WormMail.2015-01-29. Hypobiosis in sheep worms in Australia? plus more…

To: WormMail mailing list. WormMail.2015-01-29. Hypobiosis in sheep worms in Australia? plus more…

In this issue …

Main course (worms)

Hypobiosis in sheep worms in Australia? – R B Besier

Monepantel resistant Haemonchus on sheep farms in Uruguay – first report

Do hunting dogs come onto your property? (hydatids)

Dessert, coffee, cognac (sans worms)

Auden’s palindrome

Richie Benaud did not Lamb alone this Australia Day

Hypobiosis in sheep worms in Australia – is it present and is it a problem ?

– Brown Besier, Department of Agriculture and Food WA (DAFWA), Albany (Jan. 2015)

“Hypobiosis in larval nematodes has been recognised as a potential feature of some ruminant worm life cycles for many years, but there has been little discussion of whether it occurs as a routine survival mechanism for sheep worm populations in Australia. However, hypobiosis (or “developmental arrest”, or “larval inhibition”) may have implications for the effectiveness of sustainable control programs, and could be important for the development of anthelmintic resistance.

Hypobiosis is common outside Australia

As classically described, hypobiosis is a characteristic of worm strains or populations that have evolved in particular environments, where the ability to survive during prolonged periods of hostile conditions for the free-living stages is essential to ensure the continuation of the population. In this form of the nematode life cycle, at times of the year time when conditions in the external environment are becoming increasingly adverse for larval survival on pasture, some of the ingested infective larvae develop only to the fourth larval stage, and enter a dormant state rather than continuing development to the fifth larval and adult stages. Sometime later – usually months – when environmental conditions are more favourable for worm eggs and larvae, the development of inhibited larvae to the later stages re-commences.

Hypobiosis has been described in a fairly wide range of nematodes of animals and man, but for livestock has been most studied in Haemonchus contortus in sheep and Ostertagia ostertagi in cattle. The latter is seen as the condition “Ostertagiosis Type 2”, where severe scouring results from massive inflammation caused by the mass emergence of inhibited larvae from the abomasal wall. This was identified in the late 1960s as a sporadically-occurring disease syndrome, at times causing large-scale cattle deaths because the anthelmintics available prior to the late 1970s did not kill the fourth larval stage. (This condition is no longer common, although the sharp decline had not been well explained – not all cattle farmers routinely use effective anthelmintics.)

Hypobiosis has also been reported in Teladorsagia (Ostertagia) circumcincta in sheep in the northern hemisphere. In Haemonchus, hypobiosis has been reported as a routine occurrence mostly from climates with periods of either extreme cold (Canada, N. USA, UK, Europe) or extreme dryness and heat (desert environments – sub-Saharan Africa, Middle East). It appears to be a hard-wired genetic mechanism, i.e., it can potentially occur every year, and is not turned on or off in relation to particular environmental conditions in any one year.

However, there can be considerable variation in the extent of its expression, as exemplified by the sporadic occurrence of Ostertagiosis Type 2 between years and on individual properties in Australia. This could be explained by differences in larval pick-up prior to the period of developmental arrest (due to pasture management and the local environment), and factors related to anthelmintic use such as the time of application and effectiveness against the inhibited larval stage. It also appears that there are strains with a greater or lesser propensity to “go hypobiotic”, certainly between environments and perhaps within regions. This is just one of many puzzles regarding hypobiosis, such as the mechanisms to trigger its onset and then the re-development of larvae: how do they “know” when to “wake up” ? – environmental cues via hormonal routes in the animal? – changes in immunological situation due to new L3 intake ? A recent study in bovine lungworm identified differences in gene expression between hypobiotic and non-inhibited strains, but no mechanistic link was postulated.

Do we see it here ?

In Australia, there has been little overt indication of whether or not hypobiosis is a routine occurrence in a particular environment. This is presumably because modern drenches are highly effective against L4s (until anthelmintic resistance occurs) and these are usually removed before they can contribute to pasture contamination and hence influence worm populations. This may change once anthelmintic resistance affects previously highly-effective anthelmintics, although as drench failure takes time to become apparent, any effect on parasite epidemiology would also take time to be noticed.

Hypobiosis in Haemonchus contortus has long been considered a routine but largely invisible phenomenon in summer rainfall regions (especially the New England region, northern NSW), presumably due to long periods of relatively cold weather, although whether hypobiosis would be essential for population survival is debateable when compared to climates with really frigid winters. Recently, Leo le Jambre (formerly of CSIRO) has commented that hypobiosis appears to be less marked than in the early 1970s, when large numbers of inhibited L4s were routinely recovered in total worm counts. Presuming that this is a real trend, is this due to sheep management, anthelmintic effects, or environment ? (climate change, anyone ?).

I don’t know about Queensland, where dry conditions may have encouraged H.contortus populations to evolve towards hypobiosis, although this would need to be where a prolonged drought period was routine in most years as part of the normal climate. In cool temperate climates (winter rainfall regions in Australia), there is less need for H.contortus to use hypobiosis to survive: my own thesis was partly on cold-temperature tolerance in Haemonchus, and it was evident that adaptation had occurred in that the eggs from cold-winter strains could develop at up to 2 C colder than those from the tropics. The conclusion was that, in an evolutionary context, hypobiosis would only be necessary for population continuance when winters were so cold that development on pasture ceased for a prolonged period, rather than an interruption of only a few weeks, as occurs in most of southern Australia.

In winter rainfall regions in Australia, presumably the widely-used “summer drenching” program would remove inhibited worms, provided anthelmintic resistance was not severe. However, there are recent indications that Teladorsagia, at least, employs hypobiosis to survive over the hot dry WA summers, to emerge in mid-autumn once milder conditions occur. This was seen in work by Rob Woodgate (formerly DAFWA, now CSU Wagga Wagga) that led to the current “summer-autumn drench” program in WA, by which drenching adult sheep is delayed until March or April, to provide refugia for non-resistant worms. Although worm egg counts were almost always low in early summer, they had often increased to significant levels by mid-autumn. This could not be explained by over-summer pick up or faecal concentration, although the variation in occurrence between properties may be explained by differences in larval exposure in the late spring period when L3s would start to become seasonally inhibited ahead of a long period of no egg development on pasture.

Does it matter ?

There are two main potential issues of consequence if indeed hypobiosis does occur routinely in some environments.

– Sustainable worm control programs. These are generally based on the refugia concept for populations of worms not recently exposed to drenches, and in some winter rainfall regions insufficient refugia is provided by over-summering larvae. The general response is to leave some sheep untreated in summer, whether as a “targeted treatment” strategy (avoiding drenching of a proportion of the best-condition sheep) or in WA, the “summer-autumn drench” program. If worm egg counts sharply increase in autumn as inhibited larvae become adult worms, recommendations will need to allow for potential increases in pasture contamination, through additional monitoring or treatments.

– Drench resistance development. It has long been suspected that the presence of inhibited L4s may have assisted in the development of anthelmintic resistance. The L4 stage is harder to kill than adult worms, as shown by experimental data during anthelmintic development (assumed to be due to lower metabolic rate – presumably lowest for inhibited larvae – or for some species, in tissues with less blood supply than at the gut surface). For large populations of these, there will be a greater chance that some individuals would receive a sub-lethal anthelmintic dose. If this occurred when drenches were given for a strategic effect, typically ahead of periods when pasture development is minimal, these surviving (resistant) worms would have a survival advantage once the L4s reached the egg-laying adult stage.

It is intriguing to speculate that the early detection of ivermectin resistance in Teladorsagia in WA (4 years after release) may in part be related to this effect in invisible and unsuspected hypobiotic worms. Of more immediate concern, we know that many sheep owners routinely used anthelmintics that are not fully effective against adult worms – what would this mean for worms we can’t detect in resistance tests, but are even more resistant to drenches ?

Plenty of puzzles

Apart from the fundamental queries over the cues that trigger the commencement and end of hypobiosis, there are many other unanswered questions – presuming that it does indeed occur more commonly than we suspect.

– Where does it occur – only or mostly in environments where there is seasonally poor survival of the free-living stages ?

– What ages of sheep are involved, or can all be affected similarly ?

– Why is there apparent variation between seasons and properties ? – reasons and extent.

– When does pick-up occur for hypobiotic-prone larvae, and when do they re-emerge ?

– Which species are affected ?

– How should we detect and manage this ? – if it is really of consequence.

Of interest, if there are real differences between the occurrence of hypobiosis in sheep worms in response to different environments around Australia, this must have developed (or been lost if initially present) in only 200 years or so, which is very swift in evolutionary terms.”

First report of monepantel Haemonchus contortus resistance on sheep farms in Uruguay

Parasit Vectors. 2014 Dec 17;7(1):598. [Epub ahead of print]

First report of monepantel Haemonchus contortus resistance on sheep farms in Uruguay.

Mederos AE, Banchero GE, Ramos Z.

http://www.ncbi.nlm.nih.gov/pubmed/25515711 (Thanks John K).​

Do hunting dogs come onto your property?

This from SheepConnect Tasmania:

https://gallery.mailchimp.com/d8262befda5125340f6c51851/files/Hydatids_and_hunting_dogs.pdf

Auden’s palindrome

“T. Eliot, top bard, notes putrid tang emanating, is sad. I’d assign it a name: gnat dirt upset on drab pot toilet”.

I first came across this while reading a book by Alexander McCall Smith (“Sunshine on Scotland Street” (p148 hardcover edition that I am reading)).

Richie Benaud did not Lamb alone this Australia Day

https://www.youtube.com/watch?v=WpZhJcZD2H4

The characters (for the benefit of overseas readers): http://en.wikipedia.org/wiki/Richie_Benaud ; http://en.wikipedia.org/wiki/James_Cook ; http://en.wikipedia.org/wiki/Ned_Kelly (with gluten intolerance (disputed by Burke and Wills)); http://en.wikipedia.org/wiki/The_Twelfth_Man (not invited, due to parodies of Bernaud); http://en.wikipedia.org/wiki/Donald_Bradman (no answer); http://en.wikipedia.org/wiki/Ita_Buttrose (in limo, thinking ‘lamingtons’); http://en.wikipedia.org/wiki/Burke_and_Wills_expedition (in extremis) ; http://en.wikipedia.org/wiki/Sam_Kekovich (on jet ski); http://en.wikipedia.org/wiki/Lamb_chop .

Regards,

SL

2015-01-29

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WormMail.2015-01-08. Macracanthorhyncus etc

WormMail.2015-01-08. Macracanthorhyncus etc

In this issue

Worms: Macracanthorhynchus in feral pigs – NSW (Dr Bruce Watt)

Other: Subscribing to Beyond the Bale; Asparagus and smelly urine; Five promising updates in sports science; Password Security; Cyclist’s impressive dismount; Exploiting cancer cells’ metabolic quirk.

To kick off the New Year, here is something interesting and different from Bruce Watt, a Local Land Services Regional Veterinarian located at Bathurst.

Macracanthorhynchus hirudinaceus in feral pigs

Bruce Watt

Two mature feral pigs killed in August 2014, as part of a pest control program near Palmer’s Oakey, north east of Bathurst, were observed to be heavily infested with ‘tape worms.’ A worm, collected and submitted by the property owner, was subsequently identified as the euphoniously named acanthocephalan parasite, Macracanthorhynchus hirudinaceus (the giant thorny headed worm).

The acanthocephalans are wonders, within their own phylum of highly specialised vertebrate parasites, remarkably fecund (the females of M hirudinaceus producing about 260,000 highly resistant eggs per day) and yes, they are gutless, absorbing nutrients through their outer membrane. The eggs, which can live for several years, hatch when ingested by the larvae of scarabs and other species of beetles. The worm larvae eventually become encysted both in the grubs and mature beetles and infect pigs consuming them. While most pigs are only lightly infected, thorny headed worms anchor their proboscis into the intestinal wall, causing weight loss and in some cases death through intestinal perforation (Soulsby 1971). However, in one instance the parasite population caused such a high mortality in nuisance feral pigs (in Iranian sugar cane fields) that it was welcomed as a biological control agent (Mowlavi et al 2006).

M hirudinaceus can also occasionally develop in dogs that ingest beetle larvae. As an aside, some American dogs also suffer from infestations of the even bigger M ingens which is normally a parasite of racoons, with millipedes the intermediate host. However as Bowman et al (2002) observed, ‘to eat a millipede requires extraordinary cunning, frightful taste, great excitement or utter boredom on the part of the dog because the millipede gives off a potent defensive secretion. The raccoon gets around the problem by rolling the millipede about in the dust to exhaust its supply of defensive secretion, but few dogs have learned that trick.’

While a parasite that may cause emaciation and sometimes death in feral pigs is not of major concern, M hirudinaceus could also infect free range pigs and is a potential zoonosis. While M. hirudinaceus seldom matures in people there are numerous reports of its recovery in humans. In some countries people consume beetle larvae either for medicinal or dietary purposes exposing them to the risk of infection (Shapiro, Schmidt 1971).

It is increasingly claimed that entomophagy (eating insects) will help save the planet. Gaia Vince prophesied that ‘insects, which are far more efficient than cattle at transforming their feed into protein, are likely to provide a greater proportion of our dietary protein – over 2 billion people already supplement their diets in this way.’ Leaving aside that this is a straw man argument (cattle may well be less efficient at converting grain into protein than many other forms of livestock but they are remarkably efficient at converting cellulose into high quality food), let us hope that parasites like M hirudinaceus do not prove to be a thorn in the side of entomophages.

Figure 1. Adult M hirudinaceus attached to small intestine of pig. (Source: University of Pennsylvania School of Veterinary Medicine’s Computer Aided Learning program website, accessed 31 December 2014). Go to: http://cal.vet.upenn.edu/projects/dxendopar/parasitepages/acanthocephalens/mhirud.html

Figure 2. Entomophage heaven. Deep fried insects for sale Thailand. Go to: http://en.wikipedia.org/wiki/Entomophagy

REFERENCES

Bowman DD, Lynn RC and Eberhard (2002). Georgi’s Parasitology for Veterinarians, Eight Edition, pp 230-232.

Macracanthorhynchus hirudinaceus Homepage http://cal.vet.upenn.edu/projects/dxendopar/parasitepages/acanthocephalens/mhirud.html

Mowlavi GR, Massoud J, Mobedi I, Solaymani-Mohammadi S, Gharagozlou MJ and Mas-Coma S (2006) Very highly prevalent Macracanthorhynchus hirudinaceus infection of wild boar Sus scrofa in Khuzestan province, south-western Iran. Helminthologia June 2006, Volume 43, Issue 2, pp 86-91

Schmidt GD (1971) Acanthocephalan Infections of Man, with Two New Records.The Journal of Parasitology Vol. 57, No. 3 (Jun., 1971), pp. 582-584.

Soulsby EJL (1971). Helminths, arthropods and protozoa of domestic animals, pp 336-7.

Shapiro L. Life cycle of acanthocephalans Moniliformis moniliformis and Macracanthorhynchus hirudinaceus. Centers for Disease Control/Division of Parasitic Diseases and Malaria accessed 5 January 2015, http://eolspecies.lifedesks.org/

Vince, Gaia (2014). Adventures in the Anthropocene, a journey to the heart of the planet we made. p 148.

Further notes on Macracanthorhynchus hirudinaceus(SL):

From Georgi: Acanthocephala – thorny-headed worms – are a small phylum of highly specialized parasites of the vertebrate digestive track. They are not related to nematodes. These worms consist of a body and a retractable spiny proboscis – used for attaching to the host’s intestinal wall. The body is normally flattened in situ so can be mistaken for a tapeworm (as noted by Bruce, above) – but become cylindrical when placed in water. There is no digestive tract (‘gutless’, Bruce says) – nutrients are absorbed through the integument (Georgi’s Parasitology -8th Ed. 2002), a feature they share with the cestoda (tapeworms), although the two groups are not closely related (wiki).

More Macracanthorhynchus images – see here. (Accessed 2015-01-07).

From wiki: ‘The Acanthocephala were thought to be a discrete phylum. Recent genome analysis has shown that they are descended from, and should be considered as, highly modified rotifers.[5] This is an example of molecular phylogenetics. This unified taxon is known as Syndermata.’

The Merck Vet Manual article mentions M.h can ‘go’ in dogs occasionally as well.

Merck says the eggs don’t float in salt solution – a practical thing worth knowing. However the upenn page has faecal flo(a)tation (presumably using zinc sulphate solution??) as the diagnostic test to use.

Also interesting at the upenn page is Loperamide® (an opioid antimotility drug) being listed as one of the treatment options, along with ivermectin. (You learn something new every day (and then sometimes forget it the next)). So, how does an opioid work in this case? Perhaps Macracanthorhynchus worms become euphoric and lose their grip? Meanwhile the pig moves on, to paraphrase Hugh Mcl Gordon.

The female’s output of 260,000 eggs per day (noted by Bruce) makes the fecundity of Fasciola hepatica (~20,000) and Haemonchus (~ 5-10,000) look pretty anaemic.

From Radostits et al (Veterinary Medicine, 10th Ed., 2007): The prepatent period is 2-3 months and the worm lives in the host for about a year. Treatment is rarely given as the condition is usually only diagnosed at necropsy. Ivermectin in feed to provide 0.1 – 0.2mg/kg for 5 days gives good results. A single dose of doramectin is only partly effective. Control, if necessary, involves suitable disposal of manure and avoiding contact with the intermediate hosts, beetles. Sedimentation techniques are better than flotation methods for detecting eggs in faeces.

For the etymologists (c.f. entomologists) – from Georgi’s ‘Parasitology”:

Acanthocephala = ‘thorny head’

Macracanthorhyncus = ‘giant thorny trunk’

The NSW DPI Vet Lab Manual has this note:

Macracanthorhynchus spp. Not common. Heavy infection is 200 worms”, but does not, as far as I can see, indicate that you need to do a sedimentation test – as with trematodes – as opposed to flo(a)tation in a saturated salt (NaCl) solution.

Practical tip: one of the most important things in livestock parasitology is perfectly spelling and pronouncing words like naphthalophos and Macracanthorhynchus.

From the Macquarie Dictionary:

euphonious

/juˈfoʊniəs/ (say yooh’fohneeuhs)

adjective characterised by euphony, well-sounding; agreeable to the ear.

–euphoniously, adverb
–euphoniousness, noun

Other euphonious words include ‘eperythrozoonosis’ and ‘Eperythrozoon’ –especially the former – but alas, the taxonomists and molecular biologists have ruined this, now calling E. ovis, Mycoplasma ovis. See here. Equally disconcerting is Pasteurella haemolytica biotype A being reclassified as Mannheimia haemolytica (biotype A) (with Pasteurella biotype T becoming Pasteurella trehalosi (biotype T). German microbiologist Walter Mannheim is the eponym of Mannheimia. (Eponymous if not euphonious, but certainly not cacophonous. (Thank you, Bruce)).

Subscribing to Beyond the Bale

From Richard Smith (Dec 2014):

“Further to your blog entry https://wormmailinthecloud.wordpress.com/2014/12/10/wrml-sheep-worm-articles-in-beyond-the-bale-grazing-management-and-pcr-test-for-worms/ :

People can subscribe (free) to the hard copy of Beyond the Bale if they forward their name and postal address to me (richard.smith).

They are also able to subscribe (free) to the Beyond the Bale e-newsletter (that provides a link to the latest online version) via the subscribe page at www.wool.com/subscribe

Asparagus and smelly urine

In case you have wondered about this but were too afraid to ask, I came across this recently (Christmas reading):

Marcia Levin Pelchat, Cathy Bykowski, Fujiko F. Duke and Danielle R. Reed (2010). Excretion and Perception of a Characteristic Odor in Urine after Asparagus Ingestion: a Psychophysical and Genetic Study

Source and further details:

http://chemse.oxfordjournals.org/content/early/2010/09/27/chemse.bjq081.full.pdf+html

Summary by way of excerpts:

‘About 8% of the subjects studied herein did not produce this characteristic asparagus odor (sic) in sufficient concentration to be detected by the methods used here.’

‘About 6% of subjects are unable to detect asparagus odor …’

‘… the production of the asparagus metabolites was not tightly related to the ability to smell them.’

‘The urine odorant produced after asparagus ingestion may be a metabolic product or it may be a molecule found in cooked asparagus that is eliminated unchanged (Ulrich et al. 2001).’

‘The reduced ability to smell the asparagus metabolites in urine appears to be related to a single nucleotide polymorphism near the olfactory receptor gene OR2M7’

‘The genetics of odor production for some particular chemicals is well understood. For instance, the fish odor associated with trimethylaminuria is related to alleles of the FM03 gene (Dolphin et al. 1997).’ (<<< yes, the name is dolphin, Yes, I know dolphins are not fish)……’

‘People also differ in their propensity to produce axillary odor in part due to alleles of the ABCC11 gene (Martin et al. 2010). In this study, alleles of an olfactory receptor were not significantly related to the ability to produce the asparagus urine odor (although small effects might not have been detected). The major determinant of individual differences in asparagus odor production in urine remains unknown. In conclusion, this study confirmed that people with a particular allele within an olfactory gene cluster is related to the ability to smell the odor. We also report that the production of the asparagus metabolites was not tightly related to the ability to smell them. ‘

Also: https://en.wikipedia.org/wiki/Asparagus

Proust wrote more favourably that asparagus ‘‘as in a Shakespeare fairy-story transforms my chamber-pot into a flask of perfume’’ (Proust 1929).

The new news: Five promising updates in sports science

http://www.theglobeandmail.com/life/health-and-fitness/fitness/the-new-news-five-promising-updates-in-sports-science/article22159011/

Password security

https://www.schneier.com/blog/archives/2014/03/choosing_secure_1.html

If you don’t have time to read this, this is the most important para:

‘There’s still one scheme that works. Back in 2008, I described the “Schneier scheme”:

“So if you want your password to be hard to guess, you should choose something that this process will miss. My advice is to take a sentence and turn it into a password. Something like “This little piggy went to market” might become “tlpWENT2m”. That nine-character password won’t be in anyone’s dictionary. Of course, don’t use this one, because I’ve written about it. Choose your own sentence — something personal.”

Cyclist’s impressive dismount

http://www.smh.com.au/nsw/this-is-going-to-hurt-byron-bay-cyclist-talks-through-spectacular-crash-20150103-12hbbu.html

Exploiting cancer cells’ metabolic quirk

http://eatingacademy.com/nutrition/way-exploit-metabolic-quirk-cancer

Despite the name of his blog, Attia is one person whom I think is worth reading. But, ‘your mileage may differ’ (YMMD), as they say.

Bliadhna Mhath Ùr !

Regards,

SL