WRML. moxidectin in milk etc

In this issue

  • Mox in your milkshake? – WAAVP 2015 papers – Doyle, Leathwick and others
  • Moxidectin LA in ewes – Kelly et al (WAAVP 2015).
  • Macrocyclic lactones – lipophilia and secretion into milk
  • Medications in milk
  • Zolvix Plus (MPL+ABA) for cattle
  • ParaBoss incl. WormBoss – cool new logos (outdone only by the content)
  • Protein, energy, resistance and resilience – from WormBoss
  • Liver fluke – a discussion – SL
  • Congenital/ectopic fluke infections?
  • Wet and dry ewes?
  • NSW DPI digital publications
  • The K5 variant of rabbit calicivirus
  • Feral photos
  • Snake envenomation-domestic animals-Australia
  • Animal health surveillance – NSW and Australia
  • Inimitable; wasabi; stop

Mox in your milksake?

Frivolous headings aside, I first became aware of the ‘moxidectin in milk’ story when listening to a talk by Michelle Dever (Sheep CRC-supported PhD candidate, University of New England, Armidale; now with MSD) on some MLA-funded research (by Michelle and others) into worm control in prime (‘meat breed’) lambs and their mothers.  In short, they found a reduction in the worm egg counts of untreated prime lambs born to ewes treated with moxidectin pre-lambing. (This was just one of the findings). A quick search at the time found papers by the likes of Alvinerie and others reporting moxidectin in calves born to mothers treated with moxidectin.  With the benefit of 20/20 (6/6 in the metric world) hindsight, this really shouldn’t come as a surprise.

Michelle Dever and colleagues presented some of those findings at WAAVP, Perth (2013), flagging that excretion of moxidectin in the milk of ewes could have untoward consequences (“the decreased effectiveness of the … treatments in lactating ewes may be attributed to moxidectin due to its extreme lipophilic nature and excretion in milk”). See poster here: Dever M et al WAAVP_Aug13 (poster) decreased drench efficacy during lactation-ewes. frm MD nov15

In 2014, at the Australian Society for Parasitology meeting, Michelle and colleagues presented more information, including the observation that “the consequence of treating lactating ewes with long-acting anthelmintics excreted in milk could be that worms in lambs may be exposed to sub-lethal doses of the active which could hasten development of anthelmintic resistance” [Dever, M. L., Kahn, L. P., Doyle, E. K., & Walkden-Brown, S. W. (2014). Worm egg counts in lambs decreased after administration of long acting anthelmintics to ewes.  Australian Society for Parasitology, Canberra, Australia]. See poster here: Dever M et al ASP_Jun14 (poster) M Dever_17Jun14_Final (1)-WECs in lambs lower after ewes drenched-frm MD nov15

Subsequently Dever and Kahn published this paper in the journal, Veterinary Parasitology: Dever, M. L., & Kahn, L. P. (2015). Decline in faecal worm egg counts in lambs suckling ewes treated with lipophilic anthelmintics: Implications for hastening development of anthelmintic resistance. Veterinary Parasitology, 209(3-4), 229–234. doi:10.1016/j.vetpar.2015.02.018)

Matt Playford and colleagues at Dawbuts saved me time by summarising some of the papers from the recent WAAVP conference in the UK.  Here, with permission, are excerpts (italicised) from the Dawbuts spring newsletter regarding  moxidectin given to lactating ewes finding its way into the lambs.

‘Moxidectin given to lactating ewes finds its way into the lambs  – This is understandable given the lipophilic nature of moxidectin, but detailed trials on the phenomenon had not been conducted until recently. What did these trials show?’

‘* Emma Doyle from the University of New England measured the moxidectin levels in the blood and milk of LA -injected ewes. Lambs had detectable levels of moxidectin in their bloodstream up to 35 days after treatment, resulting in a sub-lethal dose being applied to all lambs. In the short term this resulted in lower worm burdens in lambs from treated ewes compared to those from untreated ewes, but in the long term it is expected that this will lead to faster onset of resistance’. (‘LA’ = moxidectin long-acting injection. Doyle et al not only measured the concentration of mox. in milk, but also the volume of milk produced as well. – Ed.) Doyle Dever Kahn.WAAVP 2015. Moxidectin transfer via milk and sub-lethal dose of the active to suckling lambs

‘* In a study that sampled milk from ewes dosed with controlled release capsules or long-acting (LA) formulation of moxidectin prior to lambing, Leathwick et al. from New Zealand came up with the following conclusions. “Treatment of ewes pre-lambing with long-acting ML anthelmintics resulted in the persistent transfer of active to the lambs via milk and in the case of moxidectin, this resulted in a significant reduction in the establishment of ML-susceptible, but not ML-resistant larvae.” These studies have answered the knowledge gap in understanding moxidectin resistance when using long-acting treatments’. 

Leathwick Fraser Miller. WAAVP 2015. Selection for anthelmintic resistant Teladorsagia circumcincta in pre-weaned lambs by treating dams with LA MOX injection

(The ML-resistant Teladorsagia isolate used by Leathwick et al (“SOL-ivm-resistant”) was resistant to ivermectin (efficacy 42%), but susceptible to abamectin (96%) and moxidectin (>99%). Moxidectin levels in milk began at ~ 45 ng/ml, declining to low levels (~1-2 ng/ml) by day 80. Abamectin fluctuated in the range 1-3 ng/ml. Reference: Leathwick, D.M., Miller, C.M., Fraser, K., Selection for anthelmintic resistant Teladorsagia circumcincta in pre-weaned lambs by treating their dams with long-acting moxidectin injection, International Journal for Parasitology: Drugs and Drug Resistance (2015), doi: 10.1016/ j.ijpddr.2015.11.001.

Paper highlights: ” [1] Long-acting anthelmintics were administered to pregnant ewes. [2] Moxidectin and abamectin were detected in ewe’s milk for >60 days. [3] Moxidectin and abamectin were detected in plasma of lambs for >60 days. [4] Abamectin treatment had no effect on establishment of larvae in the lambs. [5] Moxidectin treatment reduced establishment of susceptible, but not resistant larvae.” – Ed.)

‘* Gareth Kelly, also from the University of New England, studied LA moxidectin in ewes and found that ewes treated with the injection alone had high worm egg counts (WEC) of approximately 480 eggs per gram over the subsequent 112 days. In contrast, ewes treated with an effective primer (in this case Zolvix (monepantel)) at the time of the LA injection had an average WEC of only 50 epg. The consequences of this are that ewes treated without a primer will contaminate pastures with high numbers of moxidectin-resistant larvae (see Figure 1)’.

Figure 1. From Dr Gareth Kelly’s presentation at WAAVP, 2015.

Kelly G - WECs following moxidectin etc ewes WAAVP 2015-via Dawbuts newsletter-CROPPED

Notes for figure 1: Mox LA= single dose of long-acting moxidectin injection on day 0; MPL D0 = single dose of monepantel on day 0; MPL D0, 49 = two doses of monepantel given on days 0 and 49; MPL D0, 70 = two doses of monepantel given on days 0 and 70; Mox LA/MPL D0= primer of monepantel given on day 0 at the same time as the long-acting moxidectin; Mox LA/MPL D0,49 = long-acting moxidectin on day 0 + two doses of monepantel given on days 0 and 49; Mox LA/MPL D0, 70 = long-acting moxidectin on day 0 + two doses of monepantel given on days 0 and 70.

(Note: Moxidectin-resistant Haemonchus occurs on about 80% of farms in the New England region of NSW, where this trial was conducted. In the trial, there was severe resistance of Haemonchus to moxidectin – Ed.) Kelly G Kahn L WAAVP 2015.Managing resistance to long-acting injectable moxidectin in sheep nematodes – co-admin of unrelated actives

“Further studies by Gareth Kelly with Lewis Kahn showed that long acting moxidectin alone did have a benefit in terms of weight gain but that a primer was required to reduce worm egg counts. The bigger question is now that we have scientific evidence of the ‘lamb effect’ with moxidectin long-acting treatments how do we combat this to prevent further rapid onset of moxidectin resistance.

Also from Dawbuts:

” ZOLVIX PLUS (monepantel + abamectin) for cattle! More exciting news to come from the WAAVP conference in Liverpool, UK was details about Zolvix Plus the latest cattle oral drench. Trials have been conducted at Elanco’s research site Yarrandoo, NSW. This was the first public presentation of results of trials where Zolvix Plus was used in cattle. Dose rate of monepantel is the same as in sheep (2.5mg/kg). Efficacy appears to be similar to the two compounds used in sheep, with greater than 99% efficacy reported to the common nematode species in slaughter studies”.

Why ‘Dawbuts’?   Well, Matt , who hails from Cowra, NSW, has Japanese connections. (Cowra itself has Japanese connections). For example, his doctoral thesis, on Echinococcus multilocularis, and done in Hokkaido, was in Japanese. However, this article, by Playford and Kamiya, is in English:  http://www.ncbi.nlm.nih.gov/pubmed/1297005. The lab at Dawbuts is called the ‘Kamiya Laboratory’.

‘Dawbuts’ sounds like the Japanese word (dobutsu) for animal(s).

Macrocyclic lactones – ‘lipophilicity’ and secretion into milk

From Hennessy and Alvinerie:

“A most significant characteristic of MLs is their lipophilicity”.

“Ivermectin is arguably the least lipophilic ML, with the possible exception of eprinomectin”.

“Moxidectin is about 100 times more lipophilic than ivermectin”.

Doramectin is “less lipophilic than moxidectin, but more than ivermectin or eprinomectin..”

“Partitioning into milk is a complex process relating to physico-chemical characteristics and membrane interactions  …  The high lipophilicity of the MLs is highly conducive for partitioning into milk…  ‘(there is) considerable partitioning of ivermectin into milk” (e.g., around 5% of the dose) .. “the higher lipophilicity of moxidectin will facilitate even great partition into milk.. (but) residual concentrations (of moxdectin) in milk are below toxic limits, resulting in nil withholding periods in many countries  …     Shoop reported that saturation of the C-22,23 portion of the ML molecule* facilitated partition into milk   ….this observation led to the development of eprinomectin which is used in lactating dairy cattle with zero milk withholding time ….   Alvinerie confirmed … only 0.1% of the dose (of eprinomectin partitions into the) milk of dairy cattle…”

Hennessy DR and Alvinerie MR, 2002. ‘Pharmacokinetics of the macrocyclic lactones..”, In “Macrocyclic lactones in antiparasitic therapy”, edited by Vercruyse and Rew. ISBN 0 85199 617 5

*So, does this effect (‘saturation of the C-22,23 portion of the ML molecule* facilitated partition into milk’ ) work through increasing ‘lipophilicity’ and/or other means?


Lipophilicity?   I see lipophilic (‘tending to combine with or dissolve in lipids or fats’) in the dictionaries (Macquarie, Oxford), but I don’t see lipophilicity?   So, coprophilia, or other ‘-phila’, should be coprophilicity?

From Websters: -philia |ˈfɪlɪəcombining form denoting fondness, especially an abnormal love for a specified thing:paedophilia.• denoting undue inclination: spasmophilia.DERIVATIVES -philiac |-lɪakcombining form in corresponding nouns and adjectives.,-philic combining form in corresponding adjectives.,-philous combining form in corresponding adjectives.ORIGIN from Greek philia fondness.

Medications in milk

Further to the above (moxidectin in the milk of ewes, passing then to lambs), I was wondering: is the presence of moxidectin in milk at higher levels than, say, abamectin, entirely due to the greater lipophilicity of moxidectin?

In short, I don’t know the answer, although this article, albeit relating to human milk, is interesting:  http://www.medsmilk.com/pages/introduction

From this article:

Drugs transfer into human milk if they:

  • Are highly lipid soluble.
  • Attain high concentrations in maternal plasma.
  • Are low in molecular weight (< 500 ).
  • Are low in protein binding.
  • Pass into the brain easily.

In addition to relative ‘lipophilia’, possibly another reason for MOX being present at higher concentrations than say ABA (as in Leathwick et al above) is due to large differences in maternal plasma levels, if only due to the typically lower plasma levels of drugs when delivered by controlled release devices, especially compared to the relatively high initial blood levels achieved by long-acting injectable moxidectin.

‘Cool new logos at ParaBoss, including WormBoss

Paraboss etc -new logos 2015-11-18 Wormboss-new logo 2015-11-18

(Logos designed by Ros Kelly from ‘Pictures+Words’).

Even better than the logos, as good as they are, is the content. On the worm front, a good place to start is ‘Your Program” at wormboss.com.au

Protein, energy, resistance and resilience

‘The resistance and resilience of sheep to worms is affected by different aspects of nutrition. It is the supply of protein that is most important for regulating the resistance of sheep to worms. This is largely because worm infection results in sheep diverting protein from muscle and wool growth to the immune response and the need to repair the damaged gut. In contrast, both protein and energy are equally important in improving resilience to infection.’

Read more at: http://www.wormboss.com.au/tests-tools/management-tools/nutrition.php

A discussion regarding liver fluke

A discussion (not prescriptive or perfect!) I had with some colleagues (LLS vets) regarding liver fluke treatments:

 Hi ……………. ,

 Regarding treatment times etc:
I basically go with what fluke guru Joe Boray (who recently turned 89) suggests for SE Australia (and as outlined in his DPI Primefact on fluke): for farms with fluke, strategic treatments in order of importance: 
1 April-May (early winter, cold weather has started), +/- 
2. August or thereabouts   +/- 
3. Summer e.g. Feb.
Some may need just one (ie April-May), some need more.
So, why April-May?
 * It is at the end of a period of highest fluke transmission, i.e. highest fluke and snail activity, assuming a reasonable spring/summer/autumn. 
* The cycle grinds to a halt about then, so it is strategically good. Fluke eggs, like Haemonchus (Hc) eggs, don’t develop/hatch much when it is consistently under 10 degrees overnight. 
* BUT, just like Hc L3s, the infective stages of Fasciola hepatica – metacercariae – can survive frosts/cold in Australian winters – so are present on pasture in winter, albeit in declining numbers, just like roundworm L3s, with the decline being faster if it is dry.  So, as with Haemonchus, one needs to keep an eye out for fluke (and others) over winter, as there could be fresh pick up, even ‘tho the cycle may have stopped. Also, ineffective drenches may have unwittingly been used at the end of autumn/early winter. Additionally, grazing management might have been less than optimal and susceptible stock may be grazing heavily contaminated pastures in winter. 
* By April/May, animals in a good season could have quite a few fluke on board: adults and perhaps quite a few immatures as well. 
* Given that there might be quite a few immatures, the best flukicides are recommended for April/May, i.e. triclabendazole (TCBZ)-based flukicides (assuming no resistance), and also Nitromec(R) (clorsulon+nitroxynil+ivermectin) in cattle.  
*Other reasons: as the cycle is about to stop, you get a bigger bang for your buck by using your best drench, and stock go through winter – often a tough time nutritionally, especially for vulnerable stock – with few fluke on board.    BUT, remember that there could still be pick up of metacercariae over winter. 
* If a fluke treatment is deemed necessary in Spring, then it is a good idea to rotate to an unrelated flukicide, for resistance-management purposes. This probably means, in small ruminants, a non-TCBZ drench, e.g. closantel, which means the fluke drench won’t have high efficacy against early immatures, but hopefully Spring is one time when there won’t be many of those.
(By the way, as to ‘efficacy’, the benchmark currently used by the regulators in Australia for round worm drenches is 95% (and ‘highly effective’ usually means >98%), whereas for flukicides it is 90%).
Of course, we have mainly been talking about strategic fluke drenches.  Then there are the rescue/tactical drenches when overt fasciolosis/clinical disease, with perhaps even deaths, occur.  Along with others I have seen crashes with fluke disease, which happened in the classic fashion, i.e. stock grazing into flukey areas in a dry autumn after a wet spring and summer.  In one memorable case, occurring in one of the bad fluke localities in the New England region of NSW, sheep and cattle were dying. This was quite spectacular, as were the necropsies.   I don’t recall the details but I remember thinking at the time that the fluke program had been ad hoc, so to speak, and sub-standard.
Some issues /imponderables:
* The tests we have are just OK, and don’t really tell us much about how big the burden is and what the production impacts might be (Maybe the fluke coproantigen test is better in this regard?). In fact the tests aren’t 100% at detecting the presence or absence of fluke.   I think the fluke egg count – depending on the particulars of the method – picks up perhaps 30-40% of eggs. (Don’t quote me on that: this is just what I recall from reading Happich and Boray).   The ELISA test is said to be more sensitive, but then there are the latent or lag periods (several weeks or more)  – before antibodies go up after initial infection and then go down once infection is removed.   The faecal fluke antigen test (based on a European test kit (BIOX CT(Copro-antigen test)) and validated  and offered by the CSU Wagga lab) may have some advantages and perhaps there will be some more information along these lines soon.
So, at times we might have to do a  ‘diagnostic drench’ ( treating a sample of a mob and seeing what the response is), just as we might do with roundworm WECs in cattle. High egg counts probably mean something but low or zero ones may not.
*Negative effects of strategic drenching?   Harking back to highly effective strategic drenching programs like WormKill for sheep ( N/NSW, 1980s-1990s), the upside was fabulous worm control, especially as it was initially engineered to be robust across a range of seasons and areas, but a possible downside was increased selection for drench resistance. Likewise with ‘drench and (immediate) move’ to very clean paddocks, like cereal stubbles.
(The other upside of WormKill was that, because it was so simple, prescriptive and effective, and for other reasons, the adoption rate was around 80-90% (according to a UNE study) after 1-2 years, the highest of I have heard of any extension program in agriculture. But, there was a price to pay).
So, what about using a highly effective flukicide at the beginning of a period (winter) when the total fluke population is about to take a nose-dive?
I don’t know the answer to this. I can only wonder.   An eminent parasitologist told me 15-20 years ago that he thought that it was unlikely resistance to flukicides would develop, at least not to any extent.   The reasoning behind this was not offered – it was one of those ‘on the run’ conversations – but I guess it is because fluke has a two host/indirect cycle with a lot of the population not only being on pasture but also inside snails, and therefore not exposed to fluke drenches. (But note the fluke produced  (by asexual development and multiplication) in snails are clones. (Thanks, Peter H)). And with aestivation etc, the snails are good at surviving long periods of unfavourable conditions. But I am no expert on snails.
Anyway, we do have resistance to flukicides. The first reported case of TCBZ-resistance in the world (Overend and Bowen, Aust Vet J, 1995) came from our own back yard (northern Victoria, next to the NSW Riverina), and we have since had further reports of resistance, including Brockwell and others (from CSU Wagga etc.) reporting TCBZ resistant fluke on cattle properties in various parts of NSW and Victoria. A small Novartis-supported survey (Joan Lloyd and others) in which I was involved ~ 10-15 years ago in cooperation with various District Vets in NSW, found TCBZ resistance in one of 8 farms tested, a sheep farm in the Monaro (NSW). (The District Vet was Chris Haylock nee Venning).   Joe Boray has told me of cases of rafoxanide/closantel-resistant fluke, but I don’t know the details of these, although Overend and Bowen mention them.
Excerpt: Brockwell et al (2013) state the coproantigen test (ELISA) (CT) reflects fluke burdens in cattle, allowing for intensity of infection to be measured (various say the threshold for production losses in cattle is 30-40 flukes), and also detects fluke that survive treatment (also demonstrated in sheep by others). The authors also showed (as stated above) that coproantigen falls within 7 days after successful treatment – elsewhere (in the discussion) they say within 14 days of successful treatment – so the post-treatment collection of faeces could be done at 14 days, in line with the 10-14 days for nematodes, allowing an FECRT for nematocides as well as TCBZ to be done simultaneously.”  (Notwithstanding this, some advisers currently recommend using the coproantigen test at 28 days post-treatment – as with the fluke egg count (sedimentation test) – to check flukicide efficacy.-Ed.).
From Overend and Bowen, 1995:
‘Strains of Fasciola hepatica resistant to salicylanilides (rafoxanide,
closantel) have been identified on Australian farms (Boray 1990). In
addition, strains of F hepatica resistant to luxabendazole and
triclabendazole have been selected in the laboratory (Boray 1990).
A field isolate of F hepatica resistant to triclabendazole has now been
identified on a Victorian sheep farm’.

Congenital/ectopic fluke infections?

A veterinary colleague (Matt Ball, Virbac) raised this recently. Can calves be born with liver fluke infections?  In short, I don’t know for sure, but logically it would seem possible. If ingested larval fluke find their way through the intestine, then the peritoneal cavity, thence to the liver, presumably by some sort of chemotaxis??, then it may be that some could happen onto a foetal liver instead.

A quick search found these:

Pantelouris EM The Common Liver Fluke

On page 125 ff there was this on ectopic localization of liver fluke:

“Whilst the liver is the typical tissue sought by the young liver fluke, numerous instances are known of the parasite establishing itself and growing in other locations in the mammalian body. Incidentally, such cases cannot be detected by the demonstration of eggs in the faeces. The most usual place is the lung and the presence of flukes there has been recorded as the cause of acute pneumonia and peribronchial inflammation in sheep (Mychlis, 1959) and cattle (Catellani, 1952; Kochnev, 1950). The parasite has also been found in lymph nodules (Dziekonski, 1947), and even in the uterus of cattle, causing sterility and endometritis (Thom, 1956 – 4 cases). It is conceivable that in this way the young flukes may even come to settle in the foetus in utero. The possibility of pre-natal infection was suggested by Raillet et al. (1913) and confirmed by Bugge (1935). Enigk and Duwel (1959) found liver flukes in 50 out of 661 calves aged under 3 months. Although post-natal infection at that age is not expected normally, it cannot be excluded in principle.”

OM el-Azazy. Suspected congenital fasciola infection in a buffalo calf. Vet. Rec. 1988;122:520 doi:10.1136/vr.122.21.520

‘Congenital infections with S. japonicum have been described numerous times for different hosts, including humans, dogs, goats, cattle, sheep, rabbit and pigs’ Parasite Immunology, 2005, 27, 289–295 Blackwell Publishing, Ltd. (Vercruysse et al?)

Wet and dry ewes

The inimitable Dr Refshauge shows you how:

NSW DPI Digital Publications


The facts about the K5 variant of rabbit calicivirus (from the AVA)


Feral photos


Snake envenomation in domestic animals in Australia

Free virtual issue of the Australian Vet Journal:



“Welcome to the FREE Virtual Issue from the Australian Veterinary Journal

Published: 29 October 2015

Introduction: Australia has some of the world’s most venomous snakes. With summer approaching, pets and other domestic animals are particularly susceptible to snake bites and subsequent envenomation as snakes emerge from hibernation to seek out the summer sun.

Numerous case reports published in the Australian Veterinary Journal have identified snake bites from brown snakes, tiger snakes, red-bellied black snakes, taipans, and death adders in domestic animals, including sheep, horse and cattle. A snake bite survey conducted in a 1998 issue of the AVJ reported dogs and cats to be the most common victims of snake bite, with brown snakes the most common species contributing to envenomation of domestic animals. Despite this survey, it is difficult to quantify the frequency of snake bite in animals in Australia, because of the many unreported and undiagnosed cases of snake envenomation.

As a consequence, pet owners and veterinarians need to be vigilant in not only preventing snake bites, but also in recognising and treating animals at all stages of envenomation. Importantly, past reports in the AVJ have stressed the difference in the action of venom from Australian snakes compared with American snakes and, as such, treatment strategies vary greatly and may not be interchangeable.

Given the unique nature of Australian snakes, Australia is not only at the forefront of research into snake envenomation, antivenene and treatment, but also in the treatment of snakes themselves, as they can also suffer from cancers and infection. This virtual issue provides free, full text access to a range of papers published in the AVJ concerning snakes, from case reports on envenomation to scientific articles on blood coagulation and anitvenene kits, to the treatment of snakes with infection and adenocarcinoma. We have also included a guide to venomous snakes, as well as a link to the first of our papers on snake envenomation by Max Henry, in 1935.

N Sodhi
Editorial Coordinator”

Animal Health Surveillance Quarterly 

The latest issue of Animal Health Surveillance Quarterly (April – July 2015) is now available for download from the Animal Health Australia website by following the web link:


This issue contains the following articles:

  1. Message from the Australian Chief Veterinary Officer
  2. Approaches to support early detection of FMD in Australia
  3. Australia’s official freedom from classical swine fever
  4. Veterinary laboratory diagnosticians symposium
  5. Wildlife Health Australia
  6. Aquatic Animal Health
  7. State and territory reports
  8. Quarterly statistics
  9. NAHIS contacts

Animal Health Surveillance – NSW

Click to access ahs-issue-3-july-sept-2015.pdf

an hlth sruveillance nsw 2015-3


  1. so good or unusual as to be impossible to copy; unique.
    “they took the charts by storm with their inimitable style”
    synonyms: unique, distinctive, individual, special, idiosyncratic, quirky, exclusive,rare; Gordon Refshauge, etc.

    Yummy- all that wasabi!


    English evolves: the meaning of STOP

    We may not like it, but language is ever changing (‘going forward, evolving synergies’). One example might be the word STOP.

    Surveys show that a declining number of car drivers come to a complete halt at STOP signs.

    A young-ish policeman (as opposed to a cranky, curmudgeonly old coot) recently told me that drivers are getting worse. But when it comes to stopping, perhaps language has  changed?

    I heard of a lawyer who drove slowly through a STOP sign and was immediately swept upon by a police officer who wanted to book the lawyer for failing to stop at a stop sign. The lawyer explained to the police officer that he was a very important lawyer, and a good friend of the local judge, and that he, being an eminent lawyer, could cogently and successfully argue in a court of law that the meaning of ‘stop’ is now somewhat nuanced and could well mean ‘to slow down’ or ‘roll slowly forward’, thus fulfilling the spirit if not the letter of the law. All the while, the lawyer politely refused to produce his driver’s license, then politely declined to step from the vehicle. Eventually the officer impolitely hauled the lawyer from the car, and proceeded to vigorously beat him with his truncheon.   The lawyer screamed in pain and pleaded with the policeman to stop, whereupon the policeman, sweating with exertion, asked the lawyer if he would like him to stop or merely slow down.


    Editor (Ed.): SL.   ~ 2015-11-27

    E&OE (including stray apostrophes, various typos and errors in fact).

WRML.2015-10-05. prep weaner paddocks, refugia and resistance, horse worms, LBN, wild dogs, meat and cancer, eagle hunters, cute killers, vomiting

 In this issue:

  • Preparing weaner paddocks
  • Refugia-a powerful strategy against drench resistance (Kahn)
  • Wild dog alert – interesting research
  • Horse worm control – getting up-to-date
  • ‘Shot in the arm for sheep data’
  • Livestock Biosecurity Network-LBN
  • Meat and cancer – an alternative view
  • Kazakh eagle hunters
  • Beauty of vomiting

Preparing weaner paddocks (sheep)

‘Something I wrote for SheepConnectNSW news?   Have you subscribed?

Two worthwhile subscriptions: SheepConnectNSW and ParaBoss (includes WormBoss) Monthly News.

Good sheep worm control integrates a few different strategies. It’s not just about drenching.

Grazing management is one part of integrated worm control. The aim of grazing management is to reduce exposure of vulnerable stock to worms, notably lambing ewes and weaners. But it also aims to keep nutrition in mind: good nutrition also has a big impact on worm control.

A low worm-risk paddock is one with relatively few infective (3rd stage, ‘L3’) worm larvae. You achieve this by not adding fresh sheep manure (containing worm eggs) to the paddock during preparation time, and by giving time for a fair proportion of existing L3 larvae to die off.

Unlike earlier stages, L3 larvae cannot feed. This means they have limited energy reserves.  The warmer it is, the more they wriggle, and the faster they use up their energy reserves.  In really hot weather – e.g. over 35 degrees C – they also get cooked.

So, in warm to hot summer weather, the preparation time to get rid of say 90% of barber’s pole worm larvae is 2-3 months depending on the region. In winter months, the preparation time is about double that. It’s cooler, the larvae are more sluggish, and they conserve more energy.   By the way, most species of larvae we are dealing with survive frost.

Scour worm L3 larvae when out and about on pasture die off about as fast as barber’s pole worm larvae, but unlike barber’s pole worm, they may hang around in the faecal pellet a bit longer waiting for moist conditions.  Still, the preparation times for scour worms are broadly similar to those for barber’s pole.

Assuming a spring lambing, a lot of lambs will be weaned some time in summer. Being a warmer time of year, the preparation time for weaner paddocks will be in the 2-3 month range for the eastern third of NSW.  Check Your Program at WormBoss.com.au for details relevant to your patch.

What about feed getting tall and rank during prep. time?   Well, you can graze cattle on these paddocks.  Also, you can put sheep in for up to 3 weeks after a highly effective drench – this is sometimes called ‘smart grazing’ – because they will not be shedding worm eggs in the first 3 weeks after a drench.  BUT! – it is critical that you know by testing that the drench you used is 98-100% effective on your property. Assume nothing.

More info: http://www.wormboss.com.au/programs/tablelands-slopes/grazing-management.php

From Beyond the Bale (September):

  • Refugia – a powerful strategy against drench resistance (Assoc. Prof. Lewis Kahn)


More info: http://www.wormboss.com.au/news/articles/drench-resistance/use-refugia-to-prolong-drench-life.php

Horse worm control – getting up-to-date

Following are some links that may be of use:

“Shot in the arm for sheep data”

“Last week, federal Agriculture and Water Resources Minister Barnaby Joyce announced the government would provide $490,000 to the University of New England (UNE) in Armidale, NSW, as part of an almost $1 million project to develop a new sheep data management system in partnership with the Cooperative Research Centre for Sheep Industry Innovation (Sheep CRC).”

See “The Land” article here.

Livestock Biosecurity Network

From their brochure on the web:

‘The Livestock Biosecurity Network was established nationally in 2013 by the peak industry councils: Sheepmeat Council of Australia, Cattle Council of Australia and Wool Producers Australia. The councils pooled $5 million to fund the initiative for an initial three years using producer transaction levies, in response to industry concerns about the possible impact of diseases and pests on the farming economy. LBN has Regional Officers working in all states and territories, where they are building networks of public/private partnerships. This will facilitate the delivery of information about the biosecurity threat to sustainable farming and livestock health and welfare. The network is designed to support all jurisdictions by enhancing regional industry capability in the event of an Emergency Animal Disease (EAD) outbreak from exotic or endemic diseases.’

Meat and cancer – continued

Another link to try to add some balance in view of some of the sensational headlines and superficial reporting (the devil is oft in the detail):

Red meat, processed meat, and cancer – how strong is the evidence?

Kazakh eagle hunters

‘Interesting photos and story..   (Thanks Joy).


Sugar gliders eating swift parrots


Even the cute and cuddly can be a problem.

The beautiful act of vomiting


Science and the ‘technicolour yawn’.