Whilst trying unsuccessfully to catch a herring gull with fishing line around his leg on the River Neb in Peel, I had the misfortune of seeing this poor mallard with what I think is a nasal leech. Nasal leeches have evolved to feed from the nasal passages and eyeballs of waterbirds. They swim around in the water until they need to feed, then slither up the poor bird’s nostrils and latch on to suck their blood. They cause pain and discomfort to the bird, and can cause serious illness, blindness or even death in some birds. The most common nasal leech in Britain is Theromyzon tessulatum, commonly called the Duck Leech. The leeches can’t normally be seen when they are inside the duck’s nasal passages; I think the one I photographed must have got stuck as it tried to slither in or out of the duck’s bill.
Sharon was a young wild rook who was brought in after being found very weak and lethargic. Sadly she died within a couple of hours. A look at a sample of faeces under the microscope revealed a lot of capillaria worm eggs, and another type of egg that I had never come across before. Tiny and transparent, with bipolar plugs, the sample was full of them. Could this have been what killed Sharon?
After much googling, I came to the conclusion that the mystery eggs had nothing to do with sharonn’s demise. They are a parasite egg, but not a bird parasite – an earthworm parasite. They are sporocysts of an earthworm parasite called Monocystis. Sharon must have been eating earthworms that were infected with the parasite, and the sporocysts had passed through her digestive system without doing her any harm. In Sharon’s case they were a spurious parasite – something that looks like a parasite in your patient but is actually harmless.
The capillaria eggs, however, could be the culprit. The small worms can burrow into the bird’s crop and oesophagus, causing inflammation and anaemia and evens suffocating the bird if there are enough of them, and a heavy burden of them can kill young birds like Sharon.
This year I had the misfortune of having three juvenile birds (two House Sparrows and a Goldcrest) die suddenly and unexpectedly whilst they were being treated for coccidia. I treated the sparrows for two weeks with amprolium (Coxoid), and the goldcrest was a few days into treatment when I found him dead. The birds were lively, eating well and had no diarrhoea so I couldn’t understand why they had died.
I had a necropsy done on one of the sparrows (little Monty), because I wanted to know if his death was related to his baldness and deformed feathers, which he had when he was brought in by a member of the public as a fledgling. The necropsy revealed that Monty had died of atoxoplasmosis (also known as Systemic Isosporosis, formally known as Lankesterella), which is a disease caused by atoxoplasma parasites. These are a type of coccidia that travel in the bird’s blood and can infect all their internal organs, unlike types of coccidia that only infect the intestines.
Symptoms can include diarrhea, lethargy, wasting, and poor flight capacity.
Amprolium is not effective against atoxoplasmosis. Sufachlorpyrazine (ESB3), sulfachlorpyridazine, toltrazaril or diclazuril may be effective (Norton et al).
House Sparrow feather loss
House Sparrow deformed feathers
House sparrow deformed feathers
House sparrow poor feathering
House sparrow baldness
House sparrow alopecia
I found a couple of studies confirming that a heavy burden of coccidia can cause poor feathering in sparrows.
“Coccidians reduce general absorption, drain essential nutrients (e.g., amino acids), and stimulate the immune system (Allen and Fetterer 2002). Thus, coccidian infection during molt can induce a range of costs, including prolonged molt, reduced feather quality, and increased post-molt mortality resulting from insufficient insulation and reduced predator escape ability.” (Pap, 2011)
“primaries were lighter and shorter, and had a smaller vane area, thinner rachis and decreased stiffness, although a higher barb and barbule density, which may have various consequences for fitness through reducing flight performance.” (Pap, 2013)
Atoxoplasmosis is also one of the main causes of death in wild nestling House Sparrows
Adult House sparrows can usually live with atoxoplasma until they suffer from stress or a concurrent infection, at which point their immune system can no longer keep the atoxoplasma under control and it can multiply rapidly and kill them (Cushing et al, 2011).
Atoxoplasmosis is one of the leading causes of death in wild nestling House Sparrows and Tree Sparrows, along with E. Coli and Candida yeast infections (Pinowski et al, 1994).
Sparrow atoxoplasmosis necropsy report
Sparrow atoxoplasmosis necropsy report 2
Cushing, et al (2011) “Characterization of the Host Response in Systemic Isosporosis (Atoxoplasmosis) in a Colony of Captive American Goldfinches (Spinus tristis) and House Sparrows (Passer domesticus)” Published online before print February 10, 2011, doi: 10.1177/0300985810391114 Veterinary Pathology September 2011 vol. 48 no. 5 985-992 http://m.vet.sagepub.com/content/48/5/985.full
Norton, Terry M. et al: Atoxoplasma Medical Protocols Recommended by the Passerine Atoxoplasma Working Group: http://www.aazv.org/?545
Pap, Péter László et al (2011) “The Effect of Coccidians on the Condition and Immune Profile of Molting House Sparrows (Passer domesticus)”. The Auk: April 2011, Vol. 128, No. 2, pp. 330-339.
Gapeworm is a parasitic worm that lives in a bird’s trachea (windpipe), and causes symptoms of respiratory distress known as “the gapes”. Signs of gapeworm infestation in birds can include breathing through an open beak (“gaping”), sneezing, stretching the neck and shaking the head (Welte et al, 1986).
Gapeworm is found in a wide variety of bird species, but especially in pheasants, peacocks, blackbirds, thrushes and finches (Wit, 1995).
In England, “More than 50 percent of nestling and fledgling starlings, more than 85 percent of jackdaws, and 100 percent of young rooks were found to be infected in one study. Infection rates in adult birds were considerably lower, but they still exceeded 30 percent for starlings and rooks.” (Cole, p. 229). Another study in Chester found that 5% of faecal samples collected from adult starlings contained gapeworm eggs, and gapeworm caused heavy losses (deaths) in young chicks. These losses can be prevented in young captive birds by strategic worming in the Spring and Autumn (Cork, Susan C., 1999).
Gapeworm larvae travel through the lungs to the trachea, where they become adults and start reproducing. The larvae can cause lung damage and irritation, and lead to pneumonia (Clapham, 1939). The worms in the trachea cause inflammation tracheitis (Wit, 1995). The trachea responds by producing more mucus, which makes it difficult for the bird to breathe (Bignal et al, 1987). The gapeworm themselves also physically obstruct the windpipe, and if there is a heavy infestation the bird can asphyxiate (Bates, 1970, p. 1). This is more likely in small or young birds, as they have a narrow trachea (Wit, 1995). The worms burrow into the wall of the bird’s trachea, causing necrosis of the tissue (Fernando, 1971), and they drink the bird’s blood and can cause anaemia.
The gapeworms release eggs, which are passed out in the bird’s faeces, or may be coughed up and swallowed. These eggs do not reinfect the bird – first they must develop into larvae within the egg, and by this time they have already been excreted by the bird. Then when the infected droppings are swallowed by earthworms or other host insects, or swallowed directly by another bird, the larvae will hatch out of their eggs inside the bird’s body and migrate to the lungs, starting the cycle again.
The fact that the gapeworm uses earthworms and other invertebrates as an intermediary host explains why birds that feed on these invertebrates such as blackbirds, rooks and starling, are particularly susceptible to heavy gapeworm infestations. Even nestlings can develop heavy infestations if they are fed infected invertebrates by their parents, and some wildlife hospitals recommend routinely worming all the hand-reared blackbirds and starlings before moving them into an aviary for release (Bedford, 2016).
Worming treatments kill the adult worms who are drinking the bird’s blood, but not the larvae who are migrating through the bird’s digestive tract and lungs. Once these reach maturity, the bird will need a second dose of wormer.
Whilst young birds will develop heavy burdens of gapeworm by ingesting eggs in infected prey, adult birds develop some immunity after this initial infection and only a small percentage of adult birds are usually found to carry gapeworm, and then it is usually only a single pair of the parasites (Clapham, 1957).
Members of the thrush family (namely blackbirds, thrushes and redwings) have been found to carry a different species of gapeworm: syngamus merulae as opposed to syngamus trachea (Campbell, 1935).
Gapeworm can kill wild birds; including choughs (Stenkat et al, 2013), fieldfares, Mistle thrushes, song thrushes and sparrows (Holand et al, 2014)..
Even the successful treatment of gapeworm can be hazardous, because if a large number of the worms die and detach from the trachea at the same time, they can physically block the trachea and asphyxiate the bird, or as the dead worms break up the bird can inhale parts of them and develop asphyxiation pneumonia. Even after the worms are gone, the bird’s trachea may be permanently damaged where the worms were attached (Stenkat et al, 2013).
Bedford, Samantha, 2016. A Beginners Guide to Reading Wild Birds (fourth edition), location 607 in Kindle edition.
Clapham, Phyllis A, 1939, “On the larval migration of Syngamus trachea and its causal relationship to pneumonia in young birds”. Journal of Helminthology. Cambridge University Press
Fernando, MA, et al, 1971. “The Route of Migration, Development, and Pathogenesis of Syngamus trachea” (Montagu, 1811) Chapin, 1925, in Pheasants”. The Journal of Parasitology Vol. 57, No. 1 (Feb., 1971), pp. 107-116
Stable URL: http://www.jstor.org/stable/3277762
Holand et al, 2014. “Lower survival probability of house sparrows severely infected by the gapeworm parasite”, Journal of Avian Biology.
Meyer and Simpson, “Gapeworm infection in Choughs Pyrrhocorax pyrrhocorax: further evidence.” Richard M. Meyer and Vic R. Simpson, Zoology Department , University of Glasgow , UK Chacewater, Truro , Cornwall , UK.