Mosquitoes won't leave ducklings alone!


Apr 28, 2020
Upper Michigan
I let my almost 3 week old ducklings out this afternoon before an incoming storm. The mosquitoes were acting up like they usually do prior to rain, and were biting, me and my dogs like crazy. The ducks, though, were completely engulfed in a swarm of the insects, biting their necks and backs relentlessly. The ducks ate a good number of them, but there was no way they could contend with that many at once. Does anyone else have this issue? Biting insects targeting young fowl? Does this have to do with the food they eat? They get chick feed with supplemental niacin and bugs. Also, is this something to worry about in the first place, or will they be fine?


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The Golden State
Mosquitoes of Poultry
James R. Philips
, PhD, Math/Science Division, Babson College
Last full review/revision Oct 2013 | Content last modified Oct 2013

Mosquitoes that feed on poultry blood usually belong to the genera Culex, Aedes, or Psorophora. Large numbers can decrease egg production or cause death. Mosquitoes transmit Plasmodium gallinaceum (chicken malaria), P hermani (in turkeys), and other Plasmodium species causing avian malaria. They also transmit many viruses, including Eastern and Western equine encephalomyelitis, St. Louis encephalitis, fowlpox, and West Nile viruses. West Nile virus is transmitted from infected birds to other birds primarily by mosquitoes, particularly Culex spp in the USA, and has been found in >200 species of birds in America, including chickens, turkeys, pigeons, budgerigars, cockatiels, ducks, finches, and birds of prey. (Also see West Nile Virus Infection in Poultry.)
Removal of mosquito-breeding habitats by emptying water-filled containers, clearing pool and pond edges of emergent vegetation, draining swampy areas, and filling low areas that collect water are the best physical control measures. Insecticidal control involves chemicals such as malathion, propoxur, permethrin, chlorpyrifos, or temephos. Insect growth regulators such as methoprene and diflubenzuron are also effective. Microbial control of mosquito larvae uses Bacillus thuringiensis israelensis and, against Culex spp, Bacillus sphaericus. Screening to prevent mosquito entry, residual wall sprays, and fogging within poultry houses also aid in control.
Overview of West Nile Virus Infection in Poultry
Scott D. Fitzgerald
, DVM, PhD, DACVP, DACPV, Department of Pathobiology and Diagnostic Investigation, College of Veterinary Medicine, Michigan State University
Last full review/revision Jun 2013 | Content last modified Jun 2013

Also see Equine Arboviral Encephalomyelitis.
West Nile virus (WNV), a flavivirus related to the St. Louis encephalitis/Japanese encephalitis complex, was first isolated from the blood of a febrile Ugandan woman in 1937. The virus was first described as the cause of a West Nile fever epidemic in people in Israel in 1951; in a later outbreak, severe meningoencephalitis was seen in elderly patients. The role of mosquitoes in viral transmission was clearly delineated in a series of field studies in Egypt in the 1950s. Wild birds were identified as the reservoir of the virus around the same time. Cases of West Nile fever in horses were reported several years later. WNV was first associated with disease in domestic avian species in 1997, when flocks of young geese in Israel were affected with a neuroparalytic disease. In August 1999, the disease appeared for the first time in the Western hemisphere when wild and zoo birds, horses, and people died in the northeast USA, notably in the New York City area.
Etiology and Epidemiology:
WNV is considered to be endemic in many countries of Africa, Asia, southern Europe, and North America. Since 2001, serologic evidence of the spread of WNV into Latin America, the Caribbean, and South America has been reported. Epidemics appear in the human population at infrequent intervals in some of these countries, and there is evidence of viral transmission between Africa and Europe by migrating birds. Most outbreaks have occurred during the summer months and can continue until cold nights reduce mosquito vector activity, notably Culex spp.
Geese are the only known natural hosts of WNV among domestic avian species. Most of the flocks affected in the Israel outbreaks were 5–9 wk old, but goslings as young as 3 wk and as old as 11 wk were also affected. Adult breeding flocks were clinically unaffected, but virus-neutralizing antibodies were found. Mortality of young Muscovy ducks but not young chickens or turkey poults was induced experimentally with a WNV isolate. While chickens are not killed by WNV, they do develop antibodies against the disease and have been used as sentinels to monitor WNV presence. Neither chickens nor turkeys develop high enough levels of viremia to infect mosquitoes or transmit the virus to other animals.
The principal route of viral transmission is by the bite of a mosquito (primarily Culex spp). In the USA during 1999 and 2000, most of the viral isolates were made from C pipiens and C restvans. WNV has been isolated, RNA detected, or antibodies found in 62 mosquito species in North America. In Africa and the Middle East, the usual vector is C univittatus, and in Europe, C pipiens and C modestus. WNV has also been isolated from at least 10 tick species.
Clinical Findings:
Affected geese show various degrees of neurologic involvement ranging from recumbency to leg and wing paralysis. Affected birds are either reluctant or unable to move when disturbed. Signs of incoordination are pronounced, and some birds flip over while attempting to stand. Naturally affected geese show torticollis and opisthotonos. Mortality rates of 20%–60% have been reported, probably due to horizontal spread of the virus.
Pathologic changes include splenomegaly, hepatomegaly, and pallor of the myocardium and occasionally of the kidneys. The meningeal blood vessels are injected. Microscopic brain lesions consist of lymphocytic perivascular infiltration and neuronal degeneration. Small necrotic foci are present in the myocardium, but lymphocytic infiltration is minimal.
The tissues of choice to isolate the virus from paralytic or dead birds are the brain, spleen, and kidneys. Homogenates are inoculated into the brain of newborn mice, into embryonated eggs by the yolk sac route, or into Vero and mosquito cell line cultures. Reverse transcriptase PCR with RNA extracted from either brain material or cell culture supernatant can also be performed. Gene expression assays/probes for rapid molecular diagnosis of field-collected mosquitoes and avian tissues are also available. Immunohistochemistry can be used on formalin-fixed paraffin-embedded tissues, in particular brain and kidney, to visualize viral antigens in infected birds. Several forms of ELISA have also been developed for flaviviruses.
Neurologic signs in young geese must be distinguished from those caused by Riemerella infections, especially R anatipestifer. Other bacteria include Streptococcus gallolyticus, and Erysipelothrix, Listeria, and Salmonella spp. Neurotropic viruses include Newcastle disease, which is rare in geese, and avian influenza. Ionophore intoxication can induce paralytic signs. Aspergillus also causes brain lesions and caseous nodules in the lungs.
Prevention and Control:
Mosquito control is a mandatory component of any arboviral disease control program. Unfortunately, this is difficult to implement in a rural environment because of the distances that mosquitoes can fly or be carried by prevailing winds. Standing water and similar insect breeding sites in the vicinity of densely populated avian farms should be treated with larvicides. Poultry houses should be constructed to be insect free. Because many arboviral diseases are zoonoses, much can be achieved by cooperation with human disease surveillance agencies.
Control of WNV in geese is confined to vaccinating young flocks at risk, especially those raised during months when Culex spp are most numerous. Because of confounding factors such as possible horizontal transmission of virus, all birds in the flock should be vaccinated. Because of the age-related susceptibility to the virus, goslings should be immunized as young as possible, preferably at 3 wk old. Currently, WNV vaccines are not available commercially in North America, although several types have been developed and widely used in domestic geese in Israel. Laboratory trials have been performed with a formaldehyde-inactivated suckling mouse brain–derived product. More than 75% of geese vaccinated with a single dose of vaccine at 3 wk of age were protected, and 94% protection was achieved with 2 doses given 2 wk apart. Inactivated vaccines prepared from chick embryos or Vero cells are not protective because of their low antigenic mass. Other vaccines either approved for use in geese or under study include poxvirus vector vaccines and subunit vaccines that use WNV components such as membrane protein or envelope protein.

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