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Emerging and Re-emerging Diseases of Selected Avian Species

Pilny, Anthony A., Reavill, Drury

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Veterinary Clinics of North America: Exotic Animal Practice

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10.1016/j.cvex.2020.01.013

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Emerging and Re-emerging D i s e a s e s o f S e l e c t e d Avi a n S p ec ie s Anthony A. Pilny, DVM, DABVP (Avian Practice)a,*, Drury Reavill, DVM, DABVP (Avian and Reptile/Amphibian Practice), DACVPb KEYWORDS  Emerging disease  Re-emerging disease  Avian  Infection  Welfare KEY POINTS  The identification of emerging and re-emerging diseases of birds relates not only to scientific discovery, research, and species survival—but holds significant human health implications also.  Emerging infections can be caused by numerous factors, including previously unknown infectious agents, previously known agents whose role in specific diseases has been unrecognized, and re-emergence of agents whose incidence of disease had declined or disappeared in the past and whose incidence has reappeared.  Emerging and re-emerging diseases can have impacts on avian welfare, livestock production, and entire ecosystem health, and their recognition is of critical importance.  INTRODUCTION  The identification and significance of emerging and re-emerging diseases of birds relates not only to scientific discovery and research, but holds significant human health implications also. Two examples are bromethalin rodenticide toxicosis in wild birds living in urban areas and the worldwide disease of cercarial dermatitis (swimmer's itch). Diseases may be zoonotic or have farm production implications, present as large die-offs, and can affect zoo collections. Often, identification comes after large losses are seen and some require elimination of hosts, such as infection with exotic Newcastle disease in the poultry industry. Others can affect wild populations and affect smaller ecosystems when large die-offs are seen. Also, bird migration provides a mechanism for the establishment of new endemic disease at distances from where an infection was initially acquired. Emerging diseases can be caused by numerous factors, including previously undetected or unknown infectious agents, known agents that have spread to new a  Arizona Exotic Anim; al Hospital, 20040 N 19th Avenue Suite C, Phoenix, AZ 85027, USA; ZNLabs, 525 E 4500 South Suite F200, Salt Lake City, UT 84107, USA * Corresponding author. E-mail address: apilny@azeah.com b  Vet Clin Exot Anim 23 (2020) 429–441 https://doi.org/10.1016/j.cvex.2020.01.013 1094-9194/20/ª 2020 Elsevier Inc. All rights reserved.  vetexotic.theclinics.com  430  Pilny & Reavill  geographic locations or populations, and previously known agents whose role in specific diseases had previously been unrecognized. Agents whose incidence of disease had declined or disappeared in the past, but whose incidence has reappeared are known as re-emerging infectious diseases. The identification and our understanding of these diseases remains critical. This article summarizes selected emerging and re-emerging diseases of selected avian species and complements other avian articles in this issue. Many more diseases exist than the scope of this article allows, and many more currently remain undiscovered. Bromethalin Toxicity  Bromethalin is an odorless lipid soluble chemical, used as a rodenticide since the 1980s and designed to kill with a single ingestion. It is rapidly absorbed from the digestive tract and once demethylated to its more potent metabolite, desmethylbromethalin it readily crosses the blood-brain barrier. It acts by uncoupling oxidative phosphorylation resulting in decreased adenosine triphosphate (ATP).1,2 A decline in ATP leads to intracellular accumulation of sodium and an influx of water (cytotoxic edema) and splitting of myelin sheaths (intramyelinic edema).2–5 The salient histologic feature is of vacuolar degeneration primarily of cerebellar white matter (Fig. 1). There is no specific antidote for the toxin. Susceptibility to bromethalin varies by species, with domestic cats (Felis catus domestica) being particularly susceptible, whereas guinea pigs (Cavia porcellus) are considered resistant. In 1 tested avian species, adult Quail (Coturnix coturnix), the medium oral lethal dose is similar to domestic mice and domestic dogs. Acute toxicosis in domestic dogs and cats present with hyperexcitability, seizures, diffuse fine tremors, pelvic limb ataxia and weakness, anisocoria, blindness, abnormal nystagmus, coma, and death from respiratory arrest.2–5 Seizures tend to occur in the later stages of intoxication and are more commonly seen in cats than dogs. Chronic toxicosis appears similar to acute with a delay in the development of the clinical signs. It is possible that these domestic species could survive with subacute or chronic exposure.3,5  Fig. 1. Conure (Aratinga species). The prominent and consistent lesion of bromethalin toxicosis is of cerebellar white matter vacuolization (asterisk) with increased cellularity due to gliosis (hematoxylin-eosin stain). (Courtesy of D. R. Reavill, DVM, DABVP (Avian and Reptile & Amphibian Practice), DACVP, Salt Lake City, UT.)  Re-emerging Diseases of Selected Avian Species  The public noticed birds with neurologic clinical signs in a feral conure population in San Francisco monitored since the 1990s. In 2003, these birds were brought to Mickaboo Companion Bird Rescue, which arranged for veterinary care at area hospitals. A concerted effort was made in 2013 to determine a cause for the symptoms in these birds with chronic neurologic signs that seldom resolved even with aggressive supportive care. Based on clinical signs, histologic lesions in the brain, and positive tests for desmethyl-bromethalin in the feces, and brain and liver tissues, it has been determined that these birds were suffering chronic bromethalin toxicity. A definitive source has not been identified.6 The birds develop paresis, circling, ataxia, and seizures that are progressive until they are unable to feed themselves. The differential diagnosis based on the clinical signs includes aberrant migration of Baylisascaris, protozoal infections, such as sarcocystis, and less likely toxoplasma, paramyxoviruses, West Nile virus, avian bornavirus, lead toxicity, and trauma.6 Positive testing for bromethalin was found in all examined birds. There has been at least 1 incidence where bromethalin toxicity was suspected in bald eagles (Haliaeetus leucocephalus) and American coots (Fulica americana). The eagles were observed overflying perches or colliding with rock walls. Limb paresis and incoordination were observed in American coots. Increased mortality occurred over 2 winters in Arkansas. The consistent histologic finding was of the spongy degeneration of the white matter of the central nervous system.7 Antemortem testing is possible by bromethalin quantification in fecal samples in acute cases. Postmortem testing requires frozen tissue samples of brain and liver and seems to be diagnostic in chronic cases. Treatment of bromethalin toxicity is based on decontamination (emesis and activated charcoal) if possible, control of central nervous system signs, and supportive care. Virulent Newcastle Disease  Virulent Newcastle disease is one of the most serious reportable poultry diseases worldwide.8 Until this re-emergence, the US poultry industry was considered disease-free since the last outbreak in 2002 to 2003, the only exception being some species of wild birds implicated as reservoirs. Formerly known as exotic Newcastle disease, this is a contagious and fatal viral disease affecting the respiratory, nervous, and digestive systems of birds. The disease is so virulent that many birds die without showing any clinical signs. A death rate of almost 100% can occur in unvaccinated poultry flocks; moreover, it can infect and cause death even in vaccinated poultry. Virulent Newcastle disease spreads when healthy birds come in direct contact with bodily fluids from sick birds. In addition, the virus can travel on manure, egg flats, crates, other farming materials or equipment, and people who have picked up the virus on their hands or clothing. It has been shown to replicate in the reproductive tract of adult hens.9 Clinical signs in chickens include:  Sudden death and increased death loss in flocks  Respiratory symptoms, including sneezing, gasping for air, nasal discharge, and coughing  Greenish, watery diarrhea, lethargy, tremors, and drooped wings  Torticollis, circling, complete stiffness, and swelling around the eyes and neck Understanding the potential risks of transmission of chicken- and wild bird-origin virulent Newcastle disease in poultry is critical in outbreak response and control. Inadequate biosecurity measures poses a risk to the poultry industry of a Newcastle disease-free country, with the possibility of transmission due to contacts at the  431  432  Pilny & Reavill  wildlife-poultry interface.10 Suspected cases should be tested or verified with necropsy and reported to the respective state veterinarian or the United States Department of Agriculture (USDA). As of October 2019 the USDA has confirmed 451 premises as infected in California and 1 premises each in Utah and Arizona. This disease is not a food safety concern but more so of biosecurity for the poultry industry. Sarcocystis calchasi  The apicomplexan parasite Sarcocystis calchasi has been identified as the causative agent of pigeon protozoal encephalitis (PPE), an emerging, severe neurologic disease in domestic pigeons (Columba livia f. domestica).11,12 Pigeons serve as intermediate hosts in the lifecycle of S calchasi, and the European subspecies of the Northern goshawk (Accipiter g. gentilis) and the European sparrowhawk (Accipiter nisus) have so far been identified as definitive hosts.13 Also, several psittacine species, including princess parrots and cockatoos, have been reported as susceptible intermediate host species to natural infections.14 Clinical signs and pathologic lesions in these psittacines closely resemble PPE and include central nervous system signs of torticollis, nystagmus, ataxia, inability to stand, and star-gazing. Experimental infection in cockatiels showed development of disease similar to PPE also, and suggests possible ongoing dissemination of the parasite.15 Pigeons infected with S calchasi show a biphasic disease initially with polyuria, diarrhea, and lethargy. In the later periods of infection, central nervous signs, such as torticollis and opisthotonos associated with severe brain lesions, have been observed. Mature tissue cysts can be observed in skeletal muscles in the postinfection stage and the encephalitis is associated with the schizont stage of the parasite's development (Fig. 2). A recent report described acute death in 4 Roller pigeons naturally infected at a zoo that had schizonts and free merozoites in the liver and spleen without lesions or protozoa in the brain and muscles.16 Histologic and molecular characterization of this disease are described in white winged and Eurasian collared doves.17 All these reports suggest the disease has been found in wide-ranging areas and it is likely the parasite has been present for some time and only recently described and recognized. Baylisascaris procyonis  The nematodes of Baylisascaris species are well recognized as causes of cerebrospinal nematodiasis of North American animals. Baylisascaris procyonis is the most common cause of visceral, ocular larva migrans (OLM), and neural larva migrans (NLM),  Fig. 2. An intramyocytic thin-walled sarcocyst filled with numerous bradyzoites in skeletal muscle of a dove.  Re-emerging Diseases of Selected Avian Species  using the raccoon (Procyon lotor) as the primary host. There are 2 other Baylisascaris species that have been infrequently incriminated; Baylisascaris columnaris that cycles through skunks, and B melis of badgers. These nematode parasites have less tendency to result in OLM and NLM.18 Over 130 species of mammals and birds, as well as man, can serve as paratenic hosts.18,19 This indicates that the parasite is highly nonspecific for paratenic hosts. Larva migrans from B procyonis has also been reported in Europe and Japan where raccoons have been imported as part of zoo collections and/or have become part of the wildlife fauna.20 These large ascarid nematodes mature in the intestines of the host. Infected raccoons can shed millions of parasitic eggs per day. These will typically accumulate within communal defecation sites, which are described as latrines. The shed eggs from the primary host can survive for extended periods within the environment as well as within contaminated cages and enclosures. Birds and small mammals serve as paratenic (transport) hosts. They are infected when they ingest the eggs from contaminated environments. These eggs hatch and larval nematodes will aggressively migrate through the tissues of the paratenic hosts, commonly resulting in neurologic damage. It takes very few migrating larvae to result in a fatal central nervous system disease.20 The life cycle is completed when raccoons eat infected animals with the larvae either within the central nervous system or encapsulated in visceral tissues.18 In avian species, there have been many outbreaks within ranching situations, such as with pheasants, emus, ostriches, bobwhites, and chucker partridges.21–24 A variety of zoo birds have also succumbed to NLM when coming in contact with raccoon latrines.25 Some pet bird species have been exposed by contact to contaminated environment and/or transport containers. These have included cockatoos, macaws, Patagonian conures, and cockatiels.26,27 The clinical signs are typical for central nervous system infections: loss of equilibrium, increasing ataxia, circling, torticollis, head tilts, visual defects, and being unable to stand or walk. There may be grossly noticeable malacia and hemorrhage in the brains, although absent to minimal lesions are more common. Histologically there will be a nonsuppurative inflammatory reaction with gliosis and perivascular proliferations of lymphocytes and plasma cells. In some cases, the migration tracks can be identified. Although this is a large nematode larva, these can be very difficult to identify within sections of the brain (Fig. 3). In histologic sections, the third-stage larvae of Baylisascaris species are all similar, so species determination in cases is near impossible without epidemiologic study27–29 or molecular diagnostics. In general, it is very uncommon to see visceral lesions of the larval migrations in birds. It has been suspected in some cases where there have been granulomas identified in the heart, liver, and kidney.19,26 Experimentally in chickens extraneural lesions were limited to focal choroiditis and a larval granuloma in an extrinsic ocular muscle.30 If there are identified cases of Baylisascaris encephalitis, it is important to clean the environment. This includes identifying where there are raccoon latrines. Removal of contaminated soil or contaminated bedding material is necessary. It is also important that any cages that have housed raccoons as well as skunks and badgers should be thoroughly and fastidiously cleaned to remove any fecal material that may be supporting the nematode eggs. Schistosomes  Schistosomes belong to a large family of trematodes that use snails as the intermediate host and are found worldwide. The definitive hosts include many avian species as well as mammalian species. Some schistosomes will infect both avian and mammalian species and others are more restricted. For example, the genus Allobilharzia has been  433  434  Pilny & Reavill  Fig. 3. Scarlet macaw (Ara macao) cerebellum with a cross-section through a Baylisascaris species. This parasite is within the white matter and is supporting bilateral alae, a thin eosinophilic cuticle, and a pseudocoelomic body cavity lined by a low musculature (hematoxylin-eosin stain). (Courtesy of D. R. Reavill, DVM, DABVP (Avian and Reptile & Amphibian Practice), DACVP, Salt Lake City, UT.)  isolated only from swans31 and Anserobilharzia isolated only from geese. Avian schistosomes have been described in at least 10 orders of birds, most commonly Charadriiformes (gulls, terns, plovers) and Anseriformes (swans, geese, and ducks). Gigantobilharzia huronensis is most commonly found in passerine birds, such as red-winged blackbirds (Agelaius phoeniceus), grackles (Quiscalus spp.), and mourning doves (Zenaida macroura) that frequent freshwater habitats.32 Currently there are 20 avian schistosome species representing at least 8 genera; Allobilharzia, Ornithobilharzia, Austrobilharzia, Macrobilharzia, Trichobilharzia, Dendritobilharzia, Anserobilharzia, and Gigantobilharzia.33 Morphologic classification of schistosomes has proven difficult in both the primary and secondary hosts and further classification may rely on molecular biology and phylogenetic analyses to fully understand their life cycle.34 In humans, cercarial dermatitis is considered an important emerging disease that is driving more research in the biology of these trematodes, particularly Trichobilharzia. Trichobilharzia represents the largest genus within the family Schistosomatidae. Schistosomes are digenetic trematodes with a 2-host life cycle. They colonize many families of snails as first intermediate hosts. Most schistosome species are transmitted by the freshwater pulmonate snail families Physidae, Lymnaeidae, and Planorbidae. The cercarial stage penetrates the epithelial surface of the definitive host (mammalian and avian). They then spend their adult lives primarily within the vasculature of their host. All the members of these blood flukes live as separate males and females within the vascular system of their vertebrate definitive hosts. Most known schistosomes have a fresh water-based life cycle. This is true of all known mammalian schistosomes and most of the avian schistosomes. However, there are genera that have life cycles based in marine environments with marine snail hosts and definitive hosts primarily being Charadriiformes (gulls and terns).35  Re-emerging Diseases of Selected Avian Species  Most of the schistosomes penetrate mucosal and/or epithelial surfaces directly. The parasite may continue to migrate to other tissues, although the precise path is not fully described in many species. Based on their predilection site, Trichobilharzia spp. can be divided in visceral and nasal species.35 Visceral species migrate through the viscera and can be found in mesenteric, renal, cloacal, and portal blood vessels, whereas nasal species also may display a neurotropic mode of migration.35 With nasal schistosomes, the migration can involve blood vessels or peripheral nerves leading to the spinal cord and brain of the host. Once they reach the preadult stage in the meninges, they will start to feed on blood and then migrate via an intravascular route back to the nasal cavity. In some duck species, Trichobilharzia live in veins of the nasal mucosa where they mature and produce eggs. The miracidia hatch from the eggs directly in the tissue and leave the host during drinking/feeding by the infected birds.36 For visceral routes, many of the Trichobilharzia species will migrate to the intestinal portal veins where there may be a development of hyperplastic endophlebitis, which is characterized by severe myointimal hyperplasia that often obliterates the vascular lumen. From here, the schistosome eggs will migrate across the intestinal mucosa.31,37–39 Associated lesions in some ducks can include portal fibroplasia in the liver, nonviable schistosomes in the bile ducts, and viable adult schistosomes in the portal veins.40 The main lesions of Trichobilharzia brantae infection in Atlantic Brant geese (Branta bernicla hrota) included thrombosis of the caudal mesenteric veins with adult schistosomes in serosal and mesenteric blood vessels. The eggs in the intestinal wall elicited a fibrinohemorrhagic colitis.41 For parasite life cycles involving the digestive tract, fecal examination can identify the trematode eggs.34 The clinical signs for trematode species migrating to the central nervous system include behavioral changes, disorientation, paralysis, and death in some hosts.42 For species with intestinal vasculature migration, the vascular lesions may contribute to emaciation and death by obstruction of venous return in the intestinal and portal veins.38 The pathogenicity of the infection depends on many factors, such as parasite load, duration of infection, and preferred site of the adult trematode. The host inflammatory reactions are more significant with the immature schistosomes (dermatitis) and the eggs (usually a granulomatous inflammatory reaction).35 An unexpected natural schistosome infection was described in a pet 8-month-old female Nanday conure (Aratinga nenday). She presented for weight loss and blood-flecked diarrhea before death. A fecal examination found eggs (large 83– 134  65–78 mm) containing a miracidium. The smooth shell supported the characteristic small terminal spine or knob. On histologic evaluation, the colon and cloaca had variable epithelial hyperplasia, masses of parasitic eggs, and severe chronic inflammation. Trematode eggs were present in the lungs, liver, and kidney associated with granulomas.43 Treatment of the infection in the final avian host has been studied in an attempt to reduce the parasite load and attempt to control swimmer's itch (cercarial dermatitis). High doses (200 mg/kg IM) of praziquantel reduced the parasite load in common mergansers44 and 1 oral dose of 34 mg/bird was effective in reducing the parasites in mallards.45 Orthoreovirus  Avian orthoreoviruses belong to the family Reoviridae, genus Orthoreovirus. They infect wild and farm-raised birds and are important fowl pathogens associated with various syndromes, such as gastrointestinal malabsorption syndrome, tenosynovitis/arthritis, delayed growth, and sudden death. They have also been isolated from asymptomatic birds.  435  436  Pilny & Reavill  Scientists at the National Wildlife Health Center (NWHC), USGS, Madison, WI, have identified reovirus as the cause of death in American Crows at several locations from east to west across the United States, beginning in 2000. In January and February 2004, American Crows were found dead at the Pittock Conservation Area in Woodstock in southwestern Ontario.46 Hemorrhage and inflammation of the intestines was the most common abnormality noted, and often was accompanied by inflammation and necrosis in the spleen. In 2008, an aggressive avian virus killed thousands of crows across New York state over several weeks, according to an investigation by the state Department of Environmental Conservation alerting its significance and linking it to reovirosis. A case report of a wild hooded crow also diagnosed with the virus was seen in Finland.47 Epizootic mortalities in American Crows (Corvus brachyrhynchos) during the winter months have been recorded in North America for almost 20 years with common postmortem findings, including necrotizing enteritis, fibrinous splenic necrosis, and colitis. These findings are consistent with infection with a Reovirus sp. Reovirosis shows a clear seasonal presentation with cases occurring almost exclusively in winter months. Data from 2016 to 2017 showed that reovirosis caused up to 70% of all recorded crow deaths during winter months.48 Crows with positive orthoreovirus isolation from the spleen or intestine were 32 times more likely to die with characteristic histologic lesions of enteritis or enterocolitis and splenic necrosis than crows with negative isolation results. A new study suggested that a novel orthoreovirus was the cause of winter mortality (or reovirosis) of American Crows and placed the New York isolates in the genus of Corvid orthoreovirus. RENAL TREMATODES  Several trematode genera of the families Eucotylidae (genera Paratanaisia and Tanaisia) and Renicolidae (genera Renicola) have been identified within the upper urinary tract of a variety of avian species.49 The digenetic trematode genus Paratanasia are known parasites of the urinary tract of neotropical birds and have been identified in other regions of the world. The genus consists of 3 species: Paratanaisia bragai, P robusta, and P confusa. These have a heteroxenous cycle with gastropod mollusks acting as the intermediate hosts. These trematodes do not seem to be host-specific and have been identified in many species of birds. Most intermediate hosts are land snails. The birds acquire the infection when feeding on the mollusks affected with the metacercariae, the infective form. The adult trematodes are found developing in the ureters, collecting ducts, and renal tubules of the kidney. The birds reported as having this genus of trematodes parasitizing the kidneys include: several species of Columbiformes, Galliformes, many Passeriformes, Psittaciformes,50,51 Strigiformes, Cuculiformes, Tinamiformes, and Ciconiiformes.52,53 Renicolids are trematodes that inhabit the renal tubules and ureters of molluscivorous and piscivorous birds. The Manx shearwater (Puffinus puffinus), a migratory seabird, and the king penguin (Aptenodytes patagonicus) have been identified as the definitive hosts of Renicola sloanei. Only mild renal lesions were noted in a case report of 2 dead Manx shearwaters. Macroscopically, small black multifocal areas in the kidney were noted containing pairs of trematodes inside cyst-like structures and microscopic findings were dilation of the collecting ducts associated with accumulation of paired renicolids in the dilated ducts.54 Many other penguin groups and several terns have been identified as supporting renal Renicola, although the species was not determined. Clinically the infections were not interpreted as causing any significant disease.55  Re-emerging Diseases of Selected Avian Species  The basic life cycle consists of the excreted embryonated eggs from the host that passively infect a mollusk. After the miracidium hatches, 2 generations of sporocysts, cercariae, and metacercariae develop within the snail. The definitive host acquires the infection by eating the parasitized mollusk. In general, infected birds may have few if any clinical signs. Clinical signs noted have included poor body condition, hypothermia, inactivity, and in some cases other concurrent infections. In species considered the usual definitive hosts, the infections are considered incidental. In accidental hosts, infections with P bragai and P robusta may result in death in a variety of psittacines (South American to Australian), white-eared pheasants (Crossoptilon crossoptilon), and red bird-of-paradise (Paradisaea rubra).50–52,56 On gross evaluation, there may be no significant lesions noted to enlarged kidneys with a nodular appearance and urate stasis. With histology, these trematodes may be identified with dilated cystic spaces of the distended ureters, collecting ducts, and tubules. The adjacent renal parenchyma is generally compressed, and there may be a variable amount of inflammation, primarily lymphocytic and in some cases heterophilic with macrophages and other degenerative changes. The tubular lining cells are typically flattened and there may be interstitial fibrosis. Occasionally, eggs of this trematode can be noted within the interstitial tissue, and these typically elicit more significant inflammation.53 It seems that the primary inflammation is usually directed against the eggs as opposed to the adult trematodes. The adult trematodes may also be associated with some variable hyperplasia of the renal tubular epithelium (Fig. 4). This is suspected due to the irritation of the lining epithelium by the integument of the trematodes. Diagnosis of this infection has primarily been on necropsy. From a search of the literature, there are no reports of antemortem diagnosis, such as identifying the trematode eggs within the urine or urates. Once this trematode infection has been identified with histology, controlling access to the intermediate host is the best form of control.  Fig. 4. Brown pelican (Pelecanus occidentalis) kidney with intraureter trematodes (T), possibly Paratanasia confusa-based morphologically on the spines (arrows). There is extensive epithelial hyperplasia (E) of the ureter (hematoxylin-eosin stain). (Courtesy of D. R. Reavill, DVM, DABVP (Avian and Reptile & Amphibian Practice), DACVP, Salt Lake City, UT.)  437  438  Pilny & Reavill  Prophylactic treatment of praziquantel has been used in collections/aviaries.56 With birds in conservation programs, eliminating or preventing infections is important when considering release of infected/exposed birds and exposing naive populations to the trematodes, especially in areas supporting appropriate intermediate hosts. DISCLOSURE  The authors have nothing to disclose. REFERENCES  1. Dorman DC. Toxicology of selected pesticides, drugs, and chemicals. 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