10 Things you may not know about Ascaris suum*

Jeremy S Pittman, DVM, MS, DABVPSmithfield

Hog Production DivisionNorth Region* The Large Roundworm of Swine

“Many stockmen have erroneous ideas regarding this parasite.”

~ Robert A. Craig, Diseases of Swine, 1906

The things you should already know

▪ Direct Life-Cycle w/ Extra-intestinal migration (Roepstorff

2003, Greve 2012)

– Pig do not need to be on or exposed to dirt!

▪ Fecund female: 1 Million eggs per day (Kelley 1956, Olsen

1958)

▪ Thick walled, highly resistant eggs (Floor 1967, vd Burg 1987)

▪ “They do exist!” (NAHMS 2006, Shepherd 2010, Connor 2012,

Duff 2014, Culhane 2014, Griebel 2014)

Life cycle image adapted from: http://cal.vet.upenn.edu

Life Cycle of Ascaris suum

1. Eggs are not infectious when they are shed

▪ Eggs require time to develop to an infectious L3 larva

▪ Embryonation is dependent on temperature (59ºF-95ºF), humidity and O2 tension (Seamster 1950, Arene 1986)

– Takes 4 to 12 weeks– Faster embryonation (>82ºF) = lower survivability/infectivity– Optimum = ~72ºF

▪ Eggs shed into environment (i.e., farrowing) need 4+ wks to become infectious

▪ Key aspect to the life-cycle that allows successful control w/ basic measures

2. Worm burden is overdispursed in a population

▪ The majority of worms are harbored by a small percentage of the animals in a population (Boes

1998)

▪ Egg burden and production impact may be limited to a very small percentage of the population

▪ Impact on diagnostic methodologies– Oral Fluids > Fecals (Boykin 2014)

– Pooling > Individual

▪ Influence on measuring production impact

3. Impact in grow-finish is likely minimal

▪ Small number of pigs, experimentally challenged in 1980’s– Change in genetics, nutrition, environment, herd sizes, etc– Feed Efficiency: 5-13% (Hale 1985, Stewart 1988)

▪ Impact was linear with increasing challenge dose– Average Daily Gain: 37 g/d (Nilsson 1980), 23% (Bernardo 1990)

– Largest impact during migration phase

▪ Larger Field Studies– Impact in grow-finish was negligible and more impacted by Lawsonia (Boes 2010)

– Maximum improvement expected would be less than 1% (Bernardo 1990)

▪ Relationship with overdispursed, population dynamics?

What are the economics??

▪ Swine Industry: $87-155M in 1974-1988 (Stewart and Hale 1988)

4. USDA no longer cares about “Milk Spots”, but your packer might!▪ Loss usually experienced by packer not the

producer– Carcass weight payment method

▪ Estimated losses to liver condemnations– US: $0.27/lb to $0.30/hd (Meisinger 2004)– EU: $0.18-0.31/lb (McOrist 2007)– Netherlands: 1€ penalty/pig to farmer (van

Wagenberg 2010)

▪ Value as edible byproduct– $16.73/cwt US vs $51.80/cwt China (Marti 2011)– 2008-2011: $5-6M (AAF Canada, 2010, 2013) – Discount ~50% increments from edible inedible

(pet food) rendered (Smithfield packing 2014)

5. There are many secondary production impacts

▪ Vaccine Efficacy: M hyopneumoniae (Steenhard 2009)

▪ Respiratory Disease/Secondary Infections E. coli, IAV-S, M hyopneumoniae, Erysipelas, PCV2, CSF (Shope 1958, Underdahl 1958, Nayak 1965, Adedeji 1989, Matusyavichus 1985, Engle 2006)

▪ Acute Morbidity and Mortality (Gjestvang 2004, Culhane 2014, Trujano 2014)

▪ Reproductive Effects? (Pattison 1979, Hagsten 1994)

▪ Meat Quality? (Knecht 2011, 2012)

Images provided by Dr. Marie Culhane, UMN-VDL

6. Risk of infection: Growing site history and sow management factors are important

▪ Poor correlation between sow farm and grow-finish status when wean age is <5 wks– Twice as likely if wean age is >6 wks (Roepstorff 1991, Homgren 1998)

▪ Dx history of growing site significantly associated, sow farm status was not (Pittman 2010)

▪ Decreased association when sows washed + pre-farrow anthelmintic (De Deken 1984)

▪ Lower prevalence when sow herd washed sows (Mercy 1989)

▪ Anthelmintics alone ineffective without sanitary environmental control (Johnson 2003)

7. Immunity and Parity Distribution

▪ Immunity develops to A suum over time

▪ Mass expulsion upon entry of L4s into small intestine (Jorgensen 1975, Boes 1998)

▪ Expulsion of adults around 23 wks post-ingestion (Olsen 1958)

▪ Parity distribution (Marti 1986, Roepstorff 1998, Nosal 2008)

– Gilts > P1 > P2 > P3+

▪ Impact of diagnostic and therapeutic strategies

8. Timing of anthelmintic prior to farrowing

▪ Pre-Farrow anthelmintic treatment is common strategy

▪ Goal: Reduce transmission from dam to piglet

▪ However, if given too close to movement contamination still occurs– “We deworm when we load into farrowing!”

▪ Treatment with feed-grade/top dress anthelmintics– Majority of worms are expelled day 6-8 dpt (Pittman 2015)

– Eggs continue to be shed for 10-14 dpt (Pittman 2015)

▪ Treatment should be 14 days prior to farrowing

9. Differences in anthelmintic effectiveness†

Anthelmintic Route Larvae (L3-

L4)Adult (%

Eff)Eggs (L1-

L3)Relative

CostPiperazine Water --- 75-100 L3? $Levamisole Water --- 99-100 --- $$Ivermectin Injectable,

Feed L4 90-100 --- $$$$$Pyrantel Feed, Top-

Dress L3 96-100 L3? $Fenbendazol

eFeed, Top-

Dress L3-L4 92-100 L1-L3 $$$/$$$$Dichlorvos* Feed, Top-

Dress L4 98-100 --- $$†Chart derived from Jacela et al, 2009; Product data sheets, Boes 1998, Pittman 2015, ValleyVet.com Aug 2015* Product currently not available

10. Peri-parturient rise does not appear to occur

▪ Increase in number of eggs excreted post farrowing

▪ Common in sheep, goats and cattle

▪ Oesophagostomum and Hyostrongylus in swine?

▪ A suum: decrease in percent of animals shedding during lactation and lower EPG (Pittman 2011)

▪ Implication for herd monitor/diagnosis

– Gestation > Lactation

– Gilts/P1 > P2+

Note Sharp decrease in # shedding animals at farrowing and during lactation

Increase in EPG is driven by 1 animal with exceptionally high EPG

Questions?