 hours of examination. An apparently healthy green-cheeked conure (Pyrrhura molinae) on the same premises as the parrot from Tennessee was positive for S. enteritidis phage type 4 on a cloacal swab. These are the first reported cases of avian infection with S. enteritidis phage type 4 in the United States. Because several infectious agents were present simultaneously in the Amazon parrots, it was difficult to determine the precise role of S. enteritidis phage type 4 in the clinical presentations.
Animals↗
[Nutrition-related problems in pet birds].
The detection and correction of dietary errors plays an important role in avian medicine. Examples of diseases caused in part by a deficiency or abundance of a nutrient include hypovitaminosis A in birds of the parrot (Psittacidae) family, hypocalcemia in the African grey parrot, goitre in budgerigars, and iron storage diseases in the minah and toucan. Hypovitaminosis A can lead to metaplasia of mucous membranes, which in turn can lead to chronic rhinitis and respiratory fungal infections. Vitamin A deficiency is caused by feeding a seed based diet. Seed mixtures are often deficient in calcium, and nutritional secondary hyperparathyroidism can develop if an additional source of calcium, in the form of ground shells, is not provided. Tetanic symptoms as a result of hypocalcemia are only seen in the African grey parrot and the timneh parrot. Over supplementation of vitamin D gives rise to poisoning with polyuria and polydipsia as common initial symptoms. The exact cause of iron storage diseases in toucans and minahs is not known. A diet low in iron and vitamin C is advised as therapy. Goitre can develop in budgerigars as a result of iodine-deficient drinking water and provision of a seed mixture based on millet. An unbalanced or multideficient diet can give rise to reproductive disorders, abnormal feathers, or infections as a result of diminished resistance. It is usually not possible to relate the cause of these diseases in a simple way to the composition of the diet. Obesity, which occurs in the galah, Amazon parrot, and budgerigars, can lead to fatty liver and lipoma. A gradual reduction in weight, by means of calorie restriction, is recommended. Commercially available nutritionally balanced bird food is often effective.
Animal Feed↗
Lesions in the budgerigar vocal control nucleus NLc affect production, but not memory, of english words and natural vocalizations.
This study investigates the role of the psittacid (parrot) central nucleus of the lateral neostriatum (NLc) in the production of learned English and natural vocalizations. Anatomic data have led researchers to define NLc alternately as the parrot homologue (Paton et al. [1981] J Neurosci. 11:1279-1288) or analogue (Striedter [1994] J Comp Neurol. 343:35-56) of the songbird high vocal center. Although numerous functional and electrophysiological studies have identified the role of various songbird vocal control nuclei, few similar functional studies have been performed in parrots, particularly with respect to NLc. In this study, both novel behavioral techniques and precise neurochemical lesions have been used to investigate the role of NLc in the production of learned vocalizations. The results suggest that NLc is involved in the production of, but not memory for, learned English and natural vocalizations. Specifically, NLc lesions disrupted the amplitude of amplitude-modulated vocalizations, but did not affect the frequency of the dominant or carrier signal of these vocalizations. These data provide some of the first evidence for the functional role of a parrot vocal control nucleus.
Animals↗
Zoonotic diseases in psittacine birds: apparent increased occurrence of chlamydiosis (psittacosis), salmonellosis, and giardiasis.
Between September 1977 and November 1978, chlamydiosis (psittacoisis) was diagnosed in 52 of 128 parrots, 5 of 12 cockatiels, 2 of 5 cockatoos, 3 of 6 macaws, 1 of 22 conures, 2 of 18 lovebirds, and 6 of 76 parakeets; 2 lories and 1 lorikeet were chlamydiosis negative. Two cases of human chlamydiosis were associated with two submissions of parrots subsequently found to have active infection. Twenty parrots (including 13 that were chlamydiosis positive), 2 cockatiels, 1 macaw, 1 lorie, and 1 parakeet yielded salmonella organisms, of which 16 were identified as Salmonella typhimurium, 8 as untypeable monophasic salmonellae of serogroup B, and 1 as S arizonae. Three S typhimurium from parrots that had been treated with chlortetracycline for chlamydiosis were resistant to tetracyclines, streptomycin, and sulfonamides; another isolate was found to be resistant to chloramphenicol only. Severe giardiasis was diagnosed in parakeets originating from six aviaries.
Animals↗
Interactions between viscerotropic velogenic Newcastle diseases virus and pet birds of six species. I. Clinical and serologic responses, and viral excretion.
Clinical and serologic responses to a psittacine isolate of viscerotropic velogenic Newcastle disease virus (VVNDV) were evaluated in pet birds of six species: budgerigar, yellow-headed Amazon parrot, halfmoon conure, lesser hill mynah, black-headed nun, canary. The clinical response was most marked in the budgerigars, parrots, and conures, and only minimal in the nuns. Between post-exposure days (PED) 3 and 5 some birds developed ruffled plumage, conjunctivitis, and central nervous system dysfunction: ataxia, wing tremors, paralysis of the extremities, and tremors of the head accompanied by nodding and jerking. Mortality by PED 203 was 55% (29/52) in the halfmoon conures, 22% (23/105) in budgerigars, 29% (12/42) in parrots, and 21% (15/71) in nuns. The only clinical signs in canaries and mynahs were progressive death losses, respectively 25% (33/132) and 21% (10/48). The visceral lesions common in chickens with VVNDV were not observed in these six species. Canaries rapidly eliminated Newcastle disease virus (NDV), whereas it was detected for protracted periods in the oral and cloacal secretions of the other five species (for more than a year in parrots). Serologic evaluation by the hemagglutination-inhibition and neutralization tests also indicated prolonged NDV infections in 5 of the 6 species. The seroconversion rate observed in canaries was minimal (13%).
Animals↗
Psittacine tuberculosis.
Two cases of tuberculosis in psittacine birds were reported and the literature reviewed. One case was in a parakeet and this species was reported to be resistant to mycobacterial infection. No other case of parakeet tuberculosis was found in the literature. The other case was in a parrot. Historically, tuberculosis in parrots was common in European aviary collections, but case reports in the United States were few. The disease in parrots is of zoonotic interest, as they are unique among birds in being susceptible to mammalian strains of mycobacteria. The tuberculomatous aspect of the intestinal lesion in the parrot case described was unusual.
Animals↗
The vocal control pathways in budgerigars differ from those in songbirds.
Previous studies concluded that parrots and oscine songbirds, two taxa that have independently evolved the ability to learn vocalizations, possess similar neural circuits for vocal control. These investigations suggested, however, that the vocal control systems of parrots and songbirds may also differ in several respects. Most importantly, auditory inputs to the vocal control system derive from Field L in songbirds, but this area does not appear to project to the vocal control system in parrots. The principal aims in the present study were, therefore, to determine 1) exactly how similar the vocal control system in budgerigars is to that in songbirds and 2) whether the vocal control system in budgerigars receives auditory inputs from areas other than Field L. Biotinylated and fluorescently labeled dextrans were injected into five telencephalic nuclei of the vocal control system in budgerigars and into the physiologically identified auditory portions of the frontal neostriatum and nucleus basalis. The results indicate that the forebrain vocal control system in budgerigars is only superficially similar to that in songbirds. Many of the vocal control nuclei differ between the two taxa in both cytoarchitecture and connections. The nuclei in budgerigars that are comparable to those of the accessory loop of the vocal control system in songbirds, for example, do not form an accessory loop in budgerigars. The vocal control systems in the two taxa differ most significantly in the source of their auditory inputs. In songbirds, auditory information is conveyed to the vocal control system via Field L, whereas, in budgerigars, the auditory inputs to the vocal control system derive from nucleus basalis and the frontal neostriatum. A phylogenetic analysis suggests that the midbrain and medullary vocal control pathways are homologous across all birds, but that most of the vocal control circuits in the forebrain have probably evolved independently in parrots and songbirds.
Animals↗
Avian polyomavirus infection and disease in a green aracaris (Pteroglossus viridis).
Avian polyomavirus (APV) is one of the most significant pathogens of domestically raised psittacine birds (parrots). One or more APVs are suspected to infect nonpsittacine cage birds, but the relationship of these viruses to the APV infecting parrots remains unclear. In this report, for the first time, we fully document an APV infection in a nonpsittacine cage bird, a green aracaris (Pteroglossus viridis). Grossly, this bird evidenced generalized hemorrhage. Histologically, there was severe hepatic necrosis, splenic necrosis, and the presence of lightly basophilic to clear pannuclear inclusion bodies and karyomegaly in splenocytes and renal mesangeal cells, all characteristic lesions of APV infection in parrots. APV DNA was amplified directly from the liver by polymerase chain reaction and sequenced. The virus differed from the original APV sequence by only 24 base pairs (0.48% of the genome), demonstrating that it is a variant of the APV. A serologic survey of the remaining birds in the aviary demonstrated anti-APV antibody in two cockatoos, two cockatiels, a laughing kookaburra, a Lady Ross turaco, and five zebra finches. The remaining green aracaris was seronegative. The sequence and serologic data suggest that the APV that infected the green aracaris originated in a parrot and was capable of infecting birds from at least four orders.
Animals↗
Differential expression of glutamate receptors in avian neural pathways for learned vocalization.
Learned vocalization, the substrate for human language, is a rare trait. It is found in three distantly related groups of birds-parrots, hummingbirds, and songbirds. These three groups contain cerebral vocal nuclei for learned vocalization not found in their more closely related vocal nonlearning relatives. Here, we cloned 21 receptor subunits/subtypes of all four glutamate receptor families (AMPA, kainate, NMDA, and metabotropic) and examined their expression in vocal nuclei of songbirds. We also examined expression of a subset of these receptors in vocal nuclei of hummingbirds and parrots, as well as in the brains of dove species as examples of close vocal nonlearning relatives. Among the 21 subunits/subtypes, 19 showed higher and/or lower prominent differential expression in songbird vocal nuclei relative to the surrounding brain subdivisions in which the vocal nuclei are located. This included relatively lower levels of all four AMPA subunits in lMAN, strikingly higher levels of the kainite subunit GluR5 in the robust nucleus of the arcopallium (RA), higher and lower levels respectively of the NMDA subunits NR2A and NR2B in most vocal nuclei and lower levels of the metabotropic group I subtypes (mGluR1 and -5) in most vocal nuclei and the group II subtype (mGluR2), showing a unique expression pattern of very low levels in RA and very high levels in HVC. The splice variants of AMPA subunits showed further differential expression in vocal nuclei. Some of the receptor subunits/subtypes also showed differential expression in hummingbird and parrot vocal nuclei. The magnitude of differential expression in vocal nuclei of all three vocal learners was unique compared with the smaller magnitude of differences found for nonvocal areas of vocal learners and vocal nonlearners. Our results suggest that evolution of vocal learning was accompanied by differential expression of a conserved gene family for synaptic transmission and plasticity in vocal nuclei. They also suggest that neural activity and signal transduction in vocal nuclei of vocal learners will be different relative to the surrounding brain areas.
Alternative Splicing↗